RENAL REPLACEMENT THERAPY

CLINICAL PRACTICE GUIDELINES 2nd Edition

Editors
Dr Ghazali Ahmad Dr Hooi Lai Seong Dr Lim Yam Ngo Dr Ong Loke Meng Dr Rozina Ghazalli Dr Tan Chwee Choon Dr Wan Shaariah Wan Yusof Dr Wong Hin Seng Dato Dr Zaki Morad bin Mohd Zaher

Ministry of Health, Malaysia 2004

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PREFACE (1st Edition) In recent years clinical practice guidelines (CPG) have become a regular feature in clinical practice. Their advocate includes the clinicians, healthcare managers, patients and funding agencies. CPGs were developed for a number of reasons. They help in promoting more efficient use of resources. They may reduce inappropriate variation in clinical practice. For the practicing clinicians well developed and evidenced based guidelines offers concise, easy to follow guide, which are useful in daily clinical practice. While CPGs have generally found wide acceptance, a number of concerns remain. One major issue is the perception that guidelines limit clinical freedom and doctors are restricted to practicing “cookbook medicine”. Another issue is the concern that guidelines may be used as a standard against which to judge a complaint. Guidelines are not new; they have been in existence since clinical practice began. In the Ministry of Health guidelines were already available for many years. Very often they are department or hospital derived and reflects the practice of the consultants in the department or sometimes the view of just one senior clinician. Few are based on evidence from randomized clinical trials or other forms of scientific inquiry. The Department of Nephrology first developed its Clinical Practice Guidelines in 1984, the “Hemodialysis Manual” and the “Ward Manual”. They were developed by the doctors and paramedical staff together. These manuals served to guide doctors and others in managing routine clinical problems. In 1995 the Department together with other Nephrologists in the Ministry started developing a new set of evidence based guidelines in Renal Replacement Therapy (RRT). These were completed in 1996 and subsequently revised in 1997/8. Where evidence were available they were incorporated in the guidelines; however many aspects of the guidelines were consensus of opinion on contemporary practice with no clear or strong evidence. The process of developing the guidelines was a major learning experience even for those who worked many years in the field. For the first time long standing practices were subjected to critical review. The development of the guidelines went through various stages. Initially a consultant or specialist was given a particular area to review and he/she was expected to do an exhaustive literature search as well as study contemporary practices in a number of well-1-

known centers. He/She then prepared a draft proposal which was presented to the whole group for discussion. Amendments made were necessary before the proposal were adopted. The discussions were generally before the proposals were adopted. The discussions were generally exhaustive and comprehensive. While emphasis was given to adopting guidelines which were supported by strong evidence, consideration was also given to practical issues such as costs and other resource constraints. Where a particular recommendation based on evidence could not be adopted due to resource constraints in the next best line of action derived from consensus of opinion was accepted. The revision in 1997/8 was made following suggestions from the various nephrologists as well as based on new evidence in the literature. It is hoped that in the year 2000 a formal revision will be carried out. How well are these guidelines used and adhered to? Data from the National Renal Registry showed there is little variation in practice in Haemodialysis, CAPD and Renal Transplantation in the Ministry of Health. The practice in these particular areas has always been protocol based. To some extent compliance to guidelines in the field of RRT has been enforced through budget and other resource allocations. It is hoped that with these new guidelines, compliance will extend beyond these considerations. We trust users will find these guidelines adequate, informative and practical in their day to day practice.

DATO’ DR. ZAKI MORAD

DEPARTMENT OF NEPHROLOGY, HOSPITAL KUALA LUMPUR

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PREFACE (2nd Edition) This second edition of the Practice Guidelines on Renal Replacement Therapy came more than five years after the first. During the period there has been a number of developments in the field of Nephrology, Dialysis and Transplantation. There are new evidences on the outcome of various interventions in the field. Where appropriate they are included in this edition. The format for this edition has been the same as before and we hope users will find it as useful as the previous edition. This guideline now adds to the long list of Practice Guidelines developed by the Ministry of Health in association with the Academy of Medicine and the professional societies. Most of these guidelines are available on line as well as in hard coies which have been distributed widely. Nonetheless there are many practitioners who are unaware of the existence of these guidelines. The usage of these guidelines varied widely and in general is not optimum. It is hoped that this guideline on Renal Replacement Therapy will be better utilized. The target audience for this guideline is limited and thus it is possible to promote its effective use. We also hope to place these guidelines in both its forms (electronic and hard copies) at various point of care to make it readily accessible. Renal Replacement Therapy continues to consume a disproportionate share of the healthcare budget. Minimising practice variation and at the same time achieving the desired outcomes is important to contain costs. Practice guidelines are important tools in trying to achieve this.

DATO’ DR. ZAKI MORAD

DEPARTMENT OF NEPHROLOGY, HOSPITAL KUALA LUMPUR

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CONTRIBUTORS HAEMODIALYSIS SECTION
Section Editors: Dato’ Dr Zaki Morad, Dr Ghazali Ahmad, Dr Ong Loke Meng & Dr Rozina Ghazalli Dr Foo Siu Mei Dr Goh Bak Leong Mr Husin Harun Dr Indralingam Vaithilingam Dr Lynster Liaw Mr Mohd Sulaiman Dalimi Dr Moy Chee Hoou Dr Ong Loke Meng Mr T.S. Singam Dr Sukeri Mohamed Mr Tam Chong Chiang Dr Teo Sue Mei

CRITICAL CARE NEPHROLOGY SECTION
Section Editor: Dato’ Dr Zaki Morad, Dr Wan Shaariah Wan Yusuf Dr Ravindran Visvanathan Dr Zawawi Nordin

PERITONEAL DIALYSIS SECTION
Section Editors: Dato’ Dr Zaki Morad, Dr Lim Yam Ngo & Dr Tan Chwee Choon Dr Lee Meng Lee Dr Parameswaran Krishnan Dr Ramli Seman Dr Sunita Bavanandan Dr Clare Tan Ms Tan Poh Choo Dr R. Tharmaratnam

RENAL TRANSPLANTATION SECTION
Section Editors: Dato’ Dr Zaki Morad, Dr Hooi Lai Seong & Dr Wong Hin Seng Dr Anthony Chan Dr Goh Bak Leong Dr Liew Boon Seng Dr Liu Wen Jiun Dr Rosnawati Yahya Dr Susan Pee Dr Wan Jazilah Wan Ismail

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CONTENTS
Page HAEMODIALYSIS SECTION 1. Patient Selection And Preparation For Haemodialysis 2. Vascular Access 3. Anticoagulation In Haemodialysis 4. Intradialytic Complications 5. Long Term Complications 5.1 Anaemia 5.2 Bone Disease 5.3 Aluminium Toxicity 6. Management Of Cardiovascular Risk Factors 7. Management Of The Infective Patient 8. Nutritional Management 9. Haemodialysis Adequacy 10. Surgery And The Dialysis Patient 11. Use Of Drugs In Dialysis Patients And Treatment Of Acute Poisoning 12. Rehabilitation 13. Pregnancy During Dialysis 14. Quality Assurance Program In Haemodialysis 15. Paediatric Haemodialysis 16. Technical Aspects Of Haemodialysis 17. The Haemodialysis Procedure 18. Water Treatment Glossary CRITICAL CARE NEPHROLOGY SECTION 19. Principles And Technique In Crrt 20. Vascular Access 21. Anticoagulation 22. Replacement Fluid And Dialysate 23. Drugs And Dosage In Crrt 24. Dialysis Prescription PERITONEAL DIALYSIS SECTION 25. Patient Selection 26. Pre Dialysis Preparation 27. CAPD Systems 28. CAPD Access 29. CAPD Procedures -51 5 12 15 23 31 37 45 50 56 59 67 70 79 82 83 84 89 97 101 125 127 133 135 137 140 143 152 154 156 158 160

Immunosupressive Protocol 42. Long Term Complications After Renal Transplantation 46. Living Related Recipient Workup 38. Management Of Infection Post Kidney Transplantation 44. Malnutrition 32. Automated Peritoneal Dialysis 35. Peritoneal Dialysis In Children 34. Management Of Graft Dysfunction 43. Complications Of CAPD 31.30. CAPD Adequacy 33. Renal Transplantation And Nutrition 45. Cadaveric Transplantation 40. Intermittent Peritoneal Dialysis Glossary RENAL TRANSPLANTATION SECTION 36. Perioperative Management 39. Paediatric Renal transplantation Glossary 168 195 199 202 207 209 213 215 222 234 239 243 245 250 261 273 277 285 292 -6- . Malaysian Organ Sharing System (Moss) 41. Living Related Donor Workup 37.

HAEMODIALYSIS -7- .

3 Timing of vascular access placement A permanent vascular access should be created when creatinine clearance is: • < 20mls/min for diabetics • < 15 mls/min for non diabetics -8- . Visual acuity and hand dexterity is important for self. Financial support d.2 Socio-economic factors which have to be considered include: a.1 Patient selection and screening The decision to choose haemodialysis as the mode of treatment for end stage renal disease (ESRD) should be made after a thorough discussion with the patient and other family members and parties (e. Advanced AIDS 1.g. Family support c.1 Chronic haemodialysis is relatively contraindicated in the following conditions: a.1. An assessment of the suitability for vascular access as well as screening for HbsAg. employer). Incapacitating end stage organ failure: • Dementia • Advanced cirrhosis with encephalopathy d.1. 1. Patient’s preference Screening for haemodialysis should include physical examination to exclude unfavourable medical conditions. The final decision is made after considering coexisting medical and socio-economic factors. Advanced malignancy c. 1. Severe vascular access problems e.care haemodialysis. Access to haemodialysis facilities b.1. anti-HIV and anti-HCV should also be made. 2 Preparation for haemodialysis Timely placement of a permanent vascular access is important to: • obviate the need for temporary access and reduce catheter related complications • allow better maturation of native fistula 1. Haemodynamic or circulatory instability b. PATIENT SELECTION AND PREPARATION FOR HAEMODIALYSIS 1.

Whenever possible. Daily exit site care 2.2 Antibiotics should be started if there is an exit site infection and the catheter removed if infection is not resolving 1. endocarditis.1 Sites of temporary access SITE Internal jugular Femoral COMMENTS The right is preferred 1.3 Patients who remain febrile or still retain a positive culture after catheter removal should be evaluated for metastatic complications (e. Should be at least 19 cm long to prevent recirculation 4.4 Temporary access A cuffed tunnelled catheter should be considered if the requirement for a catheter is anticipated to be > 6 weeks. a two day trial of antibiotics and observation is reasonable c.1 When catheter-associated bacteraemia is recognised. osteomyelitis) -9- . blood cultures should be taken from both catheter lumens and a peripheral site b. < 7 days duration of HD 3.6. catheters should be removed. The dorsum of the hand is the preferred site for intravenous lines.In addition: a.6. ultrasound guided insertion of catheter should be practised.6.6 Catheter related infections 1. Table 1.g.Any suitable veins should be preserved regardless of arm dominance. 1. the catheter may be retained.5 Care of temporary vascular access • Strict adherence to aseptic techniques should be practised at each catheter contact • The exit site should be inspected at each haemodialysis session • The use of dry gauze dressing + mupirocin at the catheter exit site should be practised • The patient should be educated on catheter care 1. vertebral abscess. If an alternative site for vascular access is not available. Avoid in potential renal transplant recipients Avoid to prevent subclavian vein stenosis Subclavian 1. the catheter should be removed if the patient remains febrile or condition deteriorates 1.

8. arterial and cardiopulmonary systems must be performed. neck or chest surgery/trauma • Anticipated renal transplant from living donor: temporary access may be sufficient 1. 1. IV vancomycin in MRSA nasal carriers or recent episode of MRSA infections (15 mg/kg every 5-7 days depending on blood levels) c. a history must be taken and physical examination of the patient’s venous.2 Physical examination Physical examination of the patient’s venous.1.4 First line empirical antibiotics for catheter related infections: a. arterial and cardiopulmonary systems is important.1 History • Note any previous central venous catheter insertion. IV cloxacillin 500mg – 1 gm 6 hourly + aminoglycoside or 3rd generation cephalosporin b.8.6. looking specifically at: • Venous calibre and patency • Character of peripheral pulses • Blood pressure of upper limbs will determine suitability of vascular access • Allen’s test • Difference in arm size . Duration of treatment should be at least 2 weeks 1. the choice of a permanent vascular access should be: • Radiocephalic AVF • Brachiocephalic AVF • Transposed brachiobasilic AVF • AV graft (PTFE) • Cuffed tunnelled CVC 1. • Arm dominance: non dominant arm is preferred for AVF • Diabetes mellitus • Severe congestive cardiac failure. This is associated with central venous stenosis.7 Selection of a permanent vascular access In the order of preference.10 - .8 Patient evaluation prior to access placement To determine the type of access most suitable. Fistulae may alter haemodynamics and cardiac output • Previous vascular access • Previous arm.

9. The haemodialysis catheter conundrum. neck and chest surgeries Presence of collateral veins may indicate venous obstruction Evaluate for oedema Tourniquet venous palpation with vein mapping Signs of cardiac failure 1. GFR of 10.0 (table 1.28: S57-S59 8.1 Dialysis should be started when: a. Kidney Int 1999 5.2) and/or c. Uraemic signs and symptoms are present b. Bander. Marr.3 Indices suggestive of malnutrition • • • • • Plasma albumin < 40g/L Total cholesterol < 3. 1.• • • • • Scars of previous SVC placement. Radio.2 Dialysis should be initiated earlier in diabetics Table 1.11 - .8g/kg/day Transferrin level < 200 mg/dL Weight loss References: 1. National Kidney Foundation DOQI guidelines for vascular access 2000 2.0 = 1. Intern.24:262-293 7. Vasc.2 KT/V equivalents Kt/V of 2.5 mls/min/1. Renal CrCl of 9-14 mls/min/1. Management of infected cuffed CVC for HD: UpToDate 2000 6. Am J Infection Control 1996. 1992:3:427 4.3) develop in the absence of other causes 1. J. JASN 1995: 6:1319-1328. Bonomini. arm.73m2 3. Seminars in dialysis 1992:5:121 3. Renal urea clearance of 7 mls/min 2.9. . Schwab. Pearson. Guidelines for prevention of intravascular device related infections. Jaques.9 mmol/L Dietary protein intake < 0.9 Initiation of dialysis Dialysis should be initiated to promote wellness and not to rescue from illness.73m2 Table 1. Hospital infection control practises advisory committee. Kidney International 1985. Hakim RM. The weekly renal Kt/V falls < 2. Indices of malnutrition (table 1.

the left internal and external jugular veins.1. (Level C) • The preferred insertion site for tunnelled cuffed venous dialysis catheters is the right internal jugular vein.2.3 Vascular access catheter • Cuffed tunnelled central venous catheters should be discouraged as permanent vascular access unless patients have exhausted all other options • Tunnelled cuffed venous catheters are the method of choice for temporary access of longer than 6 weeks’ duration.1 The order of preference for placement of AV fistula: a. if possible.2 Diagnostic evaluation: a.2. (Level C) . Tunnelled cuffed catheters should not be placed on the same side as a maturing AV access. A wrist (radial-cephalic) primary AV fistula b.2 2.1 History and physical examination see Section 1. such as silicone. This is to avoid extremity ischaemia. (Atrial positioning is only recommended for catheters composed of soft compliant material.2.2 If it is not possible to establish either of these types of fistulae.1 and 1. Doppler ultrasound/venography should be done if venous stenosis is suspected b.12 - . The catheter tip should be adjusted to the level of the caval atrial junction or into the right atrium to ensure optimal blood flow. access may be established using: a.1 Patient assessment prior to access placement should include: 2. Other options include: the right external jugular vein. An elbow (brachial-cephalic) primary AV fistula (Level C) 2. Arteriography may be indicated in patients with arterial insufficiency planned for AVF.8.related complications. (Level C) • Real-time ultrasound-guided insertion is recommended to reduce insertion. VASCULAR ACCESS 2. An arteriovenous graft of synthetic material (eg PTFE) 2. Subclavian access should be used only when jugular options are not available • All cuffed dialysis catheters should ideally be inserted under fluoroscopy. A transposed brachial basilic vein fistula (Level C) b.8.2 Selection of permanent vascular access and order of preference for placement of AV fistula 2. 2.1.

(Level C) . prior to cannulation. Selective obliteration of major venous side branches will speed maturation of a slowly maturing AV fistula (Level C) c.5. (Level C) 2.3 A new primary fistula should be allowed to mature for at least 1 month.4. serum creatinine level is >350 µmol/L or c. it should be rested until swelling is resolved (Level C) 2.4.13 - .3 The following procedures may enhance maturation of AV fistula: a. (Level C) 2.2 The patient should be referred to a nephrologist prior to the need for access and for counseling about renal replacement therapy. When a new native AV fistula is infiltrated (ie presence of hematoma with associated induration and edema). but not sooner than 1 month (and preferably 3 to 4 months after construction) 2. (Level C) 2.4.5. until swelling has gone down enough to allow palpation of the course of the graft. Access Maturation 2. Fistula hand-arm exercise (eg squeezing a rubber ball)will increase blood flow and speed maturation of a new native AV fistula (Level C) b.1 Patients with chronic kidney disease should be referred for surgery of primary AV fistula when: a.4. 3 to 6 weeks should be allowed prior to cannulation of a new graft.2. creatinine clearance is <25 mL/min b.5.5.4 Dialysis AV grafts should be placed at least 3 to 6 weeks prior to an anticipated need for hemodialysis in patients who are not candidates for primary AV fistulae. reassess for revision or a new access will have to be created.1 A primary AV fistula is mature and suitable for use when the vein’s diameter is sufficient to allow successful cannulation.4.4 PTFE dialysis AV grafts should not routinely be used until 14 days after placement.2 If adequate flow (>250mls/min) is not achieved by 4 months. Ideally. Timing of Access Placement 2.5. and ideally for 3 to 4 months. even 14 days or longer after placement.5 Hemodialysis catheters should not be inserted until hemodialysis is needed. (Level D) 2.4. Cannulation of a new PTFE dialysis AV graft should not routinely be attempted. within 1 year of an anticipated need for dialysis 2. (Level C) 2.

1 Monitoring of vascular access should include clinical examination and measurement of venous pressure. For selected high risk groups (e. previous thrombosis).5. prolonged bleeding after needle withdrawal. • Stop pump (manually or by alarm). regular dynamic venous pressure. clotting of the AVF. then quickly stop ultrafiltration. Transonic method) f.6. Monitoring of vascular access 2.6.5 Patients with swelling that does not respond to arm elevation or that persists beyond 2 weeks after AV access placement should receive a venogram or other non contrast study to evaluate central veins (Level C) 2. Sample blood from arterial port. Elevated negative arterial pre-pump pressures that prevent increase to acceptable blood flow d.6.14 - .2. Kt/V) (Level C) e. • Clamp venous line between patient and drip chamber. Reduce blood flow to 25-50 ml /min • Raise venous pressure alarm limit to maximum.7 Method for access recirculation study • Blood samples must be drawn within the first hour of dialysis • Three samples are required • Draw samples from arterial and venous port simultaneously.g. Unexplained decrease in the measured amount of haemodialysis delivered (URR. graft. or altered characteristic of pulse or thrill in the AVF (Level C) b.6 Cuffed and non cuffed hemodialysis catheters are suitable for immediate use and do not require maturation time (Level C) 2. Additional investigations include: • Access recirculation • Venogram / fistulogram • Access flow (e. Persistent swelling of the arm.5. Persistently elevated venous pressure (> 150mmHg with G16 needle and > 125mmHg with G15 needle at Qb 200mls/min in 3 consecutive readings) c. blood flow. . access recirculation (if indicated) & access flow (if available) 2. Wait 30 seconds (or until alarm sounds). access recirculation or access flow (Transonic) monitoring should be done 2.g.2 Further investigations are indicated if there is evidence of : a.

8 Skin preparation for cannulation of permanent AV access a.2. Locate and palpate the needle cannulation sites prior to skin preparation b. Cleanse the skin by applying 70% alcohol and/or 10% povidone iodine using a circular rubbing motion Notes: • Alcohol has a short bacteriostatic action time and should be applied in a rubbing motion for 1 minute immediately prior to needle cannulation • Povidone iodine needs to be applied for 2 to 3 minutes for its full bacteriostatic action to take effect and must be allowed to dry prior to needle cannulation • Clean gloves should be worn by the dialysis staff for cannulation • Gloves should be changed if contaminated at any time during the cannulation procedure • New clean gloves should be worn by the dialysis staff for each patient Table 2. pull skin taut in opposite direction of needle insertion Rationale • Compresses peripheral nerve endings between epidermis and dermis • Facilitates smoother incision of skin with less surface area contacting cutting edge of needle • Enables better stabilization of graft or vessel to be cannulated Less steep angles increase risk of dragging cutting edge of needle along surface of vessel Steeper angles increase risk of perforating underside of vessel Use approximately 45 degree angle of insertion for AV graft and approximately 25 degree angle for AV fistula .1 Technique for AV Fistula/Graft Cannulation Technique After skin preparation.15 - . Wash access site using an antibacterial soap or scrub (eg 2% chlorhexidine) and water c.

16 - . there are basically traumatize the intima of the three methods employed in vessel • Rotating the axis avoids existing practice: traumatizing the intima 1. and movement and distal arterial pulses in comparison to the contralateral side.9 Monitoring for limb ischaemia All patients. and dragging cutting edge along it. Technique Rationale Once the vessel has been • Any manipulation may penetrated. Immediately rotate the axis of the needle 180 degrees and advance slowly with cutting edge facing bottom of the vessel 3. Advance the needle to desired position. . Avoid pressing cutting edge into NEVER APPLY PRESSURE intima when applying pressure BEFORE NEEDLE IS to venepuncture site for COMPLETELY OUT haemodialysis.Table 2. should be monitored for the development of limb ischaemia following AV access construction. 2. gross sensation. tingling. and impairment of motor function (not limited by postoperative pain) and objective assessment of skin temperature. Advance the needle slowly • Waiting to rotate axis avoids with cutting edge facing top traumatizing top of vessel of vessel and do not rotate while needle is taped in place axis 2.1 Technique for AV Fistula/Graft Cannulation (contd). These include sensations of coldness. then rotate the axis 180 degrees Tape the needle at the same Pressing the needle shaft flat angle or one similar to the angle against the skin moves the of insertion needle tip from the desired position within the vessel lumen Remove needle at same or angle Avoid trauma to the intima by similar to angle of insertion. numbness. particularly those in high-risk groups.

Ziegler TW. 9. Smits HF. 1996 May RE. Kidney Int 47:1364-1373. Boereboom FT. 1989 Safa AA. O'Connell RS. ASAIO J 41:M745-M749. National Kidney Foundation. 1989 Bosman PJ. Early detection of venous stenoses. 15. 4. Boereboom FTJ. 1992 Schwab S. Angle JF. Eikelboom BC. Newman GE. Roberts AC. Hye RJ. Hernanz Schulman M. Krivitski NM: Clinical measurement of blood flow in hemodialysis access fistulae and grafts by ultrasound dilution. O'Connell RS. Am J Kidney Dis 19:554-557. Koomans HA. 14. Early detection of venous stenoses. Raymond JR. Bollinger RR: Prevention of hemodialysis fistula thrombosis. Adv Ren Replace Ther 1:119-130. Knights S. Oglevie SB: Detection and treatment of dysfunctional hemodialysis access grafts: Effect of a surveillance program on graft patency and the incidence of thrombosis. Ikizler TA. Kidney Int 36:707-711. Hakim RM: Predictive measures of vascular access thrombosis: A prospective study. Bollinger RR: Prevention of hemodialysis fistula thrombosis. Kidney Int 48:244-250. Marx MV. Oglevie SB: Detection and treatment of dysfunctional hemodialysis access grafts: effect of a surveillance program on graft patency and the incidence of thrombosis. Kidney Int 36:707-711. Picus DD. 1997 Middleton WD. 7. et al: Access flow measurements in hemodialysis patients: in vivo validation of an ultrasound dilution technique. Grundlehner M. Geoly KL. Kidney Int 36:707-711. Kidney Int 52:1084-1088. Valji K. Am J Roentgenol 152:633-639. Raymond J. Tietjen DP: Forecasting thrombosis of vascular access with Doppler color flow imaging. Saeed M. Dennis PA. 10. 3. J Am Soc Nephrol 7(6):966-969. Shyr Y. Roberts AC. Dennis PA. Bollinger R: Prevention of hemodialysis fistula thrombosis. Bakker CJ. 1996 Strauch BS. Kidney Int 52:1656-1662. Radiology 199:653657. Newman GE. Radiology 199:653657. Yenicesu M. Tietjen DP: Forecasting thrombosis of vascular access with Doppler color flow imaging. Himmelfarb J. Newman GE. 1989 Schwab SJ. Cote DA: Hemodialysis access stenosis: Early detection with color Doppler US. 17. 1989 Besarab A. Moritz MJ: Utility of intra-access pressure monitoring in detecting and correcting venous outlet stenoses prior to thrombosis. 1995 .References 1. Am J Kidney Dis 21:457-471. 6. Early detection of venous stenoses. Saeed M. Schulman G. Valji K. 2000 Windus DW: Permanent vascular access: A nephrologist's view. 1998 Schwab SJ. 1997 Safa AA. Am J Kidney Dis 19:554-557.17 - . 2. Dennis P. Gizienski TA. 13. 11. 1994 Older RA. Ross RP. Ziegler TW. Blankestijn PJ: Pressure or flow recordings for the surveillance of hemodialysis grafts. 16. Geoly KL. 18. Saeed M. Hye RJ. 1993 Depner TA: Techniques for prospective detection of venous stenosis. . 1995 Depner TA. Yakub YN. 5. Melson GL: Color Doppler sonography of hemodialysis vascular access: Comparison with angiography. Grundlehner M. Sullivan KL. Wilkowski MJ. NFK-DOQI clinical practice guidelines for vascular access. Raymond JR. Bosman PJ. Yakub YN. Radiology 207:161-164. 1996 12. 1992 Krivitski NM: Theory and validation of access flow measurement by dilution technique during hemodialysis. 1995 Strauch BS. 8.

Fiskerstrand C. O'Brien J. Mihindukulasuriya J. Boraks P. Br J Haemat 101:483-486. 1979 20. Seale J. Harter H. Maeda K. Shimizu N. Trivedi H. Price J. Vernham G: Ticlopidine in the prevention of blockage of fistulae and grafts [abstract]. Anderton J: Double-blind randomized trial of the effect of ticlopidine in arteriovenous fistulas for hemodialysis. et al: Prevention of thrombosis in patients on hemodialysis by low-dose aspirin. et al: Very low doses of warfarin can prevent thrombosis in central venous catheters: a randomized prospective trial. 1998 26. Burch J. Bern MM. Larsson R. Thompson I. Ell S. Burnet M. Kawaguchi Y. Hirsh J. Thromb Res 20:255-261.19. Wallach SR. Bistrian B. Weiss LG. Dickinson JP: Effects of ticlopidine in AV-fistula surgery in uremia. Polak A. Shimizu A. Blackburn GL: Prophylaxis against central vein thrombosis with low-dose warfarin. Bern MM. Pineo G. Gonzales CA. et al: Prevention of central venous catheter associated thrombosis using minidose warfarin in patients with haematological malignancies. Williams P. Cook DJ. Kobayashi K. Gent M: Arteriovenous-shunt thrombosis: prevention by sulfinpyrazone. Kaegi A. Scand J Urol Nephrol 32:276-283. Grontoft K-C. 1986 27. Keane MS. Lokich JJ. N Engl J Med 290:304-306. Bothe A Jr. 1998 . Andrew M: Benefit of heparin in central venous and pulmonary artery catheters: a meta-analysis of randomized controlled trials. Surgery 90:216-220. Koshikawa S. 1974 21. Randolph AG. Naito C: Antithrombotic therapy with ticlopidine in chronic renal failure patients on maintenance hemodialysis: a multicenter collaborative double blind study. Haemostasis 12:180. Ann Intern Med 112:423-428. Mulec H. 1982 25. 1998 24.18 - . Champagne CD. 1980 22. Artif Organs 9:61-63. 1990 28. Majerus P. 1985 23. N Engl J Med 301:577-579. Chest 113:165-171.

Bolus dose of heparin at 50u/kg.1 Factors which favour clotting of the extracorporeal circuit Low blood flow High hematocrit High ultrafiltration rate Dialysis access recirculation Intradialytic blood. Stop the heparin infusion 1 hour before the end of dialysis . blood products and lipid transfusion Use of drip chambers (Adapted from Daugirdas “Handbook of dialysis 3rd edition”) Table 3.2 Measures to assess coagulation during dialysis 1.19 - . Visual inspection • Extremely dark blood • Black streaks in the dialyser • Foaming with clots in the drip chamber and venous trap • ‘Tethering’ b.1) 3. ANTICOAGULATION IN HAEMODIALYSIS Haemodialysis requires anticoagulation to prevent extracorporeal clotting which is contributed by several factors (see table 3. Table 3.3. Clotting time tests : ACT and PTT Table 3. Changes in the arterial and venous pressure readings depending on the location of the clot c.1 General principles The most commonly used anticoagulant in haemodialysis is unfractionated heparin. Start heparin infusion at a rate of 10-20 units/kg per hour d. this dose should be reduced in extremely uraemic patients b.3 Standard anticoagulation with heparin: Constant-infusion method a. Wait 3-5 minutes to allow heparin dispersion c.

Prostacyclin regional anticoagulation . Regional anticoagulation with citrate c. Indications for heparin free dialysis: • Pericarditis (tight heparin is also acceptable) • Recent surgery with bleeding complications • Post renal/liver biopsy • Coagulopathy • Thrombocytopenia • Intracerebral haemorrhage • Active bleeding 3. The volume of saline administered must be removed during dialysis to prevent fluid overload e.4 times 1.1 Heparin free dialysis: a.2.8 times 1. Set the blood flow rate as high as possible c.2.4 Target clotting times during dialysis Routine heparin Tight heparin Test Baseline (Desired range) (Desired range) value During End of During End of dialysis dialysis dialysis dialysis ACT 60 -150s 1.3 Other forms of anticoagulation a. 100-250 mls of saline flushes are administered every 15-30 minutes into the arterial limb d. Careful monitoring of the arterial and venous pressure alarms will be required to detect early clotting f.20 - . Low molecular weight heparin is expensive and there is no additional benefit compared to heparin in terms of dialysis related bleeding or other complications b.3.2 Tight heparin A bolus dose of heparin at 20 units per kg followed by continuous infusion at 5-10 units/kg/hour with ACT monitoring half hourly (Refer table 3. No heparin during priming b.2 Anticoagulation in haemodialysis patients at risk for bleeding A number of alternative modalities have been used: 3.4 for ACT values) Table 3.4 times (Adapted from Daugirdas `Handbook of dialysis’ 3rd edition) 3.2.4 times 1.

Henny CP.3 3. Haemost 1985. Hyperkalaemia. Haemodialysis anticoagulation.2:961 4. Pruritis. Consider switching to LMWH e. Osteoporosis References 1. Thrombocytopenia. Bleeding complications b.3 Side effects of heparin a. 54:460 5. 72: S46 . Hypertriglyceridaemia c. Fischer KG. Lohr JW. The effectiveness of a low molecular weight heparinoid in chronic intermittent haemodialysis.3. Recombinant hirudin as anticoagulant in continous haemodialysis.2002 UpToDate 9. Handbook of Dialysis – Third edition: John T.21 - . Kidney Int Suppl 1999. Daugirdas 2. Consider switching to LMWH f. Minimizing haemorrhagic complications in dialysis patients. Thromb. The options for these patients are: • Heparin free dialysis • Change to CAPD • Regional citrate anticoagulation • LMWH is not a safe substitute due to crossreactivity in >90% • Danaparoid (a heparinoid) or recombinant hirudin d. J Am Soc Nephrol 1991.

• • • • • • • 4. fits and cardiac arrhythmias.4. Decreased vascular resistance due to: • anaemia • high temperature • food ingestion • acetate dialysate d. Hypovolaemia has been implicated as a major causal factor. However. intradialytic complications still occur. hypovolaemia is not consistently reflected by blood pressure changes. Impaired plasma refilling rate due to: • high ultrafiltration (UF) rate • low predialysis haematocrit • low sodium dialysate • acetate dialysate b.2 Hypotension This is the commonest intradialytic complication.1 Causes of intradialytic complications include: Hypotension Disequilibrium syndrome Bleeding Air embolism Dialyser reaction Muscle cramps Technical: incorrect dialysate composition and microbiological contamination 4. muscle cramps. nausea. Factors causing intradialytic complications include: a.22 - . INTRADIALYTIC COMPLICATIONS In spite of advances in haemodialysis treatment and technology. vomiting. Inappropriate increase in venous capacity due to: • intradialytic ingestion of food • high body temperature • low sodium dialysate • acetate dialysate c. Hypovolaemia is sometimes asymptomatic. Cardiac dysfunction . manifesting as hypotension. Impairment of specific compensatory response will lead to hypotension.

cardiac arrythmias. pulmonary embolism and electrolyte disturbances • Carry out the following investigations : ECG. maintain it <3% of dry weight • Consider higher sodium concentration or sodium/UF profiling • Avoid heavy meals prior to/during dialysis in hypotension-prone patients • Consider use of a cooler dialysate temperature (34-36 oC) • Avoid acetate dialysate • Omit the predialysis dose of antihypertensive drugs • Use sequential ultrafiltration • Ensure haematocrit remains stable at 30% or greater prior to dialysis 4.cardiac tamponade.urea and electrolytes.arterial blood gases • • • • • • 4. Uncommon causes including: • pericardial tamponade • arrhythmia • dialyser reaction • haemolysis • air embolism • myocardial infarction • occult haemorrhage • septicemia 4.e.5 Dialysis Disequilibrium Syndrome a. blood glucose. acute myocardial infarction or ischaemia.23 - .3 Management of hypotension Lie patient in the Trendelenburg position Reduce or stop ultrafiltration depending on severity Infuse normal saline 100-250cc at a time to a maximum of 500cc Reduce blood flow rate Oxygen therapy Haemodialysis is terminated if hypotension remains after infusion of 500cc of saline • If hypotension persists exclude gastrointestinal bleeding. The disequilibrium syndrome is a set of systemic and neurologic symptoms that can occur either during or following dialysis .4 Measures to prevent hypotension • Reassessment of “dry weight” when indicated • Avoid rapid and excessive ultrafiltration • On-line monitoring of blood volume using haematocrit sensor • Avoid excessive interdialytic weight gain (IDWG).

b. Individuals with preexisting neurologic disorders, such as recent stroke, head trauma, subdural haematoma, or malignant hypertension are at increased risk. This syndrome has become rare in recent years due to improvement of dialysis delivery technology. c. The signs and symptoms are nausea, vomiting, headache, blurred vision, restlessness, obtundation, seizure and coma. Symptoms of nausea, vomiting and headache are non specific. d. The immediate treatment is symptomatic as the problem is self limiting e. The following measures may avoid disequilibrium: • Avoid aggressive dialysis. The first few haemodialysis sessions should be “gentle”, using low blood flow rates (150 mls/min) and short hours. 2 • The dialyser should be of a small surface area (0.8-1.0 m ) • Use of high dialysate sodium of at least 140 mEq/L may be useful • Use of sodium profiling 4.6 Bleeding a. Dialysis patients have a higher incidence of bleeding. The causes include: • platelet dysfunction / impaired platelet-endothelium interaction • use of anticoagulation during haemodialysis • platelet-dialyser membrane interaction leading to thrombocytopenia b. Presenting features include: • bleeding from venepunctures sites • subdural haematoma • subarachnoid haemorrhage • gastrointestinal bleeding • haemopericardium c. Management • minimal heparinisation-monitor activated clotting time (ACT) hourly; keeping ACT between 150-180 seconds or • heparin-free haemodialysis- this requires increased blood flow rate and frequent flushing with isotonic saline • blood transfusion for severe blood loss • FFP, cryoprecipitate, DDVAP (0.3-0.4 µg/kg) may be required • protamine when haemostasis is poor in heparinised patients • avoid catheter removal within 4-6 hours after dialysis

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4.7 Air Embolism a. Sources of air entry into the dialysis circuit include: prepump tubing segment, intravenous infusion set, other parts of the dialysis tubing, air from the dialysate and from an inadvertently opened end of a central venous catheter. b. The signs and symptoms depend on the volume of air entering the vascular system and the position of the patient. If the patient is sitting upright air will enter the central nervous system causing fits. If the patient is recumbent, air enters the heart causing decreased cardiac output and sudden onset of dyspnoea, cough and central cyanosis. c. Management of air embolism • Stop haemodialysis, clamp the venous return. Do not return blood to the patient. • Place the patient in the left lateral Trendelenburg position • Give 100% oxygen with or without mechanical ventilation d. Prevention • Dialysis should never be performed with the air alarm system inactivated • IV solution should be in collapsible bags • Catheter should be aspirated for return of blood and flushed with saline before connection to the dialysis circuit • Dialyser should be rinsed thoroughly with saline to expel air bubbles 4.8 Haemolysis a. Acute haemolysis is usually caused by: • dialyser/dialysate contamination with formaldehyde, bleach, copper, nitrate or chloramine • faulty dialysis equipment or procedure • kinked catheter/tube • hypoosmolar dialysate • patient- related factors b. The presenting feature is a change in colour of the blood returning to the patient from dark to brighter red. The symptoms of acute haemolysis are back pain, chest tightness and shortness of breath c. Management of haemolysis • Stop haemodialysis, clamp the venous return. Do not return blood to the patient • Blood transfusion may be necessary • Treat hyperkalemia

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• Document haemolysis by inspection of the serum sample (red),

send the blood for lactate dehydrogenase (LDH), peripheral blood film, serum haptoglobulin and serum haemoglobin • Sample of dialysate solution should be analysed, unless mechanical cause is suspected d. Prevention • Water quality to follow standard recommendation • Thorough rinsing of re-use dialysers • Care in preparation of dialysate to avoid hypoosmolarity • Monitor dialysate temperature 4.9 Dialyser Reactions 4.9.1 Type A (Anaphylactic type) a. Those with a history of atopy are at risk. Occurs usually during the first few minutes of dialysis. • Mild: Itching, urticaria, cough, sneezing, coryza, watery eyes, abdominal pain and diarrhoea • Severe: Anaphylactic reaction b. Management • Stop dialysis • Clamp blood lines- disconnect extracorporeal circulation • Assess severity • Drugs- anti-histamine/ steroid • Cardiovascular support c. Prevention • Proper dialyser rinsing prior to use • Re-use procedures prior to first use • Avoid ETO sterilised dialyser for those with history of type A dialyser reaction • Predialysis anti-histamine for those with persistent mild reaction 4.9.2 Type B (non-specific dialyser reaction) a. Typically manifestes with chest pain, may or may not be accompanied by back pain. Less severe and generally dialysis can be continued. Onset of symptom may be within several minutes of starting dialysis. b. Management • Supportive • Exclude myocardial ischaemia/ subclinical haemolysis c. Prevention • Reuse procedure on new dialyser • Try different dialyser membrane - 26 -

4.10 Muscle cramps a. Dialysis-induced muscle cramps are due to decreased muscle perfusion and contraction of intravascular volume that occurs in response to excessive ultrafltration. In some patients, leg cramps are chronic, occur during inter-dialytic interval. b. Management • Reduce ultrafltration rate • Infuse normal saline c. Prevention • Reduce interdialytic weight gain • Reduce ultrafitration rate • Reassess dry weight • Use bicarbonate dialysate • Increase dialysate Na+ • Drugs- oral Quinine sulphate 300mg ON, short or medium acting benzodiazepine. Vit E 400IU ON and carnitine have been tried • Stretching exercises 4.11 Complications due to technical faults a. This is usually due to incorrect proportioning of water and dialysate component, leading to incorrect concentration of dialysate sodium, potassium, calcium and pH. This may happen as a result of: • empty dialysate container • improper dialysate concentrate connection • machine malfunction • faulty or inactivated conductivity alarm • interrupted water supply b. Presenting features: Hypo/ Hyponatremia can cause haemolysis, cerebral hypernatremia oedema, hyperkalemia & abdominal pain Acidosis/alkalosis Acidosis causes hyperventilation & predisposes to ventricular arrhythmias Alkalosis causes hypoventilation, confusion, obtundation, stupor or coma, tetany & seizures The hard water syndrome is due to hypercalcemia in water that has been inadequately prepared - 27 -

Hypercalcemia

Hyperchloraemic acidosis

This occurs with bicarbonate dialysis due to incorrect mixing of acid/base if no pH meter is included in the system. The conductivity meter does not detect this.

c. The management is according to the underlying cause. Check urea and electrolytes, full blood count, arterial blood gas, calcium, magnesium and phosphate. 4.12 Microbial/Endotoxin contamination • The presenting features are fever and hypotension • Contamination is caused by reuse of improperly processed dialysers or contaminated dialysate • Microbial contamination can occur during any of the reprocessing steps (rinsing, cleaning, testing, and sterilising hollow fibre dialysers), but most commonly, use of contaminated water is implicated • The use of bicarbonate dialysate and high-flux dialysis is associated with an increased risk of pyrogenic reaction 4.13 Pyrogenic Reaction a. Differential diagnosis includes: • improperly sterilised dialyser • contaminated water or bicarbonate dialysate • cannulation of infected fistulae or grafts • dialyser reaction • early septicaemia b. Management is largely supportive and empirical: • antipyretic • if hypotensive, discontinue ultrafiltration and continue dialysis with caution. Saline infusion may be necessary. • hospitalisation may be required • a cluster of similar cases should prompt a review of the water used for reprocessing and water distribution and dialysate, the reprocessing procedures, and the bicarbonate system

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References
1. Daurgidas. Dialysis hypotension. A haemodynamic analysis. Kidney Int (1991) 39: 233-246 2. Daurgidas. Handbook of dialysis. 3rd Edition. Lippincott Williams & Wilkins 3. Steur R. Reducing symptoms during haemodialysis by continuously monitoring the haematocrit. Am. Jour. of Kidney Dis (1996) 27(4): 525-532. 4. Van der Sarde FM. Energy transfer is the single most important factor for the difference in the vascular response between isolated UF and haemodialysis. J.Am Soc. Nephrol (2000) 11: 1512-1517. 5. Maggiore Q. Multicentre randomised study on the effect of thermal balance on vascular stability in haemodialysis patient. J.Am Soc. Nephrol Abstract A 1473. 6. Nisselsen. Clinical Dialysis 3rd Edition (1995) Appleton & Lange. 7. M.K.Steward. Muscle cramps during maintenance haemodialysis Lancet (1992): 1049-1051. 8. Sweet SJ. Haemolytic reaction mechanically induced by kinked haemodialysis lines. Am Jour Kidney Dis. (1996) 27: 263. 9. Ahmad. Multicenter trial of L-Carnitine in maintenance haemodialysis patient.Clinical and biochemical effect. Kidney Int (1990) 38: 912-918.

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1.1 Assessment of anaemia Evaluation of anaemia in patients on dialysis should include a thorough clinical assessment to determine the cause as well as clinical impact of anaemia.1 ANAEMIA Anaemia is a common manifestation in patients with ESRD and is normochromic normocytic.30 - . gastrointestinal and uterine loss • shortened red cell survival • effects of “uraemic inhibitors” on bone marrow • severe hyperparathyroidism leading to myelofibrosis • aluminium overload • nutritional deficiencies • hypothyroidism • infection and/or inflammation • haemoglobinopathies b. 1-2 The primary cause of anaemia in chronic renal failure is erythropoietin deficiency but other factors may contribute. a. Causes of anaemia include: • erythropoietin (Epoeitin) deficiency • iron deficiency • blood loss e.5.g. LONG TERM COMPLICATIONS 5. 5. The following evaluation should be made prior to Epoetin therapy: • Full blood picture and peripheral film • Absolute reticulocyte count • Iron status – serum ferritin – transferrin saturation (serum iron x 100/TIBC) and/or – % hypochromic red cells if available (Level B) 1-2 The following work-up may be included if indicated (Level B) 1-2 • assessment of occult gastrointestinal blood loss • serum (or red cell) folate and Vit B12 level • C-reactive protein • tests for haemolysis • serum and/or urine protein electrophoresis • assess for aluminium toxicity • bone marrow examination • intact PTH .

1.1.2 Treatment of anaemia Identify and correct underlying causes of anaemia Assess clinical impact of anaemia Ensure adequate nutrition and adequate dialysis Iron supplementation (see Section 5. • Epoetin should be used when all other causes have been excluded and haemoglobin concentration remains below the target level (refer to Section 5.1.3) • • • • • • 5. iron overload and depression of endogenous erythropoietin production. sensitisation to donor HLAs (human leucocyte antigens) thus jeopardising transplantation prospects.1. Blood transfusion is discouraged because it carries the risk of transmission of viral infections. Indications for Epoetin therapy • Persistent Hb concentration < 10g/dl after evaluation for other causes of anaemia (Level C) b.4) • Ensure dialysis is adequate (Level C) .1.3 Administration of Epoetin a. Pre-treatment evaluation • Clinical evaluation to exclude other causes of anaemia • Hypertension should be controlled • Assessment of iron status and treatment of iron deficiency prior to initiation of Epoetin to achieve target iron levels (Refer to Section 5. Priority for epoietin therapy should be considered for the following: • patients preparing for transplantation • anephric patients • symptomatic anaemia despite Hb above target • patients with co-morbidities such as ischaemic heart disease • children (Level C) c.4) Folate and Vitamin B supplementation Blood transfusion should be used only when the patient is symptomatic and rapid correction of anaemia is required.5.31 - .

Dosage • Starting dose: iv 4000 units weekly in one or two divided doses (or 50-150 IU/kg/week) • Children less than 5 years may require up to 300 units/kg/ week in divided doses (Level B) ii. Adequate iron levels should be maintained (refer to Section on 5.g.d. gauge 29) should be used to minimise pain with subcutaneous injection • Site of subcutaneous injection should be rotated iii.1.4) • Target haemoglobin − Target Hb should be 10 to 12 g/dL (Level A) 13-21 − Target rise in Hb is 1 – 2 g/dl per month and target should be reached within 2 to 4 months . Method of administration • Intravenous injection is the preferred route for administration of Epoetin − although subcutaneous administration is more cost effective 3-11 the risk of pure red cell aplasia is higher with this route 12 (Level C) − if administered subcutaneously alpha epoetin should not be used (Level C) • Insulin syringe (and not tuberculin syringe) should be used to reduce wastage due to dead space when Epoetin is not available in pre-filled syringes • IV injection should be delivered perpendicularly to the injection port at the end of dialysis • The smallest needle (e. Initiation of Epoetin i. Monitoring during Epoetin therapy • Blood pressure − Blood pressure should be monitored closely during initiation or increase in dose of Epoetin and antihypertensive medication increased if necessary − Dosage interruption should be minimised • Hb response Hb level should be checked every 2 weeks at initiation or change in Epoetin dosage until Hb stabilises then every 3 months (Level C) • Iron status Serum ferritin.32 - . transferrin saturation (serum iron and TIBC) and % hypochromic red cells should be monitored every 3 months.

Epoetin dose should be increased by 2000 units to 4000 units every 2 to 4 weeks • If Hb rise is > 2. ACE inhibitors − aluminium toxicity − hyperparathyroidism − haemoglobinopathies e.g. Titration of Epoetin dosage • If Hb rise is < 0. History of seizure is not a contraindication to Epoetin therapy.5 g/dl per month or Hb exceeds the target. mutiple myeloma. Side effects of Epoetin include: • hypertension • access thrombosis Except for fits due to hypertensive encephalopathy.g.g.e.33 - . myelofibrosis. . reduce dose of Epoetin by 25 – 50% (Level C) f. myelodysplastic syndrome. rheumatoid arthritis − infections e. SLE. Resistance to Epoetin • Resistance to Epo is arbitrarily defined as failure to achieve or maintain target haemoglobin with > 300 units/kg/week (20. chronic allograft rejection. thalassemias − folate or Vit B12 deficiency − bone marrow disorders e. access infection.g.000 units/week) subcutaneously • In patients with resistance to Epoetin.g. tuberculosis. pure red cell aplasia − haemolysis − hypothyroidism g. there has been no evidence of increased risk of seizures. the following conditions should be evaluated and treated: − iron deficiency (absolute or functional) is the most common reason for resistance to Epoetin − chronic blood loss − inflammation e.5g/dl over 2-4 weeks. AIDS − malignancies − inadequate dialysis − drugs e.

5 Administration of intravenous iron a. 5. Resuscitation equipment should be available during administration of iv iron b.1. Suggested iv iron schedule • Haemodialysis patients: − Absolute iron deficiency : 100mg iron dextran or 100mg iron sucrose every HD session for 10 sessions then check iron status no earlier than 7 days − Functional iron deficiency : iv iron dextran 100mg every week for 10 weeks − Maintenance: 25mg to 100mg per week . Iron supplementation should be given to: • achieve and maintain Hb > 10g/dl • achieve and maintain adequate iron stores (refer to Section 5. Route of administration • Oral iron It is reasonable to start with oral supplementation: − At least 100mg to 200mg (2 – 3mg/kg for paediatric patients) of elemental oral iron daily should be given − Oral iron should not be taken with food and other medications particularly phosphate binders − Oral iron is often insufficient to maintain target haemoglobin and iron levels in haemodialysis patients especially those receiving erythropoietin (Level B) 22-27 • Intravenous iron − Intravenous iron has been shown to improve haemoglobin levels and reduce requirement for Epoetin in patients with and without iron deficiency 28-34( Level A) − Intramuscular iron injection is not recommended due to the risk of haematoma.1. Method of administration • Iron dextran should be given by iv infusion over 1 hour • Iron sucrose may be given by iv slow bolus (20mg/min) or by infusion d.6) (Level A) b.5.34 - .1. Patients receiving iv iron for the first time should receive a 25mg test dose c.4 Iron supplementation a. Oral iron should be stopped in patients who require maintenance intravenous iron.

1. Iron targets Table 5. The best available tests are serum ferritin. Definitions of iron deficiency • absolute iron deficiency : serum ferritin < 100 ng/ml • functional iron deficiency : serum ferritin > 100 ng/ml and TSAT < 20% or % hypochromic rbc >10% c. % hypochromic red cells and transferrin saturation: • Serum ferritin − reflects iron stores − serum ferritin should be interpreted with care in the presence of infection.• CAPD patients: − 200mg to 500mg of iron dextran infused in 250mls saline over 1-2 hours or iron sucrose 200 to 500 mg in 100 to 500 ml saline over 1 to 4 hours − The manufacturer’s recommended maximum single dose is 1000mg of iron dextran and 500mg of iron sucrose 5. inflammation or hepatitis and 1 – 2 weeks following blood transfusion or adminstration of intravenous iron • Transferrin saturation (TSAT) − reflects availability of iron − ratio of serum iron to total iron binding capacity multiplied by 100 • Percentage of hypochromic red cells − also reflects availability of iron − red cells with Hb concentration < 28g/dl or Hb < 26pg b.1 Target iron measurements Test Minimum target Serum ferritin TSAT % hypochromic red cells > 100 ng/ml > 20% < 10% Optimal target 200-500 ng/ml 30-40% Maximum level > 800 ng/ml > 50% < 2.6 Assessment of iron status a. Indices of iron status There has been no single measure of iron which accurately indicate the patient’s iron status 21.35 - .5% .

Nephro Dial Transplant 1999:14(Suppl 5):11-13 Locatelli F. Van Loo A.26(2):331-40 De Schoenmakere G.13:1642-4 Besarab A. 7. The impact of haematocrit levels and erythropoietin treatment on overall and cardiovascular mortality and morbidity – the experience of the Lombardy Dialysis Registry.36 - . Henderson WG.14 Suppl 5:19-20 Schaller R. Vaamonde CA. 2. Nephro Dial Transplant 1999:14(Suppl 5):6-7 NKF-K/DOQI Clinical Practice Guidelines for Anemia of Chronic Kidney Disease: Update 2000. Nephrol Dial Transplant 1999. Posen G. The effects of normal as compared with low 4. Wong C. Nephrol Dial Transplant 1998. Nissenson AR. Goldstein M.v. Bolton WK. Okamoto DM.346(7):46975 European Best Practice Guidelines for the Management of Anaemia in Patients with Chronic Renal Failure. Guideline 9: Route of administration of epoetin. N Engl J Med 1998. 12. 37 Suppl 1:S182-S236 Kaufman JS. Goodkin DA. 5. Lazarus JM. Reda DJ. Differences in intravenous and subcutaneous application of recombinant human erythropoietin: a multicenter trial. Target Guideline 5: Target haemoglobin concentration for the treatment of the anaemia of chronic renal failure. Thieler H. 11. Sperschneider H. Am J Kidney Dis 1995. Guideline 2: Evaluation of anaemia in uraemic patients in. Madsen JK. 339(9):578-83 Virot JS.41(5):297-302 European Best Practice Guidelines for the Management of Anaemia in Patients with Chronic Renal Failure. Duym P. Eur J Clin Pharmacol 1996. Engelmann J. Van der Goten J. Guillaumie J. Marx M. Clin Nephrol 1994. Churchill DN. Janin G. The haematopoietic effect of recombinant human erythropoietin in haemodialysis is independent of the mode of administration (i. Rifle G. Comparison of subcutaneous and intravenous recombinant human erythropoietin for anemia in hemodialysis patients with significant comorbid disease. Scigalla P.12(5):303-10 Paganini EP.Van Stone JC. Browne JK. Department of Veterans Affairs Cooperative Study Group on Erythropoietin in Hemodialysis Patients. serum erythropoietin and blood pressure following intravenous and subcutaneous erythropoietin treatment of dialysis patients. Graber SE. Conte F. Vanholder R. Dhondt A. 28(3):400-8 Taylor JE. Jensen LW. 10. et al. Fleming LW.c. Gimenez LF. Egrie JC. Eschbach JW.References 1. Comparison of dose requirement. Voigt D. Dutz W. 3. Belch JJ.18(8):552-8 Muirhead N. Intravenous versus subcutaneous dosing of epoetin alfa in hemodialysis patients. Goldfarb DS. Michel P. Laplante P. 8. Dubot P. 14.50(3):171-7 Casadevall N et al. Am J Kidney Dis 2001. Henderson IS. Chevet D. Hans S. Nephrol Dial Transplant 1998. Goodkin DA.). Pure red-cell aplasia and anti-erythropoietin antibodies in patients treated with recombinant erythropoietin. IV and SC erythropoietin. 6. Schwab SJ. 9. or s. Mactier RA. Lameire N. Subcutaneous compared with intravenous epoetin in patients receiving hemodialysis. Am J Nephrol 1992. Erythropoietin response and route of administration. Slaughter D. Artif Organs 1994.13(7):1770-5 Jensen JD. Marcelli D. Schoter KH. Fye CL. Must erythropoietin be injected by the subcutaneous route for every hemodialyzed patient? Am J Kidney Dis 1996. Okamoto DM. 15. Kleinman JG. . Egrie JC. Nadler SP. Stewart WK. N Eng J Med 2002. European Best Practice Guidelines for the Management of Anaemia in Patients with Chronic Renal Failure. 13.

Iron metabolism in patients with the anaemia of end-stage renal disease during treatment with recombinant human erythropoietin.8(12):1921-9 Xia H. Am J Kidney Dis 1997.11(2):319-22 Silverberg DS. Ebben J. N Engl J Med 1998 Aug 27. Nephrol Dial Transplant 1992.339(9):584-90 Ma JZ. Hematocrit level and associated mortality in hemodialysis patients. Arruda JA. Association between recombinant human erythropoietin and quality of life and exercise capacity of patients receiving haemodialysis. McKenzie A. Economic appraisal of maintenance parenteral iron administration in treatment of anaemia in chronic haemodialysis patients. Lazarus JM. 31.57(2):175-82 . Ismail N. Thompson J. Howarth D. Collins AJ. Int J Artif Organs 1994. Blum M.37 - . Jindal K. 32.11(6):1079-83 Allegra V et al. BMJ 1990. AmJ Nephrol 1992. 26. 23. Johns JA. 34. Lowrie EG. 28.12(3):162-9 Fishbane S.29(3):319-33 Kooistra MP. Hematocrit levels and hospitalization risks in hemodialysis patients. Horl WH. 18. 30. Hakim RM. Nephron 1991. van Es A. Bridges K. Br J Haematol 1991. Morgan AG.26(1):41-6 Anastassiades EG. Haemodynamic changes and physical performance at comparative levels of haemoglobin after long-term treatment with recombinant erythropoietin. Howarth J. Maesaka J. J Am Soc Nephrol 1997. Reduction in recombinant human erythropoietin doses by the use of chronic intravenous iron supplementation. Nephrol Dial Transplant 1996.79(4):634-9 Dunea G.10(6):1309-16 Canadian Erythropoietin Study Group. Intra-dialytic oral iron therapy.72(3):413-7 Taylor JE. Frei GL. 21. Dawborn JK. Iron management in end-stage renal disease. Shanks D. Nephrol Dial Transplant 1996. Peat N. Reduction in recombinant human erythropoietin doses by the use of chronic intravenous iron supplementation. Swagel MA. Baker LR. Maesaka J. Xia H. Tomson CR. 17. 29. Importance of iron supply for erythropoietin therapy. 25.300(6724):573-8 McMahon LP. Maesaka JK. Nephron 1996. 27. 10(11):2070-6 Sepandj F.17(5):261-4 Wingard RL. 24. 20.16. Brugnara C. 33. Regular low-dose intravenous iron therapy improves response to erythropoietin in haemodialysis patients. Owen WF. West M. Am J Kidney Dis 1995.10(3):610-9 Madore F. Frei GL.8(9):846-53 Fishbane S. Hyde K. Ebben J. Sunder-Plassmann G. Fowler R.7(12):1199-206 McMahon LP. Hirsch D. Anemia in hemodialysis patients: variables affecting this outcome predictor. Iron deficiency in maintenance hemodialysis patients: assessment of diagnosis criteria and of three different iron treatments. Ma JZ. Waters HM. J Am Soc Nephrol 1999. Struyvenberg A. A randomized controlled study of iron supplementation in patients treated with erythropoietin. Kidney Int 1996. hematocrit values in patients with cardiac disease who are receiving hemodialysis and epoetin. Austin M.26(1):41-6 Macdougall IC. J Am Soc Nephrol 1999. Monitoring of iron requirements in renal patients on erythropoietin. Subjective quality of life assessment in hemodialysis patients at different levels of hemoglobin following use of recombinant human erythropoietin. Am J Kidney Dis 1995. Bodiwala U. Dawborn JK. Peer G. Raine AE. Tucker B. Parker RA. Geary CG. Collins AJ. Intravenous ferric saccharate as an iron supplement in dialysis patients. Nephrol Dial Transplant 1993. Kaplan E. Nephrol Dial Transplant 1995. Am J Kidney Dis 1995. Gokal R. Efficacy of oral iron therapy in patients receiving recombinant human erythropoietin. Lew NL. Marx JJ. Yin JA.50(5):1694-29. Iaina A.25(3):433-9 Fishbane S. 22. Porter C. 19.

To maintain serum calcium and phosphate levels as near normal as possible • Target range of serum phosphate in dialysis patients should be 0.2(K/DOQI & EBPG < 55mg2/dl2 = 4.37 mmol/l) The calcium x phosphate product should be < 4.1 Categories of bone disease Bone disease in the patient with ESRD falls into three categories: • High turnover bone disease (HTBD): Secondary or tertiary hyperparathyroidism • Low turnover bone disease: Osteomalacia and adynamic bone disease • Mixed Bone Disease 5.5.2.2.2-2. The cold chain must be maintained for iPTH sampling from point of blood taking right up to the lab.6 mmol/l (K/DOQI 1. To prevent and reverse the development of extra skeletal calcification d. 4 .13-1.38 - . It should be carried out at least twice a year. Serum calcium/phosphate/albumin should be done every 3 months but more frequently if receiving high dose phosphate binders/high dose calcitriol/low calcium dialysate. 3 b.2 Objectives of treatment a.6 mmol/l (K/DOQI 2. For selected patients treated with DFO/pulse calcitriol/low calcium dialysate iPTH should be measured 3 monthly. Intact parathyoid hormone (iPTH) assay -measures both the mid region and N-terminal fragments of the parathyroid hormone molecule.8-1.5 1.1-2. To prevent or reverse the accumulation of aluminium in bone e.78 mmol/l .Higher values have been shown to increase cardiovascular morbidity and mortality (Level B) b.8mmol/l) • Target range of serum calcium in dialysis patients should be 2. EBPG 0.81. To reduce cardiovascular risk 5.2. 5. To prevent or suppress the development of parathyroid hyperplasia c.2 BONE DISEASE With the prolongation of life by dialysis the morbidity associated with renal bone disease will assume greater significance.4 mmol2 /l2).3 Diagnosis of renal bone disease a.

Serum alkaline phosphatase may not reflect bone turnover status.c. Desferrioxamine (DFO) test should be done if the above criteria are met (refer to Section 5.4 Medical treatment for secondary hyperparathyroidism a.the characteristic finding in osteitis fibrosa is bone loss (resorption) in the subperiosteal area. 5 (Level B) d. X-ray of hands and lumbar spine . MIBI scan) may be required to look for ectopic parathyroid glands and in cases of recurrent hyperparathyroidism. 7 (Level B) f. When severe. Additional imaging techniques (CT neck and thorax.6 (Level B) e. Control of hyperphosphataemia • A multidisciplinary approach is required to counsel patients regarding a low phosphate diet (reduce dietary PO4 to 0. Bone biopsy is desirable but this test is presently not available locally. 9 (Level C) i. Ultrasound of the parathyroid glands may be done with a high resolution transducer (7. thus should be measured 3 monthly.2.5g elemental Ca) • Aluminium hydroxide should not be used. Thallium subtraction scan. associated erosion of the tuft of the distal phalanges leads to blunting of the fingertips.81.2g/day) • Check compliance with PO4 binders (should be taken crushed or chewed with meals and titrated to the amount of food eaten) • Calcium carbonate and calcium acetate are the preferred PO4 binders (total daily amount of 6 gram should probably not be exceeded) 11 (K/DOQI 1. 8 h.3) The test is positive if the increase in serum Al level is above 50 ug/l. MR scan. g. However if unavoidable should not exceed 2-3 gm/day and used for the shortest possible duration only (4 weeks) • Increase PO4 clearance in dialysis by increasing dialysis frequency if feasible 12 (Level B) • Also use high efficiency dialysers 13 and ensure adequate dialysis . If the aluminium level is above 30ug/l on a repeat test (and serum ferritin is above100ng/ml) a desferrioxamine test should be done.5MHz) in severe hyperparathyroidism or for patients planned for parathyroidectomy. best seen on the radial side of the second and third phalanges. 10 (Level B) 5. home HD/patients on long-term aluminium exposure. Serum aluminium should be screened yearly in high risk patients eg.39 - . however increasing levels may correlate with HTBD.

Calcium control • Maintain target with calcium supplements (refer 5. Indications: • Calcific uraemic arteriolopathy (calciphylaxis) 23 • Therapy resistant hyperCa and hyperPO4 in the presence of very high PTH levels (> 800 pg/ml) 24 • Failure to reduce PTH levels after adequate trial of high dose calcitriol 24 • Intractable pruritus • Progressive extraskeletal calcification that is associated with Ca PO4 product of more than 5 • Severe and progressive skeletal pain or fractures . 2-3 times above the normal range) 17.25-0.2.40 - . 22 5.5 • IV calcitriol is required only in the non-compliant patient or if hypercalcaemia develops with oral calcitriol as there is no good evidence to support IV over oral in the treatment of severe hyperparathyroidism 19 (Level B) • Newer Vitamin D analogues may be considered 20 d.5 ug/dialysis thrice weekly and increased every month up to 2-4 ug/dialysis. monitoring iPTH and other parameters to exclude hypercalcaemia.5 or Ca X PO4 product is more than 4. Other drugs Calcium acetate . second generation PO4 binders (Sevelamer.b.5 Parathyroidectomy a. Patients already on Vit D3 should have the dose adjusted or stopped if Ca x PO4 > 4. non-hypercalcaemic Vitamin D analogues.Lanthanum) and calcimimetics may be added to our armamentarium in the management of calcium and phosphate and PTH in the future21. Vitamin D3 • The aim is to keep serum PTH at 100-200 pg/ml (i.5. hyperphosphataemia and refractory hyperparathyroidism 17 • If PO4 is above 1. 18 (Level B) (DOQI 150-300 pg/ml) • Starting dose of calcitriol is 0.e. Vit D3 should not be started.2) • If hypercalcaemia develops reduce or withdraw calcium supplements and/or calcitriol • Care should be exercised when using low calcium dialysate especially in cardiac patients and ensure hypocalcaemia does not subsequently develop to cause ventricular arrythmias or rebound increase in PTH 14-16 (Level B) c.2.

The patients at highest risk of “hungry bone syndrome” are those with the most severe hyperparathyroidism. In patients on the waiting list for transplant. 28. total parathyroidectomy without autoimplantation is contraindicated in the opinion of most experts24. Some authors also suggest starting oral calcium 2 to 3 grams per day 2 days prior to surgery. then IV pamidronate infusion 60 mg should be given 2 weeks before surgery. The preferred procedure is currently not established. DFO test should be done to exclude aluminium bone disease and treated if positive prior to parathyroidectomy c. f. very high preoperative alkaline phosphatase levels. Administer IV Calcitriol 2 ug at the end of each HD treatment.29 However there is not enough evidence to justify the use of bisphosphonates routinely prior to parathyroidectomy. If bisphosphonate is indicated. Ensure DFO is negative (see Section 5. and the elderly 27 2. (Level C) d.3) e. or oral calcitriol 2-6 ug daily beginning 3 to 5 days prior to surgery and continuing postoperatively to prevent “hungry bone syndrome” 25 (Level C).6 Preparation for Parathyroidectomy a.b. IV calcitriol may be required before and after surgery and Pamidronate may be needed to control calcium to allow for more intensive calcitriol use 5.2.41 - . Ensure patient is well dialysed (see Section 10) b. A few case reports have suggested a possible role for the preoperative administration of bisphosphonates as a means to prevent the “hungry bone syndrome”. To avoid 'hungry bone syndrome' (post-op hypocalcaemia) in patients with severe osteitis fibrosa. those patients not well dialysed with high preoperative BUN. even in patients who are hypercalcaemic 26 (Level C) g. .

8(Suppl1):47-50 7. Pons F. Mion C. Control of serum phosphate without any phosphate binders in patients treated with nocturnal haemodialysis. J Kidney Dis 1998. Nephrol Dial Transplant 1993. or aluminium overload. Uldall R. Geng Z. Canaud B. Saha HT. Kerembrun A et al. Monier-Faugere MC. Am. Kidney Int 57 (2000) 2117-2122 17. Predictive value of Serum PTH levels for Bone Turnover in Patients on Chronic Maintenance Dialysis. J Kidney Disease 1995. Kidney Int 53 (1998) 1399-1404 13. Mucsi I. Port FK. what do we need? Nephrol Dial Transplant 1998. Torregrosa JV. Ferreira A. Cannata-Andia JB. Diagnosis of renal osteodystrophy: when and how to use biochemical markers and non-invasive methods. Malluche HH. 630-640 16. Drueke TB. Parathyroid Imaging. What is the appropriate dialysate calcium concentration for the dialysis patient? Nephrol Dial Transplant (1996) 11 (Suppl 3): 91-95 15. Pasternack AI. 14.Renal Osteodystrophy: management of hyperphosphataemia. D'Haese et al. Management of disturbed calcium metabolism in uraemic patients: use of vitamin D metabolites.References Block GA. prevention and management of low-bone turnover. Vittanen VK. Kidney Int 1993:43. Am. Schomig M. Palomar MR. Bonete R. Mustonen JT. Has double-phase MIBI scintigraphy usefulness in the diagnosis of hyperparathyroidism? Nephrol Dial Transplant (1998) 13 (Suppl 3) 37-4 11. Lippert J. Gilabert R. Passlick-Deetjen J. Fernandez. Diagnosis of renal osteodystrophy: when and how to use biochemical markers and non-invasive methods. Coakley AJ.opez J. 3. Nephrol Dial Transplant 1991. DeBroe ME et al. Ouwendyk M. Nappi SE. Qi Q. Ferreira MA. Phosphate removal rate: A comparative study of five high-flux dialysers. QTc dispersion increases during haemodialysis with low -calcium dialysate. Nephrol Dial Transplant 2000. Ferreira MA. Nephrol Dial Transplant (2000) 15 (Suppl 5) 32-33 12. Nephrol Dial Transplant 2000:15 (Suppl5):15-17 6. Biochemical markers of bone turnover in the diagnosis of renal osteodystrophy: what do we have. Argiles A. increased risk for aluminium toxicity. Nephrol Dial Transplant 1995.Cruz L. Levin NW. Ritz E. Nucl Med Commun 1995: 16 522-533 10.15(Suppl 5):8-143.4:622-631 4. Ritz E. Hulbert-Shearon TE. Association of serum phosphorus and calcium-phosphate product with mortality risk in chronic haemodialysis patients: a national study. Kerr PG. Flavier JL. Sabater L.42 - . when bone biopsy is needed. Kuno T. Llovera J. Chauveau P. Nephrol Dial Transplant (2000): 15 (Suppl5): 18-24 1. when bone biopsy is needed Nephrol Dial Transplant 2000 15(Suppl5):8-14 9. Pathogenesis. Francoeur R.10:1784-1884 8.2(Suppl) 114-115.13(Suppl 3):29-32 5. Poignet JL. New insights and strategies in the diagnosis and treatment of aluminium overload in dialysis patients. Calcium kinetics and the long-term effects of lowewring dialysate calcium concentration.4:607-617 2. Pierratos A. Hercz G. Use of the low-dose desferrioxamine test to diagnose and differentiate between patients with aluminium-related bone disease. .

Nephrol Dial Transplant (2000):15(Suppl5) 25-29 25. Am J Kidney Dis 1997. Nussbaum SR. 836-844 19. Schomig M. Selective vitamin D analogs and their therapeutic applications Semin in Nephrol. Dial Transplant 1986. 1994 14 (2) 156-174 21. Shirota T. Chertow GM. Prospective trial of pulse oral versus intravenous calcitriol treatment of hyperparathyroidism in ESRD Kidney Int 1994. Llach F.14:2907-14 22. Llach F. Dinbar A et al. Hypocalcaemia after parathyroidectomy in a long-term haemodialysis patient.29:759 27. Spritzer CE. Bartholomay D. Management of disturbed calcium metabolism in uraemic patients: 3.1710-1721 20. Shinoda T. Schomig M. et al. Long term effects of sevalamer hydrochloride on the calcium x phosphate product and lipid profile of haemodialysis patients. Carroll BA. Sherrard DJ. Relationship . Immediate postoperative management of parathyroidectomised haemodialysis patients.15:507 29. Dusso A et al. Ritz E. Quarles LD. 26. Parathyroidectomy in chronic renal failure:Indications. Ritz E.43 - . Brasier AR. Nephron 1992. 84:654 28. Brown AJ. Wang M.15 (Suppl 5):30-31 23. Am J Med 1998.45. Maloney NA. Nephrol Dial Transplant 1999. Hercz G.29:S62 18. Yohay DA. Shpitz B. Biochemical aberrations in a dialysis patient following parathyroidectomy. Korzets Z. Minda SA. Hungry bone syndrome: clinical and biochemical predictors of its occurrence after parathyroid surgery. Cruz DN. Segre GV. bisphosphonates. Lobaugh BA.between Intact PTH 1-84 and Bone Histomorphometric Parameters in Dialysis Patients Without Aluminium Toxicity. Perazella MA. Calcific uraemic arteriolopathy (calciphylaxis): An evolving entity? Am J Kidney Dis 1998 32:514-518 24. Pei Y. surgical approach ant the use of calcitriol. Management of disturbed calcium metabolism in uraemic patients: Indications for parathyroidectomy. Kidney Int Suppl 1990. Am J Kidney Dis1995. Aizawa T. Potential perspectives-calcimimetics Nephrol Dial Transsplant 2000.60:482 26. et al.

If repeated level is also > 30ug/l & serum ferritin is >100ng/ml. it is no longer capable of excreting absorbed Al efficiently. 5. Shohl’s solution.1 Sources of Aluminium • drinking water • pickled foods • beer • baking powder • frozen food • water for HD (e.g.1) a.2 (Level B) b. potassium citrate) increases Al absorption from food • Although Al level in water is very low. Nevertheless it may still occur as Al is present in many substances including medications.3. As the kidney fails. home/school/office HD) • processed cheese • commercial tea/coffee • Al-based phosphate binders • Gelusil. Serum Al sampling technique .3 ALUMINIUM TOXICITY Aluminium (Al) toxicity is becoming less common now with the use of reverse osmosis for treatment of dialysate water and decline in use of Al-based phosphate binders. 5. fruit juices. proceed to desferrioxamine (DFO) test 1. continued exposure over a prolonged period of time leads to significant accumulation.3 Screening (see Fig. Serum Al screening • Serum Al screening (with serum ferritin) should be done yearly in the following selected cases 1.2 Consequences of Al overload • Bone disease • Encephalopathy • Iron & Epoetin resistant anaemia 5. 5.3.44 - .g. repeat the test one month later.2 (Level C): − home/office/school dialysis − long-term aluminum hydroxide treatment − history of Al toxicity • If the level is above 30ug/l.5. Mist.3. (Level C). Sucralfate • IV albumin Note : • Citrate (e.

Al <30ug/l but se. ferritin >800ng/ml 1 • suspected of Al toxicity ( Level C) ii. Diagnosis of Al overload in patients: • planned for parathyroidectomy (Level C) • with se. Assessment of adequacy of DFO treatment b. Procedure in Hemodialysis patients • A baseline serum Al level is obtained before a HD session. Indications for low dose DFO test: i.45 - . or se. and must be subjected to a special acidsoaking and ionised-water rinsing process before being sterilized • Blood should be collected from the venous line by dripping directly into the specimen bottle. 1. For HD patients. Heparinise the venous line only after sample collection. DFO test procedure Withold Al-containing medications for at least 48 hours before test 2.• Sample collection containers and caps should be made of colourless plastic. Al >30ug/l on 2 successive occasions & serum ferritin >100ng/ml & iPTH <650pg/ml.6 (Level B) .3.3 (Level C) Positive DFO is defined as rise in (delta) Aluminum > 50 ug/l. • 5 to 7 mls of nonheparinized blood is required for each sample. • 5 mg/kg DFO* in 150 ml of 5% dextrose is infused into the venous blood line during the last hour of the same HD session • Just before the start of the next HD session (44 h after DFO administration).4 Desferrioxamine (DFO) test a. i. • The specimen should be sent to the lab as soon as possible to avoid contamination • Al assays should be sent to reliable labs that have facilities for Flameless Atomic Absorption Spectrophotometry. This procedure is recommended to avoid contamination of the sample as plastic syringes without rubber plunger is not available. draw blood from the arterial needle line without pre-filling with heparin saline or normal saline. 1 (Level C) 5. a 2nd serum Al level is obtained * Vital signs should be closely monitored during DFO infusion.

5. Procedure in Peritoneal dialysis patients • A baseline serum Al is measured at any time of the day • 5 mg/kg DFO in 150 ml of 5% dextrose is given intravenously during the last 60 mins of a CAPD exchange. Alternatively. • A 2nd serum Al level is obtained 44h after termination of the DFO infusion or the DFO-containing exchange. Monitor dialysate water Al level 6-monthly 1. Use reverse osmosis for water treatment b. 5 mg/kg DFO is added to the nocturnal exchange for CAPD patients or the long daytime exchange for CCPD patients. They may be used temporarily for 4-8 weeks if: • serum phosphate is very high despite high dose CaCO3 • high serum calcium despite low-calcium dialysate precludes use of CaCO3 Maximum allowable daily dose of Alutab is 2-3g (6 tablets) (Level C) Conversion factor for serum aluminium : 1 umol/l = 26. Avoid foods with high Al content.ii. * Vital signs should be closely monitored during DFO infusion.3.46 - . Al level in treated water should be kept <5µg/l (AAMI standard) c. 1.6 Prevention a.8.3a) d.3. Monitor serum Al levels yearly in selected patients (see Section 5.95 ug/l . Avoid Al-based phosphate binders if possible. Patients on aluminium tablets should avoid concomitant citrate ingestion 1 e.3.6 (Level B) 5.5 Bone biopsy Bone biopsy with tetracycline labeling is the gold standard for diagnosing aluminium-related bone disease but this test is not presently available locally.

DFO-test positive without clinical evidence of Al toxicity in high risk patients iv. Dose = 5mg/kg weekly for 3 months iii. Gastrointestinal disturbances . F60. if hypotension is very severe and fails to respond to above measures or other signs of anaphylaxis/allergy e.adrenaline 1mg.3. Infections (Yersinia. Acute aluminium encephalopathy To avoid this. wheezing.g. angioedema. inform the doctor and consider s. or Alukart cartridges should be used during the HD session after each dose of DFO. anaphylaxis) iv.8 a. 9 v. retinopathy vii. give 2nd course of DFO treatment 1 (Level C) c.c. Allergic reaction (rash. Administration of DFO i. Repeat DFO test 1 month after completing treatment • if repeat DFO-test is negative. Mucormycosis) v. iii.5. DFO-test positive & patient planned for parathyroidectomy b.47 - . DFO is given 4 hours before HD if patient’s post-DFO SAl is above 300 ugl/l ii. However. Side effects of DFO treatment: i. polyflux). Biopsy-proven aluminium related bone disease (ARBD) ii. DFO-test positive with clinical evidence of Al toxicity iii. To enhance removal of DFO-Al chelate. stop DFO treatment and monitor serum Al level • if repeat DFO-test is positive. F80. Infuse over 1 hour (at a rate not exceeding 1g/hour): • during the last hour of HD if post-DFO serum Al<300ug/l or • 4 hours before HD if post-DFO serum Al >300ug/l iv. Arrhythmia viii. Ear & eye review should be documented before start of treatment ii. high-flux membranes (e. Indications for DFO treatment 1: i. rash is present.g. Hypotension Treat by temporarily stopping the infusion and giving a volume expander if needed. Cataract. Deafness vi.7 Desferrioxamine treatment 1.

48 - .treatment before PTX or high dose Vit D PTX: parathyroidectomy SAI: serum aluminium Conversion factor for serum aluminium : 1 umol/l = 26.1 Strategy for monitoring & diagnosis of aluminium related bone disease 10 DFO.test + treatment before PTX or high dose Vit D DFO.Fig 5.95 ug/l .

49 - .2 Strategy for low dose DFO treatment 10 .Fig 5.

NDT (1995) 10: 1874-1884 Barata JD et al. 9. 5. D’Haese PC et al. 2.Table 5. 6.1 Aluminium content in drugs & solutions Drug Dried gel Amphogel Maalox Alutab Alucap Sucralfate Solution Sodium chloride Dextrose 5% TPN solution (amino acids) 25% albumin Calcium gluconate Stated Al 5 mg 320mg/5ml 225mg/5ml 600mg/tab 475mg/tab 1g Calculated Al 0. AJKD Vol 34. 4. 10. NDT (1996) 11 [Suppl 3]: 74-79 Kausz AT et al. No 4 (Oct 1999): 688-693 Ostric V et al.35 mg 112mg/5ml 78mg/5ml 210mg 166mg 207mg Measured Al 0. 7. NDT 1996 Fernandez-Martin JL et al. 3rd Ed. JASN 1994 Vol 5: 469 Andia JBC.50 - . 3. NDT (1998) 13 [Suppl 3]: 78-81 Vasilakakis DM et al. .347 mg 106mg/5ml 60mg/5ml 174mg 111mg Al (mg/l) 6 72 72 1822 5 References 1. KI Vol 41 (1992): 1374-1382 D’Haese PC et al. 8. NDT (1996) 11 [Suppl 3]: 69-73 Pei Y et al. KI 1992 Vol 41: 1400-1407 Daugirdas : Handbook of dialysis.

• chronic arthropathy. cystic bone lesions. Successful kidney transplantation normalizes plasma β2 M levels.51 - .4.4. Convective treatments were associated with reduced DRA morbidity and postponed the need for carpal tunnel syndrome surgery compared to diffusive treatments. but rather eroded cavities. more than 40 years of age at the onset of dialysis therapy b.2 Risk factors for Dialysis-related Amyloidosis a. may prevent disease progression and can alleviate symptoms b. possibly by endotoxin contamination of dialysate e.4. on dialysis for > 10 years d. • destructive spondyloarthropathy • pathologic fractures 5. Beta-2-microglobulin amyloidosis (β2 M).5. These changes are not true cysts. is a unique type of amyloidosis affecting patients with renal failure.1 Introduction a. The following membrane properties are particularly important with regard to β2 M accumulation: • Highly permeable membranes provide better β2 M clearance • Adsorptive capacity. the degree of bacteriologic quality of the dialysis fluid may also play a role. Membrane adsorption appears to an important mechanism of β2 M removal • Biocompatibility membrane-induced cell activation with subsequently generated proinflammatory mediators has been incriminated in the stimulation of β2 M synthesis and in contributing to the formation of amyloid deposits and joint lesions . This condition is defined as a disabling disease in which the accumulation of amyloid fibrils consisting of β2 M deposits lead to bone and joint destruction. either before or during dialysis.3 Prevention & Management a. c. b. metabolic acidosis may stimulate β2 M production 5. A variety of osteoarticular complications have been associated with β2 M amyloid deposition in patients on long-term dialysis including: • carpal tunnel syndrome (CTS). subchondral bone cysts and/or articular erosions are a pathognomonic finding of dialysis related amyloid (DRA). those treated with bioincompatible dialysis membranes c.4 Dialysis-related Amyloidosis 5.

6. (See table 6. MANAGEMENT OF CARDIOVASCULAR RISK FACTORS Cardiovascular events are the major cause of morbidity and mortality in ESRD patients on long term haemodialysis. coronary artery disease and congestive heart failure 8 (Level A).52 - . These include factors that are not amenable to intervention.1 Hypertension 6. hypertension has been shown to be a major CV risk factor 5.2. ‘Newer’ treatable risk factors that are being increasingly recognised in haemodialysis patients should also be targetted even though the effect on survival has not been clearly established.1 In the general population. left ventricular hypertrophy and heart failure. In dialysis patients.7 (Level A).1) Table 6.4 Various factors exist which increase the risk of ischaemic heart disease. as well as those that are treatable and proven effective in the general population.1 Cardiovascular risk factors in patients on long term haemodialysis Intervention Should be treated Should be is not Intervention is possible considered possible Efficacy Effect on Effect of treatment proven in survival not not proven general proven population • Age • Hypertension • Uraemia • Hyperrelated homocysteinemia • Gender • Diabetes dyslipidemia • Hypoalbuminemia mellitus • Lipo• Increased protein(a) • Smoking • Hyperserum fibrinogenaemia • Physical phosphorus inactivity • Raised Advanced • Increased Glycation End • Hyperserum Ca Products lipidemia PO4 product • Increased • Uraemic • Hyperoxidative stress anaemia volaemia • Increased acute phase response 6.6. 1. hypertension has clearly been shown to be a risk factor for LVH. At least 80% of patients have hypertension at the commencement of regular haemodialysis. .1.3.

The aim is to keep BP < 140/90. fluid and salt restriction. subsequent dosage may need to be reduced or stopped depending on the blood pressure response to the dialysis and ultrafiltration. Less than 20 percent of hypertension in haemodialysis patients are renin dependant. Most of the major classes of antihypertensive medications may be used. If the patient is already on antihypertensive medication.6.Control can be achieved by adequate dialysis. Refractory hypertension or dialysis resistant hypertension refers to the patients at `dry weight’ requiring at least two antihypertensive medications for control. Some drugs are dialysable and dose adjustment may need to be made accordingly. Diuretics are not useful as monotherapy in patients with residual renal function and clearly has no role in anuric patients.g ischaemic heart disease. ischaemic heart disease & heart failure). Antihypertensive medications The choice of antihypertensive agents should be individualised based on the presence of other comorbidities e.2 The majority of hypertension in this population is salt and volume dependant 9-13 (Level A). Target blood pressure Current target is extrapolated from the general population. a. There is no consensus on whether target BP is based on pre or post dialysis readings. These patients may require antihypertensive medications despite adequate dialysis and ultrafiltration. achievement and maintenance of dry weight and the addition of antihypertensive medications as necessary. Management of such patients include: • reassess dry weight . left ventricular hypertrophy. d. • Correct and control the volume status using the following strategies: − Achieve target dry weight over 4-6 weeks of starting haemodialysis. Management • Thorough history and physical examination is carried out to assess for possible target organ damage (retinopathy. b.53 - .1. − Antihypertensive medication is often required at the initiation of haemodialysis until the dry weight is achieved. 14 (Level C) c. heart failure etc. As the blood pressure is expected to decrease with fluid removal on haemodialysis it is generally recommended to omit the predialysis dose of anti hypertensive medication unless indicated.

serum lipids should be regularly monitored and treated accordingly 1. Treatment is initiated if the concentrations exceed the following: • LDL. • Fluid intake should be controlled to match the urine output and insensible losses.6mmol/l) • TG > 180 mg/dl (> 2.2.2. continue to monitor six monthly. 6. Serum cholesterol may be normal but triglyceride.1 Introduction a. Once known and controlled.54 - . hyperlipidemia had been clearly shown to be a significant CV risk factor and drug therapy in this population has convincingly shown effective reduction in cardiovascular mortality.20 (Level A) b. • Maintain dry weight once this is achieved • Consider prolonged or more frequent dialysis if adequate BP control is not achieved 16-17( level B). • Revise the set dry weight when lean body mass changes.3 Dry weight Definition : dry weight is the post dialysis weight below which hypotension develops when the patient has no evidence of volume overload ie free of oedema.1. In the general population. and normal cardiac size on chest radiograph 15 ( Level C).2.21-24 6. erythropoeitin • consider other causes (eg native kidneys) 6. A third of patients on haemodialysis have dyslipidemia. 6. sympathomimetics. Interdialytic weight gain should be < 3% of the set dry weight. alcohol. 19.2 Measurement and monitoring 24: Measurement of serum lipid should be made from blood sample taken pre dialysis before heparinisation after a 12 hour fast. IDL and Lipoprotein(a) are elevated and HDL cholesterol may be reduced .1mmol/l) • HDL -Chol < 40mg/dl (< 1mmol/l) .2 Hyperlipidemia 6. Since haemodiaysis patients constitute a high CV risk group and treatment with lipid lowering drugs have been shown to be safe and effective in reducing hyperlipidemia.• assess drug compliance • consider drug effect eg NSAIDs.3 Treatment 24: a. Salt intake must be limited to < 6g daily 18 (level B).Chol > 100mg /dl (> 2.

8.10:1606-15 MacMahon S. Report on management of renal failure in Europe. Bethesda.2.1mmol/l) 6. Provide counseling on dietary modification including alcohol restriction. Statins should be used for hypercholesterolemia and combined hyperlipidemia d. 32 [Suppl 1]: S81-88 Raine AEG. McNamara PM et al. Cholesterol. Lancet 1990. Kidney Int 1996. The clinical epidemiology of cardiac disease in chronic renal failure. 5. N Eng J Med 1972.000 people in 45 prospective cohorts. morbidity and mortality in end stage renal disease.4 Target concentration 24: • LDL-Cholesterol < 100mg/dl (< 2. Parfrey PS et al.335:765-74 Prospective Studies Collaboration. Brunner FP et al. How important is volume excess in the etiology of hypertension in dialysis patients.287:781-7 Foley RN. Combination therapy is not recommended due to the high risk of rhabdomyolysis f.Role of blood pressure in the development of congestive heart failure. Parfrey PS. 9. If hyperlipidaemia remains consider drug therapy. Peto R. Am J Kidney Dis 1998. J Am Soc Nephrol 1999. Controlling the epidemic of cardiovascular disease in chronic renal disease: what do we know? What do we need to learn? Where do we go from here? Am J Kidney Dis 1998.55 - . Lancet 1995. c. Levey AS.3 Anaemia – see section 5. Impact of hypertension on cardiomyopathy.346:1647-53 Kannel WB. XXII. 3.1 References 1. Semin Dial 1999. Harnet JD et al. Beto JA.12(5):299-301 . optimal weight and physical activity/exercise.b. Liver enzymes should be monitored within six weeks of drug therapy to detect hepatotoxicity and rhabdomyolysis 6. 7[ Suppl 2]: 7-35 Parfrey PS etal. MD. 1991. Annual Report. stroke and coronary heart disease. Castelli WP. Part 1.6mmol/l) • Triglyceride < 180mg/dl (< 2. CutlerJ et al Blood pressure.The Framingham Study. Nephrol Dial Transplant 1991. National Institute of Diabetes and Digestive and Kidney Diseases. 2. In hypertriglyceridaemia use of fibrate (gemfibrozil) is recommended e. Margreiter R.prolonged differences in blood pressure: prospective observational studies corrected for the regressioin dilution bias. 4. diastolic blood pressure and stroke: 13000 strokes in 45. 6.49:1379-85 Leunissen KML et al.32: 85-906 US Renal Data System. 7.

Raj DS et al. Fink JC et al.15 [Suppl 5]:92-6 23. Semin Dial 1999. Randomised Trial of Cholesterol Lowering in 4444 Patients With Coronary Artery Disease: the Scandinavian Simvastatin Survival Study (4s).11[Suppl 2]:16-9 16. In search of ideal haemodialysis: is prolonged frequent dialysis the answer? Am J Kidney Dis 1999. Nephrol Dial Transplant 1996.12(2):87-90 22. Nephrol Dial Transplant 2000. How important is volume excess in the etiology of hypertension in dialysis patients. Lowrie EG.12(5):303-4 14.34:597-610 18. Lancet 1994. Prichard S. Dietary salt restriction and reduction of dialysate sodium to control hypertension in maintenance haemodialysis patients. Nephrol Dial Transplant 1999.B.Medical Expert Group. Nephrol Dial Transplant 1998. Nephrol DialTransplant 2000. Wanner C. Charra B. Dyslipidemia as a Risk Factor For Cardiac Disease in Dialysis Patients. Fluid state and blood pressure control in patients treated with long and short haemodialysis. How important is volume excess in the etiology of hypertension in dialysis patients. Charra . Semin Dial 1999. Commonly measured laboratory variables in haemodialysis patients: relationship among them and to death risk .13:552-3 19. Scandinavian Simvastatin Survival Study Group. Laurent G. 14: 369-75 17. Katzarski KS. Semin Dial 1999. How Important Is Volume Excess in the Etiology of Hypertension in Dialysis Patients. Clinical Algorithms On Cardiovascular Risk factors In Renal Patients. Semin Nephrol1992.12(5):296-7 12. Semin Dial 1999. Ritz E. Clinical Algorithms On Cardiovascular Risk factors In Renal Patients.344:1383-9 20. Clinical assessment of dry weight. Luik AJ et al.15[Suppl 5]:134-5 15. Charra B. Importance of hyperlipidemia and therapy in renal patients.12(5):297-9 11. Chazot C et al.56 - .12(5):304-6 13.12: 276-83 21. How important is volume excess in the etiology of hypertension in dialysis patients. Nephrol Dial Transplant 2000. Semin Dial 1999.15[Suppl 5]:128-9 10. Zuchello PC et al. Law NL. Krautzig S et al.Medical Expert Group.

57 - .5 Studies have indicated that HCV transmission most likely occurs because of breakdown in standard infection control practices. handling and storage of medication). scissors and other nondisposable items among patients should be discouraged d. In the past. Medication and supplies should not be shared among patients and medication carts should not be used f. The introduction of rigorous infection-control strategies has led to a decline in the spread of HBV infection in the dialysis units. 2 Hepatitis C infection is now a major problem in the Malaysian haemodialysis scene.9 HCV transmission within the dialysis environment can be prevented by strict adherence to infection control precautions.g. . All machines should be cleaned after each use c. The chronically infected person is central to the epidemiology of HCV transmission. Medication should be prepared and distributed from a centralised area g. clamps. 4. There should be separate clean and contaminated areas (e. 3.8. long term haemodialysis patients have a higher risk of acquiring Hepatitis B virus (HBV) and Hepatitis C virus (HCV) infection compared to the normal population. 29% of patients in the government centres were positive for anti-HCV antibody.1. 6. Hand washing should not be done in or near an area where used equipment or blood samples are handled. 1. 10 7.7.1 Universal precaution for the care of all haemodialysis patients: a. Wear disposable gloves when caring for the patient or touching the patient’s equipment at the dialysis station. MANAGEMENT OF THE INFECTIVE PATIENT Due to the nature of haemodialysis treatment and the likelihood of receiving multiple blood transfusions.1 Measures to reduce risk of transmission of virus or other infectious agents include: 7. BP cuffs. remove gloves and wash hands between each patient or station b. Sharing of ancillary supplies such as tray. In 2000. 7 Nosocomial transmission within the dialysis centre is the principal route of HCV dissemination in the dialysis population. HBV was the major cause of viral hepatitis in end-stage renal disease. Nondisposable items should be cleaned or disinfected appropriately between uses e.

5) adolescents < 20 yrs of age Adults 20 yrs of age or older 10 (1.7.1 Schedule Dosing schedule for dialysis patients: 4 dose schedule at 0.0) and other (1. and 6 to 12 months 7. repeat serologic tests every 3 months c. Confirmed positive anti-HCV patients do not require repeated serologic test 7. For children with progressive chronic renal failure.2 Repeat serologic testing Serum anti-HBs-antibody should be checked 1-2 months after completing the vaccination course Formatted: Ge . In HbsAg negative patient.2 Serological testing a. negative anti-HCV antibody. children and 5 (0. 2. an increased number of doses or both may be required to produce protective anti-HBs concentrations in adult haemodialysis patients. 1. ug (ml) Dose ug.1.2 Hepatitis B vaccine Larger vaccine doses. In newly infected HBV patient.0) Patients undergoing dialysis 20 40 (2.2. For those with negative HbsAg.2. hepatitis B vaccine is recommended early in the disease course to provide protection and potentially decrease the need for larger doses once dialysis is initiated. vaccination should be given for those with negative anti-HBs antibody status f. repeat HbsAg testing and test for anti-HBs six months later to determine clinical outcome d.0) 20 (1. (ml) Infants.1 Recommended dosages of hepatitis B vaccines Target Group Recombivax HB Engerix-B Dose. HbsAg and anti-HCV antibody should be checked 3 monthly and anti-HIV antibody yearly b. Table 7.58 - .0ml-special immunocompromised adults formulation for dialysis patients ) 7.5) 10 (0. Patients with chronic HBV infection require annual HBsAg testing to detect the small percentage of those who might lose their HbsAg e.

11.2. The disposal of bloodlines and dialysers should be made according to the recommendations of the Ministry of Health. Re-immunisation consists of 1 to 3 doses. . the need for booster doses should be assessed by annual anti-HBs testing b. • For anti-HIV positive patients who acquire the virus whilst on regular haemodialysis or newly accepted patients for haemodialysis who are asymptomatic.5 Staff of haemodialysis units should be routinely immunised 7.2.2. persistent ALT elevation and HCV RNA-positive 7. For haemodialysis patients. 7. the decision to continue the treatment will be based on similar grounds as those for nonHIV infected patients.59 - .4 Management of patients with hepatitis B/C infection • Patients positive for HbsAg and/or anti-HCV should be monitored for evidence of chronic liver disease and its complications. yearly α-fetoprotein and liver ultrasound • Hepatology referrral for possible interferon (IFN) therapy may be considered in patients who are positive for anti-HCV. Vaccine recipients who do not develop a serum anti-HBsantibody response (> 10 mIU/ml) after a primary vaccine series should be re-immunised (unless they are confirmed to be HbsAgpositive) b. A booster dose should be given if the anti-HBs concentration is less than 10 mIU/ml 7. Those who remain antiHBs-negative after a re-immunisation series of 3 doses are unlikely to respond to additional doses of vaccine. A separate area is recommended.7.3 Isolation Patients positive for HbsAg or anti-HCV antibody should be dialysed on separate machines not shared by seronegative patients. disposables should not be reused.4 Booster doses a.12 7. 3 monthly LFT.3 Management of non-responders a.5 Management of patients with HIV infection • For anti-HIV positive patients.

3. Loureiro A. 1. Sampietro M. dos Santos. Interferon therapy in haemodialysis patients with chronic hepatitis C virus infection induces a high rate of long-term sustained virological and biological response. Incidence of and risk factors for hepatitis B virus and hepatitis C virus infection among haemodialysis and CAPD patients: Evidence for environmental transmission. Multi dose heparin vial. non-B and anti-HCV antibody in dialysis patients: IJAO (1990) 13: 737 7. Okuda K. (1998) 44:98. Jorge M.Hepatitis C in dialysis and Transplantation. Portuguese Society of Nephrology. Nephrol DialTransplant (1996) 11: 201722. Patient to patient transmission of Hepatitis C virus in haemodialysis units in Turkey. Current opinion in Nephrology and Hypertension (1996) 5:497-503. Nephrol Dial Transplant (1995) 10:230-233. Universal precautions prevent hepatitis C virus transmission. National surveillance of haemodialysis associated disease in the United States. Units. Jodoul M. . 9.References J. J. M Cendorogio. Impact of dialysis room and reuse strategies on the incidence of hepatitisC virus in haemodialysis units. Tokars JI. Hepatology (1995) 23: 28 8. J. Infection Disease (1986) 153: 1549 2. M. Gill. non-A. A prospective study.60 - . Impact of infection control strategies on the incidence of dialysisassociated hepatitis in the United States. The Universitaies Clinique St-Luc (UCL) Collaborative Group. 11. 10. Mode of hepatitis C infection not associated with blood transfusion among chronic haemodialysis patients. ASAIO J. 12. 4. 13. High prevalence of a rare hepatitis C virus in patients treated in the same hemodialysis unit: Evidence for nosocomial transmission of HCV: Kidney Int (1995) 47:911-7 5. Epidemiology of hepatitis C: Geographic differences and temporal trends : Seminar in liver disease (2000) 20:1-16. Taskapan. Espinosa. Kidney Int (1998) 53: 1022-5. (2000) Vol 55-No:3/2001:220-226. Alter. Clinical Nephrology. 14. 6. Trend in the incidence of hepatitis C infection in haemodialysis unit: J Am Soc Nephrol (abstract 1995) 6: 547. Nephrol Dialysis Transplantation (1995) 10: 240246. Clinical Nephrology (2000) 55: 477-481. Annmarie W. H.

Carbohydrate metabolism Impaired glucose tolerance due to: • increased peripheral resistance to insulin • decreased beta cell sensitivity to glucose levels • increased hepatic gluconeogenesis c. dietary interview. creatinine and cholesterol are valid and clinically useful markers of protein energy nutritional status. NUTRITIONAL MANAGEMENT Malnutrition is a well recognised comorbid condition in dialysis patients that contributes to the increased mortality seen in these patients.61 - . body mass index (BMI).2 Nutritional changes in uraemia a. Lipid metabolism • Moderate increase in triglyceride levels • Normal or slight increase in cholesterol 8.g.infection • Increased circulating levels of catabolic hormones e. The following levels suggest protein-energy malnutrition: i. diaries and protein nitrogen appearance (PNA) c. PTH • Dialytic loss of amino acids and vitamins • Intradialytic hypercatabolism – dialyser bioincompatability 8. subjective global assessment. glucagons. Nutritional status should be routinely assessed.3 Evaluation of Nutritional status a. 8. Serum albumin. Albumin < 40g/L ii. nausea and vomiting • Inter-current illness e.g. This may include predialysis serum albumin.8. Cholesterl < 3.1Causes of protein energy malnutrition • Increased net protein catabolism • Anorexia.8 mmol/L . complementary measures rather than any single measure alone b. Creatinine < 880umol/L iii. Nutritional status in maintenance dialysis patients should be assessed with a combination of valid. Protein metabolism • Increased degradation of protein and amino acids • Increase in non-essential amino acids and decrease in essential amino acids b.

The response of the diabetic patient to hypoglycaemia is blunted during haemodialysis.3 Fat intake a.1 Carbohydrate intake a.2 Protein intake a.retention of a lipoprotein lipase inhibitor • dialysate (conversion of acetate to long chain fatty acids and cholesterol) . There is significant correlation between serum albumin and mortality.4. An adequate nitrogen balance is important for patients on dialysis. The lipid abnormalities of patients on chronic haemodialysis have been correlated with cardiovascular mortality. Carbohydrate should consist of more complex carbohydrates to avoid frequent peaks of glycaemia.d. Anthropometric measurements including % usual body weight.4 Nutrition in the haemodialysis patient 8. c.0 to 1. BMI. The losses are increased when glucose-free dialysate is used.62 - .4. mid arm muscle area. The amount of protein needed for positive nitrogen balance is 1.5 to 3 gram of amino acids per hour of dialysis. % standard body weight. 8. skinfold thickness. The reason for the abnormalities include: • Impaired catabolism of VLDL . b. b. The protein should be derived from animal source and they should account for at least 50% of the total protein intake. 8. circumference or diameter are valid and clinically useful indicators of protein energy nutrition status 8.4. PNA and protein catabolic rate (PCR) are valid and clinically useful measures of net protein degradation and protein intake in maintenance dialysis patients e. During hemodialysis. It is important that pre-dialysis patients should not be subjected to severe protein restriction that may deplete their protein stores. The total daily calorie requirement is about 35 kcal/kg/day. These patients should reduce their insulin intake on dialysis days and eat before dialysis. patients lose 1. estimated % body fat. Dialysis improves the abnormalities of glucose metabolism. The insulin requirement of diabetic patients may be reduced on dialysis days due to improvement of the tissue sensitivity to insulin. One important aim in supplying adequate calories is to reduce protein breakdown for gluconeogenesis.2g/kg/day.

energy requirement.4 Calcium and phosphorus a. It (maize.b. Lipid intake should be 25% of the total should be in the form of vegetable fats which contains polyunsaturated oils. A total of 1200 mg/day may be needed. Marmite Cola drinks Beer 8. hyperlipidemia includes the reduction of and reduction in carbohydrates.g. beans Heart Butter/peanut butter Brain Baked beans Canned meat Bean products Sardines Egg yolk Crabs Coconut & all coconut products Prawns Kaya Mussels Dried fruit Scallops Keropok Shellfish Ikan Bilis Mushrooms Cauliflower Evaporated milk Condensed milk Yoghurt Cheese Cocoa Chocolate Foods with chocolate Instant coffee Horlicks Ovaltine Cereals e. b. The serum phosphate should be kept below 1. • Vitamin B1 4mg/day • Vitamin B6 10mg/day • Vitamin C 100 mg/day • Folic acid 0.63 - .6 mmol/l d. Uraemia is associated with accumulation of phosphorus and low calcium level.1 Foods rich in phosphate Liver Nuts and nut products Kidney Legumes e. The dietary intake of phosphate should be limited to 800mg to 1200 mg daily c. oats Wholemeal bread Bovril. Patients on dialysis require calcium supplements if they are hypocalcaemic. Table 8.5-1mg/day • Iron supplement 200 mg /day .g. In haemodialysis the removal of phosphate is less efficient than in CAPD.4.5 Vitamins Supplements of water soluble vitamins are recommended as they are lost during dialysis.4. peas. sunflower oil) Dietary control of intake of saturated fat 8.

4. Oral diet may be started .2 g/kg/day b. wine 8. If the patient has residual urine output sodium intake should be restricted to 130-170 mmol/day (3-4 g/day) c. Total energy intake > 35 kcal/kg/day c. Water and salt as allowed by fluid balance .64 - .8.6 Sodium and water a. 8. Dietary protein intake 1.7 Recommended nutritional intake in patients on haemodialysis The nutritional prescription should be individualised and the motivation of the patient plays a vital role in ensuring compliance: a.6 Potassium Hyperkalemia may result from excessive intake of fruits and vegetables.2 Foods rich in potassium Pure fruit juices Bran Dried fruit Bran cereal Ribena Muesli Tomato juice Nuts Tomato sauce Peanut butter Vegetables Crisps Bovril.6 Nutritional support Individuals on hemodialysis who are unable to meet their protein and energy requirements with food intake for an extended period of time should receive nutritional support. Complete nutritionl assessment should be done and reversible or treatable conditions should be identified. If the patient is anuric potassium intake should be restricted to 50 mmol/day. proceeding to tube feeding if unsuccessful. Marmite Brown sauce Salt substitutes Curry powder Beer. If the patient is anuric sodium intake should be reduced to 40-80 mmol/day (1-2g/day). The amount of water allowed varies with residual urine output b. Those with adequate urine output require mild dietary restriction. lager. Interdialytic weight gain should not be > 3% of dry weight. 8. Intradialytic parenteral nutrition or daily total or partial parenteral nutrition should be considered if the former fails. Table 8.5 Management of acid base status Predialysis serum bicarbonate levels should be maintained at or above 22mmol/l and measured regularly 8.4.

d. Potassium 50 mmol/day + 25 mmol/day for each litre of residual urine e. Calcium 1.2 g/day f. Phosphate 0.8-1.2g/day References 1. K/DOQI Clinical Practice Guide for Nutrition in Chronic Renal Failure. 2. Handbook of Dialysis. 3rd Edition. John B. Daugirdas. Todd S.Ing

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9. HAEMODIALYSIS ADEQUACY 9.1 Measurement of Haemodialysis Adequacy 9.1.1 Regular Measurement of the Delivered Dose of Haemodialysis The dialysis care team should routinely measure and monitor the delivered dose of haemodialysis at least 3 monthly 9.1.2 Method of Measurement of Delivered Dose of Haemodialysis The delivered dose of haemodialysis in adult and pediatric patients should be measured using formal urea kinetic modelling (UKM), employing the single pool, variable volume model. Other methods include URR (urea reduction ratio), natural log Kt/V and the Daugirdas second generation formula: a. URR URR = (Co – Ct) x 100 Co (Ct = post dialysis BUN, Co = pre dialysis BUN) b. Kt/V natural logarithm formula Kt/V = -Ln(R - 0.008 x t) + (4 – 3.5 x R) x UF/W c. Formal urea kinetic modelling Formal urea kinetic modeling provides a quantitative method for developing a treatment prescription for a specific patient. Computational software is necessary to compute Kt/V using formal UKM. d. The single pool Kt/V (spKt/V) is a dimensionless ratio representing fractional urea clearance. K is the dialysis blood water urea clearance (L per hour), t is dialysis session length (hours, hr), and V is the distribution volume of urea (liters, L). If we deliver an spKt/V of 1.0, this implies that K x t, or the total volume of blood cleared during the dialysis session, is equal to V, the urea distribution volume. e. Formal UKM requires accurate measures of: • predialysis and post dialysis blood urea for the second dialysis treatment of the week in a thrice weekly haemodialysis schedule. • predialysis and postdialysis weights at the time of the second haemodialysis treatment of the week. f. The actual treatment time, i.e. the exact number of minutes during which the haemodialysis treatment was delivered on the second dialysis treatment of the week (not the prescribed length of treatment time or the time elapsed between putting the patient on the machine and taking him or her off).

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g. Changes in the dialysis treatment time, choice of dialysers, or operating conditions such as blood and dialysate flows can be calculated to meet the selected prescription goal. h. Formal UKM permits calculation of the normalized protein catabolic rate (nPCR). The volume of distribution term may be used to calculate the nPCR as follows: nPCR (g/kg/day) = (PCR, g/day)x (mean V/0.58) i. Use of the nPCR enables the dialysis team to perform longitudinal analysis of the patient’s nutritional status. The nPCR can be used to identify patients who might benefit from counseling about their dietary protein intake. Furthermore, it can be used to determine whether the haemodialysis dose needs to be increased because of sustained high protein intake. 9.1.3 Uniformity of Method of Measurement All patients receiving haemodialysis in the same dialysis facility should have the delivered dose of haemodialysis measured using the same method. (Level C) 9.2 Haemodialysis Dose 9.2.1 Minimum Delivered Dose of Haemodialysis (Adults Level B) The dialysis team should deliver a Kt/V of at least 1.2 (single pool, variable volume) for both adult and pediatric haemodialysis patients. For those using the URR, the delivered dose should be equivalent to a Kt/V of 1.2, i.e. an average URR of 65%. The HEMO study did not show major benefit from higher dialysis dose (Kt/V 1.7) over current recommended guidelines. (Level A) 9.2.2 Prescribed Dose of Haemodialysis To prevent the delivered dose of haemodialysis from falling below the recommended minimum dose, the prescribed dose of haemodialysis should be Kt/V 1.3. In terms of URR, a Kt/V of 1.3 corresponds to an average URR of 70%, but the URR corresponding to a Kt/V of 1.3 can vary substantially as a function of ultrafiltration. (Level C) 9.2.3 Discrepancies in Kt/V Formal UKM provides a mechanism to check for errors in the delivered dose of haemodialysis. By comparison, the value of V derived from patients’ anthropometric features is only an estimate of urea distribution volume based on body composition analysis.

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Reasons for discrepancies between the kinetically derived and anthropometric distribution volume (v) a. Kinetically Derived V Larger Than Anthropometric V • Low blood flow from the access • Inadequate dialysis performance • Dialysate flows less than prescribed • Dialysis machine programmed incorrectly • Premature completion of treatment • Pre-Dialysis BUN sample drawn after initiation of haemodialysis b. Kinetically Derived V Smaller Than Anthropometric V • Post-dialysis BUN sample drawn from the venous blood line • Post-dialysis BUN sample drawn in the setting of significant fistula recirculation • Post-dialysis BUN sample drawn following a very efficient haemodialysis in a patient with a small V (high K/V) • Post-dialysis BUN sample inadvertently diluted with saline 9.2.4 Reasons for Underdelivery of Prescribed Dose of Haemodialysis a. Compromised Urea Clearance • Access recirculation • Inadequate blood flow from the vascular access • Inaccurate estimation of dialysis performance • Inadequate dialysis reprocessing • Dialyser clotting during dialysis • Blood pump/dialysate flow calibration errors • Errors in prescribed blood and dialysate flow rates due to variability in blood pump tubing • Dialysate flow rate that is inappropriately set too low • Dialysate flow miscalibration • Dialysis leaks b. Reductions in Treatment Time • Incorrect assumption of continuous treatment time because of failure to account for interruptions. • Premature discontinuation of haemodialysis for staff or unit convenience • Premature discontinuation of haemodialysis to honour patient request or adherence. • Delay in starting dialysis session due to patient tardiness • Time on dialysis calculated incorrectly

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c. Laboratory or Blood Sampling Errors • Dilution of pre-dialysis BUN blood sample with saline • Pre-dialysis BUN blood sample drawn after the start of dialysis • Post-dialysis BUN blood sample drawn before the end of dialysis • Laboratory error due to calibration or equipment problems • Post-dialysis BUN blood sample drawn more than 5 minutes after dialysis completed 9.2.5 Frequency of Measurement of Haemodialysis Adequacy (Level C) The delivered dose of haemodialysis should be measured at least 3 monthly in all adult and pediatric haemodialysis patients. The frequency of measurement of the delivered dose of haemodialysis should be increased when: • patients are noncompliant with their haemodialysis prescriptions • frequent problems are noted in delivery of the prescribed dose of haemodialysis • wide variability in urea kinetic modeling results is observed in the absence of prescription changes • the haemodialysis prescription is modified 9.3 Blood Urea Sampling 9.3.1 Blood Urea Sampling Predialysis and postdialysis blood samples for measurement of blood urea levels must be drawn at the same haemodialysis session. 9.3.2. Acceptable methods for blood urea sampling a. Predialysis BUN samples should be drawn immediately prior to dialysis, using a technique that avoids dilution of the blood sample with saline or heparin. b. Postdiaylsis BUN sampling: Stop flow method • Stop ultrafiltration after completing haemodialysis • Reduce blood pump to 25-50 ml/min • Wait for 30 seconds • Widen pressure alarm limit to maximum • Clamp venous line in between patient and venous chamber • If pump does not stop automatically, stop pump after 30-50s • Draw blood sample from ARTERIAL port

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9.4 Duration of dialysis treatment session There are no randomized control trials comparing short with long hours. Many observational studies have suggested lower mortality associated with longer duration of treatment. • Consideration should be given to the observational studies suggesting a minimum of 4 hours for each treatment session (frequency three per week) with low flux dialysers. • Longer hours of dialysis may facilitate fluid and blood pressure control and reduce consequences of excess small and middle molecule accumulation 9.5 Dialysers The characteristics of the dialysers may influence the outcome of the dialysis process in several ways, e.g. molecular weight of cleared solute, biocompatibility and transmission of bacterial products from the dialysate. Much debate remains regarding the importance, the cause and the outcome ensuing from the use of individual membranes. Use of high flux compared to low flux membrane did not confer additional survival advantage .(Level A) 9.6 Inadequate Delivery of Haemodialysis: Troubleshooting 9.6.1 The delivered dose of haemodialysis measured by Kt/V or URR can be affected primarily by: a. clearance of the dialysers b. treatment duration c. blood flow rate d. dialysate flow rate Refer to Figure 9.1 9.6.2 If Kt/V < 1.2 or a URR < 65% on a single determination, consider the following interventions: a. Repeat the measurement of Kt/V or URR more often b. Investigate potential errors (Refer Figure 9.1) In the interim, increase the prescribed dose of haemodialysis 9.7 Clearance Less Than Assumed 9.7.1 Elements of the haemodialysis procedure affecting clearance (K) include dialyser permeability (KoA), effective dialyser surface area, blood flow and dialysate flow a. Assess fistula integrity to determine whether recirculation is present • Review arteriovenous needle placement, proximity, and direction • Verify the direction of blood flow through vascular access. - 70 -

Review actual total duration of the dialysis treatment and any intradialytic events 9. Review sampling procedures with dialysis staff 9. or problems with needle placement) g. Review the maintenance log for the dialysis machine to check the last calibration date and results e.2 Errors in Blood Sampling or measurement for calculating delivered dialysis dose. Haemodialysis treatment time (t) is the total time at the prescribed blood and dialysate flow rates with the prescribed dialysis. .2 Effective Haemodialysis Treatment Time Less Than Prescribed. Review written documentation of haemodialysis treatment. Review the following: • Blood flow rate (Qb) • Dialysate flow rate (Qd) • Type of dialyser • Extracorporeal pressures compared with previous sessions at prescribed Qb − Were pre-pump arterial pressures 200 mm Hg or higher? − Were pre-pump arterial or venous pressures close to upper limit per dialysis unit policy? f.71 - . chest pain. when Kt/V or URR was measured c.6.7.3 Consider repeating pre-dialysis and post-dialysis BUN sampling to determine Kt/V or URR again. Review pattern of dialyser clotting (review of the patient’s anticoagulation may be warranted) h. muscle cramps. then assess for possible recirculation in the vascular access. such as the Qb (hypotension. or it is the dialysis time determined to provide an equivalent Kt/V at the prevailing blood and dialysate flow rates for a particular dialyser. For delivery systems with computers.6. Review the haemodialysis log for clinical events that may have resulted in a change in treatment parameters.b. Review the hemodialysis reuse log to evaluate fibre bundle volume (FBV) of the dialysis d. review the total liters of blood processed 9.If the above still do not reveal the problem. Determine whether dialyser clearance is overestimated by reviewing formal urea kinetic modeling results in other patients using the same model of dialyser with the same prescribed Kt/V i.

72 - .Figure 9.1 Inadequate Delivery of Haemodialysis: Troubleshooting Low URR or Kt/V Adequate prescription? No Correct prescription Yes Completed prescribed time? Yes No Check dialyser integrity • Clotting • Fibre bundle volume Access function • Needle placement • Recirculation Isolated Recurrent Monitor Assess reasons • Noncomplia • Intradialytic symptoms .

Dialysis & Transplantation : A Companion To Brenner And Rector’s THE KIDNEY William F. W. Todd S. Pereira. (HEMO) study group N Engl J Med 2002. The CARI Guidelines : Caring for Australian with Renal Impairment.G. Ing Lippincott Williams & Wilkins 2. Daugirdas. Peter G. National Kidney Foundation. Handbook of Dialysis (3rd Edition) 2001 (pg. Saunders Company 2000. Brian J.73 - . 2000 Am J Kidney Dis 2001 (supp/1). B.347:2010-9 4. Sayegh. Mohamed H. Blake. . Owen. K/DOQI Clinical Practice Guidelines for Haemodialysis Adequacy. 15 – 45) John T. 5. 37 : 57 – 564 3. Effect of dialysis dose and membrane flux in maintenance hemodialysis.References 1.

haemodialysis is required to correct acidosis 1 (Level C) 10.2 Electrolytes a.5 Anaemia a.74 - . Blood transfusion may be needed depending on the type of surgery and co-morbidity c. c.1. SURGERY AND THE DIALYSIS PATIENT Patients with ESRD may need to undergo surgery either as an emergency or elective procedure.1 Fluid status a. Intravenous fluids should be given judiciously.1Preoperative management: 10. b. However.25 and serum HCO3 < 12-15 mEq/l. see Guideline on Renal Transplant Section 38 10. There is no conformity of opinion as to the safe haemoglobin level for surgery b. If dialysis is required before an emergency surgery it should be heparin-free 10.1. Serum potassium should preferably be normal at the time of surgery b. For elective surgery dialysis should preferably be done within 24 hours before surgery b.1.4 10.3 Acid-base status a. If pH < 7. Blood gases may be required for patients going for emergency surgery b. They are at higher risk of perioperative complications. Patients with cardiovascular disease should have Hb > 10 g% .1.1. 10. d.4 Dialysis a. For patients going for renal transplantation.10. Tranfusion of blood or blood products should be given during dialysis/ ultrafitration. Measurement of serum potassium should not be done within an hour post-dialysis to allow time for equilibration. Ideally patients going for surgery should be well dialysed with no significant fluid overload. patients should not be overultrafiltrated to avoid perioperative haemodynamic instability.

A blood pressure of 140/90 mmHg or less is preferred. Anti-hypertensive medication should be served on the morning of elective surgery 101. ECG. 10.5 mmol/l. 10. b.75 - .10. especially when blood urea is >35 mmol/l.1.8 Cardiovascular disease a.9 Dialysis access A label with the words ‘NO BP TAKING OR NEEDLING’ should be clearly taped to the limb with the vascular access.1 Anaesthesia Most anesthetic agents can be used in ESRD patients 1 a. (Succinylcholine increases serum potassium by 0. and is multifactorial in origin. b. CXR) should be done for adult ESRD patients planned for general anaesthesia b.2. Patients with unexplained cardiorespiratory symptoms. However.1. ECG or with multiple cardiovascular risk factors planned for elective major surgery should be referred for cardiac assessment 10. thus repeated dosing is best avoided) c.7 Blood pressure a. Other agents (including vecuronium which is cleared by the liver) may be used in reduced dosage as their half-life is increased in renal failure. Haemodialysis within 24 hours of surgery is effective in partially reversing platelet dysfunction. Induction can be accomplished with iv barbiturate & succinylcholine. abnormal signs.2 Intra-operative management 10. Premedication with commonly used drugs e. benzodiazepine & atropine can be given in normal doses. e.6 Bleeding Coagulopathy is common in ESRD patients. . Basic cardiovascular assessment (history.1. Maintenance of anaesthesia is achieved with nitrous oxide or halothane d. physical examination. Other adjunctive treatment includes use of cryoprecipitate.g. Muscle relaxant of choice is atracurium as its pharmacokinetics & duration of action is unchanged in renal failure. attempts to aggressively reduce blood pressure to normal within 24 hours of surgery are associated with intraoperative haemodynamic lability and hypotension and the risk of significant cardiovascular complication c. desmopressin.

3 Postoperative management 10. Analgesia: opiate usage should be reduced to avoid overdosage. hypotension or dehydration. PT. Infection e. Chest physiotherapy & breathing exercises. heparin-free sequential ultrafiltration should be done.2 Dialysis with tight or no heparin is usually done the day following surgery.1 Patients should be closely monitored during the immediate post-operative period. d. Hypoventilation: may occur due to prolonged sedation from side effects of drugs and uraemia in hypercatabolic state. . wound sepsis: higher risk than nonESRD patient. f. Fluid overload: this can be prevented by careful fluid management guided by strict input-output charts. e.2. APTT. Blood gases may be required following major surgery. Hyperkalaemia: Urea and serum electrolytes should be repeated after major surgery/ when blood transfusions have been given. 10. pneumonia. AVF thrombosis: may occur due to undetected prolonged pressure on AVF intraoperatively.76 - . CVP/ PCWP.3.10. c. Feel for thrill immediately post-operatively & periodically thereafter. mobilisation of patient should be started as soon as possible. Bleeding: check FBC. 10. h.g. Padding should be placed around the limb with the access. If patient becomes fluid overloaded.2 Dialysis access This must be protected during surgery.3. Cryoprecipitate/ desmopressin ± packed cells may be given if indicated. b. Hypertension: Avoid intravenous nitroprusside in the treatment of severe hypertension to avoid thiocyanate toxicity. Post-op complications to watch out for in dialysis patients: a. g. Blood pressure cuff & iv lines must never be placed in the same limb as the access.

1.1 General Principles a.77 - . Effects of renal failure on pharmacokinetics of drugs: Effects of renal failure Altered bioavailability Altered volume of distribution (Vd) Comments • Changes in gastric transit time • Vomiting due to uraemia • Oedema increases the Vd of water soluble or protein bound drugs resulting in low plasma levels as the drug stays in the extracellular space • Acidic drugs are less protein bound in renal failure but basic drugs are unaffected by uraemia. • Reduces the nonrenal elimination of drugs by decreasing hepatic hydroxylation • Higher incidence of adverse drug reaction due to accumulation of active metabolites of the drug • Elimination of drugs excreted mainly by the kidneys will be affected Altered drug metabolism Reduced renal excretion The Cockroft-Gault formula (figure 11. 1 The Use Of Drugs In Dialysis Patients 11. USE OF DRUGS IN DIALYSIS PATIENTS AND TREATMENT OF ACUTE POISONING 11.11.1) may be used for the estimation of GFR: Creatinine clearance = (140-age) x body weight (kg) 0.85) .814 X Creatinine (umol/L) (For women: multiply by 0.

• Refer to the Table 11. • Loading drug dosage is similar to that of a patient with normal renal function. For other drugs.1. the maintenance dose can be given after each dialysis. in dehydration a smaller dose is needed) • Interval extension method: The usual dose is given at increased intervals • Dose reduction method: The dose is reduced with a normal dosing interval • 3-4 doses should be given before the plasma levels are measured to ensure that the steady state has been achieved.2 Drug Prescribing In Haemodialysis • Drugs which are dialysable will need to be given post dialysis • If no information is available regarding the drug. refer to drug insert or books on drug dosing in renal failure . Principles of drug therapy in renal failure • Drugs with extensive renal elimination will require dosage adjustment.b. 11. (If oedema is present a larger dose is needed.1 for drug dosing of antimicrobial agents.78 - .

79 - .1 Dosing of antimicrobial agents in renal failure .Table 11.

) .1 Dosing of antimicrobial agents in renal failure (contd.80 - .Table 11.

) Abbreviations: D = Dose adjustment. N/a = Not applicable .81 - . I = Dosage interval adjustment Dose after = dose as for GFR < 10 mls/min should be held until after dialysis No supplement = This means that the dose given is the same as for GFR < 10 mls/mi Nd = No data.Table 11.1 Dosing of antimicrobial agents in renal failure (contd.

11.3 Management includes bladder catheterisation. Removal of the offending agent b. Replace potassium as indicated Note: Close monitoring is mandatory including dextrostix. Supportive therapy eg cardiorespiratory support Peritoneal dialysis. abandon forced alkaline diuresis c. correction of fluid deficit and correction of acidosis with iv sodium bicarbonate a. hypocalcaemia.82 - . serum electrolytes etc . Maintain urine pH 7.5-8. hypomagnesaemia c. hypokalaemia. acid-base disturbances b.5L per hour during the first hour and adjust subsequent rate accordingly • 500ml of Dextrose 5% with 50ml of 8. Infuse in rotation at a rate of 1.2.11. CVP line.9% Saline • 500ml of Dextrose 5% b.2. Give iv furosemide 20-80 mg • If urine output does not improve.1 Treatment of the patient with acute poisoning is based on 3 main approaches: a. pulmonary oedema d.2 Treatment of acute poisoning 11.4% d. cerebral oedema Note : Use with caution in the presence of: • impaired renal function • cardiac disease 11. haemodialysis and hemoperfusion are be useful adjuncts in the management of acute poisoning.5 by giving 50mls boluses of intravenous sodium bicarbonate 8. iv infusion. electrolyte abnormalities eg.2.2 Forced Alkaline Diuresis This should only be used when specifically indicated eg. poisoning with weak acids (salicylate and phenobarbitone) as this is associated with risk of: a. Measure urine volume • If urine flow < 200 mls/hour reassess fluid balance with the help of a CVP line.4% Sodium bicarbonate • 500 mls of 0. Administration of antidotes c.

4 Extracorporeal elimination a.83 - . digoxin c. Grade 4 coma. a high flux dialyser should generally be used • Hemoperfusion . N-acetyl-cysteine for paracetamol poisoning • The toxic substance is irreversibly acting eg. hypotension. organophosphorus insecticide • The substance is a rapidly acting metabolic poison eg. This method will remove many lipid soluble and highly protein bound drugs more efficiently than HD. This may also prevent hypoglycaemia.11. The advantage of this system lies in the larger adsorbent surface compared to conventional hollow fiber dialyzer 11.This is a process whereby blood passes through a cartridge packed with activated charcoal or carbon. benzodiazepines • The drug has a large Vd eg. The cartridge should be primed with D5% in order to load the charcoal with glucose first.5 Haemoperfusion .2. The priming procedures depend on the manufacturer. hypothermia and hypoventilation in those who have ingested hypnotic drugs • Progressive clinical deterioration despite the best supportive management • Impairment of normal drug excretory function in the presence of hepatic. The use of extracorporeal elimination methods is not indicated in the following situations: • When an antidote is available eg. cardiac or renal insufficiency • Intoxication with an extractable poison which can be removed at a rate exceeding endogenous elimination by the liver or kidneys b. paraquat • The drug ingested is relatively non toxic eg. The hemoperfusion circuit is similar to the blood side of a HD circuit without the use of a dialysate. Clinical indications for the use of extracorporeal elimination methods: • Severe clinical intoxication eg.Treatment and complications a. Extracorporeal methods: • Peritoneal dialysis (PD) -efficiency is lower than haemodialysis or hemoperfusion • Haemodialysis – does not eliminate short and medium acting barbiturates and non-barbiturate hypnotics • A high efficiency dialyzer should be used and for larger molecular weight drugs. .2.

The duration of the haemoperfusion depends on the amount of sorbent.2).84 - . c. Generally prolonged haemoperfusion beyond 3 hours is unnecessary especially if the sorbent amount is less than 150 gm (see Table 11. More heparin is generally required than the conventional HD: bolus 2000-3000u followed by infusion to maintain ACT twice normal d.b. The complications of this technique include: • leucopaenia • loss of clotting factors • thrombocytopaenia • hypophosphataemia • hypouricaemia • hypoglycaemia • hypocalcaemia .

3 Drugs and elimination techniques Drugs Other findings Level Salicylates Mixed respiratory alkalosis with Metabolic acidosis.100.2 Hemoperfusion devices: Manufacturer Sorbent type Asahi Charcoal Clark Charcoal Gambro Charcoal Braun XAD-4 Smith and Nephew Charcoal Amount of sorbent 170 gm 50.Table 11. Table 11.300 gm 11.3 Summary of indications for elimination techniques: Different elimination techniques should be considered in adults depending on plasma concentration of the following drugs. Antidote is 4- 75-100 mg/l 100 mg/l Level FAD HD/HP Method of elimination Dialysis (HD) is indicated if > 30 gm is ingested or if there is metabolic acidosis or mental and 85 .300 gm 350 gm 100. ethylene glycol Other findings Metabolised to formic acid and lactic acid which causes optic nerve toxicity and lactic acidosis. Renal failure Coma in severe cases 500 mg/l 750 mg/l 900 mg/l Method of elimination FAD HD/HP HD/HP (2-3 x more efficient than FAD or PD) HP All barbiturates (except phenobarbitone & barbitone) Phenobarbitone or barbitone Drugs Methanol.250 gm 100.

HD = haemodialysis.usm. PD = peritoneal dialysis Adapted from Seyffart G.methylpyranole fundoscopic which inhibits changes the formation of lactate and formic acid. HP = haemoperfusion.my 86 . Dialysis and hemoperfusion in Poisonings For further information contact Poison Centre : Tel: 04-6570099 fax: 04-6568417 Email: prnnet@prn.4 gm/l HD hypotension is an important clinical indication for HD Lithium Dialysis reduces 5 mmol/l HD the levels rapidly but a rebound phenomenon may occur 60 mg/l HP Theophylline Correction of hypokalaemia is most important and may obviate the need for HP FAD = forced alkaline diuresis. Isopropanol Significant 0. Potson index.

g. 12. REHABILITATION ESRD patients undergoing haemodialysis are typically sedentary and functionally limited as a consequence of their condition. medical complication and fear of death 12. transplantation. self image and self esteem • Associated sexual dysfunction • Impaired activities of daily living and social function • Anxieties about vascular access.2. life expectancy. This requires the integration of excellent medical care. other patients and dialysis staff 12.1 As a result of the stresses.12. 12.2 Depression is the most common psychological complication in dialysis patients. patients have substantial psychiatric morbidity manifesting as: • anxiety disorders including phobic disorders (e. Renal rehabilitation is defined broadly in terms of optimal functioning of individual patients and restoration to productive activities.3 The 5 e’s of total rehabilitation: • Employment • Exercise • Education • Encouragement • Evaluation 87 .1 Psychological stresses of dialysis • Regimentation of dietary fluid and medication intake • Dialysis procedure • The illness itself • Multiple losses and threats of loss: job. needle phobia) • depressive disorders (often situational and reactive) • panic attacks • treatment regimen non compliance • suicidal crises • other behaviour problems such as violent behaviour towards own family. Exercise and antidepressants such as the newer selective serotonin reuptake inhibitors can play a potentially large role in the treatment of depressive symptoms. Rehabilitation attempts to restore an optimal quality of life.2. freedom. psychosocial and psychiatric care and occupational rehabilitation services.2 Manifestation of psychiatric morbidity 12.

endurance and flexibility. cycling and swimming is preferred 88 . • Exercise with the least physical stress on muscles. Aerobic exercise is an excellent means of improving the physical condition of these patients.5.4 Fundamental methods to achieve optimal psychosocial rehabilitation include: • Social worker to provide assessment. 12. anxiety and depression • Cardiovascular and muscle conditioning • Improvement of lipid profile and lowering of blood pressure 12.In patients who are employed.2 Precautions • Cardiac evaluation should ideally be done prior to the start of an exercise program.5 Exercise: Exercise and physical training can add to increased physical well being and should begin at the start of the dialysis period or preferably in the pre-dialysis period. counseling and other basic services • Availability of a Consultant Psychiatrist and/or Psychologist to the dialysis program • Regular case management meetings of a multidisciplinary dialysis team that includes all professional staff 12.5. 12. bones and tendons such as walking. restoring a substantial degree of strength.1 Potential benefits of exercise include: • Heightened sense of well-being • Lessening of stress. efforts should be made to maintain employment and vocational counseling should be provided to unemployed patients who are capable of working. Initial stages of exercise should be started under observation and prescription of a specialist.

Renal Rehablitation: Obstacles. AJKD Vol 35 . sildenafil. Alteration of sexual techniques and positions to overcome problems related to impotence.emphasise the non-physical aspects of demonstration of love. CR Blagg.1 Chronic dialysis patients commonly experience sexual problems such as: • diminished sexual desire • impaired sexual response 12.6 Sex. Dialysis & Transplantation. Exercise.2 Contributing factors to sexual dysfunction include: • psychological factors • anaemia • hindrance of CAPD catheter and AV fistula • endocrine dysfunction • drugs 12. Encourage the healthy spouse to act as the active partner in love making. Life Options Rehabilitation Advisory Council. The socioeconomic impact of rehabilitation.g. AJKD Vol 36. CAPD catheter and AV fistula. Rehabilitation and the Dialysis Patient.12. MUSE References 1. Progress and Prospects for the future. AJKD Vol 24 4. The Life Readiness Program: A Physical Rehabilitation Program for Patients on Hemodialysis.Suppl. Exercise and the ESRD patient.3 Management: • Counseling and psychosocial rehabilitation • Correct anaemia • Sexual counseling .6. Cont Dial Nephrol April 1995 3. contraception and pregnancy in chronic dialysis patients: 12. • Review of the use of drugs that contribute to sexual dysfunction • Consider non-pharmacological aids and potency drugs e. fertility. No 3 (September 2000) 5.3 March 1999 2.6. Vol 3 No.6.1 (April) 2000 89 .

Available data suggests that there is no increased risk of death in the dialysis patient who becomes pregnant.31(5):756-65.1 Prescription of dialysis during pregnancy • Six sessions per week • Minimise fluid shifts • Avoid hypotension and abrupt osmolality changes • Aim to keep predialysis blood urea < 17. 1991. 1994 Jan. 3. Giatras I. Am J Kidney Dis. Infant survival is about 40%. Okundaye I. Carlson JA.8 g/kg/day 13. Am J Kidney Dis. 13. Pregnancy during dialysis: case report and management guidelines. Pregnancy and dialysis. transplantation. Malone FD.7 mmol/l • Avoid hypokalaemia and alkalosis (Level C) 13. 1998.23(1):60-3.5 kg • After 1st trimester expected weight gain of 0. Jungers P. Davison JM. and pregnancy. Dialysis.4 Birth control & contraception a. diabetes or active SLE References 1.2 Targets • First trimester: minimal weight gain of 1 to 1.31(5):766-73. Women of reproductive age on dialysis should be counselled regarding pregnancy b.17(2):127-32. 1998. Birth control is advisable: • Barrier methods are the contraceptive methods of choice • Combined OCP is an alternative in the absence of hypertension. 1998. Hou S. Am J Kidney Dis. Levy DP. 4. Hou SH. Am J Kidney Dis. Registry of pregnancy in dialysis patients.3 Additional prescription • Daily protein intake of 1. 5. Nephrol Dial Transplant.45 kg/week • Target Hb 10 – 12g% • Consider elective delivery between 34 to 36 weeks 13.13.75 to 7%. 2. PREGNANCY DURING DIALYSIS Incidence of pregnancy in woman of childbearing age on dialysis is 0.13(12):3266-72. Bagon JA et al. 90 . Frequency and outcome of pregnancy in women on dialysis. Abrinko P.

5 • Geographical equity in dialysis acceptance.3 • % of patients have delivered KT/V > 1.2 • 95% of patients have discrepancy between prescribed and delivered KT/V that is < 20% • 60% of patients have BP< 140/90 • 70% patients have Hb > 8g% • No avoidable life threatening intradialytic event • 90% of reuse dialysers perform within 80% of specification • 90% of patients expressed confidence in competence of staff and satisfaction with service provided in annual Customer Satisfaction survey • Chronic HD capacity to patient ratio < 2 • Cost effectiveness ratio < RM 25. commensurate with available resources and consistent with current scientific evidence • Commitment to ensure all future patients with ESRD will be able to access the same high quality HD treatment service delivered at a cost that is affordable to even the poorest in our community 14. as measured by male to female acceptance ratio < 1.000 per life year saved • Publicly funded dialysis acceptance rate of 50 per million population by year 2003 • No gender bias in dialysis acceptance. as measured by highest state to lowest state acceptance ratio < 3 91 .14.2 Quality objectives: • Annual patient risk-adjusted mortality rate < 15 per 100 patientyears • Life expectancy no worse than 50% expected for normal persons • 30% of patients between age of 20 and 55 who were employed premorbidly could return to paid employment • 75% of patients have serum albumin > 40g/l • 50% of patients have serum PO4 < 1. QUALITY ASSURANCE PROGRAM IN HAEMODIALYSIS (In compliance with the requirements of ISO 9002 for Ministry of Health Haemodialysis programme) 14.1 Quality Policy • Commitment to achieve and maintain the highest possible standards of quality.6 mmol/l • 95% of patients have prescribed KT/V > 1.

safe UF coefficient.4 HD machine The pump for maintaining and controlling blood flow should be accurate at low flow rates (up to 20ml/min) 15. 15. PAEDIATRIC HAEMODIALYSIS 15. high degree of biocompatibility and a predictable relationship between clearance and blood flow rates • Total extracorporeal circuit volume is < 10% of child’s estimated blood volume (80ml/kg) i.1 Introduction Children comprise less than 1% of the total haemodialysis population.73m2) = 40 x height (cm) creatinine (umol/l) 15. They should ideally be dialysed in a paediatric unit with facilities and personnel relevant to the child. 15.2 Patient selection Generally all children can be accepted for chronic haemodialysis except those who have no potential for rehabilitation.3 Indications for starting dialysis • Fluid overload resulting in cardiovascular instability • Restriction of fluid intake resulting in inadequate nutrition • School absenteeism from uraemic symptoms • GFR < 10ml/min/1. extracorporeal volume is < 8ml/kg child’s body weight • Dialyser surface area (m2) = 70 – 100% of child’s body surface area (BSA) BSA = √ height (cm) x weight (kg) 3600 92 . The preferred mode of dialysis is peritoneal dialysis but chronic haemodialysis is viable in older children and in places where PD is not available.15.e.5 Haemodialysers • Should have a low priming volume and compliance.73m2 • Reduced growth velocity • Reduced head circumference • Neurological developmental delay despite adequate nutrition Calculated GFR (ml/min/1. good care can be given in integrated paediatric and adult units with specialised staff. In areas where the population is not sufficient to justify a separate unit.

femoral or subclavian approach.50 units /kg followed by 10 .20 units/kg/hour. Activated clotting time (if used) should be kept 150 .180 seconds • Ultrafiltration rate: maximum fluid removal per session should be < 5% of dry weight and rate of removal < 0. 15. Surface (m2) Fresenius Polysulfone F3 0.1 Temporary Appropriately down-sized venous cannulas (single or double-lumen) can be inserted percutaneously into vena cava via internal jugular.2 Permanent Refer to adult section 15.as in adults (18G – 14G) 15.10 Nutrition Refer to Chapter 31 93 .6 AM-SD 400M 0.3 Asahi AM-SD 300 0.2ml/kg/min 15.9 Method of dialysis • Blood pump flow = 5ml/kg/min • Priming of the blood lines is necessary if the child is anaemic.8 AM-SD 400U 0.8.1 Locally available paediatric dialysers Manufacturer Material Model No.8 Vascular access 15.or refer to normogram Table 15.7 Needles .4 F4 0. if extracorporeal blood volume exceeds the recommended amounts.0 F6 1. Whole blood or 5% albumin can be used.7 F5 1.8. • Heparinisation: bolus 20 .8 Volume (line)/ml 30 42 63 82 40 49 49 15.6 Blood lines Volume capacity of blood lines range from 13ml (neonatal) to 30ml (paediatric) to 120ml (adult) 15.

2 Children with short stature at onset of dialysis (height standard deviation score SDS < -1.12 Adequacy • Currently no published outcome data in children with ESRD to suggest that any measure of dialysis adequacy is predictive of well-being.13 Differences with adults: • Greater size differences and dietary variations with resultant larger variations in PCR and urea generation rate • Prescription of dialysis changes with growth • In small children with relatively high clearances. it is recommended that delivered dose of HD should be equivalent to a single pool Kt/V urea of at least 1. 15. Growth rates based on age and sex are higher than expected in the youngest patients who are transplanted.11. normal height velocity for age b. ‘catch-up’ growth for those who are short at onset of dialysis 15. recombinant human growth hormone (rhGH) (Level C) 15.1 The treatment goal for children on dialysis should include: a. the 2-pool model is preferred 15.3 • Higher Kt/V values which are relatively easy to achieve (relatively low V) may facilitate growth • Measured dose of dialysis delivery should be done 3-monthly 94 .15. morbidity or mortality • Achievement of numeric targets should not be the sole determinant of adequacy of care (Level C) 15. control renal osteodystrophy c.88): a. ensure adequate nutrition f. Aim to transplant early especially if young. control acid-base balance d.11. optimise dialysis b.14 Kt/V • In the absence of specific data. correct anaemia e.11 Growth Children with CRF are growth retarded especially if renal failure starts in infancy and if the aetiology is congenital renal disease.

15. 35: S105-S136 10. Alexander SR. Jiravuttipong A. Pediatr Nephrol 2001. Brewer ED. 34: 49-54 16. Handbook of Dialysis (3rd edition). Hemodialysis in infants and small children. 5: 167-171 15. Pediatr Nephrol 1999. Bunchman TE . Donckerwolcke RA. 8: 103-106 9. National Kidney Foundation. Goldstein SL. Pediatr Nephrol 2000. Am J Kidney Dis 2000. Espinosa P. Jones CL Natural logarithmic formula: not an alternative method for estimating Kt/V in paediatric haemodialysis. Nephrology 2000. Geary DF. Sharma AK Reassessing hemodialysis adequacy in children: the case for more. 13: 401-403 5. Blake PG. Warady BA. Tom A. 562-579. Lilien MR. K/DOQI Clinical practice guidelines for hemodialysis adequacy. Watkins SL Current advances in the therapy of chronic renal failure and end stage renal disease. ideas for the future. Van Hoeck KJM.Pediatric hemodialysis: lessons from the past. Secker D. 14: 280-283 13. Logarithmic extrapolation of a 15-minute postdialysis BUN to predict equilibrated BUN and calculate double-pool Kt/V in the pediatric hemodialysis population. Rodd C Multicompartment urea kinetics in well-dialyzed children. 6. 18: 341-354. Schroeder CH. Sorof JM. Kidney Int 2000. Ing TS. Warady B. Bunchman TE. Am J Kidney Dis 2000(suppl 2). 2000. Lippincott Williams and Wilkins 2. Watkins S. 8: 135-140 7. Sharma A. 53: S64-S67 8. 33: 518-522 95 . 16: 383-390 11. Bunchman TE An update on peritoneal dialysis and hemodialysis in the pediatric population. Curr Opin Pediatr 1996. Bell L. Am J Kidney Dis 1999. Warady BA.Hemodialysis for end-stage renal disease in children weighing less than10kg. Brewer ED Natural logarithmic estimates of Kt/V in the pediatric hemodialysis population. Daugirdas JT. Optimal care of the pediatric end-stage renal disease patient on dialysis. Goldstein SL. K/DOQI Clinical Practice Guidelines for nutrition in chronic renal failure. Am J Kidney Dis 1999. Al-Hermi BE. Kohaut E. Am J Kidney Dis 1999. Harmon WE. 33: 567-583 4. Am J Kidney Dis 2001(suppl 1). Semin Nephrol 1998. Brinkman DC. Pediatr Nephrol 1994.15 Problems of patients on long-term HD As for adults plus: • growth retardation • delayed sexual maturation • psychosocial problems References 1. 2001. Comparing a urea kinetic monitor with Daugirdas formula and dietary records in children. Kidney Int Suppl 1996. Al-Saran K. Sorof JM. Brewer ED Evaluation and prediction of urea rebound and equilibrated Kt/V in the pediatric hemodialysis population. 37: S7-S64 3. 36: 98-104 14. Goldstein SL. 58: 2138-2146 12.

McCauley L. Girardin C.J Pediatr 1999. Groothof J Long-term effects of growth hormone treatment on growth and puberty in patients with chronic renal insufficiency. Am J Kidney Dis 1997. Semin Nephrol 1996. 76: 125-129 24. 12: 304-310 22. Mulder P. Ronco C Chronic renal replacement therapy in children. 14: 701-706 20. Berard E. Brendolan A. Chevallier T. 54: 1690-1696 18. Gusmano R. Chan JCM Effects of uremia on growth in children. Bell L. Harmon WE Kinetic modeling of hemodialysis in children. Tom A. Port FK. Yu J. Espinosa P. Six-Beneton A. Rodd C. Fine RN Growth retardation in children with chronic renal insufficiency. Lilien M. Cochat P. Strawderman RL. Donckerwolcke R. Jones CA. Pediatr Nephrol 2000. Lewy JE. Broyer M Recombinant human growth hormone treatment of children on hemodialysis. Agodoa LYC. Crosnier H. which index is best for adequacy? Kidney Int 1998. Hokken-Koelega A.203 23. Ettenger RB. Pediatr Nephrol 1998. De Jong R. 16: 230-241 96 . Verrina E. 7: 392-397 19. Hanna JD. Sharma A Growth during maintenance hemodialysis: impact of enhanced nutrition and clearance. Krieg RJ. Held PJ Growth rates in pediatric dialysis and renal transplant patients. 30: 193. Semin Dial 1994. Alexander SR. Yu G. 134: 464-471 21. Nephron 1997. Turenne MN. Scheinman JI.17.

c.1 Haemodialysis Machines Over the years haemodialysis machines have evolved from a simple mechanistic model to one with sophisticated microprocessor controlled processes incorporating digital displays and many features that allow individualisation of treatment. (Different ratios are used in different models).2 The main components of haemodialysis machines The standard dialysis machine consists of a blood pump.83 parts of HCO3 and 34 parts of treated water. namely central delivery and individual proportioning system. 16.83:34.1. The usual flow rate is at least 250-300 ml/min and has a direct effect on the quality of dialysis. TECHNICAL ASPECTS OF HAEMODIALYSIS 16.1. dialysis solution delivery system and appropriate safety monitors. This must be done safely by constantly measuring conductivity and temperature of the dialysate 16. Heparin infusion pump: This is a continuous infusion pump used to infuse a certain volume of heparin into the predialyser segment of the blood line to prevent clotting in the extracorporeal circuit.g Drake Willock 480. b. deaerating and appropriate proportioning of dialysate and treated water.1 The main functions of haemodialysis machines include: a. Blood related functions: • To transport blood from the patient via the blood pump to the artificial kidney and back to the patient safely b. a. Dialysis solution delivery system: • Central versus individual proportioning There are two types of dialysis solution delivery systems. heparin infusion pump. e. Blood pump: The blood pump moves blood from the access site (AVF) through the dialyser and back to the patient. 97 . Dialysate related functions: • To prepare the dialysis fluid by heating. Baxter 450/550. Two different methods of proportioning are used:− Fixed proportioning –1:1. The haemodialysis machines available in all the haemodialysis units in MOH facilities are of the latter type.16. where one part of acid concentrate is mixed with 1.

T tubes attached to the blood line permit monitoring of pressure at various points in the blood circuit: − Arterial pressure monitoring: Arterial pressure guard monitors the adequacy of arterial blood supply. • Dialysis solution circuit − Conductivity: If the proportioning system that dilutes the concentrate with water malfunctions.− Servo assisted or feedback system where conductivity can be adjusted by the use of concentrate pumps and printed circuit boards. AK 95 • Heating and degassing Incoming water has to be heated to body temperature so that dialysate sent to the artificial kidney does not cool down the blood resulting in chills and discomfort to the patient. AK 90 . The purpose of the ABD is to prevent air which may have inadvertently entered the blood circuit from being introduced into the patient. Heated water has to be free of bubbles and deaeration chambers are used. This is located distal to the venous pressure monitor. TMP monitoring is utilised in many machines to maintain accuracy of fluid removal. TMP (Transmembrane pressure) = Venous pressure – dialysate pressure d. an excessively dilute or concentrated dialysis solution can be produced. • Negative pressure: Negative pressure is used to achieve ultrafiltration or removal of excess water from the patient’s blood. e. Monitoring devices: • Blood circuit Pressure monitors. A negative pressure pump and pressure regulators have been incorporated in the haemodialysis machine.g. The ABD is attached to a relay switch which automatically clamps the venous blood lines and shuts off the blood pump if air is detected. High or low conductivity 98 . and detects clotting of the dialyser when pressure monitoring is after the blood pump − Venous pressure monitoring: To detect any kink or clot in the venous line distal to the venous chamber To help in calculation of TMP To detect accidental separation of the blood line from the fistula needle Air bubble detector (ABD).

d. “Time settings” or “pressure settings” can be used to control inflow/outflow of blood.can result in high or low blood pressure and this affects the patient severely. Use of cold dialysate causes patients to complain of cold and shivers (chills). − Bypass valve: This valve is solely responsible for diverting dialysis solution directly to the drain whenever temperature/conductivity are out of set safe limits. Only one vascular access line (needle) is needed and the arterial and venous lines are kept either closed/opened one at a time.3 Options available for haemodialysis machines a. Thus temperature sensors are used for continuous monitoring and the dialysate is bypassed when out of safety limits. Ultrafiltration controllers (UFC): Two common methods used are volumetric method and electromagnetic flow sensors. The “two concentrate” approach in preparation of bicarbonate dialysate is standard. The machine should be able to monitor the conductivity continuously. Use of Bicarbonate cartridges is an alternative. The use of dialysis solution greater than 42°C can lead to haemolysis. It is standard in all new haemodialysis machines.1. b. − Negative pressure / TMP regulator: This consists of negative pressure pumps and regulators and continuously monitors the total TMP to achieve the desired goal for fluid removal 16. Single needle dialysis: This is not commonly used but is useful in patients with poor vascular access. 99 . Sodium profiling: This option permits rapid alteration of the dialysis solution sodium concentration and is useful in haemodynamically unstable patients. Bicarbonate: Bicarbonate dialysate is preferred. − Temperature: Malfunction of the heater element in the dialysis machine can result in production of excessively cool or hot dialysis solution. − Blood leak detector (BLD): This device is placed in the dialysate outflow line and detects any blood leak from the dialyser and activates an alarm. c.

Common methods are: a. • HDF can be thought of as haemodialysis in which massive fluid removal (20-30 litres) far exceeds the desired weight loss.e. muscle cramps. Blood temperature monitor g. post treatment fatigue is reduced − improved response to Epoetin − better haemodynamic stability − improved nutritional status f. Heat b.4 Sterilisation of haemodialysis machines Machines should be bleached/sterilised and decalcified after each dialysis or at least after the last dialysis of the day.If Qb=350 ml/min. Gambro Ak100/Ak200 Ultra System ultrapure water can be produced continuously by 3filter ultrafiltration.3 x 350 x 4 x 60 = 25 Liters • The advantages of HDF are: − greater blood purification − less β 2 microglobulin related symptoms by convective clearance of β2 microglobulin e.g reduces joint pain and carpal tunnel syndrome. It is used for on line preparation of (i) Replacement fluid and (ii) Dialysis solution by proportionating ultrapure water with Bicarbonate powder cartridge. Chemical • Formaldehyde • Sodium Hypochlorite • Peracetic acid 100 . • Volume of replacement fluid = 0. the volume of replacement fluid over 4 hours = 0.g. and fluid balance is maintained by replacement of ultra-pure solution. increases mobility − better treatment comfort-the incidence of hypotensive episodes.1. This is to minimise spread of infection.03 EU/ml endotoxin).1 CFU/ml and < 0. • Ultrapure water meets stringent criteria and contains <0. • With modern HDF machines e.3 (ultrafiltration ratio) x Qb. Blood volume monitor 16. Haemodiafiltration (HDF): • Haemodiafiltration combines the advantages of haemodialysis and haemofiltration to provide the largest amount of blood purification over a wide molecular weight spectrum achievable with present renal replacement therapy.

16. The air bubble detector should be in good working condition and able to detect microbubbles/air passing through the device and clamp immediately b. blood leak detector. To ensure machine is safe for use b. air bubble detector. The conductivity and temperature readings should be within acceptable limits and stable all the time to avoid loss in effective dialysis time g. negative pressure etc d. For on line HDF. To check all calibrations which include blood pump flow rate.6 The following is a set of criteria to determine if a haemodialysis machine is safe for use: a. All audible and visual alarms should be in good working order c. To cut down cost 16. Purpose: a.03 EU/ml 101 . The dialysate lines should be free of air bubbles i.5 Preventive maintenance All machines should have a check list for preventive maintenance and this must be adhered to strictly. To detect malfunctioning parts early and cut down mean breakdown time c.1. The blood leak detector should be able to perform its function accurately within set limits k. conductivity. temperature. The heparin pump should be able to infuse the prescribed volume of anticoagulant at the set flow rate d. the ultrapure water for replacement and sterile dialysate should have < 0. The blood flow rate and the dialysate flow rates should be accurate at all times e.1 CFU/ml and < 0. There should be no leakage of fluid from the hydraulics of the machine j. The dialysate pressure/TMP/UFC calibrations must be correct to facilitate removal of fluid according to set targets f.1. Venous monitor including alarm limits must be in good working order to facilitate TMP calculation and detection of positive pressure on venous lines h.

F8) the KUf is between 6-12 ml/mmHg/hour.1 Dialyser description The dialyser is a tube with four ports. In most MOH dialysers (e.2.16. polyamide (e.2. Surface area and priming volume d. The two compartments are separated by a semipermeable membrane. F6. Ultrafiltration coefficient (Kuf) c.g. polysulfone (e. c. creatinine. uric acid. 16.g. It is commonly named as regenerated cellulose. Sterilisation method 16.2 Membrane material: There are 3 three types of membrane currently used – cellulose.2. POLYFLUX 17 S) and polymethylmethaacrylate (PMMA). F6.F60.2. cuprammonium cellulose (cuprophane) and saponified cellulose ester b.g. “Substituted cellulose”: The most commonly used is cellulose acetate. Dialysers 16. Cellulose This first generation membrane used to be the most common type. The KUf for high flux dialyser is more then 20 ml/mmHg/hour (e. The types of dialysers are parallel plate dialysers. The following define the characteristics of a dialyser: a.g. coil and hollow fibre dialysers. “substituted cellulose” and synthetic membrane.3 Ultrafiltration rate (KUf) The permeability of the membrane to water is determined by the ultrafiltration rate coefficient (KUf). F60). Cellulose acetate being a substituted cellulose membrane reduces complement activation thus increasing the biocompatibility of the dialyser. F8.2. Two ports communicate with the blood compartment and the other two with dialysate compartment. They are manufactured from synthetic materials which include polyacrylonitrile (PAN). Clearance of urea. HF80) 16. cuprammonium rayon. phosphate and Vit B12 e. Currently all of the dialysers in the Ministry’s dialysis units are hollow fibre dialysers.4 Surface area and priming volume 102 . Membrane material b. a. Synthetic membrane These membranes are not cellulose based.

103 .8 m2 with a priming volume of 60-120 ml.5.5 Clearance of urea. 16. The commonly used size for adults is 15G. Dialysers can be reprocessed either by a semi-automated or a fully automated system.2. creatinine. Artery and venous blood chambers (without filters-for easy reuse procedure) c.3 Bloodlines 16.1 In our practice universal blood lines are used. 16. phosphate and Vit B12 The clearance of a dialyser is determined by the surface area.The membrane surface area of a dialyser determines the blood volume in the dialyser.1 Dialysers are reused for the following reasons: • To reduce cost of treatment • To reduce hypersensitivity reaction to ethylene oxide gas • To reduce complement activation. Artery and venous pressure monitor lines e. For adults the dialyser surface area is between 1.2. Heparin line d.3. membrane thickness and design (refer to manufacturers’ specifications) 16. 16.2-1. This is achieved through protein coating of the membrane surface. Infusion line 16. uric acid. Other forms of sterilisation include gamma irradiation and steam sterilisation. 16. This form of sterilisation causes hypersensitivity reactions in patients who are allergic to ETO.2 The priming volume of the bloodline in adults is between 100-150 ml.4 Artery and venous fistula needles Artery and venous fistula needles range from 14 – 18G. this includes anaphylactic reactions although this is rare.5 Dialyser Reuse and Reprocessing System 16. The components of the bloodlines are: a.3. Blood pump segment b.6 Sterilisation method The most common method of dialyser sterilisation is by exposure to ethylene oxide (ETO) gas.

There should be proper care in handling formalin or any other germicide that is being used. The disinfection cycle has to be manually activated and 2-3 % formalin is filled in over a period of 2 minutes. A good ventilation system is required 104 . it ends automatically 10 minutes after being activated c.5. rinses and cleans the dialyser of residual blood and blood products with RO water b. Separate machines should be used for the following patients:• Hep B negative & Hep C negative • Hep B positive & Hep C negative • Hep B negative & Hep C positive b. fills the dialyser with an appropriate concentration of a germicide. c. No fibre bundle volume (FBV) or pressure leak test is available 16. Eye goggles or face shields.2 Semi automated reprocessing system consists of solenoid valves and timer relays a. Sterilisation and calibration of the dialyser reprocessing machine should be done regularly g.5. tests the dialyser for leaks and performance parameters (fibre bundle volume). Always ensure that the correct strength of sterilant is used for disinfection c.5 Precautions when using dialyser reprocessing systems. d. The process is activated manually b.3 Automated dialyser reprocessing system a.5. The cleaning cycle consists of Fast Rinse and Reverse Ultrafiltration (RUF) modes. a. All working areas in the reuse bay should be kept clean of blood and other biohazard materials e. face mask.4 Policies and Procedures in reprocessing dialysers There should be policies and procedures to ensure safety and effective operation of a reuse programme 16.16. Reject dialyser if FBV <80%. apron and gloves should be used. f. Reverse osmosis water should be used d. 16.5.

tight or free • amount of fluid removal required • duration of treatment • special orders e. THE HAEMODIALYSIS PROCEDURE 17.2 Vital signs observation: a. BP > 200/120 mmHg) requires medical attention • Countercheck with the patient regarding the antihypertensive drugs prescribed. BP < 90/60 mmHg) or severe hypertension (e.g. Body weight • Interdialytic weight gain should not be more than 3% of the dry weight • No weight gain may indicate good urine output. ECG monitoring may help to confirm the findings. blood transfusion. normal.1.2 Starting the patient on dialysis 17. iv therapy 105 .1. Body temperature • Hyperpyrexia requires medical attention to determine the source of infection and may require antibiotics d.17. poor oral intake or gastrointestinal loss • Excessive weight gain requires a check on oral intake of salt.1 Before commencing treatment note the haemodialysis orders: • hepatitis B.g. bicarbonate.1 General observation on receiving the patient: • Greet patient • Is he/she comfortable? • Is he/she able to walk into the unit? • Any signs of fluid overload? • Any signs of being unwell? • Is there any unusual reaction? 17. sequential ultrafiltration.g. fluid. c. volume and rate may require medical attention.g. diet and iv therapy if any 17. Pulse rate • Any abnormalities in rhythm.g.2. low calcium • heparin regime e. the dosages and the time of the last dose b. hepatitis C and HIV status • blood access • dialysate regime e. Sitting and standing blood pressure • Hypotension (e. acetate.1 Pre and post procedure checks 17.

g.g.2 Check the function of the haemodialysis machine • • • • • • • temperature conductivity blood leak detector air detector blood pump dialysate flow rate arterial. TMP monitors 17.3 Preparation of the required items • Choose the correct dialyser e.1 On the patient: To ensure that patients remain comfortable and in stable condition. type of membrane.3 Observations while on treatment 17. clearance • Use the correct haemodialysis concentrate • Ensure correct heparin dilution 17. close monitoring will help to reduce unwanted incidents e. surface area.2.g.2.2. KUf.4 On commencing treatment: • Aseptic procedure must be observed during needling • Record starting time • Record blood flow rate • Check all monitors are properly set • Set required ultrafiltration rate • Set up heparin infusion as required • Set air bubble detector 17.2 On the machine: Two hourly monitoring of the progress of treatment • remaining treatment time • venous pressure • arterial pressure • blood flow rate • TMP • heparin • extracorporeal blood condition e. blood clots 106 . clotting dialyser and unnecessary blood loss • Check vital signs at least 2 hourly 17.17.3. venous.3. hypotension.

4 Isolated/sequential ultrafiltration 17.001ml of blood • concentrate is saved during sequential ultrafiltration therapy due to inactivation of the concentrate pump 107 .4. The advantages are: • it gives fast relief of pulmonary oedema • it maintains a constant blood pressure in sipte of a large amount of fluid removed rapidly • better tolerance by the patient due to constant blood electrolytes as the dialysate does not flow through the dialyser 17.2 There are two methods of performing this therapy: a. by using an external vacuum pump The disadvantages of using an external vacuum pump are: • negative pressure is set between 400 to 780 mmHg and the danger of dialyser rupture is high • there is no blood leak detector.4. It is best performed before haemodialysis. If blood leak occurs there is significant amount of blood loss. by using the automatic device which is incorporated in the haemodialysis machine • the negative pressure is kept within 450 mmHg to prevent the risk of dialyser fibre rupture • the ultrafiltration rate depends on the KUf on the dialyser used • the blood leak detector is functioning and this detects 0. b.17.1 Definition It is a process of removing excessive body fluid before or after the actual dialysis procedure.

and accelerated atherosclerosis. 108 . The water quality standards for hemodialysis must be more stringent than drinking water since the largest contact material that the blood is exposed to during hemodialysis is the dialysis fluid. 18. To help prevent these events from occurring. The possibilities of dialysis patients exposed to greater levels of bacterial and endotoxin has increased tremendously during the last two decades with the increase in reuse. Water quality however is not limited to microbiological quality. malnutrition. is a state of chronic inflammation that may contribute to progressive inflammatory diseases in chronic renal failure such as β2-microglobulin amyloidosis. but also chemical quality.2 Quality standards for microbial purity 18. high flux dialysis and on-line replacement fluid. and all dialysis centers should develop good surveillance policies. The role of microbial contamination of dialysis water has been greatly underestimated in the last three decades. the use of bicarbonate dialysis fluid. standards for maximum allowable bacterial and endotoxin contamination must be established.1 Introduction Water use for conventional haemodialysis should be at least complied with the minimum requirements of AAMI (European Pharmacopoeia standard should be adopted if possible). The consequences of bacterial contamination besides acute pyrogenic reaction. AAMI stated that water used for diluting concentrated haemodialysis solution should have a total viable microbial count of no more than 200 cfu/ml. and that the concentration of endotoxin should be no more that 2 EU/ml.2. protein catabolism. unacceptable levels.18 WATER TREATMENT 18. While the action level are 50 cfu/ml for total viable microbial count and 1 EU/ml for endotoxin levels.1 Introduction From the early days of dialysis it is known that water used for hemodialysis must be purified. Action level denotes the concentration of a contaminant at which steps should be taken to interrupt the trend toward higher.

polyvinylidine fluoride. polypropylene. polyvinyl chloride) or appropriate stainless steel. and does not crack with age.2. treatment devices. 18.5 VC (CFU/ml) AAMI Action level* 50 European 100 1.4 Design Steps in preventing biofilm formation include the use of pipe work with linear configuration.Standard fluid Water Concentrate Viable counts (VC) ET VC (CFU/ml) (CFU/ml) (EU) 2000 200 (bicarb) 200 Dialysis Endotoxin (ET) ET (EU) 2 1 0.03 IU/ml for endotoxin levels. Dead spaces and area of slow flow and turbulence such as sharp bends should be eliminated. and precautions should be taken against the formation of biofilms. These include such materials as plastics (acrylonitrile-butadienestyrene. If unavoidable.25 0. pipes. Storage tanks should be avoided where possible.1 cfu/ml for total viable microbial count and <0. However. then an option to switch to direct feed by 109 . storage tanks and dialysis machines. 18. a smooth surface that resist corrosion.2 Biofilm The treatment system must be regularly disinfected. Avoidance of uneven surfaces such as ridges or grooves particularly at the joints is recommended. Level B 18. regenerated and changed.25 In ultrapure dialysis fluid. and are extremely difficult to remove. They form easily in any crevice or corner of containers. polyethylene.3 Material The materials of any components of water treatment systems that contact the purified water should be unreactive in nature to prevent contamination of the product water. Filters and resins must be periodically cleaned. the use of ultrapure water is strongly recommended for conventional and high-flux dialysis to prevent and/or delay the occurrence of dialysis related complications. small diameter with loop system favouring continuous high speed water recirculation even when dialysis facility is closed.2. the limits are <0.2.

A combination of a variety of water treatment devices is needed to produce water that fulfills the established standard for chemical purity for dialysis. cone shape base).bypassing the tank is recommended. 110 . dialysisproportioning machine.5 Ultrafilter In order to minimize chronic inflammation. which include: o regular cleaning of the tubing with detergent to remove organic deposits o descaling with acid solution o disinfection with chemical/or heat-sterilizing agent o a good quality assurance programme that involves all dialysis staff. and the electrolyte concentrate.3. pipe distribution system.1 Introduction Water use for conventional haemodialysis should comply with the requirements of AAMI/European Pharmacopoeia standard. (refer Appendix 1) Drinking regulation standards for water are based on a weekly exposure of 14 L with a selective gut barrier. prevention of microbial proliferation and biofilm formation relie on: • the use of two ultrafilters placed in series on the dialysis fluid pathway • regular disinfection and hygienic maintenance of the water treatment system. Storage tanks should be designed to minimize bacterial growth and facilitate routine disinfection (e. Furthermore dialysis patients having no urinary excretion ability are exposed to high risks of toxic substances accumulation. require strict protocol. Hence water used for dialysis must comply with more stringent criteria. good documentation of results and prompt corrective actions when necessary 18.g. Ultrapure dialysate is a prerequisite for on-line haemofiltration or haemodiafiltration. The production of UPD.3 Quality standards for chemical purity 18. while hemodialysis patients are regularly exposed to 300-400 L per week through nonselective dialyzer membrane.2. use of ultrapure water is strongly recommended for all dialysis modalities. Level C 18.

18. The tank should be regularly inspected for dirt particles etc and cleaned at least once a year. The minimum size should be 1500 Litres to 2000 Litres and come complete with cover. and chloramines from water supply. chlorine. a. also known as sediment filters or sand filters. iii) Softeners Softening of the incoming water is necessary to avoid the “hard water syndrome” suffered by dialysis patients due to dialysis water contamination with calcium and magnesium. activated carbon filter and microfilters • Primary Treatment involving one or more Reverse Osmosis devices • The Distribution Loop for reverse osmosis water supply to the HD stations. softener.) Raw water storage tanks The material used should be of stainless steel (grade 304) or High density polyethylene (HDPE).3. iv) Activated carbon filters Activated carbon filter is usually used as pre-treatment for removing dissolved organic contaminants. ii) Filters Pre-filters. Pre-treatment i. Carbon adsorption beds (tanks) should be sized for the 111 . sediment filters. The tank should be placed in a clean and safe environment with direct feed from the nearest main supply. remove large particles ranging from 500 micron down to about 5 micron and are generally employed to remove particles and prevent fouling of devices further downstream.2 Treatment devices The decision making process requires three key input parameters: • the purity of the water required • the quality of the municipal water supply (chemical and microorganism levels) • the amount of water required Water treatment systems can be divided into three sections: • Pre-Treatment consisting of raw water storage tanks. and to prevent calcium carbonate scale formation on other water treatment devices downstream.

and pure water forms on the product side. Distribution loop The product water distribution system should not contribute chemicals such as aluminium. All RO membranes are designed for cross-flow filtration so the feed water is separated into two streams: (a) permeate (RO water) of purified water which has passed through the membrane. and minimum rejection levels should be set. They also prevent bacteria and endotoxin passage. and the new tank placed in the last position. and the goal is 6-12 minutes (3-6 minutes per working and polishing tank(s)). The RO should provide AAMI quality water. Upon exhaustion (chlorine/chloramines breakthrough) of the first tank. the carbon media should be discarded and replaced with new.maximum of two tanks in a series configuration (one tank feeding the next) A sample port for testing the water after the first tank and before the next tank should be in place. Primary treatment i) Reverse osmosis units RO units are the most effective method of treating water. The RO membrane should be regularly flushed to prevent layering of contaminants on the membrane surface as these would reduce the effectiveness of the membrane. copper. It is advisable to use either stainless steel or crosslinked polyethylene (PEX) material for the piping system. Conductivity is the vital measurement for an RO. and (b) concentrate which has a high concentration of contaminants. or bacterial contamination to the final product water. Dissolved solids are unable to pass through the membranes enclosed. zinc and lead. A formula is used to determine Empty Bed Contact Time (EBCT). Both direct (no storage tank) and indirect (storage tank system) water distribution systems should be configured as a continuous recirculating loop designed with the proper flow and velocity to minimize bacterial proliferation and biofilm. v) Microfilters Microfilters remove intermediate sized particles of 5-1 micron in diameter and are situated in the pre-treatment and primary treatment sections of the system in order of decreasing particle size cut-off. No dead 112 . virgin carbon. b. c. The second tank should be moved to the first position.

microbial testing ideally should be carried out at least once a month. 18. The entire system should be disinfected at least once a month. Disinfection times should be according to the disinfectant instruction for use and the membrane manufacturer’s instructions for use. 113 . ensure removal of disinfectant from the system before use and verify with a test strip. • • b. After the required dwell time. 18.b and 18.3. including the distribution system and the connections to the dialysis machine.4.1 Control of Microbial Quality a.c) • The water treatment system should be designed to allow routine disinfection of the entire system.2. Ozone. a separate chemical tank with pump facility should be used.c) For a newly installed water treatment system and distribution system. System Disinfection (refer 18.Peracetic Acid (2-3%).3. before it enters the water system. Testing must also be frequent enough to pick up changes in the trend. Sodium Hypochlorite (500ppm) .2.ends or multiple branches should exist in the piping system. through to all supply outlets and diverted back to the chemical tank via the RO return loop.2. Germicides for disinfecting water systems include Formaldehyde (2-3 %). After completion of the validation. The disinfectant should be distributed to all lines and tested positive for presence of disinfectant. Chlorine dioxide and Hot water (> 80oC) To disinfect the RO water distribution Loop.4 Maintenance and Quality Control 18. The RO should be disinfected separately. and the use of simple wall outlets with the shortest possible fluid path and minimum pipe fittings are recommended.a. Hydrogen Peroxide. Frequency of microbial testing (refer 18.3. the microbial testing should be done at least once a week as part of the validation procedure for the disinfection programme. The disinfectant is introduced post RO membrane at the permeate side.2.4. • To disinfect the RO membrane a separate clean disinfectant tank is usually needed.

4.1.O sampling valve. timing and technique i). • Sampling Site o Point A Feed water (raw water) 114 .O sampling valve • Technique Using HANNA Hardness Kit o Collect water sample from sampling point into a 50 ml plastic container supplied (See diagram 2 below). o Open the Free Chlorine Test kit and check for damage. Sampling location. Daily test for hardness (Total Dissolve Solids) • Sampling location o Pre R. o Add 5 drops of reagent 1 and 3 drops of reagent 2 to the colour comparator cube. o Calculate total hardness : o Volume of titre x 30 = _________mg CaCO3 (Refer figure 18. o Titrate water with reagent supplied from a 1 ml syringe. o Note volume of reagent used after the colour change.4. (Refer figure 18. o Add 1 drop of solution B. o Observed colour change from purple to blue while adding reagent from syringe drop by drop. o Add 5 drops of solution A. Daily test for chlorine • • Sampling location o Pre R.1.i) ii). Technique Colorimetric (Using HANNA Free Chlorine Test Kit) o Run the R.c.c.i) iii). Monthly water analyses • Water for microbial analyses Samples shall be collected at a point where water enters the equipment or any point where product water is dispensed.c. o Fill the colour comparator cube with water sample from POINT A (See diagram 1) o Replace the cap and mix by carefully swirling the cube in tight circles and inverting it several time. o Determine which colour band best matches the solution in the vessel and record the results in mg/L (ppm) free chlorine.O system at least 10 to 15 minutes.

iv).c.O water First distribution point Middle distribution point Last distribution point Sampling technique (refer figure 18. Technique of culturing water-borne microorganisms i).g.o Point B o Point C o Point D o Point E o Point F • - Pre treated water R.iii) • Chemical contaminants analyses Collect sample from point C and send to analytical laboratory d.1. Collect mid stream water from sampling valve into a sterile container. Six monthly Water Analysis (refer figure 18. sterile sample tube etc. Many factors influencing the detection and quantification of micro-organism Factor Sampling place Sampling hygiene Sample storage Recommendations Direct access to the stream to be sampled. Repeat step 2 and 3.c. Samples shall be assayed within 30 minutes of collection or shall be immediately stored at 4-6 C and assay within 24 hours of collection. 24-28 C up to 7 days for water bacteria) Sample size Choice of culture medium Conditions of incubation 115 .g.4. Flush sampling valve for another few second. Immediate storage of the sample at 4 C and plating of the samples within 24 hours ( to avoid additional growth) Sufficient sample volume Appropriate culture medium ( e.4.iii) o o o o o o Flush sampling valve for a few second.1. avoidance of stagnant flow. flushing of the port Cleaning of the sample port with a bactericidal agent. Swab sampling valve nozzle with 70% alcohol or povidone iodine. nutrient for Reasoner’s 2A agar or standard methods agar for water bacteria ) Appropriate length and temperature of incubation ( e.

• As microorganisms can continue to grow in samples it is necessary to cool samples in the fridge and analyze microbial counts within 24 hours. • Pour plate technique 1 ml of undiluted sample and samples in different dilutions are added to 10 ml of the appropriate medium agar and mixed. • Standardize and document all procedures including: o sampling technique o sampling time points.g. ii). on Monday/Saturday after a long shut-down period o personnel responsible for sampling o sample storage and transport o methods for laboratory analysis o data interpretation and action protocol • Document the cleaning and disinfection procedure for the water treatment and delivery system. Endotoxin samples can be frozen and stored for a longer period of time. 72 and 168 hours. • Take an adequate sample volume: this is at least 10 ml for the determination of microbial counts and 3 ml for determining the endotoxin concentration. Determination of colony forming units (CFU) Viable microorganisms are assayed by three different methods with subsequent culturing on plates.1 to 1 ml of the aseptically collected sample are distributed over the surface of 15 ml dried culture agar on 9-10 cm culture plate with a sterile glass spreading rod. as well as any changes made.Proper sampling procedures involving sampling process. • Spread plate technique 0. The agar 116 . sample storage and transportation are all of importance. The plates are then incubated at 24 C for 7 days and colonies are counted at 48. • Samples must be transported/stored in sterile and pyrogen-free containers. • Implement aseptic conditions during sampling o disinfect hands and sampling ports with disinfectants (alcohol swab/spray) o do not use ports which cannot be properly disinfected or rinsed o rinse tap ports with an adequate volume of sample medium prior to sampling. e.

45 µm and effective in retaining microorganisms. Recoveries of bacteria compared to the counts obtained with the spread plate method may. is essential components of the cell wall of gram negative bacteria. iii). be decreased. is a state of chronic inflammation that may contribute to progressive inflammatory diseases in chronic renal failure such as 117 . the use of bicarbonate dialysis fluid and high flux dialysis. It can be more important to test water and dialysis fluid for endotoxin than for bacteria as bacteria do not pass through intact dialyzer membrane readily. Disadvantages of the method are that the organisms are submerged in the agar and the colonies tend to be smaller and do not show colony morphology characteristics. Nutrients diffuse through the filter so that colonies can grow on the filter surface. whereby it should be ensured that the filter is not inverted. or lipopolysaccharides. Why Endotoxin.should be held at 43 C in a water bath before use. • Membrane filter method Sample volumes greater than 1 ml is filtered through a sterile membrane with a pore size not greater than 0.Agar ( R2A) o Standard Method Agar ( SMA) o Tryptone Glucose Extract ( TGE) Sample incubation o At lower temperature (24-28 C ) o Duration: 7 days • e. The possibilities of dialysis patients exposed to greater levels of these microbial products has increased with the increase in reuse. which when enters the patient’s blood stream it can cause pyrogenic reactions. Measuring endotoxin levels i). The sample/agar mixed is poured onto 9-10 cm culture plates and incubated under the same conditions as described for the spread plate technique. The consequence of microbial contamination besides acute pyrogenic reaction. This filter is transferred under sterile conditions onto the appropriate culture medium on plates. Media for culturing water/ dialysate samples • Nutrient-poor agar o Reasoner’s 2. therefore.

a water softener removes calcium and magnesium by ion exchange from the feed water before it reaches the RO system. In the gel-clot method. How Bacterial endotoxin levels should be monitored using the Limulus Amoebocyte Lysate (LAL) assay.0) or dialysate concentrates with high salt content will inhibit formation of gel clot and give false negative results. However the LAL assay will not detect all pyrogenic substances derived from bacteria. 18. iii). 118 .2 Control of chemical quality a. and the pH of the sample is 6 to 7. and there are no inhibiting substances. ii).4. Water softener In typical water treatment configurations.β2-microglobulin amyloidosis.5. If the endotoxin levels in the dialysis fluid are significantly higher than in the water feeding the machine. However. Other LAL tests include the colorimetric and turbidimetric assays. Dialysis fluid samples should also be tested if a patient experiences a pyrogenic reaction during dialysis. The procedure described by the particular LAL manufacturer must be followed exactly. If sufficient ET is present. provided staff has received the necessary training. Chemical germicides with low pH (<6. The simplest form of LAL assay is the gel-clot test which can be performed in the dialysis unit. The excess calcium and magnesium in "hard" water must be removed to prevent patient injury. When Dialysis fluid should be tested routinely for endotoxin to monitor the efficacy of the dialysis machine disinfection procedure. and accelerated atherosclerosis. It is necessary to run appropriate assay control samples. a complex enzymatic reaction occurs. the disinfection schedule or the method used should be modified. protein catabolism. the solution will turn into a gelatinous clot. Hands on training of personnel are important. when a fluid sample containing ET is mixes with lysate from the blood of the horseshoe crab (Limulus polyphemus). Filter and resin maintenance i).

There are several literature reports of patient injury or death due to hemolysis when facilities did not adequately remove chloramines before initiating dialysis (FDA 1988). The AAMI -recommended maximum contaminant level for chloramine is 0. and regeneration of the water softener without bypass during treatment time. Confirm daily that there is an adequate supply of salt in the brine tank. resulting in a large sodium concentration in the softener effluent stream and potentially causing severe patient injury or death due to hypernatremia These risks can be minimized by the following monitoring and maintenance activities: • • • • Cheek the clock on the regeneration timer daily to ensure the proper setting. and some organic substances. resulting in increased hardness late in the cycle before regeneration. Check the hardness of the water softener effluent daily before beginning dialysis. Record this information on the daily water treatment log sheet.the primary practical reason for removing these ions is to prevent them from "plating" on the RO membranes. the results of excessive chlorine or chloramines are well known. resulting in high calcium or magnesium content in the water improper sizing or improper regeneration scheduling of the softener. resulting in deterioration of performance. Carbon filtration Granular activated carbon (GAC) is used in water treatment systems to remove chlorine. Each 119 .1 milligrams per liter (mg/L). The following risks are associated with the water softener: • • • failure of the softener. Validate the appropriate sizing of and regeneration schedule for the softener by periodically checking the hardness of the water softener effluent at the end of the treatment day. Use only salt designed for water softeners. While little has been published regarding the risks associated with organic materials in dialysis water supplies. chloramines. ii). Two tanks filled with granular activated carbon should be used in series.

and surveillance practices: • To prevent algae growth. arrangements should be made to replace the first tank. use only opaque housings on sediment filters. • Incorporate pressure gauges before and after all sediment filters. carbon fines. Sediment filters The sediment filter is usually placed just before the RO system to prevent dirt. The effluent of the first tank should be monitored before every patient shift to ensure that the chloramine content is below the AAMI standard level. bacterial endotoxins. If that water meets the AAMI standard. To prevent excess bacterial growth and to prophylactically guard against other contaminant build up. iii). resulting in excessive pressure build up and filter failure and thus the flushing downstream of dirt and other debris trapped by the filter. viruses) at a rate of 120 .1 mg/L. suspended materials. dialysis can proceed. If the level of chloramine exiting the first tank exceeds 0.of these tanks should have a minimum empty-bed contact time (EBCT) of 3 to 5 minutes. Whenever the pressure drop between the two gauges exceeds 10 pounds per square inch (psi) or the value recommended by the manufacturer. the filter should be changed. or other matter from damaging or plugging the RO membranes. maintenance. a sample should immediately be drawn from the water exiting the second tank. and monitor pressures at least daily. many manufacturers recommend that the filter be changed monthly even if the pressure drop does not exceed 10 psi. iv). pieces of water softener resin. Reverse osmosis systems Reverse osmosis systems use pressurized filtration (pressures capable of overcoming the osmotic pressure of solutes) to remove chemical contaminants at a rate of 95% to 99% and microbiological contaminants (bacteria. that water must not be used for dialysis. If the chloramine level in the effluent of the second tank also exceeds 1 mg/L. The risks associated with sediment filters can be minimized by the following design. Risks associated with sediment filters include algae growth in the filter housing and clogging of the filter. however.

the cause of the change should be determined and addressed. and document the results.g. resulting in either reduced flow rates or some passage of chemical contaminants. a water softener to remove excess calcium and magnesium. maintenance. which could result in a percent rejection level lower than that needed to produce "chemically safe" water for hemodialysis. and monitoring practices: • Employ appropriate pre-treatment components to protect the RO system and optimize its performance (e. • Periodically perform a quantitative analysis of the chemical contaminants listed in the AAMI standard (table 1). • progressive membrane failure. which could clog the RO system. Such alarms also alert the dialysis staff to any massive failure of the system. Performing a reduction ratio analysis on "worst-case" tap water will allow the dialysis staff to estimate that minimum percent rejection level. particulate filtration for removal of silt. These risks can be minimized by the following design. carbon filtration to remove excess chlorine. • bacterial colonization. • Equip the RO system with a continuous monitor for conductivity. which would "scale" on the RO membrane. and. Data on such parameters as pressure and flow rate are important in evaluating the safe and effective operation of the system.. which can be set to activate visible and audible alarms if the percent salt passage exceeds two times that validated when the membranes were initially installed. © 1998 Association for the Advancement of Medical Instrumentation AAMI WQD 121 . resulting in possible pyrogenic reactions or septicaemia. Such alarms indicate to the facility that cleaning or other service of the RO system may be necessary to maintain proper operation and cost-effectiveness. • Monitor other RO system parameters daily.approximately 99%. allowing large amounts of chemical or microbiological contaminants to pass downstream. The following risks are associated with the use of RO systems: • membrane failure. which would also damage the RO membrane. Whenever any significant change occurs in pressure or flow rate. a temperature-blending valve to assure a feed-water temperature for optimum RO system performance).

pressure < 15 psi) o Product water pressure (20-40 psi) o RO filter pre / post (max. R.b Frequency of maintenance and testing i). iii) Monthly • • • Change guard filter if the pressure difference is more than 15 psi Change bacteria filter at the R. storage tank if pressure difference is more than 15 psi.O. Weekly Maintenance • Multimedia Sand Column Manual / Auto regeneration (backwash) 3x/week (Monday. Wednesday & Friday)* • Carbon Column Manual /Auto regeneration (backwash) 3x/week (Tuesday.O. • Document in R. o Reject water flow rate o Product conductivity o Test hardness of post-softened water o Test the chlorine/chloramines of the product water ii). water for bacteria culture and endotoxin level. (40gm in 10 liters of water) 122 .O. Water daily log sheet o Raw Water pump pressure (30-90 psi) o Guard filter in / out (diff. Daily • 15 minutes after starting R. Thursday & Saturday)* • Softener resin Manual /Auto regeneration once per week (Sunday)* • Municipality water Frequency depends on pre and post pressure difference of column. Check the UV light at the R. 3 Monthly • Chemical wash of the R.* iv). 15 psi) o Product water flow rate.O. storage tank. membranes with Citric Acid and NaOH. diff. chlorine and hardness test.O.O.

o Indication: hardness test positive after a few regeneration of softener resin for a few days. Carbon Column o change as recommended in the service manual which is usually once in 2-4 years.4.v).1. Sampling location. Softener Resin change as recommended in the service manual which is usually once in 2-4 years. c. timing and technique (refer 18. vii). 6 Monthly • Inspection of the Raw water tank o physical examination of the raw water tank o ball float valve o presence of impurities in the water o cleaning of the tank if necessary Pre and post R. o indication: chlorine/chloramine test positive or traces after a few regeneration of carbon column for a few days. water for analysis inclusive of TBC and Endotoxins o AAMI standards Disinfection of R. water distribution piping o peroxide base disinfectant – 3% o formaldehyde – 4% • • vi). viii).O.c) 123 . Multimedia Sand Column o change as recommended in the service manual o depending on the usage but usually once in 2-4 years.O.

flow should divert to drain in the event of bed exhaustion. there should be an audible and visible alarm and permeate flow should divert to drain. audible and visible alarm should be provided to indicate bed exhaustion. or an alarm should sound. and chlorine/chloramines should be monitored after every shift. • Failure analysis of the complete system must demonstrate safe operation in the event of a single component failure.Recommended Features of Water Purification Systems Component/System Feature • A Total Dissolve Solids (TDS) indicator should be provided for product quality as well as percent rejection • The TDS alarm should be temperature-compensated Reverse osmosis • Whenever the product quality alarm is activated. Complete system 124 . maintenance. Carbon filters Water softeners • Two tanks should be installed in series (i. Deionization • If used for primary purification.5 Checklist FDA. worker/polisher configuration). • Each component of the system must be labeled with the name and address of the supplier. • Regeneration lockouts should be included • Product water must meet all applicable industry and government standards and should pass a leachables test. • A temperature-compensated. • Deionization should only be used when carbon filters are installed for pretreatment (to prevent formation of nitrosamines).18. • All water-contact materials should be appropriate for this use and should pass a leachables test • There should be a 6-minute empty-bed contact time (EBCT) for chlorine removal and a 10-minute EBCT for chloramines removal. • The user must be supplied with clear and adequate instructions for startup. and troubleshooting of the system. • All water-contact materials should be appropriate for this use and should pass a leachables test. • Ultrafilters or submicron filters should be provided on the product water output line for removal of bacteria and endotoxin. monitoring.e.

WATER TREATMENT SYSTEM LOG Mon DATE VALVES OPEN Water Supply Raw water tank inlet Raw water pump inlet/outlet Sand/Carbon/Softener Guard filter inlet SERVICE MODE / TIMER CHECK Multimedia Sand column Softener resin Carbon column 1 Carbon column 2 Brine tank (adequate salt) GAUGE READINGS Pressure pre multimedia sand Pressure pre softener Pressure pre carbon 1 Pressure pre carbon 2 Pressure Guard filter in Pressure Guard filter out Pressure pre RO filter Pressure post RO filter Permeate pressure Permeate flow Reject flow Permeate conductivity WATER TESTS Post Softener Hardness LOGGED BY: CHLORAMINES TESTS (<0.1 mg/L) Before 1st patient shift (initials) Before 2nd patient shift (initials) Before 3rd patient shift (initials) AUDITS (initials) * Suggested daily water treatment system log Tue Wed Thu Fri Sat 125 .

i: Pre R.4.1.O membrane 126 .Figure 18.O sampling valve (daily test for chlorine and hardness) Raw water Dialysis machines Sediment filter Carbon Filter (x2) Softener Sampling R.c.

Figure 18.1.4.iii: Sampling sites for water for microbial analyses E Dialysis machines Raw water A F D Sediment filter Carbon Filter (x2) Softener R.O membrane B C 127 .c.

Lead.001 0.005 0.09 0.2 mEq/L) 70 (3. Zinc Aluminum Arsenic. Barium.00 0. CHEMICAL CONTAMINANTS MONITORING • Should be performed at least yearly if prepared by DI or RO.3 mEq/L) 8 (0.014 0.0 mEq/L) 0.10 0.01 0.10 2.Appendix 1 Table 1 – AAMI standard for hemodialysis water quality MICROBIOLOGICAL MONITORING • Should be performed at least monthly. • Total viable microbial counts shall not exceed 200/ml in water used to prepare dialysate.20 0. • AAMI maximum levels of contaminants* Contaminant Calcium Magnesium Potassium Sodium Fluoride Free chlorine Chloramines Nitrate (as N) Sulfate Copper.1 mEq/L) 4 (0.00 100. more frequently if prepared with lesser level of treatment.50 0. Silver Cadmium Chromium Selenium Mercury Suggested Maximum Level (mg/L) 2 (0. or 2000/ml in proportional dialysate exiting the dialyzer.0002 128 .

as long as conductivity of water is being continuously monitored. 129 . b) 230 mg/L (10 mEq/L) where sodium concentration of the concentrate has been reduced to compensate for the excess sodium in the water.a) The physician has the ultimate responsibility for ensuring the quality of water used for dialysis.

25 IU/ml (action level 0. turbidimeter or chromogenic) or other validated techniques.1 cfu/ml < 0.25 IU/ml Fungi and yeast: < 10 cfu/ml EDTNA/ERCA Guidelines for the control and Monitoring of microbiological contamination in water for dialysis Total viable count:<100 cfu/ml (action level 25 cfu/mi) Endotoxin: <o0. Dialysis fluid purity Bacteria: < 100 cfu/ml Endotoxin: < 0.03 IU/ml UPD must be further purified for used as substitution fluid Tryptone Glucose Extract Agar or Reasoner’s 2A Culture at 20 to 220C for 7 days Malt Extract Agar or Sabouraud’s Dextrose Agar Culture at 20 to 220C for 7 days LAL assay (gel-clot.Appendix 2 Recommendation ERA-EDTA Best Practice Guidelines for Haemodialysis: Section IV. turbidimeter or chromogenic) with detection limit of 0. Dialysis fliuid samples must be diluted to prevent interference Incubation conditions for bacteria Incubation conditions for fungi and yeast Endotoxin test method 130 .125 IU/ml) Suggested limit for fungi and yeast: 10 cfu/ml At least weekly during validation phase At least monthly during normal maintenance Minimum requirement for water used for production of dialysis fluid Frequentcy of monitoring water used for production of dialysis fluid for microbiological contamination Frequency of monitoring dialysis fluid for microbiological contamination Requirements for ultrapure dialysis fluid (UPD) Weekly during validation phase At least quarterly during normal use (more frequently if used for ‘online’ production of substitution fluid) Regular checks to optimize disinfection cycles A representative sample of machines should be tested for endotoxin each month Undetectable bacteria level Undetectable endotoxin level UPD can be used as substitution fluid Tryptone Glucose Extract Agar or Reasoner’s 2A Culture at 20 to 220C for 7 days Tryptone Glucose Extract Agar or Reasoner’s 2A Culture at 20 to 220C for 7 days Limulus Amoebocyte Lysate (LAL) assay (gelclot.03 IU/ml < 0.

Blood Purification. 1990 Apr. 2000 Ward RA: Ultrapure dialysate: A desirable and achievable goal for routine hemodialysis.16(5):448-456. Microbial and endotoxin contamination in water and dialysate in the central United State. Nephrol Dial Transplant 15:578-580. Good dialysis practice. 58.References: 1. 1995. 11. Nephrol Dial Transplant (1998) 13:949-954. Brunet P. 4.pp 738-750 Arvanitidou A: Microbiological quality of water and dialysate in all haemodialysis centers in Greece. Artificial organ.Kidney International. Semin Dial 13(6):378-380. 8. E. 12.Nephrol dial transplant(1998) 13 (Supp 5):17-20.Suppl. Vol 25. Vol 1-1998 Pabst Science Publisher Robert A Laurence: Quality of hemodialysis water. S-112-119. 14. 3. Klein E. Am Jour of Kidney Disease. 2000 Lonnemann G: The quality of dialysate: An integrated approach. 2001 AAMI Dialysis Monograph 3rd Edition 131 . Harding GB: Bacteriology of hemodialysis fluids:are current methodologies meaningful?.Vol. 2000 Lonnemann G: Chronic inflammation in hemodialysis: The role of contaminated dialysate. 76(2000)pp. Berland Yvon: Water quality and complications of haemodialysis. Kidney Int 76(S112-119). Lonnemann G :assessement of the quality of dialysate. 14(2):136-45. 13.No 5(May). 10. Blood Purif 18(3):214-223. 5. Pass T: Culture of dialysis fluids on nutrient-rich media for short periods at elevated temperatures underestimate microbial contamination.Artif Organs. A 7-year Multicenter study. 7. Lonnemann G :The quality of dialysate: An integrated approach. 9.1992 Oct. 2000 Tielemans C: Are standards for dialysate purity in hemodialysis insufficiently strict? Semin Dial 14(5):328-329. 15. 6.1996.Bonnie-Schorn: Water Quality in Hemodialysis. 2000 Lonnemann G: Should ultra-pure dialysate be mandatory? Nephrol Dial Transplant 15(Suppl 1):55-59.14(2):85-94. 2.

Glossary AVF BP BUN CAPD CRF DFO EBPG EPO ESRD GFR Hb HD HDF K/DOQI Kt/V KUf LMWH PCR PD PO4 RO URR Arteriovenous fistula blood pressure Blood urea nitrogen continuous ambulatory peritoneal dialysis chronic renal failure Desferrioxamine European Best Practice Guidelines erythropoeitin end stage renal disease glomerular filtration rate haemoglobin haemodialysis haemodiafiltration Kidney Disease Outcomes & Quality Initiatives K = urea clearance t = time on dialysis V = total body water volume Ultrafiltration coefficient Low molecular weight heparin protein catabolic rate peritoneal dialysis phosphate Reverse osmosis Urea reduction ratio 132 .

CRITICAL CARE NEPHROLOGY 133 .

19.1 There is insufficient evidence for the effectiveness of CRRT over intermittent haemodialysis in patients with acute renal failure.2.1. 19. 19.1 Convection : flow of solute across a semipermeable membrane with solvent which is dependent upon transmembrane pressure. The ultrafiltrate produced is replaced in part or completely with appropriate replacement solution to achieve blood purification and volume control. Solute clearance is mostly diffusive.2.3 However.1 Definitions 19. 134 . 19.1.2 Continuous Venovenous haemodialysis(CVVHD) Slow countercurrent dialysate flows into the dialysate compartment of the dialyser.5 Predilution: replacement fluid infused prefilter.2.7 Ultrafiltration control system (UFC): technique whereby ultrafiltrate production is controlled by volumetric pump.1. The replacement fluid can be infused either before(predilution) or after the filter(post-dilution).1. Ultrafiltration in excess of replacement fluid results in weight loss. Most observational studies have reported improved survival with CRRT. 19.1.4 Post dilution: replacement fluid infused post filter. Solute removed may vary depending on the choice of membrane. beginning and terminating in a vein. 19. some reported poor outcome.19: PRINCIPLES AND TECHNIQUE IN CONTINUOUS RENAL REPLACEMENT THERAPY (CRRT) CRRT is any extracorporeal blood purification therapy intended to substitute for renal function over an extended period of time and applied for. Fluid replacement is not administered.3 Replacement fluid: special solution used to replace ultrafiltrate during haemofiltration or haemodiafiltration 19.1 Continuous Venovenous Haemofiltration (CVVH) Blood is driven through a highly permeable membrane by a pump via an extracorporeal circuit originating from a vein and terminating in a vein. 19.1.6 Ultrafiltrate: plasma water and ultrafiltered solute produced during ultrafiltration or haemofiltration of blood. 4. Blood flow is pump driven.1.5 19. or aim at being applied 24 hours a day.2 Diffusion: flow of solute across a semipermeable membrane driven by a concentration gradient.2 Types of CRRT 19.

19.2.3 Continuous Venovenous Haemodiafiltration (CVVHDF) Combines both the process of CVVHD and CVVH. Fluid replacement is routinely administered to maintain desired fluid balance. Fluid replacement can be infused either before or after the filter. Solute removal is both diffusive and convective. 19.2.4 Slow Continuous Ultrafiltration (SCUF) Similar to CVVH but no fluid replacement required. Volumetric control of ultrafiltration is necessary to maintain the ultrafiltration rate. Table 19.1 Mechanism of function and membrane type.6,7,8
CVVH CVVHD CVVHDF

SCUF Low Low No Poor 100-200 0 High flux

Diffusion Clearance Convective Clearance Fluid Replacement Middle Molecule clearance Blood Flow mls/min Dialysate l/hr Membrane type

Low High Yes Good 100-200 0 High flux

High Low No Poor 100-200 1-2.5 Low flux

High High Yes Good 100-200 1-2.5 High flux

19.3 19.3.1 19.3.2 a. b.

Recommendation for Clinical Practice: Arteriovenous therapy should be reserved for settings in which venovenous therapy cannot be provided because of absence of adequate equipment or personnel.8 (Level D) Choice of treatment Studies have shown relative equivalence between convective (CVVH) and diffusive (CVVHD) clearance for low molecular weight solutes.2,9,10,11 (Level A). Convective transport provides higher clearance for middle /high molecular weight molecules. 3,10,11 There is considerable variability based on membrane type.1

135

(Level A) c. Data is inconclusive on adsorptive ability of membranes for proinflammatory mediators and its clinical impact.4 (Level D) d. There is no data comparing patient outcome between convective and diffusive therapies. 19.3.3 Recommendations for clinical practice: No recommendations regarding use of convective therapies compared to diffusive therapies can be made. 19.4 Indications for CRRT in patients with ARF There is no consensus on exact indications of CRRT.12 Some criteria for the decision to start CRRT have been proposed. 13

19.4.1 Non obstructive oliguria (urine output < 200mls/12hr) or anuria. 19.4.2 Severe metabolic acidosis 19.4.3 Azotaemia (blood urea > 30 mmol/l) 19.4.4 Hyperkalaemia (K+ > 6.5mmol/l) 19.4.5 Suspected ureamic organ involvement (pericarditis, encephalopathy) 19.4.6 Progressive severe dysnatraemia (Na > 160 or< 115mmol/l) 19.4.7 Hyperthermia (core temperature > 39.5oC) 19.4.8 Clinically significant cerebral or pulmonary oedema 19.4.9 Coagulopathy requiring large amounts of blood products in patients with pulmonary oedema 19.4.10 Overdose with dialysable drugs 19.5 Non-renal indication for CRRT There is insufficient evidence to recommend the use of CRRT for non renal indications. 12,14 19.6 Patient Selection CRRT is usually used in 19.6.1 Severely ill patients in intensive care. 19.6.2 Haemodynamic instability. 19.6.3 For continuous removal of fluid, toxic substances eg. in septic shock, ARDS, cerebral oedema. 19.7 Timing of initiation of CRRT No recommendation on the timing of initiation of CRRT but treatment should be started early before complications develop.15,16

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19.8

Decision to stop CRRT Decision is influenced by 19.8.1 Haemodynamic status 19.8.2 Urine output 19.8.3 Volume status 19.8.4 Staff availability 19.8.5 Cost 19.8.6 Circuit clotting.
.

Figure 19.2.1 CRRT techniques: CVVH R V P Uf Qb = 100- 200 ml/min Qf = 10-20 ml/ min V

Figure 19.2.2 CRRT techniques: CVVHD

P

`

V V
Dialysate Out Qb = 100- 200 mls/ min Dialysate In Qf = 1-5 ml/ min

137

Figure 19.2.3 CRRT techniques: CVVHDF

P R V
Dialysate out + Uf Dialysate in

V

P
Qb = 100-200mls/ min Qd = 16-40 ml/ min Qf = 8-15mls/min

Figure 19.2.4 CRRT techniques: SCUF

P V
UFC

V

Uf
Qb = 100- 200 ml/min Qf = 2-8 ml/min

Key: V= Vein Qb= Blood flow Qd= Dialysate flow UFC= Ultrafiltrate controller

R= Replacement fluid Qf= Ultrafiltration rate P = Blood pump

138

References.
1. 2. 3. 4. 5. 6. 7. 8.

9.
10. 11.

12. 13. 14.

15.
16. 17. 18.

ADQI: Workgroup 1,2001. Definition and Nomenclature, Reporting of CRRT Techniques. Kruezynski K, Irvine-Bird K, Toffelmire EB, et al: A Comparison of continuous arteriovenous haemofiltration and intermittent hemodialysis in acute renal failure patients in the intensive care unit. ASAIO Journal 1993:39; 778-781. Bellomo R, Farmer M, Parkin G, et al: Severe acute renal failure: A comparison of acute continuous haemodiafiltration and conventional dialytic therapy. Nephron 1995:71;59 -64. Bosworth C, Paganini EP, Cosentino F, et al; Long term experience with continuous renal replacement therapy in intensive care unit; acute renal failure, Contrib Nephro 1991 : 93:13-16. Van Bommel, Bouvy ND , So KL. et al: Acute dialysis support for critically ill: intermittent hemodialysis versus continuous arteriovenous haemodiafiltration . American Journal of Nephrology 1995;15:192-200. ADQI, 2001: Workshop 5, Operational Characteristic . Rinaldo Bellomo, Claudio Ronco, Critical Care Nephrology, Kluwer Academic Publishers,1998 ,1169-1176. Rinaldo Bellomo, Claudio Ronco, Ravindra Mehta, Nomenclature for Continuous Renal Replacement Therapies. Am Journal of Kidney Disease, Nov 1996,, Vol 28;no 5,Suppl 3, S2-7. Robert Udhall; Vascular Access for Continuous Renal Replacement Therapy: Seminar in Dialysis, March-April 1996, Vol 9, No. 2, 93-97. Davenport A, Will EJ, Davison AM et al, Changes in intracranial pressure during haemofiltration in oliguric patients with Grade V Hepatic Encephalopathy. Nephron,89:53;142-146. Ronco C, Bellomo R, Brendolan A, et al, Brain density changes during renal replacement in critically ill patients with acute renal failure. Continuous haemofiltration versus intermittent hemodialysis. J Nephrology, 1999:12 :173178. ADQI:2001,Workshop 2, Selection of patients for acute extracorporeal renal support in general and CRRT in particular. Bellomo R, Ronco C: Continuous haemofiltration in the intensive care unit. Critical Care 2000:4:339. Miet Schetz, Non renal indications for renal replacement therapy, Kidney International, Nov 1999, Vol 56; Suppl 72,S88-99. Lettering LG, Reynolds HN, Scalea: Outcome in post traumatic acute renal failure when continuous renal replacement therapy is applied early versus late: Intensive Care Medicine, 1999; 25; 805-813. Proceedings of 2nd International Course on Critical Care Nephrology May 2225; 2001. Mehta RI, Letteri JM: Current Status of renal replacement therapy for acute renal failure. American Journal of Nephrology 1999:19:377-382. Rinaldo Bellomo; Choosing a Therapeutic Modality; Hemofiltration versus Haemodiafiltration; Seminar in Dialysis Vol 9, No. 2, March – April 1996, 88-92.

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20. VASCULAR ACCESS

20.1 Introduction 20.1.1 Central venous catheter provide rapid and easy access in the critically ill patients 20.1.2 CRRT can be operated with the use of a single double lumen catheter inserted in any central vein but require the use of a blood pump to circulate the blood through the extra corporeal circuit. An air bubble detector monitoring system is required to avoid air embolism.1,2
20.2 The placement of catheter can be at: 20.2.1Femoral vein a. The insertion is located approximately 1-2 cm below the inguinal ligament and 1 cm medial to femoral artery. b. Cannulation of femoral vein for central access is the primary choice in critically ill patients. c. Usage of femoral catheter should be restricted to 2 weeks.3,4 (Level C). 20.2.2 Internal jugular vein(IJV) a. IJV cannulation has become more popular. b. The right IJV is preferred, offering a shorter distance to reach the right atrium. 5 20.2.3 Subclavian vein a. Cannulation of subclavian is associated with subclavian vein stenosis and thrombosis, especially when a semirigid or poorly haemocompatible catheter is used. 5,6 b. The right subclavian is preferred to reduce the distance from insertion site to right atrium. c. The left subclavian is more difficult to cannulate and is exposed to higher risk of thrombosis. 7 d. A straight tipped guide wire should never be used in the subclavian or jugular veins as they may perforate the apex of the right ventricle and cause cardiac tamponade. Jtipped guide wires should be used. 7,8 . Movement of the patient is made easier if catheters are Inserted in the IJV or subclavian compared to if they are in the femoral area. 20.3 Catheter length used. 3,7 (Level C) 13.3.1 (R) Subclavian or internal jugular vein 13.3.2 (L) Subclavian or internal jugular vein 13.3.3 Femoral (R + L) 15 cm 19-20cm 25-35cm

140

Ash. Vol 16. Seminar In Dialysis. 1118-1123. 293-297 William T. Fatal hemothorax caused by subclavian hemodialysis catheter. 86. (Level C) References: 1. Use of tunnel femoral catheters to prevent catheter related infection. Rita A Mankus. et al. Vascular Access for renal replacement therapy. No 6(December). Critical Care Med. Ackerman. 624-628. 80. BB. No 2: 93-97.2001. 1992. 1998. Frequency. 1998. Am J Kidney Dis. Vanholder.Artificial Organ 1994.1114-1124. Kluwer Publisher. Comparison of Blood Flow and Hydraulic Resistance between the Mahukar catheter. A prospective randomized multicenter trial. Theodore F. Robert Udhall. Vol 144. Stephen R. Saad. Ann Intern Med. No 8.4. Advantages and disadvantages. 87-92.3. Catheter related infections and their prevention. Edward Worly. 1177-1 4. Critical Care Nephrology. Leonard Mermel. 1685-1687. Mestres P. Cimochowski. 1998. 38 :96-101. Bacteraemia associated with tunneled.Workgroup 5. ASAIO. Superiority of internal jugular over the subclavian access for temporary dialysis.4. Micheal Wanscher. 1998. M Klinger. No 8. ADQI . Leblanc Martin. Pirrung KJ. Fabrice Bruneel. et al. Am J Kidney Dis. 1998. Arch Intern Med.130 .De Moor.729735. Bambauer R. Ringoir . Is there enough evidence to recommend tunneling for short term use. 1996: Vol 9. 1998.4 Ideal position of tip of central venous catheter. Vanita Jarssal. S. 5 6 7 8 9 10 11 12 13 14 15 16 141 . R. Barbara L. therapy and prevention of infection associated with large bore catheter. Vol 34. Robert Udhall. 2. Measurement by ultrasound velocity dilution. 3. Jean Francois Timsit. Vol 21. Subclavian vein hemodialysis catheters. John Stephen Tapson. 31. C Ronco. m532-m534. the Tesio Twin catheter and the Ash Split catheter. No. Thrombosis caused by polyurethane double lumen subclavian catheter and hemodialysis. 2001. Rouben. George E. E. Christian Smith. R. I Wikiere. 54. ASAIO Journal. Karger Publisher. Jens Jorgen Frifelt. Mcgee.7 20.154-161.20.1 Subclavian or Internal jugular: Just above junction between superior vena cava and right atrium. . Prolonged cannulation of femoral vein is a safe method of temporary vascular access for hemodialysis. G La Greca. Critical Care Medicine. James M Sutton. Christine Cheval. Vaussenat F. 1991. Adreas Pierratos. Bellomo. K. Vascular Access for Continuous renal Replacement Therapy.E Rutherford. Nephron. et al. No 6.2 Femoral Vein: In the inferior vena cava. 20. 1999. Operational Characteristic. 1990. Vol 26. Bosc JY. W Weyde.4. et al. Proceeding of the 2nd International Course in critical care nephrology Vienna May 22-25 . Critical Care Med. Accurate placement of central venous catheters. Effective blood flow and recirculation rate in internal jugular vein catheter. Nephron. Blood purification in intensive care . cuffed hemodialysis catheters. 1984. 1315-1316.

3. Platelet count >100.6 21.1.2 Moderate risk group a.000/ul with coagulopathy.000-5.1. 142 .5 Heparin infusion should be stopped once there is evidence of bleeding or severe heparin induced thrombocytopaenia.2. in CRRT the patient’s exposure to anticoagulation is much more prolonged. Non uraemic: 90seconds. 21.3 21. reduces efficiency of therapy and may affect patient’s outcome.3. thus increasing the risk of bleeding and other side effects. Anticoagulation is therefore routinely used to optimize filter life. 21.21: ANTICOAGULATION One of the major drawback of CRRT is frequent filter clotting. followed by continuous infusion 5-10unit/kg/hour. 4 21.000unit heparin bolus is given into inflow limb (prefilter). which requires a repeat ACT/ PTT one hour after dose alteration. 21.3 Low risk group a. initial dose of 1.3.0002.2 Partial thromboplastin time is aimed at 1. 21.5-2. 5 21.filter blood sampling is preferred in patients without bleeding risk and prevention of filter clotting is the main goal.000/ul with coagulopathy.3. or requiring systemic anticoagulation for other reasons.3. Immediate post-operation d. Normal platelets and no coagulopathy.1.7 21. 21. b.1 High risk Group a.1 Monitoring of anticoagulation profile should be done one hour after starting CRRT and every 4-6 hourly unless there is a change in heparin dose.3 Post. This increases the cost of treatment. Unlike intermittent haemodialysis. Platelet count <100. Liver failure c.0 X control or ACT at 150-200 second { Normal ACT value for uraemic patients: 100 seconds (62-138sec).000unit/L heparin (except in severe bleeding or heparin induced thrombocytopaenia) is flushed into the extracorporeal system and drained out prior to connection.3 Normal Heparin 4 For those without contraindication.4 Systemic sampling is used in patients with bleeding risk.1 Bleeding risk stratification:1. Patient with bleeding. 21.2 Priming: 1-2 liter normal saline containing 2.

15 21.7.5.6. Maintenance: 10-14mg every 4-6 hours or infusion at the rate of 0.5 Heparin Free: 21. 21.7 Regional Heparinisation 21.2 Priming with saline is appropriate 1.1 LMWH may have a role in CRRT.1 Used in patients with moderate risk of bleeding. 6.4 Low Dose Heparin: 1 21. but so far the reported experience in continuous dialysis is insufficient for us to make a strong recommendation.3 Maintenance dose:5 unit/kg/hour. Target : 0.21.7. Monitoring: a Measure anti Xa level.25 U/ml ( Level of >0.1Heparin is infused into inflow limb and protamine is infused on the return line.6.4 -0. Enoxaparin 21.2 Citrate References: Please refer to chapter 23 143 . Fraxiparin b.45 U/ml have been shown to be associated with bleeding complication.7. 21.5.6. 1.6 Low Molecular Weight Heparin(LMWH) 21.4.2Dosage: 1mg of protamine will neutralizes approximately 100units of heparin.2 Types of LMWH available : a. (Level B) 21.3 Flushing of the system (prefilter) with 100ml-250ml saline every hour or more frequent if necessary.8. b.6 mg/kg/day.1 Prostacyclin. 21. 21.9.6ml (>50kg) every 12hourly. Fraxiparin : 0.6.5. 21.7.10.4. 21. 21. 14.2 No data available regarding bolus dose at initiation.4. 21.8. 21.3In CVVHD it has not been shown to prolong filter life nor to reduce bleeding complications compared with low dose UH36 .1 For high risk patients. b.4.4ml( <50kg) or 0.3 Recommended dosage: a. 21.8 Alternatives For Anti-coagulation in CRRT: 21.8. Enoxaparin: Initial dose: 40mg.8-13 (Level D) 21.

45% saline + 75ml 8.17 Fluid with high glucose content results in hyperglycaemia and should be avoided.22 : REPLACEMENT FLUID AND DIALYSATE To maintain fluid balance in haemofiltration or haemodiafiltration the replacement fluid used during CRRT should contain physiological concentrations of electrolytes.13 c. During CVVH/CVVHD there is a loss of bicarbonate up to 1.8meq).1Lactate based solution: Ringer’s lactate (caution in hyperkalaemia) a. d.18 22. Most commercially available solutions do not contain phosphate and supplementation is generally required at some stage during CRRT.1. Data does not show any survival benefit. Lactate is converted to bicarbonate in the liver on an equimolar basis at rate of 100 mmol/hour.5ml 10% CaCl2 (10.9% saline + 5ml 10% CaCl2 (7mEq) Solution B: 1L 0. lactic acidosis and high volume haemofiltration. If Haemasol is not available the following formula can be used: 17 i) Single Bag Formulation: 1L 0. Indications are: hepatic failure.1 Types of replacement fluid: 22. Controlled trials (not all randomized) have shown that during CRRT. b. 22.1. Haemasol® 32 mmol/l HCO3 a. except in patients with extreme electrolyte imbalance.19-23. Lactate levels are generally higher with lactate solutions and may confuse the interpretation of blood lactate level.45% saline + 35ml 8.4% NaHCO3 (35meq) + 10ml 23.5meq) 144 . ii) Two-bag Formulation: Solution A: 1L 0. b. 16The serum concentration of phosphate and magnesium should be monitored and replaced accordingly.4% NaHCO3 (75meq) iii) Four Bag Formulation: Solution A: 1L 0.g.000 mmol/day and these needs to be replaced.9% Saline + 7.2Bicarbonate based solution e. lactate or bicarbonate buffered solutions have similar efficacy for correction of metabolic acidosis.4% NaCl (40meq) +2ml 10% CaCl2 (2. but it provides better control of acidosis and cardiovascular stability. Lactate based replacement fluid is safe and effective for reversal of acidosis in the majority of ICU and acute renal failure patients.

6ml 50% MgSO4 (6.4% NaHCO3 It is not advisable to use saline solution as the sole replacement fluid as it does not contain buffer 7.1 Replacement fluid can be given either pre-filter (pre-dilution) or post filter (post-dilution) with their own advantages and disadvantages.2.5 In patients who have no contraindication for anticoagulation. 145 .2 Pre-dilution fluid replacement is believed to enhance filter patency during CRRT and to reduce need for anticoagulant.45% Saline + 150ml 8. 22. 22.2.24 22. 22. 22.4 Combination of pre-dilution and post-dilution is needed when extracorporeal clearance is limited by achievable blood flow. CVVH is generally performed with an average UF rate between 1 and 2 liters per hour.2.allow high UF rate .4meq) Solution C: 1L 0.45%Saline Solution D: 1L 0.3 Pre-dilution enhances achievable ultrafiltration rate (important in high volume CVVH) and may be considered in patients with frequent clotting.Reduce solute clearance because of dilutional effect -Required large amount of replacement fluid -Require more porous membranes and larger surface area in high volume UF Post –filter -Higher solute clearance Disadvantages -Efficiency is limited by filtration fraction (25 % from Qb).2 Recommendations 22.6 In CVVH (for post-dilution mode) ultrafiltration rate should not exceed 25% of blood flow. post-dilution is preferred.9%Saline + 1.25 Table 22 : Advantages and disadvantages of pre and post filter replacement fluid Advantages Pre-filter .Reduced use of anticoagulant .solute clearance can be increase by increase UF rate .2. 22.Solution B: 1L 0.2.2.

5% dextrose.6. However a reduction of body temperature below 35oC should be avoided. except in high flux dialysis where dialysate should be sterile because of back-filtration.6 Physical properties (temperature & sterility) of replacement fluid and dialysate 46 22.5meq/l. Ca:1.g Peritoneal dialysis solution 1.4 Dialysate Flow Rate 22. the bacteriological requirements for CRRT dialysate are less clear.4. b.5 Recommendation: In hypercatabolic ARF patients on CVVHD/CVVHDF. Sources: Haemosol solution: Content Na: 140mmol/l .1 Lactate based e.1 Most patients undergoing CRRT show a decrease of body temperature.30-31 22.3 g/hour absorption) an increase in the mean serum glucose is seen especially at higher dialysate flow rates.6 ml/min to 40 ml/min. the clearance of small solute is increase from 8. a. Glucose: 0 22.6-0.75mmol/l. K: 0. (Level D) 22. 22. As a result of the large glucose load (5. Lactate: 3mmol/l. Bicarbonate buffered dialysate is required for patient with impaired lactate metabolism.22.2 Bicarbonate based solution (Haemosol) a. Although lactate metabolism may be impaired in acutely ill patients. 29 22.8gm – 7.2 The efficiency of small solute removal during high dialysate flow rate in CVVHD is enhanced by using a large surface area filter (0.6.4. Sodium concentration in PD solution is 132mmol/l which is lower than optimal may result in mild hyponatraemia. HCO3: 32.30 22.5%) has been shown to be safe and effective in both continuous haemodialysis and haemodiafiltration.3 Dialysate Types: 22.2 Whereas the use of sterile substitution fluid is imperative. the clinical consequences of which are illdefined. References: Please refer to chapter 23 146 .3. the dialysate flow rate can be increased from 1000 ml/hour to a maximum of 2500 ml/hour.5mmol/l. the use of lactate buffered solution (PD 1.26-28 c.3. Cl: 109.0mmol/l. Mg: 0.9m2).1 With increasing Qd from 500ml/hour to 2500ml/hour in CVVHD.

25-0.5g q8-12h 0.8g q4-6h 3-4g q6-8h 20-60mg q24h 200-400mg q24-48h 100-200mg q12h 200mg q24h 147 .5g q12h 150-300mg q6h 250-500mg q6h 0.1 Low protein binding 23.23: DRUGS AND DOSAGE IN CRRT 23. Thus.75-1.5g q8h 1-2g q6-8h 12.5mg/kg q6h 0.5-1g q6h 0.5-1g q8h 12.1.6-1.75-1.1.5g q8h 0.75g q12h 150-300mg q6h 0.5mg/kg q8h 1g q18h 6mg/kg q48h 250-500mg q12-24h 100-200mg q18h 1g q24-48h 500mg q8-12h 0.1.5-1g q6h 0. Equal GFR:30ml/min 5mg/kg q12-18h or 15mg/kg q48-72h 1mg/kg q12-18h or 4mg/kg q48-72h As for amikacin 250-500mg q8h 1-2g q12h 1g q8-12h 1-2g q24h 1g q12h 0.5mg/kg q8h 1g q8h 6mg/kg q24h 250-500mg q6h 100-200mg q12h 1g q12h 500mg q8h 0.2 Twenty liters of daily ultrafiltrate correspond to a urea clearance of 14ml/min.1 Drug remove by CRRT that requires a dose adjustment has: 23.3 Low non-renal clearance Examples are aminoglycoside. the dosage of a drug should be calculated as for a patient with GFR of 14ml/min.6-2.5-1g q6h 7. Fosfomycine and flucytocine 23. Vancomycin.5-1g q6h 0.4g q4-6h 3-4g q4h 20-60mg q24h 200-400mg q24h 100-200mg q12h 200mg q24h Dose in CVVH 2l/hr.2 Low volume distribution 23.5-1g q6-12h 0.5-0.5 q12 7.5mg/kg q6h 0. Drug Dosing in CRRT Drugs Amikacin Gentamicin Netilmicin Cefaclor Cefoperazone Cefotaxime Ceftazidime Ceftriaxone Cefuroxime Aztreonam Chloramphenicol Ciprofloxacin Clindamycin Erythromycin Imipenem Meropenem Metronidazole Sulphamethoxazole Teicoplanin Tetracycline Trimethoprim Vancomycin Amoxycillin Ampicillin Penicillin G Piperacillin Amphotericin B Fluconazole Itraconazole Ketoconazole T1/2 GFR<15 30-90hr 20-60 35-75 3 3 15-35 13-25 12-24 17 6-8 3-7 6-9 4 6 4 7 7-21 20-50 60-230 60-100 20-50 200-500 * 7-20 6-20 3-5 24 100 25 8 Usual dose 5mg/kg q8h or 15mg/kg q24h 1mg/kg q8h or 4mg/kg q24h As for amikacin 250-500mg q8h 1-2g q12h 1g q6h 1-2g q8h 1g q12h 0.

5-1g q4-6h 50-100mg q3-4h 100-400mg q8-12h 250-500mg q24h 1mg/kg q24h 250-500mg q6h 10-40mg q6-8h 60-180mg q4h 200-400g q12h 100-150mg q12h 160mg q6-12h 10mg/kg q8-12h 0.5 * 0.7 12 100 20 * 20 1.5 * 140 24 3.8 * * * 0.5-10units/h 5-15mg q2-3h 40mg q8h 2g/24h 100-200mg q6-8h 10mg q8h 50-100mg q8-12h 2-8mg/hr 5-10mg q5-6h unchanged 10-20mg q24h 1-4mg/hr 0.5-8mg q24h 160mg/400mg q18h 4mg/kg q24h 15mg/kg q24-36h 250-500mg q12h 25mg/kg q24h (max.5mg/kg q8-12h 80-250mg q12h unchanged unchanged Not recommended Not recommended Unchanged Unchanged Unchanged Unchanged 50-150mg q6-8h 5mg q8h Unchanged Unchanged Unchanged Unchanged Unchanged 50% 0.3-1g q12h 40-80ug/kg/h 40-80mg q8h 0.4 2 16 10 * 2.5 5.8 4.5-1.Co-trimoxazole Pentamidine Ethambutol Ethionamide Pyrazinamide Rifampicin Acyclovir Ganciclovir Zidovudine Amiadarone Carbamazepine Chlorpromazine Cimetidine Cyclophosphamide Cyclosporin Digoxin Flecainide Frusemide Haloperidol Hydrocortisone Ibuprofen Indomethacin Insulin Isosorbide dinitrate Isosorbide mono Lignocaine Mexiletine Metoclopramide Metoprolol Midazolam Morphine Naloxone Omeprazole Pancuronium Paracetamol Pethidine Phenobarbitone Phenytoin Prednisolone Procainamide Propranolol Pyridostigmin Quinidine Ranitidine Sotalol Theophylline Valproate Vecuronium Verapamil Warfarin * 118 20 * 9 9 20 30 2 600 15 30 5 3.5g qd) 600mg q6h 5mg/kg q8h 5mg/kg q12h 200mg q8h 10-15mg/kg/24h 200-400mg q8-12h 10-50mg q8h 200-400mg q6h * 2-5mg/kg/24h 250ug q24h 1-2mg/kg q8-12h 20-80mg q8h 0.5-5mg q8-12h 50-250mg q6h 400mg q8h 25-50mg q8h 0.5-1g q6-8h Unchanged 100-200mg q8-12h Unchanged Unchanged 250-500mg q12h Unchanged 60-120mg q6-8h Unchanged 50-75mg q12h 80mg q8h Unchanged Unchanged Unchanged Unchanged Unchanged *data not available 148 .5 * * 6 * 12 15 * 5 * 160mg/400mg 12h 4mg/kg q24h 15mg/kg q24h 250-500mg q12h 25mg/kg q24h (max 2.1-2mg * * 2.2.5mcg q24h 0.5g qd) 300-600mg q6h 5mg/kg q12-24h 5mg/kg q24-48h 200mg q8h unchanged unchanged unchanged 100-200mg q6h 50-75% usual dose unchanged 62.5 3.

1999. Continuous Renal Replacement Therapy Component Selection: Replacement fluid and dialysis solutions. Continuous haemofiltration with a low molecular weight heparin enoxaparine: Report on two cases: Int. 910-917. 1999.. Blood purification in intensive care: 2001. Brunet. Ronco. monitoring.over study. is bicarbonate or lactate buffered solution better ? Contrib Nephrol. efficiency and safety. Anticoagulation with Low Molecular Weight Heparin during continuous hemodialysis in intensive care unit. 116. C. 1999. Karger. 12. Vol. Mann. Anticoagulation: Seminar in Dialysis: April 1996. pharmacokinetics. Seminars in dialsysis. Poul. JH et al. Singler. Am J Kidney Disease. 9.2(Mar. Nephrol. . 1997. Herve. 1997. 1997. 9. Nephrology: 2001. P et al. Ronco. 17:717-720. 13. Blood Purif. Hory. dosing considerations. R et al. 41: 125. 237-242. Vol. 20. Lorenzini JL et al. Chest. RF et al. 93. No. MH.Hirsh. manufacture guideline. 7. 1985. Mechanism of action. 19. M. AN et al. 12. H et al. 17. 2. Anticoagulation with low molecular weight heparin (fragment)During continuous hem dialysis in the intensive care unit. Contrib. 1987. Critical Care Med. Jeffrey. M et al. 1998. 3. Vol..L. 27: 2224-2228. 38-47. Comparison of lactate –versus acetate base hemofiltration replacement fluid in patient with acute renal failure. Continuous venovenous hemodialysis: Technical considerations : Up to date ACTest System. Reeves. Solute transport in continuous hemodialysis. 123. Blood purification in Intensive Care. S et al. R. 221-224. Morgera. Heparin and LMWH. Basel. Jeffrey. 1995. Acid Base balance and substitution fluid during continuous hemofiltration. Continuous arterivenous hemofiltration: Optimal therapy for renal failure in an intensive care setting? Autralia NZ L Med. 8. 5. PM. Nephrol Dial Transplant. C. 107-111. AJKD: 1998. S et al. Comparison of lactate and bicarbonate buffered hemofiltration fluids: use in critically ill patients. Continuous Renal Replacement Therapy: An Update. Vol. 26. Critical Care Nephrology. 56 suppl 72. 1996. 14 15 16 17 18 19 20 21 22 23 24 149 .313-322. S37-40. RF et al. 4. A control trial of low molecular weight heparin (dalteparin) versus unfractionated heparin as anticoagulation during venovenous hemodialysis with filtration. B et al. Mehta. Nehru. 114: S498-S510. 1998.molecular weight heparin (letter). Heering. Nadroparin versus daltaparin anticoagulation in high volume continuous venovenous hemofiltration – double blind randomized cross. 10. 1995. M. Guidelines to the use of enoxaparin in slow continuous hemodialysis: Contrib. 132. Bicarbonate dialysate for continuous renal replacement therapy in intensive care unit patients with acute renal failure. 562-571. Artif Organs. J Clin Pharmacol Theraphy Toxicol: 1991. 1993. 6. 1212-1217. 32. 1993. 717-720 Bellomo. A et al. Vol.Apr). a new treatment for acute renal failure. 9: 112-118. ACJ et al. Ren Fail. 32(2): 8 Palevsky. 1199-1211. Organ. Kierdorf. Kidney Int. Am J Kidney Dis. Thomas.References: 1. 155164. Continuous venovenous hemofiltration in ARF. 34(3) Sept: 486-497. J et al. 11. 1991. Artif. De pont. 15.132. 29:89-91 Wynckel. 1990. Leblane. Continuous arteriovenous hemofiltration with a low.

Dis 21: 400. 1672-1676. 107-111.25 26 27 28 29 30 31 32 Ronco. 2. Am. Paleevsky. C. R et al. Bonnardeaux et al. suppl 160-164. A prospective comparative study of continuous arteriovenous hemodialfiltration and continuous venovenous hemodialfiltration in critically ill patients. Intensive Care Med. 1991. J Kidney. Evaluation in technology and nomenclature. Crit. 1993. J Kidney. Slow continuous UF and dialysis for the treatment of acute renal failure. P et al. effect on insulin concentration and glycemic control in critically ill patients. 150 . Bellomo.20. 343. No.404.Vol. Kidney Int. Paleevsky. 53. Bellomo. 1992. influence on major nutrition balance. 17. 1996. Bellomo. 1991. Diffusive and convective solute clearances during continuous renal replacement therapy at various dialysate and ultrafiltration flow rate. J Am Soc Neprhol. Dis 34(3): 486. suppl 66. 2.9. P et al. Solute clearances with high dialysate flow rates and glucose absorption from the dialysate in continuous arterioveneous hemodialysis. Care Med. S et al.. Vol. CRRT. R et al. Am. 399-402. Acute continuous hemofiltration with dialysis. 1998. 1999. R et al. Brunet. Am J Kidney 1992. Continuous AV hemofiltration in the critically ill. Seminar in dialysis. Dis 19: 31-38.492.

Multiflow 60 or100 b. increasing ultrafiltrate flow rate or both c.1.e (QD or QD +QUF) 24.5. CVVHD and CVVHDF include: a.7 (Level D) 24. 24.2 Solute clearance can be increased by a.1. the use of synthetic membranes with high hydraulic permeability is appropriate.3.2 Based on hydraulic permeability. These are also called haemofilters.4.1.1. they can be classified into a.3 Optimisation of CRRT therapies 24.3.1 No accepted method to assess filter function in CRRT 24.1 Small solute clearance is proportional to hemofilter or haemodialyser effluent flow rate i.4 Fluid removal can be maximized by using a haemofilter with high ultrafiltration coefficient . 4.7(Level D) Examples of haemofilters/haemodialysers suitable for CVVH. Low flux: ultrafiltration coefficient (Kuf) 4-8 ml/hr/mmHg b.2 24. High flux: Kuf > 20ml/hr/mmHg Kuf: is defined as the coefficient of hydraulic permeability of the membrane.2 Some useful indicators of filter function include: 151 .4.3. AN 69 c.24: DIALYSIS PRESCRIPTION 24.1.3. F40 d. 24.3 Higher molecular weight clearance can be achieved by increasing ultrafiltration rate using a haemofilter/ haemodialyser with high UF coefficient 24. using a hemodialyser with greater surface area 24.4 Most membranes in CRRT are high flux membranes made of synthetic polymers.2. PAN-50 24.4 Assesment of menbrane function7 24. increasing dialysate flow b.1 Membrane characteristics determine solute removal and water permeability 24.1 Membranes for CRRT 24.5 There is inconclusive evidence that the biocompatibility of the membrane affects mortality in critically ill patients with acute renal failure.6 24.2 Recommendations for clinical practice 24.3.1 Based on current evidence.3 High flux membranes also have higher porosity and increased sieving coefficients for larger molecules 1.

Filtration fraction < 0. effluent flow rate from the filter. 24.4.g urea clearance)23 24.Data also suggests that adequate metabolic control is achieved when urea clearances equal or exceeds 2 l/hr. (Quf) Ultrafiltration rate (-) not recommended.7.6. 16. Table 24:Variables used to measure clearance for the different forms of CRRT Variable Qb Qd Quf CVVH ++ CVVHD ++ CVVHDF + + (Qb) blood flow.6. (++) Best 24.5. 152 . Markers of clearance have been suggested to be used as a basis of CRRT dosing (e. Dialysis dose in CRRT 24. or Quf for CVVH provided the Qeff < 50% Qb for CVVHD / CVVHDF. (Qd) dialysate flow rate.23 24.1. However the appropriate target clearance is not clear22.6 (CVVHD/HDF) c.2 Duration of filter use should not exceed 48 hours. (+) Recommended.22 a.23 There is no consensus on which approach is best.7( level D) 24. ultrafiltration rate for CVVHDF.This is equal to the sum of QD.2 Various methods for dialysis quantification and prescription including urea kinetic Modeling and direct quantification techniques have been described.6. urea clearance may be equated to Qeff. urea equilibration ratio and filtration fraction may be used to assess filter function although there is no proven benefit. 24.17 One study 18 suggests higher doses of clearance improved survival.2 (CVVH). Recent data suggest renal replacement therapy dose may affect outcome in critically ill patients with ARF.7 Recommendation for clinical practice: 24.1 The optimal technique for CRRT quantification in ARF remains to be determined. 22.6. Urea equilibration ratio (≅ dialysate urea /blood urea) > 0.1 Transmembrane pressure monitoring. CVVHDF.7 (Level D).Urea sieving coefficient (≅ ultrafiltrate urea /blood urea) > 0. SCUF).5.6.6 (CVVH) b.3 For CRRT modalities (except predilutional CVVH. urea sieving coefficient.22 (level A) 24. dialysate flow rate and Quf.5 Recommendations for clinical practice 24.

Arterial blood gas 24. Daily full blood count e.4 Baseline parameter required: a. magnesium f.8. Renal profile.6 Monitoring Parameters: a.3 Markers of clearance should be used for CRRT dosing.1 Primary service should contact Nephrology Referral team to evaluate patient for CRRT 24. random blood sugar c. Serum calcium. magnesium.3 Prescription orders should be written up by Referral Team before the procedure is started and this should be reviewed every 8-12 hourly. Central venous pressure b.7.7. arterial blood gases four hourly then prn when stable 153 . Hepatitis screen g. Filtrate urea/blood urea ratio daily. activated clotting time e. 24. Blood pressure d. Heart rate 24. Change filter if ratio < 0. PT.5 Haemodynamic parameters required a. Daily serum calcium.8.7 For CVVH. specific target levels of azotaemia control cannot be recommended 24. ACT/APTT: 1 hour after initiation then 4 – 6 hourly and after 1 hour of any change in anti-coagulation b. Liver function tests d.24.22 (Level D) 24.8.8. Daily serum lactate f. phosphate. 24. Blood urea / serum electrolytes 6 hourly initially then bd once stable c.8. APTT. Vascular access should be inserted 24.6 g. Full blood count count b. ultrafiltration of at least 35 ml/hr/kg is advocated. Pulmonary artery wedge pressure if available c.8 Initiation of CRRT 24.2 Based on the lack of data currently. phosphate d.2 If appropriate.8. the Referral Team/ICU specialist will notify Critical Care Nephrology/ Haemodialysis Unit to set-up the CRRT system.

5%PDSolution (Prisma/Hospal only) (Potassium addition see Table) 154 .9 Sample of CRRT prescription form (Hospital Kuala Lumpur) Date Time Start Finish NAME AGE: SEX: Aquarius DIAGNOSIS Prisma Hospal INDICATION: RN: TYPE OF THERAPY SCUF CVVHDF CVVH CVVHD DIALYSATE: BICARBONATE: Bicaflac / Hemosol LACTATE: 1.24.

DIALYSATE FLOW RATE: REPLACEMENT: BICARBONATE RINGER`S LACTATE SALINE REPLACEMENT FLOW RATE: Pre-filter Post-filter BLOOD FLOW RATE: ANTICOAGULATION: SALINE FLUSH: HEPARIN: BOLUS (units/hr) (See Table) ACCESS: FEMORAL SUBCLAVIAN Reason for Termination : Filter clotting Change of Modality Procedure Name of Doctor: Low BP Renal recovery Death MAINTAINANCE: IJC 155 .

9 15 mmol/l 5.Potassium Replacement in Dialysate Serum K (mmol/l) K addition (per 5L bag) 50 mmol/l < 3.5.9 40 mmol/l 4.4.5 3.0.3.4.5.0 or more 0 mmol/l ANTICOAGULATION Start @ 5-10 u/kg /hr (± intial bolus) Check APTT @ 4 hrs then 6 hrs followed by every 24 hrs APTT Heparin dosage Increase by 400u/hr < 40s 40-60s Increase by 200u/hr 61-80s No change Inform Doctor > 80s References 156 .4 30 mmol/l 4.

Greenberg A. 38: 691-696. Chandran P. Hakim RM. ADQI: Workgroup 4: Membranes 2001. 17. Effect of the dialysis membrane in the treatment of patients with acute renal failure. Lang SM. 2. Van Bommel EF. 116:62-65. 8(6):709 -713. 16. 28:1161-1165. Lancet 1994.Hakim R: A multicenter comparison of dialysis membranes in the treatment of acute renal failure J Am Soc Nephrol. Ronco C. Konig A. Palevsky P: Dialysate and blood flow dependence of diffusive solute clearance during CVVHD. 354:1337–1341. 8.Biocompatible membranes in acute renal failure: prospective case-controlled study. 1992. 7. Tolkoff RN. 6. International Multicentre Study Group. Contribution Nephrology 1995. 22. 23:99-107.: Prospective comparison between hemofiltration and hemofiltration with dialysis. 34:486-492. ADQI: Workgroup 3: Solute Control (Treatment Dose) 2001. 3. Kidney International 1999. Removal of platelet activating factor in experimental arteriovenous hemofiltration. Dobis C. 20. Bloom R. What`s new: Current Opinion in Nephrology and Hypertension 1999. 11. 10. Himmelfarb J. Crtical Care Med 1995. ASIO J. 9. 3:1516 –1521. 9:257–266. Haider MC. 19. 5. Jorres A. Parker RA. 12. Lancet 1999. . Storck M: Comparison of pump driven and spontaneous hemofiltration in postoperative ARF: Lancet 1991: 337:452. Schiffl H. 26:1995-2000. Brumet S. Parker RA. 18. N Engl J Med 1994. Rondo C. Wingard: . 2000: 56:26-30. Clark W: Role of renal replacement therapy quantification in Acute renal failure: Am J Kidney Dies 1997:30(5 Supply 4: S 10-S14) 157 . 344:570–572. Wingard RL. Strasser T. Clark WR. 13. 331:1338– 1342. Ronco C : Hemodialysis filters. Leblanc M: Diffusive and Convective solute clearance during CRRT at various dialysate and ultrafiltrate rates: Am J Kidney Dis 1999. 21. Lysaght MJ : Effect of membrane composition and structure on solute removal and biocompatibility in hemodialysis. Blood purification 1995: 14:255. 56: 2005-2015. Homely P: Effect of different doses in Continuous venomvenous haemofiltration on outcome in acute renal failure: a prospective randomized trial: Lancet. Critical care Med 1998. Haemodialysis-membrane biocompatibility and mortality of patients with dialysis-dependent acute renal failure: A prospective randomised multicentre trial. Maxvold NJ.1. 15. Gahl GM. 1998.Cytokine kinetics during continuous hemofiltration. Relton S. Van Bommel: Acute dialytic support for critically ill: intermittent hemodialysis vs continuous arterovenous hemodiafiltration: American J of Nephro 1995:15(3):192-200. ADQI. Hamburger RJ. et al. Kellum J Diffusive vs Convective: Effect of mediators of inflammation in patients with severe systemic inflammatory response syndrome. Clark WR: Extra corporeal therapy requirements for patients with ARF: J Am Soc Nephi (in press) Chime CS: Protein catabolic rate in patients with ARF on CAVH: J Am Soc Nephrology 1993. Critical Care Med 2000. 23. 4. Held E. Laurie Gnarred: Urea Kinetic Modeling for CRRT: Am J Kidney Dies 1997:30(5 Supply 4: S2-S9). Kraus MA Acute dialysis catheter recalculation studies. 14. Working group 5: Operational Characteristics 2001.

PATIENT SELECTION 158 .PERITONEAL DIALYSIS 25.

and cardiovascular disease 159 .Ideally continuous ambulatory peritoneal dialysis (CAPD) is best suited to patients who are independent. patient preference should determine the modality of therapy.1 Once other psychosocial factors are eliminated. medical factors play a role in the choice of modality only in a minority of patients. Although the evidence is controversial. Medical Factors • • • • • • • • • • • Age Cerebro and cardiovascular disease Diabetes mellitus Blindness Peripheral vascular disease Severe pulmonary disease Lumbar disc problems Inflammatory bowel disease Previous extensive abdominal surgery Timing of referral Vascular access In adults. They should be physically and mentally capable of performing the procedure. When the above characteristics are not available particularly in the very young and old patients. In new patients starting dialysis.2. some diabetics and other ‘high risk’ patients with severe cerebro. disciplined and motivated to care for themselves. the following factors may influence the choice of CAPD: 25.1. Psychosocial factors • • • • • • • Patient preference and motivation Concern with body image Occupation Economic considerations Home and workplace environment Family support and availability of assistant Distance from nearest haemodialysis (HD) centre 25. a fully committed and reliable trained assistant must be available.

Vascular access problems 2. Abdominal hernias. Colostomy. 26. nephrostomy and ileal conduits. ileostomy. CAPD may be indicated in the following circumstances: 1. CAPD is the dialysis modality of choice for children (vascular access is often problematic in this group of patients). The rapid change in solute transport and rapid shifting of volume within compartments during HD may result in HD being potentially more hazardous in these situations. 25. 8.4. neurological and rheumatological disorders resulting in physical disability can make CAPD impossible to perform unless assisted. Relative Contraindications 1. PRE-DIALYSIS PREPAPARATION 160 . Poor vision. Severe diverticular disease of the colon.may be better managed on CAPD. These can lead to contamination of the catheter exit site. Chronic obstructive airways diseases. Psychological problems A psychotic. Hernias may need to be repaired before CAPD is started. 6. 7.3. 5. For patients already on haemodialysis. Absolute Contraindications Extensive peritoneal fibrosis and adhesions arising from previous surgery or inflammatory bowel disease. 2. Unstable cardiovascular status on HD 25. Morbid obesity. belligerent or uncooperative patient cannot be expected to succeed in CAPD. Chronic backache from preexisting lumbar disc disease. 4. 3.

Repeated percutaneous insertion of temporary dialysis catheters should be avoided. The conditions that may indicate that dialysis is not yet necessary even though weekly Kt/V is below 2.4 A weekly Kt/V of 2. The dose of dialysis should be gradually increased to the recommended minimal targets of total weekly Kt/V.73 m2 . 26.0 approximates a renal creatinine clearance of 9-14 mL/min/1. Complete absence of clinical signs and symptoms attributable to uraemia.0 include: 1. 2.3. Counselling and education Pre-dialysis counselling. Local data has shown that CAPD technique survival is adversely affected if the antecedent renal replacement therapy was intermittent peritoneal dialysis by repeated percutaneous insertion of temporary dialysis catheters. careful psychological preparation and assurance can alleviate fear. Dietary protein intake as estimated by urea kinetics > 0.1. 161 . However such teaching plans should also be flexible and adaptable to patient needs. Timing of catheter insertion It is important that the catheter is inserted on an elective basis preferably before dialysis needs to be initiated. Early Start of CAPD Evidence that an early start of dialysis will improve outcome has been derived from studies showing that late referral to the nephrologist has detrimental effect on ESRD patients.8 g/kg/d) 3.3 The PD committee of the NKF-DOQI recommends that some form of chronic dialysis be initiated once the weekly Kt/Vurea drops below 2. 26.26.2. anxiety and stress associated with the insertion of the Tenckhoff catheter. Stable or increased oedema free body weight. 2.5 The catheter break-in should be delayed for 10 to 14 days after the insertion. CAPD Units should have a formal educational plan and checklist to ensure consistency.8 g/kg per day (nPNA ≥ 0. subsequent CAPD procedures and changes to their lifestyle.0.

The belt line of the patient is identified preferably in the sitting and standing position. References 1. Jungers P. 26. the patient should empty the bladder and an enema may be given to patients who are constipated. One dose of parenteral cephalosporin is given intra-operatively. 4. 5. Early referral to the nephrologist and timely initiation of renal replacement therapy: a paradigm shift in the management of patients with chronic renal failure. The tunnel site is marked on the skin in such a way that the exit hole will be created at least 2 cm below the belt line.5. Pereira BJ. Prior to the operation. 3. 1996. Treatment modality selection in 150 consecutive patients starting ESRD therapy. Am J Kidney Dis 1997: 30(supp. Detrimental Effects of late referral in patients with chronic renal failure: a case control study. Indications for switching from CAPD to HD4 1. patients should have a good bath with soap.4. Prichard SS. et al. 1999 (suppl. Perit Dial Int. Kidney Int. 2. First Report of the Malaysian Dialysis and Transplant Registry 1993. Development of mechanical and technical problems. and all questions answered in a reassuring way. 3.2): S70-3 Lim TO. Page B. 5. Am J Kidney Dis 1998. 3. 31(3): 398-417 NKF-DOQI Clinical Practice Guidelines – Initiation of dialysis. 2. water and hibiscrub. Inadequate solute or fluid removal. On the day prior to the surgery. 2. Inadequacy of dialysis on CAPD with consistent failure to achieve target Kt/Vurea and creatinine clearance. 4. The patient is briefed regarding the operation including risks and possible complications. 41): S170-3 Obrador GT. Unmanageably severe hypertriglyceridaemia Unacceptably frequent peritonitis or other PD-related complications. High transporters may have poor ultrafiltration and/ or excessive protein losses. 162 . Pre catheter insertion preparation 1.26. 4. Zingraff J. 16:69-72.

Table 27.1.25-0. The volumes available are 1.e. CAPD Solutions Several types of solutions are available in clinical practice in different volumes and glucose concentrations. hypertonicity and formation of advanced glycosylation end products (AGE) and glucose degradation products (GDP). Role of new PD solutions • • • • • Improved UF Prolonged technique survival Improved membrane viability Nutritional management Reduced glucose load.2. CAPD SYSTEMS 27.2 132-134 1. 2. magnesium. calcium.5% and 4.5. peritonitis and sclerosing peritonitis.27 Osmolarity (mmol/L) 346 396 pH 5.75 0.75 Chloride 96 96 Lactate 35-40 35-40 4.36 2.0. 1. They are formulated with electrolytes including sodium chloride.25-0.75 96 35-40 27. and lactate as a precursor of bicarbonate. 1.2. As dextrose is the osmotic agent. 2.2 5.25-0.1 27.25% 3.5%.25%.86 485 5.75 1.1. New PD Solutions The long term use of standard PD solutions may be responsible for some of the complications of PD namely ultrafiltration failure.0. 2.75 Magnesium 0.27. various strengths are available i.1: Composition per 100ml PD solutions Dextrose strength 1.5 and 5.0-1.0 litres.5% 2.2 Ionic Concentration (mmol/L) Sodium 132-134 132-134 Calcium 1.75 0.5% Glucose 1. 163 . Factors of concern are unphysiological pH.0-1.0-1.

Kluwer Academic Publishers Jones MR. Substitution with amino acids in PD fluids may correct this loss.2. Khanna R.3 (Level B) 27. Unfortunately. magnesium and glucose. 2. Gehr TW.2.2 (Level B) Disadvantages of amino acid: ♦ Due to rapid absorption its use as an osmotic agent is limited.2.27. It is safe and efficacious and especially useful for patients with UF failure. Replacement of amino acid and protein losses with 1. Bicarbonate solution Bicarbonate solutions have been shown to reduce infusion pain and should also provide a more physiological environment for the peritoneal membrane. it is difficult to prepare and store and is incompatible with calcium. nausea and vomiting 27. Perit Dial Int 1997. Burkart JM et al. 18:210 Peers E. 17:22-26 164 .3.5% mixture of glucose polymers that is isosmolar. Textbook of Peritoneal Dialysis.2. Icodextrin It is a 7. Thus it has to be stored in double chamber bags to be mixed immediately before use. Gokal R. Recent trials showed that once daily intraperitoneal amino acid solution leads to positive nitrogen balance. Icodextrin overview of clinical experience. ♦ Metabolic acidosis may be seen in 50% of patients. ♦ Associated with loss of appetite.4. Amino Acid solution A high percentage of patients treated with PD are malnoursished due to continued loss of amino acids and proteins.25% dextrose. 2nd Ed 2000.2% amino acid peritoneal dialysis solution. As it is removed from the peritoneum by lymphatic absorption the osmotic gradient is better preserved than glucose and its ultrafiltration capacity is equivalent to dextrose 4. 3. Krediet R and Nolph K eds. A 2% amino acid solution produces equivalent UF to 4. Perit Dial Int 1998. References 1. alkaline supplements may be needed.25%. Gokal R.

The downward directed exit is associated with decreased incidence of exit site associated peritonitis. PD ACCESS Chronic PD catheters are made of soft materials like silicone rubber or polyurethane.1.2. Catheters available in Malaysia. (Flush before fill). The standard two cuff straight Tenckhoff catheter is still the most widely used access device because it satisfies the needs of most patients and there is no conclusive evidence that other catheters are superior1. 28. CAPD Connectology Some of the systems currently available are as follows: 28. Double Bag System This system is similar to the Y-disconnect system except that the two bags are permanently connected to the upper two branches of a long Y-set while the short branch is connected to the PD catheter only during exchanges. Swan Neck Catheter:Dual cuff with a pre-formed 150-degree bend in the tubing between the cuffs designed so that the catheter can be placed in an arcuate tunnel. The Y-Disconnect System2. 1. 2.2. The exchange is completed by disconnecting the Y-set (and both dialysate bags) from the peritoneal catheter which is then capped off. Straight Tenckhoff Catheter:Double cuffed straight catheter with perforations of 1 mm over the inner-most ten cm. 28. followed by flushing of the Y-set lines from the new bag to the empty drainage bag. Then the previous peritoneal exchange is drained followed by inflow of fresh dialysate. Both internal and external segments are directed downwards.28. 165 .2.2. the exchange is initiated by spiking a new dialysate bag. 28.3 In the Y-set method.1.

In: The Cochrane Library. 28. 9:159. Trans ASAIO 1988. Prospective controlled trial of a Y. Nephrol Dial Transplant 1993. Khan I. 34: 433. Stay safe a new PVC free system for peritoneal dialysis: results in a multicentre trial.6 (Level A) This system is particularly suitable for those with impaired dexterity. Perit Dial Int 1989. flush. 166 . Lawrence P. Krichgessner J. 2003. Oxford: Update Software. Issue 1. 6. Grant A.sets in CAPD. Lancet 1983. Peritontis in CAPD: a multicenter randomized clinical trial comparing the Y. Double bag or Y-set versus standard transfer systems for continuous ambulatory peritoneal dialysis in endstage renal disease (Cochrane Review).e.This has been shown to significantly reduce peritonitis rate as it eliminates the need for spiking of the dialysate bag. A.2:642. Major reduction of CAPD peritonitis after introduction of twin bag system. Wallace S. References 1.Y. (A-non-disconnect Y) This is also a double-bag system closed with a special irreversible clamp which is removed at the next exchange. 21: 596. Burkatt JM.3. 2. inflow and automatic closing of the system with a pin.2. Campbell M. Tielens E. The Stay-Safe system This is another double-bag system in which the drainage bag and the dialysate bag are connected to the tubing lines by a special disc.connector and disinfectant to prevent peritonitis in CAPD. Comparison of peritonitis rates using standard spike versus Y.N. 28. outflow. Nube MJ. 3. Int J Artif Organs 1998.2. Cody J.5 By turning the disc all the exchange phases can be performed i.4. 5. Canadian CAPD trial group. Van Biesen W. MacLeod A.connector disinfectant to standard system. 4.D. et al. Daly C. Donaldson C. Vale L. Schilling H.8: 1237.4.

or paramedian (deep cuff at the medial edge of the rectus musculature) to give good deep-cuff fixation and minimise herniation and fluid leaks. catheter insertion should be undertaken under operating theatre. CAPD PROCEDURES 29.9% saline and observing if 30-40 ml is easily aspirated. 167 . c. Catheter Insertion Ideally. usually on an inpatient basis.1. f. e. Techniques to accomplish this include infusing one litre of peritoneal fluid over 5 minutes and allowing an equal time for drainage.1. or injecting 60 ml of 0. The implantation must be performed by a competent and experienced operator. This has been found to decrease the risk of peritonitis associated b. Recommendations2 a. sterile conditions. Peritoneal entry should be lateral (deep cuff in or below the rectus musculature). The deep cuff should be placed in the musculature of the anterior abdominal wall or in the preperitoneal space. The catheter should be tested to ensure that there is adequate inflow and outflow without leakage. After proper positioning of the catheter tip. Although several techniques have been used. in a planned manner. The implantation technique has a significant influence on the complications and outcome of the chronic peritoneal catheter.29. Check for catheter patency. d. Care should also be taken to avoid mechanically stressing the cuff material. The exit site should be facing downwards or laterally. The deep cuff should never be placed within the peritoneal cavity. Good results have also been obtained with the cuff placed within the posterior rectus fascia. the peritoneum is closed tightly around the catheter below the level of the deep cuff using a pursestring suture. The procedure must be regarded as an important surgical intervention demanding care and attention to detail equal to any other surgical procedure.1 29.3 The subcutaneous cuff should be located near the skin surface and at a distance of at least two cm from the exit site.1. the common practice is by surgical implantation under direct vision.

A titanium adapter is attached to the end of the catheter. 168 .3.2. The catheter is clamped and disconnected from the tubing and re-soaked in povidone iodine for another 5 minutes. with exit site or tunnel infection. The Tenckhoff catheter and the extension tubing is soaked in 1% povidone iodine for 5 minutes. Optimally. Catheter break-in and post implantation dialysis. The catheter is then flushed with 5000 units of heparin in 8 ml of distilled water and capped. Upward-directed exit sites should. preferably by automated cycler may be carried out with the patient in the recumbent position. Showers should only be advised 4 – 6 weeks after implantation. Only sponge baths are advocated during the initial healing period. Clean the exit site and surgical wound with 1% povidone iodine and rinse with normal saline. c. Initial exit site dressing changes are done by properly trained nursing staff. This can be facilitated by the use of a bent stylet or any device that will add rigidity to the catheter. Post operative catheter care. If peritoneal dialysis is required during this period. CAPD should not be initiated for 10-14 days after catheter implantation. The approach given below is adapted from current Malaysian CAPD practice which has been found to be similar to ISPD practice. b. be avoided. 29. d. e. 29. a. There is little evidence to support the superiority of one approach over the others. The volume per exchange can be gradually increased over the next few days to a maximum of one litre. in general. (Level B evidence) The intra-abdominal portion of the catheter should be placed between the visceral and the parietal peritoneum towards the pouch of Douglas and should not be placed within loops of bowel or directed in omental tissue. small volume exchanges of 500 ml. Cover with sterile gauze and non-occlusive dressing.g. The dressing should not be changed for at least 7 days unless there is obvious bleeding or signs of leakage or infection.

protecting the tunnel and exit site from trauma. If patient is sensitive to iodine. c. The exit site should be patted dry after cleansing. Assess patient's domestic environment. Exit site care includes a. Familiarise the patient on the components of PD catheter. cleansing the exit site c. Chronic care of the healed exit site. 3. Start exit care training on the tenth post-catheter insertion day. e. However. However certain recommendations are given below based on evidence if available. Educate the patient on: 169 .e self care and being trained to do so.4. Optimal care of the exit site has not been determined. a. b. CAPD Training Program When CAPD is decided on:1. Decide who is to be trained with the patient. b. d. Speak to patient and spouse or other family members about what CAPD involves i. The exit site should be cleaned with povidone iodine and rinsed with saline. f. 29. assessment of the exit site b.29. or current practice. dressings may help keep the exit site clean.5. anchoring and immobilising the catheter d. 2. It is important not to forcibly remove crusts or scabs during cleansing because this may cause a break in the skin and increase exit site infection. Mupirocin cream should be applied at the exit site after cleansing. normal saline dressing can be used after bathing using liquid soap. 4.2 a.4 (Level B) Use of dressing has not been shown to affect the incidence of exit site infections. The exit site should be inspected and cleansed daily or every other day. protect it from trauma and immobilise the catheter. Only showers and not long baths are recommended.

5.

the rules to follow when handling/touching the catheter. catheter exit site care. catheter complications, their causes, prevention and management. hand washing procedure and its importance. c. Hand out "shopping list" of essential equipment to patient to make purchase. Check when training is to be started and let the patient and partner know about it.

29.6. Schedule of Training For CAPD Patients DAY 1 Objectives Nursing management 1. 2. 1. 2. 3. Provide adequate dialysis. Introduce patient to CAPD. Evaluate patient's dialysis requirements and set the time for the exchanges (usually 4 exchanges daily). Assess patient's anxiety and learning capacity. Impress on importance of record keeping of exchanges, blood pressure, weight and temperature.

Patient/Partner

1.

Demonstrate taking blood pressure, temperature and body weight. 2. Observe first exchange procedure and do subsequent exchanges under close supervision. 3. Learn to record all exchanges. 1. 2. 3. 4. 5. 6. Normal kidney function. Basic theory of PD. Emergency phone numbers. Aseptic technique (clean/dirty/sterile). Record keeping. Personal hygiene.

Teaching Topics

170

DAY 2 Objectives

1. 2. 3.

Provide adequate dialysis according to patient's needs. Enforce self care. Understand principles of CAPD. Evaluate patient's dialysis treatment. Supervise exchange procedure. Explain the following terms • clean and dirty, aseptic & sterile • disinfection • contamination • areas which are considered sterile & non-sterile in PD Learn to take blood pressure, weight and temperature. Carry out exchanges as stipulated. Learn exit site care. Record all exchanges correctly. Define how fluid & waste products are removed in CAPD. Describe the importance of keeping to dialysis prescription to achieve adequate dialysis (i.e. not omitting any exchanges). Describe fluid removal and how to regulate ultrafiltration with different dextrose concentrations

Nursing management

1. 2. 3.

Patient/Partner

1. 2. 3. 4.

Teaching Topics

1. 2.

3.

171

DAY 3 Objectives

1. 2. 3.

Provide adequate dialysis according to patient's needs. Participation of patient in exchange procedures Inform patients about CAPD complications Evaluate effectiveness of exchange schedule and dextrose concentration used Supervise exchange procedures. Monitor blood pressure, weight and temperature. Carry out exchanges as stipulated. Carry out exit site care under supervision. Record all exchanges correctly. Review fluid management Dietary management Complication - peritonitis -exit site infection - leakage/hernia. Contamination

Nursing management

1. 2.

Patient/Partner

1. 2. 3. 4.

Teaching Topics

1. 2. 3.

4.

172

DAY 4 Objectives

1. 2.

Provide adequate dialysis according to patient's needs Encourage patient's independence Assess patient’s independence & proficiency in performing exchange procedure Monitor vital signs. Perform catheter & exit site care independently. Perform exchanges as stipulated. Problem solving (troubleshooting). Medication/diet. Disconnect system.

Nursing management

1.

Patient/Partner

1. 2. 3.

Teaching Topics

1. 2. 3.

DAY 5 Objectives

1. 2. 3.

Encourage patient independence. Evaluate dialysis schedule effectiveness. Re-educate on symptoms & signs peritonitis. Evaluate patient's independence and proficiency in procedures Retrain procedures where necessary Perform procedures independently Peritonitis a) Symptoms and signs b) Causes c) Prevention d) Early detection & reporting e) Treatment protocols Follow up care Disposable & dialysate indenting & storage

Nursing management

1. 2.

Patient/Partner Teaching Topics

1. 1.

2. 3.

173

End of Training 1. Training should not end until both the staff & patient are comfortable with the patient / carer’s ability to care for himself/ herself independently. 2. Schedule a return appointment, one to two weeks after completion of training to assess progress & discuss problems.

References
1. 2. 3. 4. Golper TA, Brier ME, et al. Risk factors of peritonitis in long term peritoneal dialysis: The Network 9 peritonitis and catheter survival studies. Am J Kidney Dis 1996; 28(3):428-436 Gokal R, Alexander S, Ash S, Chen TW, et al. Peritoneal catheters and exit-site practices toward optimum peritoneal access: 1998 update.( Official report from the ISPD). Perit Dial Int 1998; 18(1):11-33 Stegmayr BG, Hedberg B, Norrgard O. Stylet with a curved tip to facilitate introduction of new Tenckhoff catheters and reposition of displaced ones. Eur J Surg 1993;159(9):495-7 Thodis E, Passadakis P, Panagoutsos S, Bacharaki D, Euthimiadou A, Vargemezis V. The effectiveness of mupirocin preventing staphylococcus aureus in catheter-related infections in peritoneal dialysis. Adv Perit Dialysis, 2000; 16:257-261

174

30. COMPLICATIONS OF CAPD 30.1. Technical Complications of CAPD 30.1.1. Hernia a. Incidence: 10-25% b. Predisposing factors • • • • • • Children Older females Multiparity Post-operative leak at time of catheter insertion Previous hernia repair/laparotomy Higher fill volumes: studies so far do not support this to be a factor leading to hernia formation.

c. Common sites • • • • Incisional or through catheter placement site Inguinal Umbilical Epigastric

d. Treatment Surgical repair is indicated to prevent strangulation and incarceration especially in small hernias.1 (Level C) Peri-operative management of CAPD patients undergoing hernia repair.2 • Pre-operative imaging is only indicated in those in whom diagnosis is unclear. • CAPD may be continued till day of operation. • Drain peritoneal dialysate immediately prior to surgery. • Post-operative management remains controversial and the following have been followed. - HD for 2-4 weeks2 - Immediate resumption of CAPD but on smaller fill volumes 2 - Resumption of CAPD 3 days later3,4 - Cycler PD using small fill-volumes.

175

a. • Recurrence of abdominal wall oedema HD for 4-6 weeks Resolve Restart CAPD Recur surgical repair Permanent HD • Recurrence of Genital oedema Radiologic investigation (refer above section) Patent processus vaginalis Repair Leak Permanent HD 30. Treatment Various options have been practiced.1. • Bed rest and cessation of CAPD • Keep intra-abdominal pressure low by cycling PD in supine position. Genital and abdominal wall oedema Oedema of the scrotum/ penis.6 (Level C) 30. Prevention Paramedian incision for PD catheter insertion has been found to reduce the incidence of incisional hernias. • CT scan b. Early leakage (<30 days after insertion of PD catheter) • Overt leak • Subcutaneous leak or genital swelling 176 . the following may be helpful. • Radiocontrast (preferably non-ionic) into abdominal cavity.1.2. labia majora or abdominal wall may result in poor ultrafiltration and inadequate dialysis. • Technetium 99 dialysate fluid into abdominal cavity.3.e. Leakage a. Causes • • Leak through soft tissue plane from catheter insertion site Patent processus vaginalis to labia/scrotum then leakage into surrounding soft tissue. or HD if vascular access is available. To distinguish the cause of genital oedema.5.

Inflow obstruction Causes: • Kinking • Intraluminal debris 177 . Signs & symptoms • Diminished drainage • Pale patch around catheter or surgical scar.4. Outflow obstruction Causes: • Intraluminal – debris or blood clot • Extraluminal .1. a.incorrect catheter placement at implantation b.omental wrap .stool filled bowel enwrapping the catheter . • Increasing abdominal girth • Genital swelling Diagnosis and treatment (See section on genital swelling) 30. It can also present later together with a PD related complication such as peritonitis. Inflow and Outflow Obstruction Outflow and inflow obstruction are most frequently observed within 2 weeks after catheter implantation.occclusion of catheter holes from pressure exerted by adjacent organs .Recommendations: • Can be prevented by a break-in period of about 2 weeks. b. Late leakage (>30 days after catheter insertion) This may be difficult to diagnose. • Persistent leak after resting will need surgical repair. small volume PD in recumbent position if HD is not feasible. • Withhold PD temporarily for 1-2 weeks – HD if patient needs dialysis.tip entrapment in peritoneal pockets from adhesions .

Laxatives .Open surgical revision or replacement.Instillation with fibrinolytic agents – urokinase/streptokinase 12. . • These various techniques have not been evaluated in randomized clinical trials. Caution: increased risk of peritonitis and bowel perforation.000 u in 2 ml heparin (10.Interventions such as fluoroscopically guided stiff wires or stylet manipulation or intraluminal brushing.000 units) into catheter for 2 hours Invasive approaches: . 178 .Body position change .Flushing with heparinised saline.Recommendations • • Establish type of obstruction by examination and evaluation Try non-invasive approaches: . Other rare complications include: Sclerosing encapsulating peritonitis Kidney stones Haemoperitoneum Hydrothorax Chyloperitoneum. .

Crusting alone is not indicative of infection. however granulation tissue is more commonly seen and pain and erythema are frequently absent. tenderness. Definitions. swelling and discharge are absent. b. Chronic exit site infection Exit site infection lasting for > 4 weeks. Tunnel infection Erythema.2. c.2. Pain. exuberant granulation tissue and oedema.1.8.2. a. Erythema may be present but with a diameter <13 mm. d. oedema and/or tenderness over the subcutaneous pathway and may be characterised by intermittent or chronic. It represents low grade infection and most progress to overt infection if untreated. Symptoms are similar to acute infection.30. It may be a sequelae of untreated or inadequately treated infection or recurrence of resolved acute infection.2 Exit-Site and Tunnel Infections 7. Acute exit site infection Purulent and/or bloody discharge from the exit site which may be associated with erythema of >13 mm in diameter. Pathogens • Staphylococcus aureus – majority • Peudomonas aeruginosa • Staphylococcus coagulase negative 179 . 30. accompanied by regression of the epithelium and presence of granulation tissue in the sinus. Equivocal exit site infection Purulent and/or bloody drainage only in the sinus that cannot be expressed out.9 30. It is associated with increased risk of peritonitis. purulent bloody or gooey discharge.

quinolone for gramneg. Topical mupirocin Cauterise slightly exuberant and exuberant granulation tissue.Table 30. quinolone for gram-neg. organisms. First generation cephalospori n for grampos. If initial therapy: first generation cephalospori n for grampos. vancomycin for MRSA. Gram Stain Acute infection Culture and sensitivities on exudate Gram Stain Chronic infection Culture and sensitivities on exudate Gram stain Tunnel infection Palpation of cuff and tunnel Culture and sensitivities and Gram stain of exudate (spontaneous or after pressure on cuff) U/S of cuff/tunnel Cauterise slightly exuberant and exuberant granulation tissue. organisms.1. Treatment of exit-site and tunnel infections Equivocal infection Evaluati on Culture and sensitivities on peri-exit smear. 180 . vancomycin for MRSA Cauterise slightly exuberant granulation tissue. If previously treated: add synergistic drug or change antibiotic according to culture and sensitivities. organisms. organisms. Initial antibiotic therapy based on Gram stain results Initial therapy Cauterise slightly exuberant granulation tissue with copper sulphate crystals or silver nitrate solution.

consider catheter removal. Continue therapy 7 days past achieving a good appearance. Consider chronic antibiotic suppression. If no response in 2 weeks. Use rifampicin as a second antibiotic for staph infections. remove catheter. if no improvement after a month of treatment. Adapted from 1998 update on peritoneal catheters and exit site practices toward optimum peritoneal access 7 181 . Re-evaluate every 2 weeks. Response to systemic antibiotic therapy is excellent with cure occurring in almost all instances. organisms on culture. remove catheter. reculture monthly. If infection recurs repeatedly after achieving a good appearance: 1. consider cuff shaving 2. Adjust therapy according to culture and sensitivities. synergistic antibiotic. suspect cuff infection and treat as such.48 Hours Change to neomycin or gentamicin ointment if gram-neg. Adjust antibiotic according to culture and sensitivities Followup Evaluate weekly. If no remission: 1. If accompanying peritonitis. Evaluate every 2 weeks. reculture every 2 weeks if no improvement on appropriate therapy. Continue to treat for 7 days after achieving a good appearance. Most acute infections respond favourable to therapy. Adjust therapy according to culture and sensitivities. reculture if no improvement Substitute another appropriate antibiotic or add a second. If accompanyin g peritonitis. If accompanying peritonitis. change to systemic antibiotic based on initial culture and sensitivities . consider catheter replacement. 2.

3.3. Peritonitis10 Peritonitis is a common clinical problem in patients on CAPD and the main cause of technique failure.5 • Gram negative • • • bacteria • Pseudomonas • 1.4 • 6.4 • Enterobacter • 2.2 • MRSA • 1.2 • Staph epidermis • 13.4 • E.2.4 • 0 • 1.3.1 • 6. Diagnosis In a patient with cloudy fluid and/or abdominal pain and/or fever. aureus • 3.1 • 0 182 . Microorganisms causing CAPD peritonitis Table 30.1.3 • 10.2 • 0 • 2. coli • 3.6 • 3.8 • 7.7 • Kelbsiella • TB • 0 • 1. Clinical manifestations of peritonitis Symptoms Cloudy effluent Abdominal pain Fever Nausea/vomiting/chills Drainage problems Signs Abdominal tenderness Fever 30. 30.3 • 3.3.2 • 8. 30.4 • 2.2.3. Principal pathogens causing peritonitis in CAPD patients in Hospital Kuala Lumpur • Microorganism • % total organism isolated • • 1998 • 1999 • 2000 • Gram positive • • • bacteria • Staph.30.9 • 10.6 • 2.2 • 5.3 • 3.8 aeruginosa • Acinetobacter • 3.6 • 2. an elevated cell count of >100 WBC per mm3 with at least 50% polymorphs is supportive of the diagnosis of peritonitis.

183 . draw up sediment and place 1 drop on bacteriological culture plates. refrigerate but do not freeze sample.3. • Perform Gram stain and microscopy from sediment Materials • Blood agar plate • Chocolate agar plate • EMB agar plate or MacConkey agar • IMA agar plate • BHI/Blood agar plate or Sabourod’s plate • BacT/Alert fan blood bottle or BACTEC bottle Procedure • Microscopic examination • Perform gram stain on sediment . transport sample at room temperature.4. • For immediate delivery. • 50 –100 ml peritoneal effluent should be concentrated and cultured to maximize bacteria recovery rates. • Decant supernatant aseptically. • For delayed delivery (>1 hour after collection).6 • • 5.6 30.• • Fungal Culture negative • • 6. • Vortex to re-suspend sediment. Laboratory investigation a. Incubate plates in carbon dioxide (5%) at 35 oC for 48 hours and hold the blood bottle for 5-7 days in the BacT/Alert or BACTEC Blood System. Processing • Place effluent sample into two 50 ml tubes and centrifuge for 15 minutes at 3000g.Culture Bacteria : Using Pasteur pipette. Diagnostic Workup of Peritonitis Specimen Collection and transport10 The sample should be obtained from the first cloudy bag as it has the greatest probability of yielding a positive culture.1 58 • • 9.3 54. Place 5 mL of sample into blood culture bottle.1 43.

It is reported to be of symptomatic benefit. Wrap plates and incubate in 30 oC incubator for 4 weeks. • One to three rapid exchanges in succession are carried out without addition of antibiotics. Stain sample according to Pappenheim for evaluation. . The usual number of CAPD exchanges is then continued with maintenance doses of antibiotics.5. Heparin at a dose of 500-1000 U/L may be added to the regular regimen until dialysate effluent clears. Initial Empiric Antibiotic Selection 10 184 .3. but does not appear to offer any specific therapeutic benefits. Management of peritonitis10 Once the diagnosis of peritonitis is suspected and the suggested work-up completed the following steps for treatment are initiated either at home or in the hospital.Fungus : Inoculate BHI/blood agar or Sabourod’s agar and IMA plates with the sediment. The resolution of peritonitis is monitored clinically and by serial effluent white cell counts. Dialysate fluid with loading doses of recommended first line antibiotics is instilled and allowed to dwell for at least 6 hours. Cell differential Spin peritoneal effluent sample (200 uL) in a cytocentrifuge (1:10-1:100 dilution in physiological saline for leucocyte count > 1000) at 8000g for 7 minutes. Appropriate changes in antibiotics are made if necessary.Haematology Effluent polymorphonuclear leucocyte count Count unspun sample using a counting chamber or haemocytometer. • • • • • • a. culture and antibiotic sensitivity are available. The CAPD team should review the patient’s technique in an attempt to determine whether errors in technique have contributed to the episode of peritonitis. This regimen is continued until the results of gram stain. 30. The duration of antibiotic therapy is dependent on the culture and sensitivity results.

it should be noted that penicillins deactivate aminoglycosides. In patients with residual urine volume of < 100 ml/day. in combination with ceftazidime as first line empiric therapy.Although there is no clear evidence. the expert committee in ISPD recommends a first-generation cephalosporin. cephazolin (1gm daily in the long dwell). In Malaysia. Empirical antibiotic selection Residual urine output Antibiotic cephazolin ceftazidime gentamicin amikacin cloxacillin <100ml/day 15 mg/kg BW once daily 1g/bag once daily 0.6mg/kgBW/bag daily 2mg/kgBW/bag daily 250 mg/bag >100ml/day 20mg/kgBW once daily 20mg/kgBW/bag once daily not recommended not recommended 250 mg/bag * once daily dose should be given in long dwell exchange. However.11 185 . Table 30. since first generation parenteral cephalosporin is not yet widely available.3. cephazolin in combination with an aminoglycoside can be used. *Aminoglycoside given as a single daily dose may result in less ototoxicity and nephrotoxicity and improved bacterial killing in association with prolonged post-antibiotic effect. cloxacillin is used instead although there is no evidence available in the literature for its use.

ND ND LD 250MD. ND mg. ND mg p. ND mg mg.Table 30. MD 250 mg Ampicillin 250-500 ND MD 125 or MD.. MD 125 mg Penicillins All LD same as anuric Piperacillin 4000 mg ND LD 4 g IV.o..d.i. MD 50 mg 186 .4.d.i.6 mg/kg MD 8 mg by 25%) 25%) Netilmicin 0.d. mg p. ND Amoxicillin 500 mg. Dicloxacillin 250-500 ND 250-500 MD. MD increase 125 mg by 25% Cephalothin 15 mg/kg ND LD 500 MD..o. Antibiotic dosing recommendations for CAPD patients with and without residual renal functiona CAPD intermittent CAPD continuous dosing (once/day) dosing (per litre exchange) Drug Anuric NonAnuric Nonanuric anuric Aminoglycosides * (Increase MD 24 mg Amikacin 2 mg/kg (Increase all doses all MD by Gentamicin 0. MD. ND IV. mg p.i. b. q.d.o.6 mg/kg MD 8 mg Cephalosporins All LD same as anuric Cefazolin 15 mg/kg 20 LD 500 MD mg/kg mg.i. ND mg p.o. b. MD 125 mg Ceftazidime 1000-1500 ND LD 250 MD. 250-500 b.d. q.i.

d.d. + rifampin 600 mg p.o. b. MD 200 mg LD 1000 mg.d.57d 400 mg IP.. 15-30 mg/kg q. 1 g b.o.. 100 mg q.12 hr As intermittent ND 100 mg q. 400 mg p. q.o.d.d.12 hr Isoniazid 300 mg p..12 hr ND 187 . iv 200 mg q.o.. then 1 g q.d. then 200 mg p.i. ND ND LD 50 mg. b. 300 mg p.. ND ND ND ND All LD same as anuric NA ND Amphotericin Flucytosine Fluconazole Itraconazole Antituberculars NA 2 g LD. MD 25 mg As intermittent ND ND Others Vancomycin Increase doses by 25% ND MD 30-50 mg/L LD 400 mg. MD 250 mg As intermittent As intermittent Increase MD by 25% ND Teicoplanin Imipenem/ cilastatin Aztreonam ND ND ND Metronidazole Rifampin Antifungals 250 mg p.5 mg As intermittent As intermittent 100 mg q.i.d. q.d..o.i.Quinolones Ciprofloxacin Ofloxacin 500 mg p.o.i.d. MD 40 mgb LD 500 mg.d. q.o.i.12 hr ND ND 100 mg q. b. NA ND MD 1. b...

+ pyridoxine 10 mg/d Combinations All LD same as anuric ND LD 1000 mg.12 hr ND The route of administration is IP unless otherwise specified. especially when using intermittent regimens. MD = maintenance dose. q. ND = no data. b.+ pyrazinamide 1.d. nonanuric = >100 mL/24 hours. There is no evidence that mixing different antibiotics in dialysis fluid (except for aminoglycosides and penicillins) is deleterious to the drugs or patients.o. q.o.d. therefore probably an increase in dose by 25% is warranted.1-2 mg p.o.i. but these are predominantly renally excreted.i. Therapeutic Drug Monitoring: for vancomycin and aminoglycosides * Avoid if possible in patients with residual renal function 188 . MD 100 mg Cotrimoxazole 1920 mg ND LD 1920 ND p.. a Ampicillin/ sulbactam 2 g q. or hepatically metabolized and renally excreted..d. = once per day. drug is extensively metabolized and therefore there should be no difference in dosing between anuric and non-anuric patients. IP = intraperitoneally. LD = loading dose. q. Do not use the same syringe to mix antibiotics.5g p. "ND" means no data. and then in 1 bag/day × 7 days. b This is in each bag × 7 days.o. CAPD patients with residual renal function may require increased doses or more frequent dosing. NA = not applicable. For penicillins: "No change" is for those predominantly hepatically metabolized. then in 2 bags/day × 7 days.d. "NA" = not applicable. = four times per day.. that is. IV = intravenous. q. These data for CAPD only. = twice per day. days MD 480 mg p. Anuric = <100 mL urine/24 hours.

MRSA = methicillinresistant S. Modification of treatment based on culture and sensitivity Enterococcus Other gram-positive Staphylococcus organism aureus (Coagulasenegative staph) At 24 to 48 hours Stop Stop ceftazidime or Stop ceftazidime or cephalosporins aminoglycoside aminoglycoside Start ampicillin Continue Continue 125 mg/L/bag cephalosporin cephalosporin Consider adding aminoglycoside If ampicillinIf MRSA.Table 30. MRSE = methicillin-resistant enterococcus. catheter colonization. Choice of final therapy should always be guided by antibiotic sensitivities. VRE = vancomycin-resistant enterococcus. start vancomycin Duration of therapy 14 days 21 days 14 days At 96 hours If no improvement. 189 . aureus. start vancomycin clinically not vancomycin responding. re-culture and evaluate for exit-site or tunnel infection. etc.5. start If MRSE and resistant.

190 . MD 200 mg/L Continue cephazolin/cloxacillin and Multiple gramnegatives and/or ceftazidime and add metronidazole. ciprofloxacin 500 mg.8 hours. Gram improvement stain.i. Treatment recommendations if a gram-negative organism is identified on culture at 24 to 48 hours Duration of therapy Single gramAdjust antibiotics to sensitivity 14 days negative organism < 100 mL urine. 500 mg 21 days q. consider surgical intervention IV = intravenously.6. IP = intraperitoneally. Treatment strategies if peritoneal dialysis fluid cultures are negative or not performed Continue initial therapy Duration of therapy If clinical Continue treatment 14 days improvement If no clinical Repeat cell count. b. or rectally anaerobes If no change in clinical status. or imipenam/cilastatin LD 500mg/L.d. and culture at 96 hours Consider change to vancomycin. p. adjust therapy 14 days accordingly If culture negative.o. aminoglycoside > 100 mL urine.o. or piperacillin 4 g IV q.Table 30. consider infrequent 14 days pathogens and/or catheter removal Table 30.12 hours or sulfamethoxazole/trimethoprim 960 mg/day p. aminoglycoside > 100 mL urine.o.7. ceftazidime Pseudomonas/ Continue ceftazidime and add 21 days stenotrophomonas < 100 mL urine. p. IV.. continue ceftazidime/ aminoglycoside If culture positive.

8. or IP 200 mg daily If organism resistant.tropicalis. but 50% in those in whom the catheter was left in place. Timing of catheter reinsertion – no evidence but current practice recommends catheter reinsertion at least 4 weeks after catheter removal. Management of fungal peritonitis 10.13 (Level C) Fungal peritonitis in CAPD patients accounts for about 5-10% of peritonitis episodes among CAPD patients. Krusei Non-yeast spp Table 30. C. glabrata . non-albicans e. Loading dose 2 g IV. If no clinical improvement. • • • • Imidazole/triazole plus flucytosine combination is as effective as amphotericin B in treatment of fungal peritonitis. C.12.d. consider itraconazole IP 100 mg 12 hourly 191 .albicans C. Therapy with antifungal agents should be continued after catheter removal for at least an additional 10 days longer. maintenance dose 1 g q. Clinical presentation does not differ from bacterial peritonitis but should be suspected in culture –negative peritonitis or peritonitis not responding after adequate doses of conventional antibiotics. parapsilosis. 200 mg po. Mortality at 1 month was 15% in patients in whom the catheter was removed within a week of diagnosis.g. Type of fungus C. iv. C.b. remove catheter and continue therapy for 10-14 days after catheter removal with fluconazole 200 PO daily and flucytosine 1 g IV after hemodialysis. . C. duration of therapy 4-6 weeks. Treatment of fungal peritonitis At 24 to 48 hours Flucytosine Fluconazole At 2-4 days If clinical improvement.

Empirical treatment should be commenced based on previous culture while awaiting culture results. Chest X-Ray and Mantoux test may not be helpful. There is high risk of optic neuritis with ethambutol.3. Catheter removal and reinsertion PD catheter removal should be considered when peritonitis is unlikely to resolve with catheter in-situ. Streptomycin should be avoided. Management Of Tuberculous Peritonitis 10.. The timing of catheter replacement should be 4 weeks following catheter removal although the optimal period is not known. Treatment: Anti-TB drugs should be started with removal of catheter at diagnosis. Inadequate dosing has been found to predispose to relapse. Relapsing Peritonitis Definition: Peritonitis caused by the same organism occurring within 4 weeks of completion of the antibiotic therapy. rifampicin and pyrazinamide together with pyridoxine should be prescribed for 9-12 months. Early peritoneal biopsy should be considered in the presence of non-resolving peritonitis with lymphocytosis. laparotomy or percutaneous peritoneal biopsy.7. (Level B) 30.6.c.14 • • Tuberculous peritonitis is uncommon and accounts for less than 4% of peritonitis episodes among CAPD patients. Peritoneal membrane biopsy is best obtained at the time of catheter removal. Smear and culture may be negative and diagnosis may be from tissue obtained through peritoneoscopy. At least three anti-TB drugs – isoniazid.3. • • 30. Isolation of mycobacteria from peritoneal effluent is difficult. These include: • • • • • • Fungal peritonitis Tuberculous peritonitis Perforated bowel Persistent exit/tunnel infections Peritonitis not responsive to second line antibiotic treatment Relapsing peritonitis not responding to treatment. 192 .

d.i. adjunctive therapy should be considered on an individual basis and may include the following: a.Table 30. Management of relapsing peritonitis Organism Management Coagulase neg/pos cephalosporin for 4 weeks staphylococcus MRSA/S. consider catheter removal and surgical exploration. Thrombolytic therapy may be occasionally useful in patients with recurrent peritonitis (Level C). cephalosporin 193 . 30.3.epidermidis vancomycin for 4 weeks.metronidazole b. Prophylactic Antibiotic use Short term antibiotic prophylaxis may be considered in the following situations: a. Coagulase pos Search for occult tunnel infection staphylococcus Enterococci Ampicillin plus aminoglycoside Look for intra-abdominal abscess Consider catheter removal if no response after 96 hours Gram negative bacilli Evaluate for intra-abdominal abscess. Invasive procedures associated with transient bacteraemia (level C) • dental procedures – amoxycillin 2 g prior to procedure • genito-urinary instrumentation: ampicillin plus ceftazidime/aminoglycosides • gastrointestinal .9.8. Antifungal prophylaxis with oral nystatin at a dose of 500 000 u q. Adjunctive therapy for peritonitis In patients who are being treated for peritonitis.g.3. 30.9. Technique break • Although no data is available. current practice recommends 1-2 day course of antibiotics e. 15 b.ampicillin plus ceftazidime/ aminoglycosides +/. during and for a few days after the course of antibiotics (Level B).

18 In view of this fact. In some patients. Hence. the constant energy source may exacerbate malnutrition. METABOLIC COMPLICATIONS IN CAPD16 30. 30. Continuous contact between the peritoneum and glucose-based solutions may induce peritoneal mesothelial damage by nonenzymatic glycosylation leading to the formation of advanced glycosylation end-products ( AGE’s). hypertriglyceridaemia and premature atherosclerosis. Metabolic complications of glucose absorption Uraemia per se is associated with hyperinsulinaemia.4. and the proven benefit of lipid-lowering therapy in the general population.4.30. PD patients have a 15 to 25 fold higher annual rate of cardiovascular mortality. Hyperlipidaemia Peritoneal dialysis is associated with the following abnormalities. Icodextrin may be considered in the event of problems with ultrafiltration although evidence is still lacking.17 • increased total and LDL cholesterol concentration • increased apolipoprotein B concentration • decreased HDL cholesterol concentration • decreased apolipoprotein AI concentration • increased triglyceride concentration • preponderance of small dense LDL particles • increased lipoprotein (a) lipid Hyperlipidaemia (in particular elevated LDL) as well as increased small dense LDL particles and lipoprotein (a) in the general population has a strong association with coronary artery disease (level A evidence). The average carbohydrate load of 100-150 g of glucose per day through CAPD exchanges amplifies the abnormalities in carbohydrate metabolism and leads to metabolic problems such as obesity.4. 194 .g. use of hypertonic glucose-based CAPD solutions should be minimised wherever possible and alternative solutions e. Evidence in the dialysis population is still not available. When compared with a non-uraemic cohort.1.2.

Tzardis PJ. Johnston JR. Hyper/hypokalaemia a. Lutes R A randomised trial of Staphylococcus aureus prophylaxis in peritoneal dialysis patients: mupirocin 8. Manouras AJ et al.54(5):318-9 Gokal R. Piraino B. Serum potassium levels should be monitored regularly. Kidney Int. Holley J. Nephrol. 6. 7. Haride IR et al. • References 1. Chen TW. Jureqicz WA. However there are no long term trials with lipid lowering treatment in the dialysis population so the value of this approach is still uncertain. Rigby RJ. Oreopoulos DG. Postgrad Med J. Lord RHH. 2. 1986. Stegmayr B. Abdominal hernias complicating CAPD. 4. 1993. Khanna R. Piraino B. 6:271-274 Sepnce PA. Mathews RE. Peritoneal catheters and exit-site practices toward optimum peritoneal access: 1998 update. Surgery. Joffe P. Twardowski Z. HDL and LDL should be measured every 6 to 12 months • It may be reasonable to treat hyperlipidaemia with diet and lipid lowering agents (level D evidence). 3. J. Improved results with a paramedian technique for the insertion of PD catheters. 40(Suppl 49) S75-80 Morris-Stiff GJ. Danielson A.( Official report from the ISPD). Alexander S. 1985. Prowant B. Abdominal and inguinal hernias in continuous ambulatory peritoneal dialysis patients. Am Surg.Serum cholesterol. 1988. Bowrey DJ. 161:585-587 Apostolidis NS.150(3):357-60 O’Connor JP. triglycerides. 195 .18(1):11-33 Bernardini J. Holmes C. Perit Dial Int 1998. Ash S. Gynecology & Obstetrics. 1998. 30. Vas S.4. Slingeneyer A. 74:699-670 Wetherington G. Filo RS. Hypokalaemia Causes: Ongoing losses through dialysis solution Poor nutritional intake Treatment: Oral supplement to raise serum potassium concentration to > 3 mmol/L and 3.3. Nichols K. 5. Robison RJ. Management of inguinal herniae in patients on CAPD: an audit of current UK practice. Moncrief J. The incidence of postoperative hernia as related to the site of insertion of permanent peritoneal catheter. Leapman SB. Complications of peritoneal dialysis related to increased intraabdominal pressure. Bargman JM. Am . Am J Surg 1985.5 mmol/L in patients on digoxin or history of cardiac arrhythmias.

17.Y. Cheng SW. A prospective randomized control study of oral Nystatin prophylaxis for Candida peritonitis complicating continuous ambulatory peritoneal dialysis.20 Suppl. 12. Lui SL. Vas S. Adult peritoneal dialysis-related peritonitis treatment recommendations:2000 update. Fungal peritonitis in patients on peritoneal dialysis: incidence. Passadakis P.B. 16. Euthimiadou A. Lo CY. Fang GX. Kluwer Academic Publishers Prichard S. 18. Gokal R. . 14. Choy. Gallagher N. Ioannidis JPA. 9(Suppl Dec):S16-23.9. Chan TM.Nephrol 1985. Epidemiology of cardiovascular disease in chronic renal disease. 13. Chan PC. Chan MK. Br Med J 1996. Textbook of Peritoneal Dialysis 2nd edition. Lo WK. Ramsey PG. Lo WK. Sarnak MJ. 27: 695-700 Thodis E. Optimal treatment and long-term outcome of tuberculous peritonitis complicating continuous ambulatory peritoneal dialysis. Cheng IKP. Perit Dialysis Int Vol. Am J Kidney Dis. Am J Kidney Dis. The effectiveness of mupirocin preventing staphylococcus aureus in catheter-related infections in peritoneal dialysis. Adv perit dialysis. Fungal peritonitis complicating peritoneal dialysis: Report of 27 cases and review of treatment. 11.2 : S154-S159 Foley RN. calcium ointment 2% applied to the exit site versus cyclic oral rifampin. Ahmad S. 28(5):747-751. 2000. Cappelleri JC. Khanna R. Single or multiple daily doses of aminoglycosides: a meta-analysis.Cheng IKP. Cheng IKP. Panagoutsos S. Parfrey PS. Boeschoten E. Lau J.71:407-416. Krediet R and Nolph. clinical features and prognosis: Am J.1996. Am J Kidney diseases. eds. 16:257-261 Keane WF. Q J Med 1989. Johnson RJ. J Am Soc Nephrol. 10. Gokal R. Riella M. Chan CY. Major and minor risk factors for cardiovascular disease in peritoneal dialysis. Piraino B. Vargemezis V. Bailie GR.1996. 1996. 15. Holmes CJ. 28 :549-552. Perit Dial Bull 2000.5:169-175. 20: 610-624 Barza M. Golper TA. Kawaguchi Y.312:338-345.K. 196 . Chan TM. Daniel Tak-Mao Chan. Bacharaki D. Poon JMP. 1998.

DAPD Standard dose PD Standard dose PD High dose PD High dose PD or HD Preferred dialysis prescription 197 .30. Ultrafiltration Failure in CAPD 30. Baseline PET prognostic value Solute transport High High average Low average Low Predicted response to CAPD UF Poor Adequate Good Good Excellent Clearance Adequate Adequate Adequate Inadequate Inadequate APD.1. The Peritoneal Equilibration Test (PET)1 The PET defines the peritoneal membrane’s clearance and ultrafiltration characteristics by measuring the dialysate to plasma ratios of creatinine and dialysate glucose at specific times under standard conditions.10.5. The peritoneal equilibration test results Table 30. a PD regime can be more accurately selected to optimise dialysis.5. Once the membrane permeability is identified.5. Results from the PET classify patients into four basic groups as shown below: Figure 30.

3. 2. 4. Dialysate for creatinine. urea and glucose. soak injection port with methylated spirit/povidone iodine for 5 minutes. 198 . urea and glucose. 3. Label the specimen 0 hour PET. Obtain 10 mls sample of effluent for creatinine. At 0 hour: 1. Measure and record effluent volume. Ask patient to roll from side to side. 6. Then drain 200 ml of effluent into drain bag. Then drain 200 mls of effluent into drain bag. Using aseptic technique. creatinine and glucose. 2. Using aseptic technique. Obtain 10 mls sample of effluent for creatinine. At 2 hours: 1. At 4 hours 1. At 4 hours after initial infusion.Standard Peritoneal Equilibration Test (PET) Procedure Initiate after 8 – 12 hours overnight dwell of standard CAPD.5% dialysate by infusing over 10 minutes. 4. drain exchange over at least 20 minutes. 4. Reinfuse remaining 190 ml of effluent. The following samples are sent for analysis: 1. Record time infusion is completed – considered the 0 hour. urea and glucose testing. soak injection port with methylated spirit/povidone iodine for 5 minutes. 6. Two hours after initial infusion obtain blood sample for blood urea. 5. Label specimens 2 hour PET. Under aseptic technique obtain 10 ml sample of effluent for creatinine. 7. Drain dialysate completely from patient over 20 minutes and note volume drained. 2. with patient in vertical position. 2 and 4 hours. Reinfuse the remaining 190 ml of effluent. 3. Advise patient to ambulate or sit. urea and glucose at 0. Perform exchange procedure with 2000 ml Dextrose 2. 5. soak injection port with methylated spirit/povidone iodine for 5 minutes. Using aseptic technique.

Inappropriate tonicity . • Exaggerated contrary mechanisms . Ultrafiltration (UF) failure in simple terms can be defined as the failure of peritoneal fluid removal to match the volume balance needs of the patient being treated by PD i.High transport status .2. • Inadequate provision of ultrafiltration conditions . failure to maintain volume homeostasis.Obstruction and other catheter malfunctions 199 .2 Input dependent cause • Excessive salt/water intake Output dependent causes • Uncompensated loss of residual renal function. 8-12% of CAPD patients were transferred to HD yearly because of membrane failure.25% dextrose solution may be considered abnormal. Blood for creatinine.Loss of functional peritoneum • Mechanical failure of dialysis procedure . 30.Aquaporin deficiency . Causes of UF failure. urea and glucose at 2 hours. or a net UF volume of <400 ml after a 4 hour dwell using 4. Once the values are obtained. the calculations can be made and the values plotted onto the PET graph as shown below.4 a.5. Ultrafiltration Failure in CAPD From the Malaysian dialysis and transplant registry.Lymphatic/tissue reabsorption • Failure of peritoneal response .e.2. Note the range in which the patient’s values fall and use the prognostic value table shown above to select the appropriate PD regime.Long dwells .Mismatch of prescription and PET status.2.5% dextrose solution according to standard PET. A net UF volume of <100 ml after a 4 hour dwell using 2.

5 Mechanical causes Enhanced reabsorption Aquaporin deficiency Disruption of Inherent high Peritoneal space Recent peritonitis Long term PD c.Dietary indiscretion/compliance • Deficient education • Complex regime • Burn-out Appropriate prescription • Dwell time • Dialysate tonicity Mechanical problems • Leaks • Obstruction • Entrapment • Mal-position Evaluation of peritoneal membrane function Ultrafiltration response Modified PET – 4.81 drain volume< 2400 ml/4 hrs small solute profile (PET) High average/ low average 0. Diagnosis Volume / fluid overload Evaluation for reversible causes .25% 2 Litres drain volume > 2400 ml/4 hrs re-evaluate clinically Low transport D/P Cr < 0.81 > D/P Cr > 0. Treatment General Guidelines (level C) • • • • Routine standardised monitoring.b. including awareness of PET status Dietary counselling concerning appropriate salt and water intake Protection of residual renal function Loop diuretics if residual renal function present 200 .5 High transport D/P Cr > 0.

201 . Gokal R.15(6):22630. A randomized multicentre clinical trial comparing isosmolar Icodextrin with hyperosmolar glucose solutions in CAPD. Moore H. 7: 138-147 Mujais S: Ultrafiltration failure. Raymond Krediet and Karl Nolph eds. 3. Peers E. How to measure ultrafiltration failure: 2. 2nd Ed 2000 Mistry CD. 1997. Ramesh Khanna. Nielsen M. Prowant B. In Ram Gokal. and the MIDAS Study Group.• • • Enhanced compliance by education Hyperglycaemia control Preservation of peritoneal membrane function CAPD • • • • Avoid long dwells Use of night. Textbook of Peritoneal Dialysis. 2. Roppe B. Twardowski ZJ. Nolph KD. 1995. Ryan L.27% or 3. Peritoneal Equilibration Test. Perit Dialysis Bul. Perit Dial Int. 1987.time exchange device Tailoring prescription to transport profile determined by PET Use of icodextrin for long dwells3 APD • • Avoidance of long dwells with low glucose concentrations Use of short day dwells even when no additional exchange is needed for clearance References 1. 17: 125-128 4.86% glucose? Perit Dialysis Int.

31. Measures of protein energy malnutrition Category Measure Minimum frequency of measurement in PD patients 3 monthly Predialysis or 1. Malnutrition is strongly associated with increased morbidity and mortality in patients with end-stage renal failure from both international studies and local renal registry data.g. Adequate nutritional support and dialysis treatment alone is insufficient unless the co-morbid and inflammatory conditions are adequately treated.1. co-morbidity e. inflammation.1. no single measurement that provides a comprehensive indication of protein-energy nutrition status.associated with the uraemic syndrome. Periodic assessment of nutritional status should be part of the routine care of dialysis patients to ensure early recognition of malnutrition and institution of appropriate therapy. There is however. MALNUTRITION Evidence from both cross-sectional and longitudinal studies1-3 suggest that up to two-thirds of patients on haemodialysis and CAPD are malnourished (Grade B evidence). below8: Table 31. and increased protein catabolism.6 (Grade B evidence) Two different types of malnutrition exist in dialysis patients 7. chronic heart failure. Measurements stabilized serum that should be albumin performed routinely in all patients Subjective global Every 6 months assessment (SGA) nPNA Every 3-4 months 2.1. • Type 2 or “cytokine-driven” malnutrition . This may be reversible with adequate dialysis treatment and nutritional support.31. Measures that Skinfold thickness As needed 202 .5. • Type 1 . Hence a combination of measures is recommended as in Table 31.4.marked hypoalbuminaemia.

g.cholesterol As needed As needed As needed As needed 31.e. might suggest the need for a more rigorous examination of protein-energy nutritional status Mid-arm muscle area. if low. have a high content of essential amino acids. cost/limited access to food .regular review ± modification based on the patient’s medical and social conditions If DPI remains inadequate Oral energy and protein supplements 203 .creatinine .3 g/ kg BW/ day11.suggestion of alternative food sources if palatability is a concern . Clinically useful measures which.identification of any specific issues e.urea nitrogen .2. The recommended dietary protein intake (DPI) for clinically stable CPD patients is 1. circumference/diameter Predialysis or stabilized serum .2 – 1.may be useful to confirm/ extend the data from measures in Category 1 3. (Level C) NB: Both protein and caloric intake recommendations should be based on ideal rather than actual body weight At least 50% of the protein intake should be of high biological value i. Patients who do not have an adequate DPI should be managed in a stepwise manner as in the flowchart below: Inadequate DPI Counseling from a trained dietician Should include .

3. avoidance of drugs which exacerbate anorexia prevention and control of hyperparathyroidism maintenance of vitamin D homeostasis correction of acidosis optimal treatment of catabolic comorbid conditions provision of adequate dialysis minimisation of the use of hypertonic glucose-based dialysates 31. High dose folic acid supplementation has been shown to reduce homocysteine levels. 31. 31.6.9.7. 31. Supplementation of water soluble and not fat soluble vitamins is recommended.4.1.6.6. 31.6.and polyunsaturated fats. The recommended daily energy intake for CPD patients is 35 kcal/ kg BW/d for those < 60 years of age and 30-35 kcal/kg BW/d for those 60 years or older10.3. prevention of peritonitis 31.12 ( Grade C evidence) 31. Consideration should be given to adequacy of dietary intake of mineral and trace elements.6. It is recommended that only up to 30% of energy intake is in the form of fat.6.5. timely initiation of dialysis 204 . intraperitoneal amino acids and parenteral nutrition should ideally be implemented if above measures fail but this is dependent on availability of resources. 31.2. 31. 31.8. Specific attention should be given to factors impacting on the patient’s nutritional status which are independent of nutrient intake.5.6. Carbohydrate should be predominantly in the form of starch.6.6. 31.6.4.Other measures eg enteral feeding. 31. with preference for mono.6. 31.

17: 462-71 4. Kidney Int 1982. New strategies for the management of malnutrition in peritoneal dialysis patients. Gabella P. Adequacy of dialysis and nutrition in continuous peritoneal dialysis: association with clinical outcome J Am Soc Nephrol 1996. Lim TO. Nutrition and adequacy of dialysis. Moran J. DeVecchi A. Laidlaw S Kopple J. Canada-USA (CANUSA) Peritoneal Dialysis Study Group. Death risk in hemodialysis patients: the predictive value of commonly measured variables and an evaluation of death rate differences between facilities. 21: 849-861 10. Lindholm B. 205 . Furst P. Blumenkrantz MJ. Clin Nephrol 1988. 20:271-275 8. Am J Kidney Dis.Vonesh EF. Lindholm B.2 : S166-S171 12. 2000. Lindholm B. Am J Kidney Dis 1990. Lew NL.20 Suppl. nitrogen balance and nitrogen losses in patients treated with continuous ambulatory peritoneal dialysis. Protein and energy intake. Kidney Int 1989. Am J Kid Dis 1991. Monteon FJ. Kopple JD. How do haemodialysis and CAPD compare? Kidney Int Suppl 1993. Kopple J. Marckmann P. Young GA. Eleventh Report of the Malaysian Dialysis and Transplant Registry 2003.35(6 Suppl 2):S1-140 9. Steinvinkel P. Ramello A Use of amino acids in peritoneal dialysis solutions. Alvestrand A.40:S39-S50 2.7: 198-207 6. Effect of energy intake on nutritional status in maintenance haemodialysis patients. Nutritional assessment of continuous ambulatory peritoneal dialysis patients : an international study. Kidney Int 1993. 29 : 75-8 3. National Kidney Foundation DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure.44: 1048-57 11. Nutritional status of patients on haemodialysis and peritoneal dialysis. 15 : 458-82 5. Slomowitz LA. Coburn J. Perit Dial Int 2000. Lindholm B. Bergstrom J. Kuala Lumpur 2004 7. Lowrie EG. Lim YN (Eds). Bruno M. Perit Dialysis Int 2000. et al. Grosvenor M.References Bergstrom J. Metabolic balance studies and dietary protein requirements in patients undergoing continuous ambulatory peritoneal dialysis.35:704-11 1. Scalamogna A. Heimburger O.

1: Reasons for discordance: a. and both measurements have been shown to be associated with outcomes in studies. BP control.8 (peritoneal Kt/V) did not result in poorer outcome. renal osteodystrophy. Recent studies have increasingly shown that renal clearance and peritoneal clearance are not equivalent and a lower total Kt/V of 1. phosphate control. Hence although the target Kt/V value is still not defined. Kt/V urea should be the minimum target of adequacy 32. and total creatinine clearance > 60L/ 1.1. there should be a minimum peritoneal Kt/V of at least 1. causes for the discrepancy should be sought and patient monitored closely for signs of under-dialysis.32.73m2 should be used to measure delivered PD dose as each measure provides slightly different information. (Level B) The K/DOQI guidelines recommends a total Kt/V of > 2. correction of anaemia. Amount of residual renal function and its relative contribution to Kt/V and CrCl b.(Level A). • measurement of delivered dialysis dose • dietary protein intake.1. nutritional status.73m2 per week. 32. When there is a discordance between weekly Kt/V urea and CrCl.9 Other parameters – protein intake. CAPD ADEQUACY GUIDELINES Delivered dose of CAPD should be routinely measured and monitored as clinical signs and symptoms may be unreliable indicators of adequacy and studies have shown correlation between delivered dose of CAPD and patient mortality and morbidity. Dwell time d. (Level B) Dialysis adequacy should be assessed by • clinical parameter . Difference in peritoneal transport of urea and creatinine c. PD dose and total solute clearance Both total and peritoneal weekly Kt/V urea and total and peritoneal weekly creatinine clearance(CrCl) normalised to 1. sodium and fluid removal and BP control should be considered in the assessment of adequacy of dialysis treatment.Influence of patient size on normalisation 206 .6 and peritoneal creatinine clearance of 45 L/week.0 per week.dry weight.

Patient performs first bag exchange.3. The 24 hour urine collection should begin in the morning and the first morning specimen should be discarded.3.3. Save all exchanges in the next 24 hours period i. 24 hours urine a. This should be done on the same day as the dialysate collection. glucose and albumin 32.32. creatinine. Obtain blood sample for urea. Collect every subsequent urine specimen including the first morning urine sample of the following day. Perform an exchange the next morning and save. Frequency of measurement • 2-4 weeks after initiation of CAPD • 6 monthly thereafter Measurement of dialysis dose should be done when the patient is clinically stable. f. b. a. and discard b. For patients who void > 3 x/day.2. e. c. 3 and 4 c.2. d.3. Sending specimens to the lab 10 mls of mixed effluent for urea and creatinine Blood for urea.3.1. 24 hours dialysate a. and should be delayed for > 4 weeks after resolution of peritonitis. Protocol for Kt/V measurement 32. 48 hr urine collection is recommended 32. 24 hr urine collection is sufficient but for patients who void < 3 x/day. Using syringe. Weigh all 4 bags separately. d. aspirate 1 % of dialysate volume from each bag into a container and mix thoroughly g. Bring urine to the CAPD unit NB. 32. h. Draw 10 mls of the above mixed effluent for creatinine and urea. Bring all 4 bags of effluent to the CAPD unit. Record total volume of effluent per 24 hours.e. Record the time of first urine specimen c. b. creatinine. albumin and glucose 24 (or 48) hours urine for urea and creatinine 207 . exchanges 2.

7(2):198-207 3. a Prospective.1. albumin level ( target > 35 g/L) b.30(Suppl 2) : S67-136 2. Critique of CANUSA. Oreopoulos DG. Nutritional assessment Nutritional status should be monitored regularly as there is a correlation between nutrition and dialysis dose. Ramos A. Nephrol Dial Transplant 1995 Oct.4. Mujais for the Mexican Nephrology Collaborative Study Group. nPNA ( target > 1g/kg/day) c. A longitudinal study. Prognostic factors in CAPD patients: a retrospective study of a 10-year period. Moran J. Zubani R . Blake PG. There is also strong indirect evidence linking survival with nutritional status. Churchill DN. Nolph KD. Clinical practice guidelines for peritoneal dialysis adequacy. Adequacy of dialysis and nutrition in continuous peritoneal dialysis: association with clinical outcomes. Oreopoulos DG. Faller B. Correa-Rotter R. Nephrol Dial Transplant 1995 Dec. J Am Soc Nephrol 1998. both at initiation of dialysis and on follow up 32. Maiorca R. CANUSA Peritoneal Dialysis Study Group. Subjective global assessment (SGA) References: 1. National Kidney Foundation Dialysis Outcomes Quality Initiative.16:448-56 7. Perit Dial Int 1996. Kidney Int 1999. Burkart J. Churchill D. Increased peritoneal membrane transport is associated with decreased patient and technique survival for continuous peritoneal dialysis patients. J Am Soc Nephrol 13: 1307–1320. 2002 208 . Perit Dial Int 1996. randomized. Keshaviah PR.Vonesh E. controlled trial.32. J Am Soc Nephrol 1996 Feb.55:1131-49 8. Blake PG. Paniagua R. Brunori G. Measurements of nutritional status : a. Hedelin G: Schaffer P. The optimization of continuous ambulatory peritoneal dialysis. Thorpe KE. Recommended clinical practices for maximizing peritoneal dialysis clearances. Page D. Am J Kidney Dis 1997. Amato D.16:243-5 4. The CanadaUSA (CANUSA) Peritoneal Dialysis Study Group.9: 1285-92 9.4. Predictive value of dialysis adequacy and nutritional indices for mortality and morbidity in CAPD and HD patients. 10(10):1905-11 5. Effects of increased peritoneal clearances on mortality rates in peritoneal dialysis: ADEMEX.10(12):2295-305 6. Genestier S.

4.1100ml/m2. Adequate Dose of Peritoneal Dialysis 33. using exchange volume of 900 . Solutions used are as for adults except that volumes of 1. It is the opinion of the DOQI Work Group that since the nutritional requirements per kg of body weight are higher in children than in adults. 33.1 33. 33.3. Catheter insertion. Catheters commonly used are as for adults except for the size – paediatric and neonatal straight double cuff Tenckhoff catheters are commonly used.5L and 1. scaling of intraperitoneal fill volume by body surface area (BSA) is recommended. partial omentectomy may be helpful in preventing catheter obstruction3 . The recommendations for adult patients apply to children as well.2. may have to be higher than PD doses in adults4 . morbidity or mortality. Higher fill volume used compared to CAPD because of enhanced tolerance to the intraperitoneal fill volume in the supine position in APD.3. CAPD : usually 4 – 5 exchanges.2 A fill volume of 900 – 1100 mL/m2 is recommended for most paediatric patients to achieve a theoretical weekly target Kt/Vurea of > 1.1.9.4.1. There are currently no definitive outcome data in paediatric patients to suggest that any measure of dialysis adequacy is predictive of well being. APD : usually 8 – 10 exchanges over 8 – 10 hours at night. 33.1. Weekly dose of CAPD.1.33.2. and especially small infants who have very high protein intakes. Theoretically this will result in a weekly target Kt/Vurea of greater than 1. In addition. 209 . In children. PERITONEAL DIALYSIS IN CHILDREN CAPD/APD is the preferred form of dialysis for children with ESRD.9 for the average patient. the PD doses in children. 33.0L are available. Chronic peritoneal dialysis prescription 33. Access.3.

or PO q 2448H (max dose 200 mg) __ 50 mg/kg IV 25-37. Weekly dose of APD. or mortality.0 g) Aminoglycosides 25 mg/L 12 mg/L __ Amikacin 8 mg/L 4 mg/L __ Gentamicin 8 mg/L 4 mg/L __ Netilmycin Penicillins Formatted: Ge Formatted: Ge Formatted: Ge Formatted: Ge Formatted: Ge 210 . Table 33. __ Fluconazole IV. Treatment of peritonitis in children5 The Guideline for the treatment of peritonitis in children is similar to that for the adult patients with the exception that aminoglycosides should be avoided unless absolutely indicated.33.4.5 Flucytocine or PO (max mg/kg PO q dose 2.) Loading dose Maintenance Intermittent dose therapy Glycopeptides 500 mg/L 30 mg/L Vancomycin 30 mg/kg q 5-7 days 200 mg/L 20mg/L Teicoplanin 15 mg/kg q 5-7 days Cephalosporins 250 mg/L 125 mg/L Cefazolin/ 15 mg/kg q24H cephalothin 200 mg/L 125 mg/L 15 mg/kg q24H Cefuroxime 500 mg/L 250 mg/L 30 mg/kg q24H Cefotaxime 250 mg/L 15 mg/kg q24H 125 mg/L Ceftazidime 250 mg/L 125 mg/L Ceftizoxime Antifungals __ 1mg/kg/day Amphotericin B 1 mg/kg IV IV __ 3-6 mg/kg IP.5. morbidity.1: Paediatric Antibiotic Dosing Recommendations (Administration should be via intraperitoneal route unless specified otherwise.0 g) 24H (max 1. Again there are no definitive outcome data in paediatrics to suggest that any measure of dialysis adequacy is predictive of well being.2. 33.

Schooling 33. Table 33.6.2.6.7. Quality of Life Issues. 33.6.6. Nutrition.3. Minimal restriction of physical activities 33.Piperacillin Ampicillin Oxacillin Amoxicillin Quinolones Ciprofloxacin Combinations Ampicillin/ Sulbactam Imipenem/ Cilastin TMP/SMZ Others Metronidazole Rifampin __ __ __ 250 -500 mg/L 50 mg/L 1000 mg/L 500 mg/L 320/1600 mg/L __ __ 250 mg/L 125 mg/L 125 mg/L 50 mg/L 25 mg/L 100 mg/L 200 mg/L 80/400 mg/L __ __ 150 mg/kg IV q 12 H __ __ __ __ __ __ __ 35-50 mg/kg/d PO in 3 doses 20 mg/kg/d PO (max 600 mg/day) 33. Growth and developmental progress measured serially 33.1.2: Nutritional parameters and appropriate minimum schedule of testing or measurement for patients on HD and PD 6 Minimum Interval Parameter Below 2 years 2 years and Over Length 3 Monthly Not applicable *+ Standing height Not applicable 3 mo Head circumference Monthly 3-4 mo until 36 mo+ Estimated dry weight Monthly 3-4 mo + Weight/height index Monthly 3-4 mo+ Z score or SDS height 3 monthly 6 mo for chronological age Serum albumin Monthly 3 Monthly+ Serum bicarbonate Monthly 3 Monthly+ Skinfold thickness No agreement 3-4 mo+ Midarm 3-4 mo 3-4 mo+ 211 .

3: Daily dietary recommendation for children on CAPD Infants Children / Adolescents Minimum of RDA for Minimum of RDA Energy height age for age 3.5 g/kg ht age 5-10 years 2.5 (>7yr) 212 .age 2-5 year 3-4 g/kg Protein 2.0 (<7yr).0 g/kg ht.4-0.2-2. 1.5 g/kg ht age >12years Sodium Potassium Calcium Phosphorus Vitamins: Water soluble Fat soluble Trace elements Zinc (mg) Copper (mg) 1 mmol/kg 3 mmol/kg and restriction supplement as necessary may be liberalized supplement avoid supplementation 5 0. + opinion Monthly 6 mo 3-4 mo+ 6 mo+ Table 33.0g/kg ht age 10-12 years 1.circumference Dietary interview Urea kinetic modelling * evidence.5-2.7 26 – 100 mmol/day if necessary 25-50 mmol/day if necessary supplement as necessary generally 240 ml milk/day supplement avoid supplementation 10-15 0.

Suppl 2 (June). Nolph KD. Salusky I. Am J Kidney Dis 30:S67-S136. Nicholson M. 6:610-624 K/DOQI Nutrition in Chronic Renal Failure. 11:330-332. Tranaeus A. 20. Piraino B. Burton P. In: Gokal R. 14:236-9. International Society for Peritoneal Dialysis (ISPD) Advisory Committee on Peritonitis Management in Pediatric Patients. 35:6. 2. The textbook of peritoneal dialysis. Peritoneal dialysis in children. Holloway M. Kandert M. Dordecht: Kluwer Academic. Kohaut EC. 1994:591-637. The effects of changes in dialysate volume on glucose and urea equilibration. 3. Eds. Balfe JW. Donnelly P. Warady BA. Mujais S. 213 . 4. Veitch P. The Role of omentectomy in Continuous Ambulatory Peritoneal Dialysis. Divino J. Waldo FB. Walls J. Verrina E. Perit Dial Int 2000. ISPD Guidelines/recommendations. Harvey E. Alexander S. Perit Dial Int 1994. NKF-DOQI Peritoneal Dialysis Adequacy Work Group Members (1997) NKFDOQI clinical practice guidelines for peritoneal dialysis adequacy. Am J Kidney Dis. Schaefer F. S105-S136 6. Perit Dial Int 1990. Honda M. Bienfeld M. 2000. 5.References: 1. Consensus guidelines for the treatment of Peritonitis in Pediatric Patients receiving peritoneal dialysis. Alexander S.

Patients with limited self-sufficiency d. High average and high transporters b.3.2.2.1.1. NIPD – nightly intermittent peritoneal dialysis. CCPD – continuous cycling peritoneal dialysis.34.4. This may be preceded by several rapid flushes of dialysis solution at diagnosis to help reduce 214 . 34. CTPD may be the only way that some larger or anephric patients can achieve target clearance rates c.1.1. Modification of APD regimen for treatment of peritonitis: The initial (24 – 48 hours) treatment of peritonitis should include a prolongation of the dialysate dwell time to 3-6 hours until there is clearing of the peritoneal effluent.73 m2 b.1. APD performed only at night with complete fill and drain of the peritoneal cavity 34. Peritoneal transport characteristics c. NTPD – nightly tidal peritoneal dialysis.1. CTPD – continuous tidal peritoneal dialysis. Total prescribed dialysate volume per session 34. These latest two modalities are also called PD plus therapy 34. Patients with hernias or leaks 34. The various APD techniques available are: 34. Fill volumes – 40 mL/kg or 2. APD performed only at night with partial fill and drain of the peritoneal cavity 34.5 L/1. AUTOMATED PERITONEAL DIALYSIS (APD) APD includes every type of peritoneal dialysis performed with the aid of a cycler. The efficiency of APD is affected by a. APD performed at night (tidal modality).3.2. but with the addition of one or two daytime dwells 34. with the addition of one(CTPD1) or two(CTPD2) daytime dwells.1. Prescription and delivery of APD 34. Children e.2. APD performed at night. Patient selection criteria for APD: a.2.

or maintenance dosing if patient continues on APD. the patient may return to a more standard APD regimen or be converted temporarily to standard CAPD regime. Data on dosing of antibiotics for patients on APD is lacking but generally follows that for single daily dosing for CAPD. When the effluent demonstrates clearing which typically occurs within the initial 48 hours.abdominal pain. 215 .

Contraindications 35.5. then draped. 216 . 35.1.3. aneurysm.6.6. INTERMITTENT PERITONEAL DIALYSIS 35. Indications 35.4.1. Under aseptic conditions. A small skin incision. Acute renal failure 35.4.2.2 If necessary.3.1. 11). The puncture site is usually in the midline – about one inch below the umbilicus.2. slightly smaller than the diameter of the catheter is made using a sharp pointed scalpel blade (No. 35.9. The operator should be masked. scrubbed and gloved. Procedure 35.g.2.1.3. polycystic kidneys.2.3. shave the area between the umbilicus and pubic symphysis.1. 35. Electrolyte imbalance unresponsive to conservative measures 35. 35. 35.2. Avoid puncturing a previously scarred site.35. pregnancy 35.7. Congenital absence of diaphragm Large pleuroperitoneal fistula Diffusely infected abdominal wall.3. The catheter should be removed as soon as possible. The area is infiltrated with 3-10 mls of 1-2% lignocaine down to the peritoneum with a 21G or 23G needle. Severe fluid overload not responsive to conservative measures 35. the periumbilical area is cleaned with povidone iodine only.1. 35.5. In unconscious or ill patients. 35.8.2. Consent for first peritoneal dialysis 35. High blood urea or rapidly rising blood urea with metabolic acidosis 35. Do not cut the muscle layer. Acute poisoning 35. The bladder must be emptied.1. Recent major abdominal operation Large abdominal masses e. The catheter must be checked carefully by withdrawing the stilette from the catheter for any breakages before insertion.3.3. 35.3.3. the bladder may need to be catheterised. 35.2.3.1.4. End stage renal disease as temporary treatment 35. 35. 35.2.3.3.1.3.1.5.

Suturing is not necessary unless there is leakage. Bleeding from the insertion site can be stopped by a pursestring suture.4. vital signs monitoring and PD chart should be kept up-to-date.4.35. changing peritoneal dialysis solutions or injecting drugs into bags.12.3.2. The subsequent cycles are retained for 20-40 minutes per cycle and drained in 10-15 minutes. At the termination of the procedure. The first 6 cycles are rapid exchanges with heparin. 35.11. The stilette is then withdrawn and the catheter gently pushed in. The duration of dialysis depends on the needs of the patient.1.3. directed towards either iliac fossae. The catheter and stilette are introduced while controlling the length with the dominant hand until the peritoneum is pierced.3.4. 35. The current practice is 60 cycles for first PD and 40 cycles for subsequent PDs.3. Oversee the first 3 cycles of dialysis to ensure good flow. Skin sutures are unnecessary if a retaining knob is present. 35.4. 217 . the catheter is removed and the puncture site covered with gauze and plaster. leakage and ultrafiltration every two hours. 35.B. serum electrolytes and creatinine should be requested according to patients needs. N. Gauze with povidone iodine is applied around the puncture site.10. Check for turbidity. 35.4. Reminder: 35.4. Exchange volume: adult 1000 – 2000 ml Children 20-50 ml/kg body weight 35. Blood urea and electrolyte results to be reviewed by the doctor and potassium chloride to be added into dialysate if necessary. 35. Turbid effluent must be noted to the doctor. 35.5. The required volume of dialysate is instilled into the abdomen.4.4. Ensure strict aseptic techniques at all times and especially when preparing the PD sets of fluids and lines. The peritoneal cavity may be pre-filled with dialysate using 14-18G branula before introducing the actual PD catheter.3.3. Blood urea.13. Input and output chart. In stable patients. This is to reduce the risk of puncturing any viscus in the peritoneal cavity. 35.4. 35. once daily should be more than sufficient. Cover with plaster.6.

5. 35. One gram of potassium chloride available in 10 ml ampoule is equivalent to 13. Patient complains of severe abdominal distension or pain.8.5.5.2. Check blood sugar in diabetic patients. Stop dialysis immediately. 35.1. hypotension. Inform doctor immediately in the following situations: a.8.6.5. Never flush catheter under non-sterile conditions. If dialysate is • heavily blood stained • Turbid/cloudy • Faecal matter present.5.35. 35. Run rapid cycles with heparinised dialysate solution at 500 U per litre till good flow is obtained. 35. Poor inflow or outflow. 35.3. tachycardia.4. 35. e.6. Nursing guidelines in acute peritoneal dialysis. 35. 35. f.7. fever.4. d. Abnormal vital signs e. 218 . Spike all the way in. Do not use dialysate solution that is past the expiry date or looks turbid. d. Change position of the patient. Do not add drugs from open medication ampoules that have been left open for some time into the dialysate bag.7.5.5. NB. tachypnoea.5.g. Patient complains of severe/progressive breathlessness after starting PD.4.5. Actrapid may be needed.5. 35. c. Leakage of dialysate from the abdomen or anywhere along the dialysis set. If there is poor drainage: a. 35. c. Hence adding 3 ml to one litre would result in dialysate with 4. Check for fibrin clots.0 mmol/l of potassium. Wash hands each time before spiking solution bags. b. Collect effluent for cell count and culture and sensitivity. b. The outlet tubing should not dip into the drainage container. Do NOT touch the part that spikes into the bag.9. Check for kinking of the external drainage tubes. Avoid dismantling any part of the dialysis system once it is set up.3 mmol of potassium. Dialysate drainage bag should not touch the floor. 35. Ensure asepsis at all times.

Resuture immediately.Check for kinking .2.Drip and suck. b. 35. but vital signs stable. . . Transfuse cryoprecipitate. Damage to viscera. and remove dialysis catheter.35. culture and sensitivity. stop dialysis immediately. . d.Check site of leakage. . Peritonitis (refer section on CAPD peritonitis) 219 .5.Check for blockage by blood clots and fibrin.Re-insert if necessary. . stop the dialysis. Consider blood transfusion and DDAVP. Mechanical complications a. c. Leaking dialysate. Tubings – change dialysis set. Blood stained effluent .6. collect specimens for inspection.6.Start antibiotics – ceftazidime plus metronidazole. .10. It should clear with successive cycles.Change position of patient. One to two days of IP antibiotics e.6. 35. Stop dialysis and refer surgeon immediately.Purse string suture. Bleeding from puncture site. Send PD fluid for cell count and culture and sensitivity at start and end of PD and when the effluent is turbid. resuscitate as for patient with hypovolaemic shock. e.Convert to HD.If there is faecal material in the effluent. . patient in shock. Complications: 35. Poor drainage . . cephalosporin group may be needed.If heavy. Exit site .1. .If heavy. run rapid cycles. If bleeding does not stop after the first few cycles. .g.If mild observe.

GLOSSARY PD APD CAPD IPD CCPD HD ISPD NKF-DOQI PET Kt/Vurea nPNA UF BW BSA AGE GDP MRSA peritoneal dialysis automated peritoneal dialysis continuous ambulatory peritoneal dialysis intermittent peritoneal dialysis continuous cycling peritoneal dialysis haemodialysis International society for peritoneal dialysis National Kidney Foundation Dialysis Outcomes Quality Initiative peritoneal equilibrium test urea kinetic modelling normalised protein nitrogen appearance ultrafiltration body weight body surface area advanced glycation end-products glucose degradation products methicillin resistant staph aureus 220 .

RENAL TRANSPLANTATION 221 .

1. There was a small increase in blood pressure but this increase was insufficient to result in increased prevalence of hypertension 4 36.2 Selection criteria 36.2.3 Morbidity (Table 36.1. consideration can be given to emotionally related donor7 (Level B) 36. Psychological risk1 Minor feelings of depression are common in the immediate post operative period.4 Assurance that donor may withdraw at any stage of pre transplant assessment 36.6 (Level B) There is no increase in proteinuria.1: Summary of the incidence of early complications after donor nephrectomy Complications Incidence Atelectasis 15-30 % Paraesthesia / nerve injury 6% Urinary tract infection 5% Pneumothorax 5% Wound infection 3% Blood transfusion 2% Pneumonia 1% Splenectomy 0.1.1 Short term risk a.3 Results of graft and recipient survival is dependent on the centre (refer to Renal Registry) 36.3 % Pulmonary embolism 0. LIVING RELATED DONOR WORKUP 36.5.05 %1.2.1 Siblings / parents are the best donor1.1)2 Table 36. Surgical risk Mortality rate of 0.3 (Level B) In the absence of a relative.2.2 Age 222 . more so if the graft fails 36.3 % b.2 Long term risk to renal function is minimal4.36.1 Patient information 36.03 – 0.1.

Donation is safe if: • stone disease is inactive for the last 10 years. amphetamines.3 Contraindications to renal donation1.g. Severe cardiac and pulmonary disease l.2.g. Proteinuria / haematuria (refer to 36. The cysts may be either unilateral of bilateral • Between 30 to 59 years of age. Coagulopathy i.4 HLA A. Drug abuse e.17.1 Absolute contraindications a.4) b. at least 2 cysts must be present in each kidney • Over the age of 60.4) c. Hypertension > 140/90 mmHg d. Impaired renal function (refer to 36.4.2.3. Psychiatric illness e. Transient gestational diabetes 15 g. 223 .3.3.12 Biological age is more important than chronological age 36. Infectious disease eg.Exclude those who are < 18 and > 65 years of age8.6.3.9.11.13 (Level A) 36. 2 cysts establish APKD. Family history of type 2 diabetes mellitus with impaired glucose tolerance test f.10.4. • donor has only passed 1 stone so far. HIV m. Diabetes mellitus e. • there is no evidence of stones on current radiographic studies. 4 cysts must be present in each kidney 36. Systemic illness with potential to develop renal disease j.14 36. B. Pregnancy n.18 b. psychotic disorders h.3 ABO compatibility1. Adult polycystic kidney disease (APKD).2 Relative contraindications a. DR phenotypes3 (Level A) Priority should be given to the donor with 1 or 2 haplotype match 36. heroin and cocaine k. For donors who are relatives of recipient with adult polycystic kidney disease use of US kidneys to rule out APKD is according to the following criteria 16 (Level B): • Donor of less than 30 years of age. History of nephrolithiasis. Obesity: BMI > 30 15. Living related donor < 30 years old if recipient is type 1 diabetic c.

coerced or induced to donate.21 provided the HCV genotype is similar (Level D).d. Final decision should preferably be based on genotyping • Recipient who gets a kidney from someone without Alport’s syndrome may develop anti glomerular basement membrane disease 36. psychiatrist. fasting triglyceride and cholesterol Referral for cardiology assessment is indicated for: a.20. CXR. donors who are 35 years or older with coronary risk factors e.g. 36. The rest of the family should also be seen to obtain collateral and feedback information. dyslipidaemia.21. family history of coronary heart disease.4.g. social worker. There is no difference in liver disease prevalence over a period of 10 years. The potential donor should be seen individually and given sufficient time to decide. male donor who is more than 45 years old b.4 Donor assessment 36. Donors who are relatives of recipient with Alport’s syndrome 1 • Male relatives without haematuria can become a donor • Female relatives without haematuria might be a carrier and she should consider that her child may inherit the disease and require future transplantation.1 Motivation and psychosocial status assessment The motive to donate to the potential recipient should be entirely altruistic. the potential donor should be independently assessed by another person outside the transplant team e.4. Malignancy (donation is possible if tumour is cured) e.22 f. obesity 224 .2 Cardiovascular assessment ECG. c. Other members of the transplant team including the dialysis staff should interact with the potential donor so that a continuous assessment of the motivation can be made and further doubts cleared. smoking. HCV RNA positive recipient is relatively safe19. The potential donor should not be under duress. Hepatitis B or C infection • HBsAg positive and HBeAg negative donor can be accepted if the recipient is HBsAb positive (titre >10mIU/l) • Renal donation from HCVAb positive donor to HCVAb positive. In doubtful cases and in cases involving spousal donors. female donor who is 50 years old or premature menopause.22 Caution: Superinfection with a new genotype can occur unless HCV genotypes in donor-recipient are matched.

5 76 Table 36. Fasting blood sugar (glucose tolerance test if indicated) c.4 97 35-44 133 20. Renal profile b. Investigations include the following: a. Exclude < 80 mls/min/1.2: Renal function as determined by creatinine clearance according to age range17 Mean creatinine Standard Mean minus 2 Age clearance deviation standard deviations range mls/min/1. uric acid d. Urine cystine.4 90 30-38 115 10.73 m2 24-29 123 16.36.4.6 70 61-68 96 25.0 93 45-54 127 17.73 m2 (years) 17-24 140 11. 24 hour creatinine clearance (X3).8 93 40-49 121 23.5 45 70-78 89 19.7 117 25-34 140 21.5 87 65-74 109 16. 36.4.3 74 51-59 99 14. uric acid. phosphate (X3).73 m2 or < 2 standard deviations of the mean8.3 Respiratory assessment Potential donor with chronic smoking history and symptoms of chronic lung disease should be referred to a respiratory physician and anaesthetist for assessment. Abnormally high results should be assessed individually e.4 Assessment of donor renal status A full history and examination should be carried out with particular attention to the recipient’s primary renal disease and any history of familial renal disease. calcium. Serum calcium and phosphate.3 93 55-64 120 16.17 Table 36.3: Renal function as determined by inulin clearance according to age range17 Standard Mean minus 2 Age Mean creatinine deviation standard deviations range clearance (years) mls/min/1.9 49 225 .

24 hour urine protein (X3). Can be performed on obese patients h. If GFR contradicts the 24 hour urine creatinine clearance.28. Earlier return to work d.f. Urine microscopy (X3) h.25 (Level C) or Gadolinium-enhanced magnetic resonance angiography26 (Level C) could be an alternative 36.5.1 First introduced in 1991 36. Exclude if > 300 mg /day8 g.5.5 Laparoscopic donor nephrectomy Laparoscopic donor nephrectomy can be performed with morbidity and mortality comparable to open donor nephrectomy in established centres27. Selective renal angiography. Screening of • HIV • HBV (including HBeAg in HBsAg positive cases) • HCV antibody • Toxoplasmosis • Cytomegalovirus (See section on: Prevention of CMV disease post transplantation) 36. Longer operating time b. Screening and treatment of • Syphilis • Tuberculosis • Urinary tract infection b. proceed to Cr EDTA scan l.2 Benefits of laparoscopic versus open method are: a. Improved cosmetic results f.29 (Level B) 36. Less blood loss e. Less analgesic requirement c. Ultrasonography of the kidneys i. IVP k. Spiral CT angiogram23.5 Assessment of potential risk of transmitting infection to the recipient a. KUB j. Technically more demanding 226 . Multiple renal vessels are not a contraindication 36.4.3 Disadvantages of laparoscopic method: a. DTPA renography. Shorter hospital stay b. No deaths reported g.24.5.

Surgical implications of obesity. Choban PS. 130: 112-121 Ravine D et al.4 Relative contraindication to laparoscopic method: a. Transplant Proc 1992. Ad Hoc Clinical Practice Guidelines Subcommittee of the Patient Care and Education Committee of the American Society of Transplant Physicians. Should elderly donors be accepted in a living renal transplant program? Clin Transplantation 1994. Kidney Int 1993. Lancet 1994: 343: 824-827 British Transplantation Society and The Renal Association. 19. 66: 1694-1697 2. 8. 12. N Eng J Med 1995. Ravenscraft M. Kasiske BL. Right sided donor nephrectomy References 1. Russell WS. 60: 322-327 Kerr SR et al.36. 5. Donor hepatitis C virus status does not adversely affect short term outcomes in HCV + recipients in renal transplantation. 15 (suppl 7) Kasiske BL et al. 11. Ann Rev Med 1998. 7: 2288 Richard DM. Organ and Tissue Donation for transplantation. Transplant Proc 1998. et al. 15. 333: 333-336 Margaret JB et al. 162-199 The EBPG Expert Group on Renal Transplantation. Lancet 1992. Evaluation of ultrasonographic diagnostic criteria for autosomal dominant polycystic kidney disease. Kidney Int 1995. Ramos EL. 6. 7. 78: 27-39 Morris RD et al. 17. 30 : 3118-3119 Kumar A et al. J Am Soc Nephrol 1996. Cook DJ et al. ABO incompatibility in cadaver donor kidney allografts. 10. Surgical Clinics of North America 1998. Use of elderly living related donors in renal transplantation. Am J Epidemiology 1989. 3. Long term effects of reduced renal mass in humans. Forty-five years of followup after uninephrectomy. 8: 523-526. To use or not to use? Transplantation 1999. 13.). Nephrol Dial Transplant 2000. 67: 999-1004 Kim YS et al. The evaluation of living renal transplant donors: clinical practice guidelines.662 adult white women. 20 years or more of followup of living kidney donors. 9. Obesity and hereditary in the etiology of non-insulin dependent diabetes mellitus in 32. Transplantation 1995. Arnold Publication. 1997. 227 . Jeremy C (eds. Transplantation 1998. Living donors > 50 years. 16: 4549-4552 Kasiske BL. Transplant Proc 1987. High survival rates of kidney transplants from spousal and living unrelated donors. 18. 48: 814-819 Narkun-Burgess DM et al. Impact of donor age on long term graft survival in living donor kidney transplantation. 2000 Flancbaum L. 16. Stephen VL. United Kingdom guidelines for living donor kidney trans-plantation. Evaluation of living renal donors. 49: 215-34 Ali MK et al. 43: 1110-1115 Najarian JS et al. 24: 1325-1326 Kanematsu A et al. 4. The Living Organ Donor. 340: 807-810 Terasaki PI et al. European Best Practice Guidelines for Renal Transplantation (Part 1).5. The evaluation of prospective renal transplant recipients and living donors. Prior open upper abdominal surgery b. 14.

Annals of Surgery 1997. Transplantation of kidneys from donors with hepatitis C antibody into recipient with pre-transplantation anti-HCV. J Am Soc Nephrol 2000. Assessment of living renal donors with spiral CT. Transplantation 2000. J. Lionel G et al. Dominguez-Gil B et al. 57: 21752186 28. Aust N. Kavoussi LR. Trasplantation in the patients with hepatitis C.20. Ratner LE et al. Surg 1999. The use of spiral computed tomography in the evaluation of living donors for kidney transplantation. Transplantation 1999. Kidney Int 2000. Z. 195 (2): 457-62 24. Preoperative evaluation of living renal donors with gadoliniumenhanced magnetic resonance angiography. 63: 229-233 228 . Laparoscopic donor nephrectomy. Bakker J et al. Transplantation 1995.a comparison with the open approach. Morales JM and Campistol JM. 67: 8 27. Transplantation 1997. Flowers JL et al. 59: 643-645 25. Morales JM et al. 226 (4): 483-489 29. Alfrey EJ et al. 47: 236-240 21. The use of spiral computed tomography angiography for the assessment of the living kidney donors. 69: S404 22. 11: 1343-1353 23. Rubin GD et al. Comparison of open and laparoscopic live donor nephrectomy. Kidney Int 1995. Laparoscopic assisted live donor nephrectomy. 69: 217-219 26. Radiology 1995. Ten years experience in transplantation of kidneys from HCV positive donors into HCV positive recipients.

1)3 Table 37.3 Severe cardiovascular disease e.4 37. infiltrating At least 2 years Wilm’s tumor At least 2 years Bladder : In situ None Invasive At least 2 years Uterus : In situ cervical None Invasive cervical 5 years Uterine body At least 2 years Testis At least 2 years Thyroid At least 2 years Breast At least 5 years Colorectal At least 2 years Prostate At least 2 years Lymphoma At least 2 years Skin : Melanoma At least 5 years Squamous cell 2 years Basal cell None 37.1.2 Malignancy (Table 37.6 37.g.1.5 (Level C) 229 .1. ventricular arrythmia1 (Level C) 37.g.8 Diabetes mellitus with multiorgan failure Psychiatric illness e. asymptomatic None Large . amphetamines.1 HIV infection1.2 (Level C) 37. diffuse disease on coronary angiogram.1. alcohol. psychosis4 Noncompliance1.5 37. valvular heart disease.1.1. ejection fraction of < 35 %.1.37.7 37.1. cocaine.1: Guidelines for recommending tumor free waiting periods for common pretransplant malignancies3 Site Waiting period Renal: Incidental.1 Contraindications to transplantation 37.4 (Level C) Active substance dependence or abuse e.g. LIVING RELATED RECIPIENT WORKUP 37. heroin4 Chronic active hepatitis or cirrhosis4.

and preemptive renal transplantation with possible liver transplantation should be considered.12 Secondary GN a. Body mass index c. d. Body weight b.11 Primary renal disease. Delay for at least 1 year prior to transplantation. Membranoproliferative glomerulonephritis type II (MPGN II).37.1. Patients between the age of 55 and 65 years of age are not at a significantly increased risk of post transplant morbidity as long as they do not have significant vascular disease. 37.1. Patients with end stage renal disease due to the following aetiology may be transplanted with caution: a.9 Age: > 55 years old.3 Consideration should be given on an individual basis.1.6 e.2 Dialysis and nutritional status 37. Transplant should be considered one year after end stage renal failure and the circulating anti GBM titre is no longer detectable in the blood. Triceps skin fold thickness d. Haemolytic Uraemic Syndrome (HUS) or Thrombotic Thrombocytopaenia Purpura (TTP).1 Potential renal transplant recipients should be adequately dialysed to achieve good control of blood pressure. 37.1. 2 c. Focal segmental glomerulosclerosis b. b. Fabry’s disease 37. Stable ANCA and asymptomatic for at least 6 months prior to transplantation.2 Potential renal transplant recipients should have the following assessment : a. optimum status of hydration and acquire satisfactory nutritional status 37. 37. Mid arm circumference (MAC.) 230 . Oxalosis.10 Any disease with an expected survival of less than 5 years or with a resultant poor quality of life.2. Disease should be inactive for at least 6 months prior to transplant as assessed by clinical and serological status. Patients can be treated with orthophosphate and pyridoxine. c. Idiopathic crescentic GN or Wegener’s or microscopic polyangiitis.2. Systemic Lupus Erythematosus (SLE). Antiglomerular basement membrane (Anti GBM) disease.

a suspicious renal tract abnormality or an unknown primary renal disease in a young patient). Serum albumin Patients on continuous ambulatory peritoneal dialysis (CAPD) may undergo renal transplant without Tenckhoff catheter removal prior to transplantation provided they are free from peritonitis or catheter related infection for at least 4 weeks.2 Assessment of respiratory system Full history and examination. obesity 37. The following investigations should be routinely carried out in potential recipients • KUB. smoking. CXR Potential recipients with chronic smoking history and symptoms of chronic lung disease should be referred to a respiratory physician and anaesthetist for assessment 37. CXR. Pap smear. diabetes mellitus. dyslipidaemia. 231 .4 Similarly.6 In men: testicular and per rectal examinations 37. mammography. ECG Further assessment by cardiologist is indicated for the following cases: a. • Ultrasonography of kidneys / ureter.3.g. female recipients who are 55 years old or premature menopause c. recipients who are 35 years or older with coronary risk factors e. haemodialysis patients may undergo renal transplant with an indwelling central venous dialysis catheter provided there is no evidence of catheter related infection. family history of coronary heart disease.3.4 Urological evaluation a.3.e.3.3 Assessment of the gastrointestinal system Routine upper GI endoscopy should be performed in order to detect subclinical peptic ulcer disease (not routinely done in children unless symptomatic) 37. male recipients who are more than 45 years old b. • Micturating cystourethrogram (if there is a history of recurrent urinary tract infection.3 Assessment of medical and psychiatric status In women: breast and pelvic examination. 37. In those over 40 years old or over 35 years old with a family history of breast carcinoma.1 Assessment of the cardiovascular system Full history and examination.

HCVAb • If HBsAg is positive. renal transplant should be deferred until the enzyme has decreased to a level less than twice normal on 3 consecutive occasions separated by two weekly intervals between each reading. Following liver biopsy the patients should be treated as follows: • If there is chronic active hepatitis (CAH). Refer hepatologist for treatment of chronic hepatitis B and C • Treatment of chronic hepatits B: Treatment is indicated when HBsAg + > 6 months. past history of femoral catheterisation. If there is chronic persistent hepatitis or milder disease with ALT less than 2X normal renal transplant may be carried out. MRA/angiogram when indicated 37. negative HBeAg with or without raised liver enzymes c.13 d. Routine assessment include ALT. HBsAg.8.5 Assessment of pelvic vasculature For selected patients e.3. Indications for liver biopsy4.11. renal transplant is contraindicated.10. chronic hepatitis on biopsy. referral to urologist is required for further evaluation which may include a urodynamic study c. long-term HD or increased iPTH.3. CT scan.9. HBV DNA +. HBeAg +.1) b.g. Doppler US studies. For patients with suspected urological disorders.11 (Level B) • Patients with HCVAb or HCV PCR positive with or without elevation of liver enzymes • Patients with positive HBsAg.6 Assessment of the liver status a. Treatment with either Interferon α-2b 5 232 .12 (Level C) • If the liver enzymes is more than twice normal. • If HBsAg is negative and HBsAb is negative. the patient should have HBeAg and HBV DNA tested. the patient should be immunised with Hepatitis B vaccine (refer table 7. raised ALT (2X above upper limit).b. The following group of potential recipients should be referred earlier to the transplant surgeon • All diabetic patients • Patients with a history of recurrent urinary tract infections • Patients with raised PSA level • Patients with adult polycystic kidney disease • Patients with severe peripheral vascular disease 37.

18 • Treatment of chronic hepatitis C: Treatment is indicated when HCVAb +.14. 233 .22.3. Patients should be treated with erythropoeitin after exclusion and treatment of underlying factors which contribute to anaemia 37. Alcohol and substance abuse (at least 6 months of documented abstinence) c.15 or Lamivudine 100 mg daily for at least 1 year. Blood transfusion for correction of anaemia is strongly discouraged. Past psychiatric history / treatment e. 21 37. a referral to a counselor or a psychiatrist should be made prior to further pretransplant evaluation.16.7 Assessment of the haematological system Potential recipients should have haemoglobin of at least 8 g/dl before transplant.19.4 Dental evaluation All potential recipients should be assessed by a dentist for dental clearance.21.17.9 Obesity Attempts should be made for the potential recipients to achieve an ideal body weight (weight reduction should be carried out for potential recipient whose BMI> 30). Noncompliance with dialysis / medications b. Treatment is interferon α-2b 3 million units 3X per week for 6 to 12 months. In children a full developmental assessment should be made If indicated. Pegylated interferon 2a may be considered at a weekly dose of 135ug for 48 weeks with close monitoring for toxicity.3.8 Psychological assessment 4 All potential recipients should be assessed psychologically with particular attention paid to the following areas: a. HCV RNA +. raised ALT (2X above upper limit).million units daily or 10 million units 3X/ week for 3 to 6 months13.3. chronic hepatitis (moderate to severe) on biopsy.20. 37. Family support d. 37.

Respiratory CXR just prior to transplantation should be done 234 .1 Screening for infection according to organ / system a. ENT Surveillance cultures should be taken from ear.1: Management of HCV infection in dialysis patient on the waiting list for renal transplantation23 HCV Ab POSITIVE PATIENT ON DIALYSIS HCV RNA -ve HCV RNA +ve LIVER FAILURE / CIRRHOSIS LIVER BIOPSY Normal Chronic Hepatitis Liver Cirrhosis IFN for 12 months RNA -ve RNA +ve IFN + Ribavirin RNA -ve Waiting list for renal transplantation Defer renal Tx ? RNA +ve To consider double liver-kidney transplantation 37.Figure 37.5 Management of pretransplant infection (1–2 weeks pretransplant) 37.5. nose and throat. Chronic suppurative otitis media should be excluded b.

2 The following 6 cross matches should be performed by complement-dependent cytotoxicity (CDC) method: 235 . Cutaneous and genital warts should be treated pretransplant g. Herpes Simplex Ab i.2) h. A six month period of observation after completing anti TB treatment is desirable before transplantation is undertaken b. Toxoplasma IgM antibody of > 1:4 is regarded as significant and the patient should be treated pretransplant c.29 Refer to figure 37.6.6.2 Screening for specific infection a.27. Renal Unit.25. The first is done at the initial part of the assessment and the second preceding the transplant e.c. Tuberculosis (TB) Any suspicion of active TB (radiological or clinical) should be thoroughly investigated and adequately treated.28. HBV Potential recipient who are HBeAg and HBV DNA positive in spite of treatment are excluded from transplantation f. Cytomegalovirus (CMV) IgG Ab against CMV is used for screening 37. HIV Screening by ELISA should be done twice during the pretransplant assessment. Genitourinary tract Mid stream urine for C & S if potential recipient still having significant urine output d. Singapore General Hospital) 37.6 Acute rejection prophylaxis 37. Epstein Barr virus Ab j. subject to liver histology.5.24.26. Varicella Zoster Ab (refer to table 45. Miscellaneous • CAPD catheter – dialysate for cell count and C & S and exit site swab for C & S if indicated • Central venous catheter – exit site swab for C & S 37. HCV Screening is done by detecting HCV antibody HCV antibody +ve patients can be considered for renal transplantation.1 White cell cross match is done at the early stage of donor workup and one week prior to transplant (adapted from Guidelines for lymphocytotoxic cross match procedures.1 for details (Level C) d.

6. IgG and especially IgM anti HLA class II antibodies indicate a less certain risk. Anti human globulin (AHG) enhanced T cell cross match d.30 There remains considerable doubt about the degree of positive B lymphocyte crossmatch in influencing transplant outcome.4 Many studies have confirmed that the historical crossmatch result is not relevant in sensitised recipients of a first transplant. T cell cross match detects anti HLA class I antibodies while B cell cross match detects both anti HLA class I and II antibodies. contraindicate transplantation. B cell cross matches are also more sensitive than T cell cross matches in identifying class I antibodies. T cell cross match (standard) b. Conversion of a positive cross match to negative after pretreatment of recipient serum with DTT indicates the presence of IgM antibodies. Many centres would ignore a historical crossmatch result in first graft but not in regraft recipients. Presence of autoantibodies in recipient sera can cause false positive crossmatch.3 All T cell positive crossmatches i. DTT treated B cell cross match 37.e. Dithiothreitol (DTT) treated T cell cross match f.2: Standard white cell crossmatch results and their implications Transplant Current Cell Historical (Test done (Test done within 1 week of months before transplant) transplant) T + No Yes + No Yes B No + Yes + No + + 236 . usually IgG. AHG enhanced B cell cross match e. B cell cross match (standard) c.2. The situation is less certain when the recipient of a historical positive. 37.6. current negative crossmatch has become sensitised by loss of a first graft. AHG enhanced cross matches are more sensitive than the standard CDC (SCDC) method in detecting lymphocytotoxic antibodies.30(Level C) Table 37. presence of IgG or IgM anti HLA class I antibodies.a.

In international organ sharing algorithms. 237 .37.5 Panel Reactive Antibodies (PRAs) PRAs are anti HLA antibodies against T & B cells from a panel of donors selected to represent the HLA specificities.6. Anti HLA specificity of antibodies produced by the patient A sequential record of antibody specificities over time can be used to avoid donors with those specificities and therefore diminish the likelihood of rejection episodes. Patients with PRA>20% should have enhanced immunosuppression. b. Percentage of PRAs Its value determines the likelihood of a negative cross match. The results are expressed as the % of panel cells that show positive antibody reactivity. Those with high % of PRAs are more likely to have a positive cross match and to be excluded from transplant. the PRAs value is used to increase queue points to improve patient’s chances of receiving a cadaveric transplant. Serum screening determines: a.

2: Algorithm for white cell cross match T cell XMatch SCDC + SCDC − AHG + AHG − B cell XMatch SCDC + or AHG + SCDC − or AHG − DTT + DTT − Delay 3 months and repeat T & B cell XMatch DTT + (IgM has converted to IgG) DTT − Continue transplant workup. Needs enhanced immunosuppression post transplant Continue transplant workup Transplantation excluded 238 .Figure 37.

Transplantation 2000. 3. NIH consensus development conference panel statement: Management of hepatitis C. Hepatitis C virus infection and renal transplantation. Ann Intern Med 1993. Mohamed HS. 21: 355-358 Venkateswara K et al. Transplantation 1996. 102: 2091-2097 Lok ASF. 62: 297-299 Kasiske BL. Eleanor LR et al. The long term virologic and pathologic impact of renal transplantation on chronic hepatitis B virus infection. UpToDate 2000. Nephrol Dial Transplant 1999. 29: 257-263 Ozdogan M et al. Hepatology 1999. 94: 3576-3582 Mathurin P et al. 6: 1-34 Fornairon S et al. 12. European Best Practice Guidelines for Renal Transplantation (Part 1). Kasiske BL et al. 13. Effect of alpha interferon treatment in patients with hepatitis Be Ag positive chronic hepatitis B. Handbook of Kidney Transplantation. 29: 889-896 Pereira B. 10. Histological impacts of hepatitis virus infection in haemodialysis patients: Should liver biopsy be performed before renal transplantation? Artif Organs 1997. 8(3) Lai C et al. Interferon therapy for chronic hepatitis B virus infection. 22. J Am Soc Nephrol 1995. A Little Brown Handbook. Efficacy and tolerance of interferon alpha-2b in the treatment of chronic hepatitis C virus infection in haemodialysis patients. 78: 27-39 Ramos E. 6. Value of liver biopsy in the evaluation and management of chronic liver disease in renal transplant recipients. UpToDate 2000. UpToDate 2003. 9. Transplantation 1994. Evaluation of the potential renal transplant recipient. 57: 490-497 The EBPG Expert Group on Renal Transplantation. Hepatology 26 (supp 1): 2S-10S Chopra S. The evaluation of prospective renal transplant recipients and living donors. The evaluation of candidates for renal transplantation. 2. 8. 11. 1996. Treatment of chronic hepatitis C virus infection: Recommendation. 21. 14. 20. 8(3) Wong DKH et al. 4. Lamivudine treatment of chronic hepatitis B virus infection. 14: 2704-2709 239 . Histopathological features of hepatitis C in renal transplant candidates. The evaluation of renal transplant candidates: Clinical practice guidelines. a meta analysis. A controlled trial of interferon with or without prednisone priming for chronic hepatitis B. Surg Clin North Am 1998. Impact of hepatitis B and C virus on kidney transplantation outcome. 119: 312-323 Lok ASF et al. 2nd edition. Am J Gastroenterol 1999. Am J Med 1993. 7 (3) Martin P et al. Hepatology 1999.References 1. 16. 94: 241250 Lok ASF. Nephrol Dial Transplant 2000. 15. 11(2) Campistol JM et al. 15 (suppl 7) Danovitch G. Efficacy of lamivudine in patients with hepatitis Be antigen negative/ hepatitis B virus DNA-positive (precore mutant) chronic hepatitis B. 19. N Eng J Med 1998. 339: 61-68 Tassopoulos NC et al. A one year trial of lamivudine for chronic hepatitis B. Gastroenterology 1992. Chronic hepatitis C infection in patients with end stage renal disease: characterisation of liver histology and viral load in patients awaiting renal transplantation. 1999. 69: 1479-1484 Sterling RK et al. UpToDate 2000. UpToDate. 5. 17. 7. 18. 8(3) National Health Institiutes (NIH) of Health Consensus Development Conference Panel.

65: 930-936 28. An Edward Arnold publication. Pereira BJG et al. A manual of renal transplantation. 11: 1343-1353 24. A prospective study of hepatitis C virus infection in renal allograft recipients. Transplantation 1996. 29: 608-614 27. Hanafusa T et al. Transplantation 1998. Knoll GA et al. Roth D et al. The impact of renal transplantation on survival in hepatitis C positive end stage renal disease patients. J Am Soc Nephrol 2000.23. 1994. 52-66 240 . Transplantation 1996. Rostaing L et al. Kidney Int 1998. Allen RDM. 61: 886-889 29. Impact of hepatitis C virus duration and hepatitis C virus genotypes on renal transplant patients. Chapman JR. Kliem V et al. 53: 1374-1381 26. 62: 1417-1421 30. Retrospective study on the impact of hepatitis C virus infection on kidney transplant patients over 20 years. 66: 471-476 25. Morales JM. Campistol JM. Effect of hepatitis C infection and renal transplantation on survival in end stage renal disease. Am J Kidney Dis 1997. The long term course of hepatitis C after kidney transplantation. Transplantation in the patient with hepatitis C. Transplantation 1998.

4 Determination of any intercurrent problems that may preclude or complicate surgery (e. CMV status. 38. examined and sent for cell count and culture.3 38.2 38.2. viral status and infective screen as well as pre-transplant sensitisation.1 Renal profile 38.1 38.1.7 Knowledge of the donor status is important. cytotoxic cross-match result.2. femoral catheter insertion.1. obesity (if present).2. 38. previous abdominal surgery.2.1. PERI-OPERATIVE MANAGEMENT 38.1.1 Specific issues to be addressed: 38. recent onset of cardiac or respiratory disease. position of Tenckhoff catheter if on CAPD.1 Assessment of recipient’s fluid status (to keep 1-2 kg above dry weight in adults if possible). URTI.6 Ca2+.6 The site of vascular access should be clearly marked and demonstrated to the OT staff.1.2. uncontrolled BP).2 38. particularly serum potassium.1.38. and serum electrolyte levels.2 Organise dialysis before transplant. volume status.5 38. Decision to dialyse a patient depends on the timing of the previous dialysis. fever.4 38. PO4. LFT FBS/RBS FBC PT/APTT Urine C&S 241 .3 CAPD patients should have their usual exchanges until day of transplant.2. 38.1 38.2 Immediate pre-transplant investigations: 38.5 Document residual urine. 38.1. then the peritoneal dialysis fluid should be drained from the abdominal cavity.g. Protection of the vascular access site is advisable using non-circumferential padding to reduce the risk of occlusion by inadvertent external occlusion.

1 Central line to be inserted in OT 38.8 38.2.5 Immunosuppressive protocol Refer to chapter 40 for prophylactic/induction therapy 38. EDTA tube) 38.3 Urology Specialist Nephrology Specialist 38.2.8 Perioperative prophylactic antibiotic drugs are beneficial in reducing the incidence of wound infections (not UTI).6.4 Prophylactic antibiotic is recommended3.7 38.2.2 38. In 242 .5.11 Cross match 4 units packed cells 38. ear CMV serology (if not available) Chest radiography 38.10 38.6.7.6.4 To maintain CVP at 10-15 cmH2O2 (Level D) Urinary catheter to be inserted Anaesthetist to document clamp and release time 38. (Level C) The regimen depends on local bacterial epidemiology but should attempt to cover Staph.38.2.3. aureus and common enteric coliform bacteria. although there is considerable variation in practice. Instilling antibiotic into the bladder is of no additional benefit9.6.10 ECG 38.5 Measures to decrease the likelihood of delayed graft function entail maintenance of adequate blood pressure and fluid status with IV colloid or crystalloid (the latter being preferable). throat.3.6 Intra-operative management 38.12 Cyclosporin or tacrolimus level (for LRRT only.3. before serving cyclosporine or tacrolimus on the morning of operation.3 38.2.4.6.2.1 Urology or Nephrology consultant 38.9 Swabs: nasal.3 Consent for donor nephrectomy: 3 signatures required for LRRT: 38.6.2 38.

7. microbiology.10 Wound drain To be removed at the discretion of urologist 243 . output.1 Isolation nursing until all tubes/drains removed 38. CVP).4 Daily investigations: biochemistry.4 Bladder washout should be only done under strict aseptic technique by urologist if deemed necessary 38.4 Use normal saline alternate with D5%.8. haematology.3 If patient is adequately hydrated but remains anuric. and urinalysis 38. it is common practice to administer mannitol before the kidney is reperfused.9.3 Proper hand wash before and after examining the patient Hourly fluid balance (input.8.1 Indwelling bladder catheter should be inserted in OT 38.8.8 Intravenous fluids2 (Level D) 38.7.5 CVP line to be removed at the discretion of nephrologist 38. aim to keep patient well hydrated 38. use Hartmann’s solution or K+ supplement 38.8.2 38. restrict intravenous fluid to 500-1000 ml/day 38.9 (Level D) 38.9.5 Catheter usually removed at Day 5 or at the discretion of urologist 38.3 If urine output declines (< 100 ml/hour) or blood clots present to inform doctor immediately 38.7.8.9. daily weight 38.9 Bladder catheter 38.9.2 If patient is adequately hydrated with good graft function. if K+ < 4.1 Aggressive replacement.living related transplant. replace previous hours’ urine output 38.2 Urine output to be measured hourly 38.9.7 Post-operative care 38.7. which helps to trigger an osmotic diuresis2.

12.12.13.11 Stents If there is an internal J stent ensure removal by 3 months post transplant or earlier if patient has UTIs 38. to commence when renal function is stable 38.3 Cotrimoxazole 480 mg at night. MSU 38.12 Investigations 38. Mg2+.4 CMV prophylaxis in high risk recipients 244 .13.13. delayed graft function or sudden drop in urine output 38.2 Nystatin 250 000 units gargle and swallow qid for 3 months 38.1 Renal profile twice daily for 48 hours then daily (can be altered at the discretion of nephrologist) 38.5 Cyclosporin / tacrolimus level 3 x a week or when indicated 38. PO4 3 x a week 38.4 LFT.38.1 Intravenous ranitidine 50 mg tds for 2 days then change to oral ranitidine 150 mg bd for 3 – 6 months 38.6 Doppler US Day 1. Ca2+.13 Other medications 38.3 Chest radiography 38.12.2 Daily FBC.13.12. or immediately if primary non-function.12.7 DPTA scan as indicated (usually done on Day 2 – 4) 38.12.12.

3: 12 References 245 . Goodman CM. 13(7): 1637-41 8. Kidney Transplantation: Principles and Practice. A prospective randomized controlled trial of perioperative antibiotic prophylaxis in renal transplantation. Castelo Filho A. J Urol 1992. Transplant Int 1990. Handbook of Kidney Transplantation. Kyllonen L et al. Nephrol Dial Transplant 1998. Wound infection following renal transplantation. Midtvedt T. Risk factors for nosocomial urinary tract and postoperative wound infections in renal transplant patients: a matched-pair case-control study. Danovitch G. 2001.1. Routine perioperative antibiotic prophylaxis in renal transplantation. Wey SB. 147(4): 9948 5. Wenzel RP. Rudolf LE. Int Urol Nephrol 1990. 3. Rees AJ. Hartmann A. 1(2): 93-6 9. A Manual of Renal Transplantation. Westervelt FB Jr. Infect Control 1980. 1994 Cohen J. Prophylactic antibiotics therapy with cefamandole and tobramycin for patients undergoing renal transplantation. 2. Ekland B. Pestana JO. Aust NZ J Surg 1984. Chapman J. J Hosp Infect 1988. Brekke IB. Lapchik MS. Survey of antibiotic prophylaxis in European renal transplantion practice. Salmela AD. Judson RT. Townsend TR. The effects of intravesically applied antibiotic solution in the prophylaxis of infectious complication of renal transplantation. 5th edition 10. 2nd edition Allen R. Mandell GL. Silva Filho AP. 1996. 11(4): 357-63 4. Morris P. 54(3): 223-4 7. 22(2): 173-9 6. Midtvedt K. Hargreave TB. Williams G.

acoustic schwannomas. glioblastoma multiforme. ependymomas and well differentiated teratoma. regardless of age. ganglional cell tumors. The Council of Europe has recently published an international consensus on the prevention of neoplastic disease in transplantation and classified primary brain tumors according to acceptability for organ donation1 • Brains tumors that do not exclude the donor from organ donation are: benign meningiomas. anaplastic oligodendroglioma (Schmidt C & D). Physicians caring for the potential donors should be encouraged to make early contact with the tissue organ procurement (TOP) team or the HKL transplant coordinator for assistance in the further management of the donor and the donor family (Tel. low grade oligodendrogliomas. anaplastic and malignant meningiomas. pineoblastomas. intracranial sarcomas. epidermoid cysts. HIV positive serology or a history of activities with high risk for HIV infection c. History of cancer other then non invasive brain tumor.2 Contraindications 39. 246 .1 Absolute contraindication (Level B) a.2.39. medulloblastoma. Acute hepatitis b. Severe untreated septicaemia or septicaemia of unknown origin b. or 013-3759887) 39. pineocytomas. choroid plexus papillomas. No: 0326942704 or 03-26942705 during office hours. chordamas and primary cerebral lymphomas. colloid cysts of the third ventricle. haemangioblastomas. pituitary adenomas. pilocytic astrocytomas (astrocytomas grade I). CADAVERIC TRANSPLANTATION 39.1 Selection of donors Any comatose patients with irreversible cerebral damage who appears likely to progress to brain death prior to terminal circulatory failure should be considered as a potential donor. malignant ependymomas. gliomatosis cerebri • Tumours where the donor should not be considered for organ donation: Anaplastic astrocytoma (grade III). craniopharyngiomas. germ cell tumours (except well differentiated teratomas). • Tumours where the donor can be considered for organ donation depending on characteristics: low grade astrocytoma (grade II). non melanotic non metastatic skin tumor.

Poisoning. Spinal reflexes may be present 247 .4 Determination of brain death Any potential donor should be adequately assessed. Unconscious.2 Relative contraindication (Level C) a. Defensive movement of head.2. No reaction to speech. Spinal reflexes in trunk or extremities may be seen d. sedation. Limit may be set as CrCl >60ml/min as acceptable. Very elderly donor (>70 years)2 b. Hepatitis B immunoglobulin should be given prior to transplantation. Suboptimal or non acceptable renal function It is recommended that donors should be evaluated on the basis of renal function (calculated creatinine clearance). Body temperature > 330C c.7.5 (Level B) Recipients for suboptimal kidneys or dual kidneys should have given their informed consent prior to transplantation 39.8 (Level C) 39. Long term insulin dependent diabetes mellitus d. extremities and trunk on painful stimuli absent. 50-60 ml/min as marginal and <50 ml/min as non acceptable for single kidney transplant.4 Non acceptable kidneys may be considered for dual transplant.1 Hepatitis C positive donors Hepatitis C positive donors may be accepted for seropositive recipients if the recipient’s PCR for HCV is also positive.4. Spontaneous muscular movement in area innervated by cranial nerves absent.4.6.3 age and vascular disease. Hypertension or other condition with impaired renal function e.39. electrolyte or acid/base disturbance are excluded 39. and metabolic.3. Known cerebral disease that can cause total cerebral infarction b. 39. Spontaneous breathing absent c.2 Clinical criteria a. The clinical neurological examination to confirm brain death should include: 39.1 Basic criteria for clinical neurological examination to be used a.3.3 Special situations 39. Severe vascular disease c.2 Hepatitis B positive donor Hepatitis B positive donor may be accepted for transplantation to recipients with Hepatitis Bs antibody. touch or pain b.

248 . Corneal reflexes absent bilaterally g. dopamine may be added as an inotropic support.5 Support of the potential donor and optimisation of organ function Any comatose patient with irreversible cerebral disease should be identified as a potential donor and monitored carefully awaiting determination of brain death.1 Maintain a CVP of 10cm H2O. 39.5.5. Apnoea test shows absence of spontaneous breathing 39.15 If this cannot be reached using fluids alone.3 A urine output of 100 ml/hr.5.2 A systolic arterial pressure of 100 mmHg. (Level C) The best treatment of diabetes insipidus is vasopressin or one of its analogues.4 Maintain normal values of blood gas analysis.14 (Level C): 39.5. Laryngeal reflexes absent k. Doll’s eye movement absent h. Reactions of pupils to light absent f. The management of a potential donor should be similar to normal ICU care and simplified goal for management should be to13. 39. Blood volume can be increased with crystalloids and colloids 39.e. Cardiocerebral reflexes absent (eye bulb pressure) i. A positive end expiratory pressure of 5cm H2O is advisable to retard the development of atelectasis. evaluation and consent for organ donation. Blinking reflexes on sound stimuli absent j.

Renal transplantation with limited donors. 16: 31-41 Sola R. 66: 1159-1163 Alfred EJ. To what extent should the good results obtained be attributed? Transplantation 1998. 5. 7. Wright TL. 13. Transplantation 1995. 8. Castellano G et al. Scandling JD et al. Committee of experts on the organisational aspects of cooperation in organ transplantation. 2. Gleb AW. Organ donation management and outcome: a 6 year review from a level 1 Trauma Centre. Cattran D et al. 4. 338: 221225 Sanchez-Fructuoso Al. The multiple organ donor: Identification and management. 9. 64: 1142-1146 Morales JM. Levey AS. Outcome of transplantation of non heart beating donors kidneys. 11: 350-358 Soifer BE. 1997 Karpinski J. Factors influencing early function of cadaver renal transplants. Cecka JM. Trauma 1990. Lancet 1995. Prats D. Lopez Navidad et al. 345: 484-487 Widell A. Hepatitis C superinfection in hepatits C virus infected patients transplanted with a HCV infected lidney. Booster MH. 4: 455-477 Wijnen RMH. 345: 1067-1070 Cho YW. Standardisation of organ donor screening to prevent transmission of neoplastic diseases. 110: 814-823 Nygaard CE. Transplantation of kidneys from donors with hepatitis C antibody into recipient with pre transplantation anti HCV. and organ transplantation: Reducing the risk through donor selection. Torrente J et al. Transplantation of kidneys from donors whose hearts have stopped beating. Chisholm GD. Transplantation 1999. Cell Transpl 1995. Campistol JM. Prediction of creatinine clearance from serum creatinine. 3. Nephron 1976. 47: 236-240 Periera BJ. A controlled study of hepatitis C transmission by organ transplantation. Infectious disease transmission through cell. Renal transplantation from non heart beating donors: a promising alternative to enlarge the donor pool. Lajoie G. Schmid CH. 14. Lancet 1969. Council of Europe International Consensus. Diamond DL. 12. Ann Int Med 1989. 67: 1162-1167 Cockcroft DW. Lancet 1995. 551-552 249 . Kidney Int 1995. Kootstra G et al. Persson NH et al.References 1. Townsend RN. 30: 728732 Caroll RPN. Shackman R. 6. 15. Outcome of kidney transplantation from high risk donors is determined by both structure and function. Mansson S. J Am Soc Nephrol 2000. 60: 642-647 Eastlund T. N Eng J Med 1998. Guirado LL. Lee CM. Gault MH. Terasaki PI. Gjerston DW. 10. When should expanded criteria donor kidneys be used for single versus dual kidney transplants? Transplantation 1997. 11. tissue.

1. Patients with any disease or illness with expected survival of less than 5 years or with a resultant poor quality of life are not eligible.1 Positive HIV serology 40.2 Symptomatic or asymptomatic patients with positive stress test should be further assessed by a cardiologist and treated appropriately.8 Active substance abuse 40. nondiabetic patients > 55 years old or diabetic patients > 35 years old.1 Cardiac assessment (including cardiac stress test and echocardiogram) is required for asymptomatic.1.1.1 Exclusion criteria Patients aged less than 2 years old or above 60 years old are disqualified.2 Preregisteration assessment 40.1.3 40.1.6 Positive hepatitis Be antigen Active liver disease Severe cardiovascular/cerebrovascular/pulmonary disease Dementia or psychosis with no underlying treatable disease Malignancy of limited life expectancy 40. 40. 40. Presently only cadaveric kidneys are distributed based on the criteria drawn up by the MOSS committee.2.2.7 Oxalosis (not contraindicated for combined liver and kidney transplantation) 40. This will include the following patients: 40. named the Malaysian Organ Sharing System (MOSS).40.4 40.1.1.2 40.1. Any Malaysian citizen with end stage renal failure can register with MOSS as a potential renal recipient. This system is to ensure an equitable distribution of cadaveric organs.5 40. 250 . MALAYSIAN ORGAN SHARING SYSTEM (MOSS) Malaysian Society of Nephrology (MSN) and the Ministry of Health of Malaysia initiated the development of a national organ sharing network in 1999.

1 HLA antigens (A.3. Med J Malaysia 1999. 54 : 537-538 251 . This decision can only be made by a nephrologist.3 40. the donor and recipient should be the same ABO blood group type.40. Candidates with limited life expectancy (<1 year) without renal transplant will be placed into the medical emergency list (SOS).3. One of the two kidneys will be allocated to the procurement centre.3.4 Panel reactive antigen (10 points) * Waiting time (20 points) Logistic score (6 points) *Due to logistic reasons.3 Criteria for prioritisation With rare exception. Reference Wong HS. B and DR) matching * (12 points) 40. Candidates on the SOS list will receive top priority in receiving a cadaveric kidney. HLA antigens & PRA are presently not used as selection criteria.3. Candidates will be selected based on the following scoring system: 40. Malaysian Organ Sharing System.2 40.

5 mg daily in selected patients (e.g.10. Hydrocortisone 200 mg IV stat on call to theatre and postoperatively and 8-hourly until patient is tolerating orally b.2.1. stable recipient with severe steroid toxicity) 41.20 as induction immunotherapy.4 b.11.2 Immunosuppressive agents 41.2 Cyclosporin a. dose of Neoral is 10 mg/kg/day given pre transplant c.15. (Level A) 41.14. Prednisolone may be reduced to 5 – 7. For living related renal transplantation.2. Hydrocortisone is replaced by prednisolone 20 mg daily when allowed orally d.5 mg per month till the dose of 10 mg daily is reached e. tacrolimus may be used instead of cyclosporin. In highly sensitised recipients i.20 can be used as induction immunotherapy when acute tubular necrosis or delayed graft function is anticipated and in highly sensitised recipients.5/monoclonal antibody6 or anti-ILII antibody7.8. (Level A) However Anti-IL II antibody has minimal side effects and is easier to use.3.1 The immunosuppression regimen may be modified in the following situations: a.19. multiple blood transfusion and previous history of transplant. Neoral 8 mg/kg/day to begin 5 days pre-transplant b. multiparous female. IV Methylprednisolone 500 mg at anastomosis for cadaveric renal transplant in addition to the above c.1 The standard immunosuppression regimen The standard immunosuppression regimen (adult1. IMMUNOSUPPRESSION PROTOCOL 41. Prednisolone is tapered off beginning at 3 months post-transplant. For cadaveric transplant. cadaveric transplantation in children.19. mycophenolate mofetil (MMF) and prednisolone.1 Corticosteroids a.41.12. PRA >20%.2.13. Dose of Neoral is adjusted according to trough levels or C2 Trough levels • Less than 6 months post-transplant: 250-375 ng/ml • 6 months or more post-transplant: 100-250 ng/ml 252 . Polyclonal4.16 and LRRT in children18) consists of tacrolimus / cyclosporin. and/or the use polyclonal5/monoclonal antibody 6 or anti-ILII antibody7.e. 41. by 2.9.

administration of these two agents must be spaced apart and the dose of MMF is reduced to 500 mg twice a day. Oral Azathioprine is given at 1.5 mg/kg/day b.1 ug/ml • 7–12 months: 0.5 Azathioprine a. mycophenolate mofetil is given 1 g twice a day per oral (dose in children 600 mg/m2/dose 12 hourly) c.7 ug/ml • 1-2 months: 1. For cadaveric transplant.3 mg/kg/day given per oral when called to operating theatre. If leucopaenic mycophenolate mofetil should be stopped • It can be safely withheld for a few days up to 2 – 3 weeks for severe side effects 41.2. Dose is adjusted according to trough levels: • Less than 6 months post-transplant: 10-15 ng/ml • 6 months or more post-transplant: 5-10 ng/ml 41. On call to theatre.2 mg/kg/day in divided doses d.9 ug/ml • more than 12 months: 0. Azathioprine will be omitted in the following situations: • Recipients who are HBsAg positive and/or Anti-HCV antibody positive • Recipients with post-transplant chronic active hepatitis • Recipients with chronic hepatitis and progressively rising serum transaminase 253 .5 ug/ml • 2-3 months: 1. c.2.2. mycophenolate mofetil is given 1 g per oral b. e.4 Mycophenolate mofetil a. Post-transplant. For living related renal transplantation. tacrolimus is given at 0. Dose is reduced or omitted if total white counts are < 4000/mm3 d. Dose reduction is indicated if haematologic or gastro-intestinal side effects develop • Dose reduction is done in 30 – 50% decrements.3 ug/ml • 4-6 months: 1.3 Tacrolimus a. dose of tacrolimus is 0. When tacrolimus and mycophenolate mofetil are used. Post-operatively.8 ug/ml 41.C2 levels • Less than 1 month: 1.2 mg/kg/day to begin 5 days pre-transplant b. tacrolimus 0.

d. 20 mg bolus if > 8 yr Oral MMF 300 mg/m2/dose stat dose before going to OT Tacrolimus 0.d.1 mg/kg/dose b. dosing or tacrolimus 0.8 post-transplant 41. Azathioprine can be resumed at lower dose once counts are normalised 41.2.2 mg/kg/day b. dosing or tacrolimus 0. Daclizumab – 1 mg/kg stat IV on call to theatre and at week 2.d.6 ATG/ALG Refer to Chapter 42 41.1 mg/kg/dose b. D2 Prednisolone 60 mg/m2/day b.3.7 Anti-Interleukin II antibody a.6. Basiliximab – 20 mg IV is given on call to theatre and at day 4 post-transplant b.1 Cadaveric Renal Transplantation Day of Transplant D0 IV Basixilimab 10 mg bolus if < 8 yr.4.2 Living Related Renal Transplant D – 5 Oral Cyclosporin 10 mg/kg/day in b.d. Oral MMF 600 mg/m2/dose bd (reduced by 50% if used in combination with tacrolimus) D1 IV Hydrocortisone 5mg/kg/dose tds 254 .d.d. dosing Oral MMF 300 mg/m2/dose bd Tacrolimus 0.1 mg/kg/dose b. D4 Repeat IV Basiliximab 41.3 Paediatric immunosuppressive regime Immunosuppressive protocol for paediatric kidney transplantation is as follows:41.d. Oral MMF 600 mg/m2/dose bd (reduced by 50% if used in combination with tacrolimus) D0 IV Methyprednisolone 600 mg/m2 BSA prior to anastomosis of vessels Oral Cyclosporin 10 mg/kg/day in b.• In the presence of leucopaenia (<4000/mm3).2 mg/kg/day b. IV Methyprednisolone 600 mg/m2 BSA just prior to anastomosis of renal vessels D1 IV Hydrocortisone 5 mg/kg/dose tds Oral MMF 300 mg/m2/dose bd Tacrolimus 0.2.3.d.

Gonwa T et al. N Engl J Med 1983. European Multicentre Trial Group.d. The long term effect of prophylactic OKT3 monoclonal antibody in cadaveric kidney transplantation – a single centre.3. A randomised clinical trial of cyclosporine in cadaveric renal transplantation. Morrell R et al. Abramowicz D.start tapering the dose 1 week post-transplant and taper 10 mg/week till 10 – 12. Transplantation 1999. References The Canadian Multicentre Transplant Study Group. dosing or tacrolimus 0. 986-989 4. 67: 411-415 1. 6. A randomised clinical trial of cyclosporine in cadaveric renal transplantation. Oral MMF 600 mg/m2/dose bd (reduced by 50% if used in combination with tacrolimus) Prednisolone 60 mg/m2/day bd dosing Oral Cyclosporin 10 mg/kg/day in b. Brodie J. dosing or tacrolimus 0. 255 . De Pauw L et al. Oral MMF 600 mg/m2/dose bd (reduced by 50% if used in combination with tacrolimus) 41. Moore R. Antithymocyte globulin (ATGAM) in renal allograft recipients. 314: 1219-1225 3. 69: 834-841 10. Transplantation 1979.D2 Oral Cyclosporin 10 mg/kg/day in b. Multicentre randomised trial comparing tacrolimus and cyclosporin in prevention of renal allograft rejection. The Canadian Multicentre Transplant Study Group. 54: 433-437 7. Slakey D. Amlot P et al. Randomised trial of tacrolimus (Prograf) in combination with azathioprine or mycophenolate mofetil versus cyclosporin (Neoral) with mycophenolate mofetil after cadaveric kidney transplantation. Transplantation 1997. A prospective randomised trial of tacrolimus/prednisolone versus tacrolimus/prednisolone/mycophenolate mofetil in randomised transplant recipients.d. 28: 294-302. 309: 809-815 2. Callaluce R et al. Cyclosporin in cadaveric renal transplantation: one-year follow-up of a multicentre trial. Goldman M. Lancet 1983. Cyclosporin / tacroloimus – follow adult schedule b. N Engl J Med 1986. 64: 436-443 9.randomised study. Johnson C.3 Guidelines for drug dose tapering in paediatric renal transplant recipients a.2 mg/kg/day b. Prednisolone . prospective .d. Transplantation 1992.5 mg daily if renal function is stable and cyclosporin / tacrolimus is within the desired range. 350: 1193-1198 8. Johnson C. Ahsan N. Nashan B. European Tacrolimus Multicentre Renal Study Group. Transplantation 2000. A prospective randomised comparison of quadruple versus triple treatment for the first cadaver transplant with immediate graft function. Scantlebury V et al. Randomised trial of basiliximab versus placebo for control of acute cellular rejection in renal allograft recipients. Transplantation 1996.Analysis at three years. Shapiro R. 56: 827-831 5. Lancet 1997. Jordan M. Wechter W.2 mg/kg/day b.d.

63(1): 39-47 12. Transplantation 1998. 1999. A comparison of the effect of cyclosporin versus antilymphocyte globulin on delayed graft function in cadaveric renal transplant recipients. Burke JF et al. The International Mycophenolate Mofetil Study Groups. Paed Nephrol 1997. European Mycophenolate Mofetil Multicentre Cooperative Study Group. 68: 391-396 16.11. Mycophenolate mofetil in renal allograft recipients: a pooled efficacy analysis of three randomized. clinical studies in prevention of rejection. 61: 10291037 13. Mathew T. Transplantation 1997. Lancet 1995. Tricontinental Mycophenolate Mofetil Renal Transplant Study Group. A blinded randomised clinical trial of mycophenolate mofetil for the prevention of acute rejection in cadaveric renal transplantation. Halloran P. Reduction of the occurrence of acute cellular rejection among renal allograft recipients treated with basiliximab. doubleblind. United States Simulect Renal Group Study. Clin Transplant 2000. 65: 1450-1454 14. Tomlanovich S et al. Tricontinental Mycophenolate Mofetil Renal Transplant Study Group. A blinded long-term randomised multicentre study of mycophenolate mofetil in cadaveric renal transplantation: results at 3 years. 34: 296-303 17. Transplantation 1999. Transplantation. Transplantation 1996. Michael HJ. Transplantation 1999. European Mycophenolate Mofetil Multicentre Cooperative Study Group. 345: 1321-1325 15. Francos GC. 11: 49-64 19. Placebo control study of Mycophenolate Mofetil combined with cyclosporin and steroid for prevention of acute rejection. 67(2): 276-84 20. Am J Kidney Dis 1999. US Renal Transplant Mycophenolate Mofetil Study Group. Mycophenolate Mofetil in cadaveric renal transplant. achimeric anti-chimeric antiinterleukin-2-receptor monoclonal antibody. Mycophenolate Mofetil in renal transplant: 3-year results for placebo controlled trial. 48: 805-808 18. Renal transplantation. chronic dialysis and chronic renal insufficiency in children and adolescents. Meier-Kriesche et al. The effect of daclizumab in high risk renal transplant population. The 1995 annual report of the North Paediatric Renal Transplant Cooperative Study. Kahan B. 14(5): 509-13 256 .

1 Causes: a.1: Causes of acute graft dysfunction First 3 months After 3 months Acute rejection Acute rejection Calcineurin inhibitor toxicity Calcineurin inhibitor toxicity Urinary obstruction Urinary obstruction Recurrence of 1o disease Recurrence of 1o disease Drugs Graft renal artery stenosis Infections Drugs Infections 257 .1. Vascular thrombosis c.42. Hyperacute rejection Figure 42. MANAGEMENT OF GRAFT DYSFUNCTION 42.1: Approach to primary non-function Primary non-function Urgent Doppler Flow present Hyperacute rejection ATN Refer urologist No flow Consider antilymphocyte Avoid CSA 42.2 Acute graft dysfunction Table 42. Acute tubular necrosis b.1 Primary non function Definition: failure of graft to function immediately post anastomosis 42.

1 Causes: a. Ureteric stenosis b.2: Clinical approach to acute graft dysfunction Acute allograft dysfunction Exclude nongraft related causes e.Figure 42. drugs / infection Obstruction Doppler US No obstruction Refer urologist Flow present No flow Calcineurin inhibitor level DTPA scan / Angiogram Raised Normal Refer urologist Response Reduce dosage No response Allograft biopsy Calcineurin inhibotor toxicity Disease recurrence Rejection ATN 42.3 Obstruction 42.3. Others 258 . Perinephric collection c.g.

DTPA scan with frusemide c. Magnetic resonance angiography3 (Level C) • Increasingly utilised to screen for renal artery stenosis d.2 Investigations: a. Ultrasound scan b. Renography (DTPA with Captopril)4 (Level C) • Perform before and after an ACE inhibitor • Useful in predicting the physiological significance of a moderately severe stenotic lesion • Negative renography is less likely to respond to intervention 42. Surgery • Difficult due to extensive fibrosis and scarring • Should only be considered in patients with resistant hypertension or with proximal atherosclerotic disease6 • Success rate 60-90% 259 .3 Management: Consult urologist. Doppler US1. 20% recurrence rate 5 • Stent deployment results in better results b. All obstruction must be dealt PROMPTLY to avoid permanent graft dysfunction 42.3 Treatment a. Retrograde/antegrade pyelography 42. Sudden deterioration in BP control b.4 Renal artery stenosis 42.1 Consider if: a.2 (Level C) • Preferred screening modality • Operator dependent c.3. Angiography • Gold standard • Invasive b.4. Spiral CT angiography e. Recent onset of hypertension c.3. Angioplasty • Success rate 80%.4. Graft dysfunction in the presence of hypertension 42.2 Diagnosis: a.4.42.

9 (Level B) c.1 Recommendations: a. (Level C) b.5.42.9 (Level B) 42. Reporting of biopsies should be standardised according to an internationally agreed scheme to reflect the histopathological pattern and severity of the rejection episode. The biopsy result can be used to guide the intensity of anti rejection therapy and to assess long term prognosis.7. graft tenderness or fever when other causes of acute graft dysfunction has been ruled out.5.2 Banff classification of acute rejection Table 42.2) and to do a graft biopsy to confirm clinical diagnosis of acute rejection. Acute rejection should be suspected in patient with stable graft function who experience rapid rise of plasma creatinine concentration of more than 20-25% over their baseline with or without decrease urine output.8.5 Acute rejection 42. It is recommended to exclude other causes of graft dysfunction (see figure 41.2: Banff classification 199710 Class Histopathological Findings Grade I A Interstitial infiltration (>25% parenchyma affected) Foci of moderate tubulitis (> 4 mononuclear cells/tubular cross section/group of 10 tubular cells Interstitial infiltration (>25% parenchyma affected) Foci of severe tubulitis (>10 mononuclear cells /tubular cross section /group of 10 tubular cells Mild to moderate intimal arteritis found in at least one arterial cross section Severe intimal arteritis (>25% loss of the luminal area) Type I rejection (tubulointerstitial) Grade I B Type II rejection (vascular) Grade II A Grade II B 260 .

15. Steroid resistant rejection (Banff I B and above) • Response is usually evident after 5 days of treatment • Use of polyclonal/monoclonal antibody has to be weighed against risk of infection (e. 261 . Severe acute rejection (Banff II B or III) ii.14.g.21.13. high CMV risk.17 (Level B) • Rejection reversal in 67-98% of cases • Main problems : cost and adverse events • The use of anti-T-lymphocyte antibody therapy are reserved for: i. hepatitis Be antigenaemia) In cases where the acute rejection is resistant to corticosteroid therapy and treatment with anti-T-lymphocyte preparation does not provide optimal response. Second rejection episodes within 2 weeks of previous rejection iii.5.16. Corticosteroids11 (Level C) • Corticosteroid treatment is most widely used • 500 mg of methylprednisolone for 3 days • In children 300-600 mg/m2BSA/day IV methylprednisolone for 3 days • Response to treatment is identifiable by day 5 of treatment b. Antilymphocyte or Monoclonal Antibody12.22 "Rescue therapy" include replacing cyclosporin with tacrolimus.18.Class Histopathological Findings Transmural arteritis and/or arterial fibrinoid change and necrosis of medial smooth muscle cells occurring in association with lymphocytic inflammation of the vessels No intimal arteritis Foci of mild tubulitis Type III rejection Borderline/ suspicious of rejection 42.20.3 Treatment of acute rejection episodes Treatment of first acute rejection episode a.19. a change in baseline therapy may be considered.

3: Protocol recommendation for Polyclonal Antibody use Adapted from drug insert Usage : only histologically confirmed acute rejection Dosage : ATG 10-15mg/kg/day for 10 to 14 days (see dosage table for different brands) : ALG for 10 to 14 days (see dosage table for different brands) Prophylactic treatment: 1 hour prior to each administration IV chlorpheniramine 10 mg (children 0.Figure 42. Pulse steroids : Remains the mainstay of treatment of acute rejection • IV Methylprednisolone : Doses range from 5–10 mg/kg/day for 3– 5 days followed by maintenance corticosteroid dose at prerejection level or recycled back down from the high levels used posttransplant • Oral prednisolone: Oral prednisolone pulses 3–5 mg/kg for 3 days followed by tapering the dose back to baseline levels over 2–3 days b. FBC Treatment of Acute Rejection In Children 6 a. Tacrolimus23 This agent has been used successfully to reverse episodes of acute rejection that are refractory to treatment with steroids and OKT3 262 . OKT3 Approximately 20 – 30% of rejection episodes will not respond to high-dose steroids but up to 90% of these can be reversed by OKT3 c.1 mg/kg) Antipyretic agent: paracetamol 1 g 6 hourly (children 15 mg/kg) Administer via central venous line as an infusion Dose of Azathioprine/MMF should be reduce or stopped according to TWC Monitoring: daily renal profile.

Contraindication: 1.Oral paracetamol 0.Stop cyclosporin / tacrolimus and restart 3 days before completion of the course .Children (dosage): body weight < 30 kg : 2. Fluid overload (>3% above dry weight) 3.Administer premedication 15-60 min before first and second dose: .Monitoring: daily FBC. serum sickness 2.Dosage adjustment for other immunosuppressive treatment: .Administer as a bolus injection through a peripheral line .Dosage: . .Figure 42. renal profile. CXR before OKT3 263 .IV chlorpheniramine 10 mg (children 0. Use with caution in patients with past history of seizures . Hypersensitivity e.g.5 mg OKT3 body weight > 30 kg : 5 mg OKT3 .Should only be given for histologically confirmed acute allograft rejection . use paracetamol prn for fever .Continue MMF.4: Protocol recommendation for OKT3 use Adapted from Danovitch 1996 / Drug insert . patient should be oedema free and within 3% of dry weight and have normal CXR .5 to 1 g (children 15 mg/kg) Premedication is not required for remainder of the course.IV methylprednisolone 5-8 mg/kg .Use high dose diuretics.Adults: 5 mg daily for 10 to 14 days . dialysis or ultrafiltration to achieve euvolaemia in a volume overloaded patient .Before administration of first dose.1 mg/kg) . reduce dosage if patient is leucopaenic.

6.3 No proven effective specific treatment at present.5: Flow diagram of management strategy for acute graft rejection Suspected Rejection Pulse IV Methylpred No or partial response Response Allograft biopsy Maintain Immunosuppression Biopsy proven Cellular Rejection IA ± IB Vascular rejection Cellular Rejection (>IIA / + IB) Monoclonal Antibody/ Polyclonal antibody Suboptimal response Rescue therapy 42. However general measures to retard the progression of the renal failure should be instituted 42.2 Characterised by a gradual and irreversible deterioration in renal function 42.6.Figure 42.6.4 Start withdrawing immunosuppression when allograft function is severely impaired 264 .6.1 Usually occurs after 6 months 42.6 Chronic allograft nephropathy 42.

5 No controlled prospective studies have been performed to determine the best method for withdrawing immunosuppression. The absence of cellular or vascular rejection strongly suggests cyclosporin toxicity.0 mg/kg and refer patient for graft nephrectomy b. Time interval post-transplant ii. Acute toxicity • Clinical features suggestive of acute cyclosporin toxicity include : i.e. The frequency of monitoring should be guided by the following factors: i.25 • Acute toxicity is usually reversible with cessation of therapy • Some commonly used drugs can interact with cyclosporin metabolism resulting in toxicity • Cyclosporin blood monitoring is useful adjunct in preventing nephrotoxicity. Recommendation24 (Level D): a.7. Early graft failure (< 1 year) • To consider graft nephrectomy with withdrawal of immunosuppression 42. Change in cyclosporin dosing 265 . Tremor • There is no characteristic feature of cyclosporin toxicity on histopathological examination of allograft biopsy. Late graft failure (> 1 year) • Stop Azathioprine/MMF when in advanced renal failure • Withdraw Cyclosporin / Tacrolimus on starting dialysis • Taper Prednisolone by 1 mg/month until drug is discontinued watching for adrenal insufficiency • If patient develop symptoms of allograft rejection. Hypertension iv. Deterioration in graft function iii.7 Calcineurin inhibitor (Cyclosporin / Tacrolimus) toxicity Calcineurin inhibitor` toxicity is one of the causes of renal allograft dysfunction and it is difficult to differentiate from acute rejection clinically 42.42.1 Cyclosporin toxicity There are two forms of cyclosporine toxicity i. start a 5-7 days of prednisolone at dose of 0. Acute cyclosporin toxicity: histology may be normal.6. Hyperkalaemia iii.5 to 1. a. Increased cyclosporin blood level (Note: nephrotoxicity can occur with normal cyclosporin level) ii. acute toxicity and chronic toxicity.

55. Shamlou et al. Little. hyperkalaemia and hyperuricaemia References Baxter GM et al. Magnetic Resonance Imaging 1997.2 Tacrolimus toxicity a. 15: 13 4. Transplantation 1999. Kamath S et al. Transplantation 1999. Boston 1996 7.27. If this is not seen. International Standardization of criteria for the histologic diagnosis of renal allograft rejection. Danovitch G. J Vasc Interv Radiol 1998. Solez K. Loubeyre P et al. Kidney Int 1999. Histological outcome of acute cellular rejection in kidney transplantation after treatment with methylprednisolone. The possibility of drug interaction • In patient with suspected cyclosporin nephrotoxicity the dosage should be reduced. there is no effective treatment modalities that have been shown to be effective in preventing chronic cyclosporin nephrotoxicity 42. Lucon et al. 67: 1430-434 1. mycophenolate mofetil) may ameliorate renal dysfunction in patients with cyclosporin induced nephrotoxicity.iv. Radiology 1994. 190: 153 5. 44: 411-422 9.7. Colour Doppler ultrasound in renal transplant artery stenosis: Which Doppler index? Clinical Radiology 1995. 68: 642-645 10. Treatment of recurrent transplant renal artery stenosis with metallic stents. Johnson DB et al. 50: 618 2. The Banff 97 working classification of renal allograft pathology. Solez et al. Chronic cyclosporin toxicity • Leads to chronic allograft failure26 • Chronic cyclosporin toxicity: stripe fibrosis. Dean De. Radiology 1997. Racusen. Transplanted renal artery: Detection of stenosis with colour Doppler. As nephrotoxic as cyclosporin 28 b. glomerular ischaemia. 713-723 11. Handbook of Kidney Transplantation 2nd Ed. Axelsen RA. May cause hyperglycaemia. Brown and Company. 9: 639 6. Captopril renography and the hypertensive renal transplant patient-predictive test of therapeutic outcome. allograft biopsy is indicated b. 203: 661 3. Sierre SD. A blinded retrospective analysis of renal allograft pathology using Banff schema. Kidney Int 1993. A prospective study. Gadolinium enhanced magnetic resonance angiogram of renal transplant. 266 . Transplantation 1999. 67: 737-741 8. Improvement in graft function usually noted in 48-72 hours. The Banff working classification of transplant pathology. microcalcification • Reduction of cyclosporin dose and replacement with nonnephrotoxic immunosuppressive drugs (e.g. Mazucchi. Pascual M et al. et al.28 (Level C) • At present. The clinical usefulness of renal allograft biopsy in the cyclosporin era. Raynauds AC.

10: 131-135 21. The efficacy of OKT3 in vascular rejection. Transplantation 1996. Transplantation 1991. 66: 29-37 18. Paedr Nephrol 1996. Norman D. Miller BW. Transplant Proc 1997. Transplantation 1998 . Suppl: 139 28. Plasma Exchange and Tacrolimus . 20: 759 26. A comparison of tacrolimus and cyclosporin for immunosuppression in liver transplantation. FK506 "Rescue" For Resistant Rejection Of Renal Allografts Under Primary Cyclosporine Immunosuppression. A randomized clinical trial of OKT3 monoclonal antibody for acute rejection of cadaveric renal transplants. A Multicenter Trial of TACROLIMUS (Tacrolimus) Therapy Refractory Acute Renal Allograft Rejection. 46: 523-529 17. Efficacy of OKT3 as primary therapy for histologically confirmed acute renal allograft rejection.Shapiro R et al. 51: 312-315 15. J Am Soc Nephrol 1991. Weiss MA. Kamath S. Transplantation 1998. et al. 8 (3) 25. Transplantation 1998. Transplant Proc. Results of double blind. Tokat Y. 30: 1297-1298 23. Transplant Proc 1988. The US Multicenter Liver FK 506 Study Group. Dean D. Refractory rejection Metaanalysis Group. Thistlewaite JR et al. Transplantation 1994. 66 (11): 1460-1464 22. 313: 337-342 13. Transplantation 1998. Clinical Transplant 1996. Ducloux et al. 10: 720-722 24. Schroedrer TJ. 1998. First MR. Withdrawal of Immunosuppression after renal transplant failure. randomized multicentre phase III clinical trial of Thymoglobulin versus ATGAM in the treatment of acute graft rejection episodes after renal transplantation. Uslu A. Shield C. 331: 1110 267 . Howard E. 2: S45 27. N Engl J Med 1994. Houde et al. Ortho Multicentre Transplant Study Group. Peddi VR et al. 29: 2805-2806 14. Improved renal allograft survival in children treated with FK506 (tacrolimus) rescue therapy. Corey. Histopathology of cyclosporine nephrotoxicity. Prednisone-mycophenolate mofetil double therapy for cyclosporine A toxicity in kidney transplantation. Jordan M. Transplantation 1997. Pascual M. Jordan ML. 64: 1428-1432 16.12. Effectiveness of second course of OKT3 monoclonal anti T cell antibody for treatment of renal allograft rejection. Up To Date 2000. Mihatsch et al. Transplantation 1988. Metaanlysis of TACROLIMUS and mycophenolate refractory rejection trials in renal transplantation. Cyclosporine induced chronic nephropathy: an obliterative microvascular renal injury. Mycophenolate Mofetil in renal transplant recipient with cyclosporine associated nephrotoxicity. 62: 594-599 19. Myers et al. ATG versus OKT3 in the treatment of steroid resistant rejection following living related donor renal transplantation.Mycophenolate Rescue for Acute Humoral Rejection in Kidney Transplantation. et al. Saidman S. Woodle ES. 57 :860-865 20. The Mycophenolate Mofetil Renal Refractory Rejection Study Group. Gaber AO. 65: 1504 29. Rescue therapy with Mycophenolate Mofetil. Brennan. N Engl J Med 1985. Woodle ES.

stents. Fluid collections or devitalized tissue d.1. 43. Prophylactic immunosuppressive protocol employed and treatment for acute rejections b.1) 43.2 43. hyperglycaemia. Bleeding or multiple blood transfusions Post-op management a. Metabolic abnormalities (malnutrition. Catheters.1) 43. Open wounds. Suboptimal nutritional status d. foreign bodies (catheters.1 General guidelines for infection recognition1 The following factors may assist in the identification of the causative pathogen and initiation of therapy (Table 43.1: Risk factors for infection post kidney transplantation1 Pretransplantation (Recipient) Medical Condition a. Graft injury or prolonged ischaemia c. Anastomotic breakdown or leak c. Immunosuppression for chronic conditions eg steroid. and intubation b. Leukopaenia 268 . Infection with immunomodulatory viruses (CMV. Early re-exploration or retransplantation e. stents). Diabetes mellitus c. MRSA.3 Pretransplantation donor screening Pretransplantation recipient screening 43. Neutropaenia c.4 Acquisition of community and hospital acquired pathogens e.g. pseudomonas species. cytotoxics b.1.1. ureamia) e.5 Net state of immunosuppression a.43. Prolonged procedure or anaesthesia b.1.1 The temporal occurrence of presumed infectious episode relative to the date of transplantation (see Figure 43. pneumococcus. EBV) Table 43. fluid collections and devitalised tissues d. MANAGEMENT OF TRANSPLANTATION INFECTION POST KIDNEY Infections related to transplantation procedure and opportunistic pathogens can adversely affect the outcome of kidney transplantation.1. Unrecognised or inadequately treated infection Perioperative Post-transplantation Surgery a. VRE 43.

Pre-op antibiotic exposures b.2. c.3 Systemic inflammatory response The presence of more than one causative agent must be considered e. 269 . Duration of hospitalisation Perioperative Graft ( donor) a. Microbial contamination of preservation fluid Post-transplantation Nosocomial infection a. Multiple agents b. may include: 43. Antibody induction and treatment for acute rejection.2.Pretransplantation (Recipient) Altered bacterial colonisation a. Unrecognised infection in allograft c.g. Prolonged antibiotic therapy b.2 Diagnosis of infection Diagnosis of infections post kidney transplantation can be difficult due to attenuation of the usual clinical signs and symptoms of infection by alterations in the immune response.2.1 Graft rejection 43. Bacteraemia or sepsis b. CMV disease facilitating other opportunistic infections. In transplant recipients. Increased antibiotic resistance Immunosuppression a. 43. fever also has a more expanded differential diagnosis which in addition to infections.2 Adverse effect of medication Treatment with antibodies (OKT3 and polyclonal antibodies) for acute rejection may cause fever and signs and symptoms suggestive of aseptic meningitis and pulmonary infiltrates. Fever may be absent in the presence of infection due to immunosuppression. Steroid – pulse and maintenance dose 43.

culture of blood. Specific pathogens should be sought in addition to common bacteria.3 Diagnosis of pneumonia Includes radiological examinations. 43.4. sputum.3 Nocardia – modified acid-fast staining. bronchoalveolar lavage (BAL).6 Mycobacterium tuberculosis Fungi 270 .4.4 Diagnosis of pneumonia Includes radiological examinations. Specific pathogens should be sought in addition to common bacteria.2 Pneumocystis carinii – fluorescein labeled antibody of BAL or sputum. sputum. culture of blood. 43. pleural fluid. bronchoalveolar lavage (BAL). transthoracic fine needle aspirate.4. pleural fluid. and transbronchial lung biopsy. tracheal aspirate.1 Legionella pneumophila – direct fluorescent antibodies of antigens in respiratory specimens. 43.4 Cytomegalovirus (CMV) – antigen detection using DEAFF from respiratory fluid and blood.4.4. tracheal aspirate.4. and transbronchial lung biopsy.1: Time table for occurrence of infection post transplantation2 43.Fig 43. 43. transthoracic fine needle aspirate. 43.5 43. such as: 43.

1 Prophylaxis therapy Peri-operative antibiotics prophylaxis may reduce the incidence of wound infection. Probable organism c. skin nodules or necrotic tissues should be swabbed and biopsied when appropriate.7 Treatment of infection In severe infection. Intravascular access and catheter tips should be cultured. Suspected anatomical site of infection b. 43. 43. prolonged course of antibiotics may promote emergence of resistance organisms and increase the risk for Clostridium difficile colitis.43. Aspiration and drainage of any collections. 43.6 Diagnosis of wound and other infections Wound infections.1) f. Net state of immunosuppression Initial empirical treatment for suspected severe bacterial infection should be broad spectrum. However. Time since transplantation (see fig 42.2 Empirical therapy For patients with suspected bacterial infections. Previous anti-microbial therapy e. If suspected. The choice of therapy should be guided by the available clinical information such as: a. Patients with diarrhoea should have stool examination done including detection for clostridium difficile. Antibiotic dosage also needs to be adjusted for renal impairment. The choice of broad spectrum antibiotics should have good Gram negative coverage according to local bacteriological and susceptibility pattern.7. Local antibiotic susceptibility pattern d. A number of antibiotics interact with cyclosporin metabolism and the level has to be monitored and adjusted accordingly. empirical therapy may be started while waiting for results of bacteriological studies. The implementation of anti-microbial therapy can be considered under the categories of prophylaxis therapy. either percutaneously with ultrasound guidance or surgically should be performed. and effective against Gram positive and 271 . immunosuppressive therapy may need to be reduced or stopped.5 Diagnosis of urinary tract infection Clean catch mid-stream urine specimen for culture. 43. The duration of treatment should be minimised. empirical therapy and definitive therapy.7. tips of ureteric stents should be cultured.

8 Mycobacterial infection3 Can occur as early as one month post-transplantation. treatment is changed to appropriate narrow spectrum agent (see specific therapy). Imipenem). If patient deteriorates or did not improve. At the same time consider changing antibiotics (e. and sensitivities are available. Pathogens (suspected/proven) Antibiotics 3rd generation cephalosporins Gram negative Gram positive: Aerobic: Staph aureus (MSSA) Staph aureus (MRSA) Staph epidermidis (MRSE) Streptococcal Listeria Anaerobic: Clostridium perfringens Clostridium difficile Legionella Pneumocystis Norcadia Cloxacillin Vancomycin Vancomycin Penicillin + Gentamicin Ampicillin + Gentamicin Penicillin Oral Vancomycin or Metronidazole Erythromycin* + Rifampicin* Cotrimoxazole + Pentamidine Dapsone+Trimethoprim Cotrimoxazole . 272 . The duration of therapy is based on the resolution of clinical signs and symptoms of bacterial infections. Table 43. aggressive search for source of infection should be performed.g. Ceftriazone. If a specific pathogen is isolated.3 Specific therapy Therapy is focused on the specific organism isolated to avoid superinfection. Imipenem * cyclosporin dosage needs to be adjusted 43. ESBL producers. 43. mycobacterium and fungal infections. Unusual presentation of mycobacterium tuberculosis and non tuberculous mycobacterial disease may delay diagnosis.2: Pathogens and recommended antibiotics. including search for MRSA.7. Amikacin. usually of 10 to 14 days duration.Gram negative bacteria. Minocycline.

Patients with previous mycobacterial infection are at risk of reactivation.1 Treatment Treatment is intravenous cotrimoxazole (20 mg/kg/day trimethoprim and 100 mg/kg/day sulphamethoxazole) given 6 hourly for at least 2 weeks. The dose of cyclosporin may need to increase by 3 to 5 folds with the use of rifampicin. and central nervous system. hypoxia and diffuse interstitial infiltration or focal consolidation on chest radiography.9 Pneumocystis carinii infection Occurs from 1 month post-transplantation onward. non-productive cough. 43. breathlessness. Rifampicin Isoniazid daily for 2 months daily# for 4 to 10 months *In certain situations. whichever is longer. 43. If intolerant of rifampicin. Caution: With the use of rifampicin. If there is no improvement after 4 to 5 days. and may involve skin. pyrazinamide and ethambutol is given for 18 to 24 months. or 12 months after cultures are negative. Chemoprophylaxis for mycobacterial is currently not given routinely. Bronchial alveolar lavage and transbronchial biopsy are good diagnostic methods. Presents with fever. whichever is longer. Rifampicin (R) Isoniazid (H) Pyrazinamide (Z) Vitamin B6 * Then if susceptible. joints and bones. combination of daily isoniazid. Patients may have disseminated disease. Alternatively Dapsone (100 mg/day) and Trimethoprim (15 mg/kg/day) may be used but caution on the use of dapsone and 273 .9. add in pentamidine infusion at 4 mg/kg/day. # Daily dosing to avoid fluctuating cyclosporin level. ethambutol (E) or ciprofloxacin may be added. If intolerant to isoniazid. or 12 months after cultures are negative. the dose of cyclosporin should be doubled and the cyclosporin dose should be adjusted with close monitoring of cyclosporin level. combination of ERZ daily for 2 months then ER for 12 to 16 months.

3 Cryptococcosis May cause meningitis.5 (Level B) 43.4 Histoplasmosis Usually causes acute pulmonary syndrome. Treatment of meningitis is with intravenous amphotericin B followed by fluconazole. 43.6 The routine use of OKT3 and polyclonal antibodies for induction should be avoided in transplant recipients who are positive for 274 . Chemoprophylaxis with oral co trimoxazole 80/400 daily or inhaled pentamidine 300 mg/month may be required for at least 3 months post treatment.10. Evidence of candida in the blood or disseminated infection of the lungs or other organs must be treated with intravenous amphotericin B or fluconazole.cotrimoxazole combination which may cause haemolysis in G6PD deficiency. 43.4 (Level A) However the duration of chemoprophylaxis is unclear. 43. Itraconazole is an alternative.2 Chemoprophylaxis Chemoprophylaxis for pneumocystis carinii pneumonia with co trimoxazole 80/400 daily is recommended for the first 6 months after renal transplantation and during treatment for acute rejection. urinary catheter and vaginal swab may be sufficient to justify local or topical treatment. and by vaccination of the recipient.10. dermatological. and other organ specific disease. pulmonary.10.9. Treatment is with intravenous amphotericin B or itraconazole.10. 43. Less severe disease can be treated with fluconazole alone 43. skin and central nervous system.1 Candidiasis Oral nystatin may be helpful as prophylaxis during period of intensified immunosuppression (first 3 months after transplant).10 Fungal infection 43. Treatment is with intravenous amphotericin B. Culture of candida from the mouth. This can be prevented by careful pre-transplant donor and recipient screening.2 Aspergillosis Usually presents with pneumonia but may disseminate to gastrointestinal.11 Hepatitis B virus (HBV) infection The outcome of HBV hepatitis is unfavourable in renal transplant recipients as it may lead to progressive liver damage.

Azathioprine is omitted from HCV carriers undergoing kidney transplantation. viral replication recurred when therapy was discontinued and one patient developed lamivudine resistant viral mutant. CMV is associated with immunomodulatory derangements that can lead indirectly to opportunistic superinfections. recipientnegative (D+R-) kidney transplant patients. In HCV positive recipients. CMV infection is the presence of CMV viraemia with mild fever without evidence of tissue invasion.1 Diagnosis 275 . 43.10 (Level D) Early referral to hepatologist is desirable.7 (Level D) Azathioprine is omitted from HBV carriers undergoing kidney transplantation. and development of post transplant lymphoproliferative disease.12 Hepatitis C infection HCV hepatitis may develop progressive liver disease in the long term but at a slower rate than HBV hepatitis.8 (Level D) Currently there is no effective treatment for HCV hepatitis.13. allograft rejection. The biggest concern regarding the use of interferon-alpha is precipitation of acute rejection. azathioprine withdrawal had been shown to reduce the incidence of progression of viral hepatitis to cirrhosis in a small study. It may be asymptomatic. particularly after the use of anti-lymphocyte antibodies. Two small studies demonstrated clearance of HBV DNA in renal transplant recipients by Lamivudine 100mg daily. hepatitis. CMV disease refers to symptomatic or tissue-invasive acute CMV infection eg pneumonitis. the use of OKT3 and polyclonal antibodies should be avoided.hepatitis B surface antigen (HBsAg). nervous system and gastrointestinal involvement. 43.9.13 Cytomegalovirus (CMV) infection and disease CMV infection occurs primarily after the first month of transplantation and the risk is dependent on the serological status of the donor and recipient. 43. haematological. (Level D) In HBV seroconverted recipients.8 (Level D) Treatment of active HBV hepatitis is limited. The risk of CMV infection is greatest in donor-positive. Such patients should be monitored for raised liver enzymes and viral replication by HBVDNA PCR. Interferon-alpha may precipitate acute rejection. However. (Level D) Azathioprine should be stopped in HCV seroconverted recipients and in those with hepatitis. Early reduction of immunosuppression may be useful in preventing severe liver disease.

IV ganciclovir 5 mg/kg bd for at least 14 days.5 – 50 kg 750 mg tds 25 – 37.13. 43. CMV DNA if available c.5 daily >400 10-24 1.3 Monitor during treatment a. Intravenous ganciclovir for at least 2 to 4 weeks. liver enzymes b. Direct early antigen fluorescent foci (monoclonal antibody against pp65. Daily full blood count. throat washing b.25 3x/wk after HD b. DEAFF). blood. given that life threatening disease is difficult to treat successfully once it is established.25 daily On dialysis <10 1. Upper and lower GI endoscopy and biopsy d. dosage according to renal function Table 43.400 25-49 2.5 kg 500 mg tds 276 . in urine.13. CMV DNA PCR c.2 Treatment of CMV disease11 (Level C) a. followed by oral 1000 mg tds for 2 to 12 weeks b. prevention by either prophylaxis or pre-emptive therapy is the most effective approach. renal profile.3: Dosing of ganciclovir Serum Creatinine (umol/l) GFR (ml/min) Dose (mg/kg/dose) <130 70 5 bd 130 – 220 50-69 2. Bronchio-alveolar lavage e.4 Prophylaxis therapy Modalities of prophylaxis therapy (dose adjustment required for renal impairment)13 a. Repeat cultures for CMV as necessary Overall.5 bd 220 .15: > 50 kg 1000 mg tds 37.13. Foscarnet 180mg/kg/day may be used instead of ganciclovir especially in ganciclovir resistant CMV Note: Acyclovir has no role in treating CMV disease while CMV immunoglobulins and intravenous immunoglobulin have uncertain value. Serology (IgM and IgG) is less helpful 43.a. Oral ganciclovir 1000 mg tds for 2 to 12 weeks In children14. 43.

c.5: Prophylaxis therapy12 Donor (D) Immunosuppression recipient (R) regime serological status D-/R+/-antilymphocyte therapy D+/RConventional D+/RD+/R+ D+/R+ D-/R+ D-/R+ Antilymphocyte therapy Conventional Antilymphocyte therapy Conventional Antilymphocyte therapy Recommendations Not needed Prophylaxis (Level B) Prophylaxis (Level A) Discretionary (Level C) Prophylaxis (Level A) Discretionary (Level C) Prophylaxis (Level A) 277 . predictive test to detect infection • Depending on test sensitivity may not identify all individuals at risk of disease Preemptive therapy Treatment administered for a brief period if laboratory tests indicate a high risk for CMV disease • Exposure of fewer individuals to drug • Reduce duration of exposure • Minimizes emergence of resistant CMV Table 43. • Prolonged exposure may result in development of resistance • Requires sensitive. Table 43. Oral valacyclovir 2000 mg qds for 90 days Oral acyclovir 800 mg qds for 12 weeks. d.4: Definitions of prophylaxis and pre-emptive therapy 11 Strategy Definition Advantages Disadvantages Prophylaxis Treatment administered before and at transplantation to prevent CMV disease Easy to administer • Risk of unnecessary exposure of low risk individual to a drug.

14. Zoster: oral acyclovir 400 mg/dose 5x/day (< 2 yr) .13. pancreatitis and disseminated intravascular coagulation. 43. In younger children. hepatic failure. pneumonitis. 43.2 Treatment Chickenpox: intravenous acyclovir 500 mg/m2/dose tds should be instituted immediately. 278 .1 Prophylaxis on exposure Prophylactic varicella-zoster immune globulin (VZIg) given to seronegative children within 72 hours of accidental exposure can modify the disease in 75% of cases. 43.14 Varicella-zoster (Level C) The most commonly seen manifestation in older paediatric transplant recipients is dermatome-restricted herpes zoster.11 Therefore. 800 mg/dose 5x/day (> 2 yr) (dosage adjustment will be needed in renal impairment) In chicken pox discontinue azathioprine until 2 days after the last new crop of vesicles has dried up.14. there is no guideline on pre-emptive therapy. primary varicella infection can result in rapidly progressive and overwhelming infection with encephalitis.5 Pre-emptive Currently there is insufficient data to recommend routine screening for CMV infection (presence of viraemia).43. The dose of other immunosuppressive agents will depend on the clinical situation and response to therapy.

Prophylactic oral ganciclovir after renal transplantation – dosing and pharmacokinetics. 3. 11 (supplement 15): S49-50 Recommendations for the Outpatient Surveillance of Renal Transplant Recipients. 66: 407-409 Recommendations from the IHMF Management Strategies Workshop: The Challenge of CMV Infection and Disease in Transplantation. Recommendations for the Outpatient Surveilance of Renal Transplant Recipients. 2nd edition. 156: 177-188 Recommendations for the Outpatient Surveilance of Renal Transplant Recipients. 12: 6-9 279 . 8. 2. 14. 15 (supplement 7): 75 David-Neto E. Paedr Nephrol 1997. 11: 665-667 Guido Filler. Infectious complications of kidney transplantation and their management. Nephrol Dial Transplant 2000. Skolnik PR. 12. Young LS.1994. Lau J. Transplantation 1998. 15 (supplement 7). 6. In: Handbook of Kidney Transplantation (Danovitch GM) 3rd ed. 10. Da Fonseca JA. et al. 2002 Ioannidis JPA. J Am Soc Nephrol 2000. Lamivudine inhibits hepatitis B virus replication in kidney graft recipients. Henry S et al. 4. Transplantation 1999. Practice Guidelines for the Control and Management of Tuberculosis. Kubak BM. J Am Soc Nephrol 2000. Clinical approach to infection in the compromised host. 64: 1624-1627 Goffin E. Paedr Nephrol 1998. 7.References 1. Horsman Y et al. Holt CD. Transplantation 1997. single center. Plenum. prospective study on azathioprine withdrawal. in Clinical Practice Guidelines of the American Society of Transplantation. Arch Intern Med 1996. 2001. S45-46 The EBPG Expert Group on Renal Transplantation: European Best Practice Guidelines for Renal Transplantation (part 1). 11 (supplement 15): S50-51 The EBPG Expert Group on Renal Transplantation: European Best Practice Guidelines for Renal Transplantation (part 1). 9. 11. Nephrol Dial Transplant 2000. in Clinical Practice Guidelines of the American Society of Transplantation. J Am Soc Nephrol 2000. Efficacy and safety of lamivudine on replication of recurrent hepatitis B after cadaveric renal transplantation. Sacks HS: A meta-analysis of the relative efficacy and toxicity of Pneumocystis carinii prophylactic regiments. 71-74 CMV infections following renal transplantation – effects of antiviral prophylaxis : a report of NAPRTCS. 13. 11 (supplement 15). Cappelleri JC.pp 221-262 Rubin RH. Lippincott Williams & Wilkins. 68: 976-980 Rostaing L. in Clinical Practice Guidelines of the American Society of Transplantation. Pegues DA. eds. 2000. The impact of azathioprine on chronic viral hepatitis in renal transplantations: a long term. 5. 15.

A desired body mass index of 20 –25 kg/m2 is considered healthy. Increased caloric intake may occur after transplantation primarily because of enhanced appetite associated with steroid use. weight and body mass index (weight in kg divided by height in metres squared) b.5 Potassium intake Patients who have normal functioning graft will usually not encounter problems with serum potassium.44. RENAL TRANSPLANTATION AND NUTRITION 44. Potassium supplementation or restriction is necessary in some cases. 44. 44. 44.1 Dietary modification The first 21 days after successful transplantation should focus on a diet of optimal protein and energy intake as well as restrictions of total fat.1.1 Obesity a.5 gm/kg/day. Incidence: Approximately 40% of renal transplant recipients are obese one-year post transplant.1. Dietary cholesterol should be < 300mg/day.2 Nutritional complications post-transplantation 44. saturated fat. 44.1. mono-unsaturated fatty acids and saturated fatty acids should be 1:1:1. cholesterol and simple sugars to restore nitrogen balance and minimise clinical symptoms of post-transplant diabetes and hyperlipidaemia. May have adverse effect on coronary vascular disease.1 Calorie intake Adequate calorie intake of at least 35kcal/kg/day (range of 35 to 50 kcal/kg/day) a.2 –1.1.2 Protein Protein intake is recommended at 1. 280 .3 d.2 Detected by height. A diet with moderate sodium restriction to 1 –2 gm/day is recommended if there is hypertension.1. 44. 40%-50%: Carbohydrate b.4 Sodium intake Sodium intake is restricted to 2-4 gm/day.3 Fat The ratio of polyunsaturated fatty acids. > 25 kg/m2 is overweight and >30kg/m2 is obese.1 (Level C) 44.2. < 30%: Fat Calorie intake is aimed at achieving or maintaining desired body weight. c.

8 • Age • Body weight • Sex • Pretransplantation lipid levels • Renal dysfunction • Proteinuria • Drugs eg.5 Reported changes in serum lipid levels are: ↑ triglyceride ↑ total cholestrol ↑LDL cholesterol ↑apolipoprotein B a. Malnutrition is associated with increased risk of infection.7. Treatment • Weight reduction • Increase exercise • Dietary modification as recommended for non transplant population (National Cholesterol Education Programme) Step 1 Intake of saturated fat 8% to 10% of total calories Fat intake of 30 % of total calories Saturated fat intake < 300mg/day 281 . Prednisolone. delayed wound healing and general debility.44.2 Malnutrition Incidence: 10% of patients exhibit low serum albumin levels at 1 year and 20% at 10 year after transplantation. β Blockers.4 Suspect malnutrition in the presence of low serum albumin (although factors other than calorie intake may contribute to hypoalbuminaemia).2.3 Post transplantation hyperlipidaemia Incidence: 60% of patients exhibit total cholestrol levels > 240mg/dl (high risk). Consequences of hyperlipidaemia • Correlation with chronic allograft nephropathy • Development of cardiovascular and peripheral vascular disease c. Pathogenesis of hyperlipidaemia in renal transplant patients: (multifactorial)6. Cyclosporin etc b. Sirolimus. Diagnosed by the presence of low serum albumin levels. 44.2. Corticosteroid accelerates the protein catabolic rate and frequently creates a negative nitrogen balance. Diuretics.

Management • Diet modification • Exercise • Weight loss • Cessation of smoking • Metformin • Sulfonylureas • Insulin .2. then proceed to Step 2 Step 2 Intake of saturated fat to 7% of total calories Saturated fat intake < 200mg/day • Drug therapy Drug therapy is indicated if dietary modification fails (Refer to chapter 45) 44. Treatment with insulin is also required during periods of stress and intercurrent illness.10 a. Predisposing factors: • Tacrolimus • Family history of diabetes mellitus • Prednisolone • Cyclosporin b.half of patients with PTDM may require insulin.If Step 1 fails.4 Post transplantation diabetes mellitus (PTDM) Incidence : Peak incidence in the first year post-transplant affecting 3% to 4% of patients.11 282 .

Ding Z et al. 48: 37 8. Hyperlipidaemia after renal transplantation: natural history and pathophysiolology. 51: 343-47 1.References Edwards MS. Factors influencing weight gain after renal transplantation. Summary of the second report of the National Cholestrol Education Program (NCEP) Expert Panel on Detection. Diabetes mellitus after renal transplantation in the cyclosporin era : analysis of risk factors. 79: 554 7. 239: 407-415 6. Vathsala A. Roth D. Massy ZA. Transplantation 1993. 47:278-281 11. Lipid abnormalities in cyclcosporin prednisolone treated renal transplant recipients. Johnson CP Gallagher-Lepak S. Steiner G. Serum albumin and mortality after renal transplantation Am J Kid Dis 1996. Posttransplantation hyperglycaemia: Increased incidence in cyclosporin treated renal allograft recipients Transplantation 1989. Milgrom M. Cattran DC. (6): 843-6 2. Zhu YR et al. Weinberg RB. Wideroe TE Hyperlipidaemia in renal transplant patients. Wilson D et al. J Int Med 1996. Dahl K. Renal transplantation diet recommendations: results of a survey or renal dietitians in the United States J Am Diet Assoc 1990. Aakhus S. Massy ZA. Schoenberg L et al. 56: 822-27 4. Delaney V. Doster S. 283 . Transplantation 1991. Should obese patients lose weight before receiving a kidney transplant? Transplantation 1997. 269: 3015 10. 64: 597-604 3. Ann Inter Med 1991. Sumrani N. Transplantation 1989. Evaluation and treatment of high blood cholesterol in adults(Adult Panel 11). 7: 971 9. Modlin CS Flechner SM Goormastic M. JAMA 1993. 27: 117-123 5. J Am Soc Nephrol 1996. Kasiske BL: Post transplantation hyperlipidaemia: Mechanisms and management. Ma JZ et al. Esquenazi V et al. Guijarro C.

10.5.1 The following steps may be taken to lower the IHD risk in patients (Level B): a.1 Cardiovascular disease 17% of deaths in renal transplant are due to cardiovascular disease. Low dose aspirin* (75 – 150 mg/day)14. Exercise 30 minutes 3 – 4 times a week16 h.14.5.16. (Level B) All renal transplant patients are considered at high risk of IHD.17 * caution in patients at risk of bleeding 284 . Control diabetes mellitus (HbA1C < 7% and FBS < 7 mmol/l) f.6. Weight kept at body mass index < 30 i. Table 45.9 family history of left ventricular age IHD hypertrophy male sex hypertension acute rejection smoking high LDL levels diabetes mellitus low HDL levels Elevated body mass index.1. Blood pressure < 125/75 mmHg if proteinuria > 1 g/day and < 130/85 mmHg if < 1 g/day13 c. Other suggestions (Level C)6: • Treat polycythaemia when PCV > 55%14 • Folic acid supplement (5 mg/day) to reduce homocysteine levels8.9.16 g. LONG-TERM COMPLICATIONS TRANSPLANTATION AFTER RENAL 45. hyperhomocysteinaemia. Stop smoking14.45.8 45. increased lipoprotein A and increased circulating inflammatory factors (CRP.3.1 The death rate from cardiovascular disease is 10 – 20 times increased in the younger age groups.15 e.1: Risk factors for IHD post renal transplant2. ACEI and beta blockers for hypertension13 d.1.11.12 If they had an old myocardial infarction (MI) they are considered very high risk.11 It is recommended to aggressively modify identifiable risk factors to lower cardiovascular risk.1.7. fibrinogen) are associations.8. Decrease LDL cholesterol (refer to 44.3 on lipid lowering therapy) b.4.

left ventricular hypertrophy. Diuretics Metabolic side effects. Secondary causes include20. anaemia. Methyl dopa Sedation. Useful in fluid overload a. Alpha blockers useful in benign prostatic hypertrophy.45. cardiovascular disease. Minoxidil Hirsutism and fluid retention. Useful in IHD. oedema common. Table 45.20 Renal function should be closely monitored. Table 45. Suspect a secondary cause of HT if: • Hypertension is poorly controlled despite good compliance and maximum anti-HT drugs • Malignant hypertension • Recent onset hypertension • Hypertension with progressive graft dysfunction b. liver damage. hyperkalaemia.13 It is assumed the patient has no acute rejection. channel verapamil and amlodipine elevate cyclosporine blockers levels.g. palpitations.18 Treatment is to protect from cardiovascular complications and injury to the allograft. has decreased salt intake and is limiting weight gain. obesity are taken into account. antagonists13. asthma.13 Beta blockers Lipid side effects. Contraindicated in renal artery stenosis. hypercholesterolaemia.3: The following anti-hypertensives are used with caution Agent Notes Decreased GFR. The management is similar to other cases of hypertension. Useful in uncontrolled hypertension. diabetes mellitus.1. Vasodilators Postural hypotension.21: 285 . Diltiazem.13. dehydration.2 Hypertension The incidence of hypertension post renal transplant is 60 – 80% with the use of cyclosporine and tacrolimus. ACE inhibitors and AII receptor cough. Worsens peripheral vascular disease. heart block. Comorbid factors e. Nifedipine causes gum hypertrophy.2: The following anti-hypertensives may be used in renal transplant recipients19 Agent Notes Calcium Headache. Useful in HT with proteinuria or posttransplant erythrocytosis. is on the lowest steroid and cyclosporine dose.

22. 5 – 10 mg/day simvastatin and 20mg/day lovastatin. simvastatin and atorvastatin) which cause myopathy.16.1.2. start if total cholesterol is 4 or LDL > 3 mmol/l.31.67) Cholesterol usually will not change with diet modification. Cholesterol lowering in renal transplant recipients: (Level A) For primary prevention start with HMG CoA reductase inhibitor (statin) if total cholesterol is 7 or LDL > 5 mmol/l.14 (Level A) b.9 Statins reduced the incidence of cardiac deaths and non fatal myocardial infarction in renal transplant recipients.91 mmol/l29 (>1.3 Lipid lowering therapy Lowering LDL cholesterol in patients with IHD or in high risk patients for primary prevention leads to clinical benefit beyond a doubt.37 mmol/l9 • Secondary prevention: target LDL < 2.27. LDL. In postmenopausal women with IHD there was no effect of HRT on decreasing IHD.• • • • Graft renal artery stenosis Chronic allograft nephropathy Recurrent or de novo glomerulonephritis (active urine sediment with CRF) Chronic cyclosporine toxicity 45.33.26. Patients should be screened at least once during the first 6 months and again at 1 year after renal transplant with fasting total cholesterol.1 mmol/l (180 mg/dl). in the latter reduce the dose to half.2.36 286 .30. Thereafter annual screening with fasting lipid profile.25.g.26 With IHD.02586) (Conversion from mmol/l to mg/dl cholesterol: x 38. Fibrates should not use in combination with statins. e.28 (Level A) a.25 • Primary prevention: target LDL < 3.32 There are 2 classes of statins: hydrophilic (pravastatin and fluvastatin) which do not cause myopathy and lipophilic (lovastatin.55 mmol/l is protective) *(Conversion from mg/dl to mmol/l cholesterol: x 0. graft function or IHD risk may warrant additional screening.23. Caution as statins may interact with cyclosporin. Statins are the drugs of first choice for decreasing LDL.34.35 In the former class maximum dose can be used.23.59 mmol/l 13 Further guidelines are to start if HDL < 0. Changes in immunosuppressive therapy.24. Fibrates may be used for hypertriglyceridaemia and decreased HDL: target TG < 2.2.22. HDL and TG.

14 (Level B) Intravenous pamidronate 0.53 Graft loss 60% compared to 23% if no recurrence 75 – 85% second graft failure in children if first graft is lost to FSGS. Hormone replacement therapy is recommended for post-menopausal women. (Level D) Table 45. renal transplant (Tx) within 3 years of nephrotic syndrome and rapid progression to ESRF are associated with recurrence 20 – 30%.6.43.51.44. after 6 months and then every 12 months if results are abnormal. 10 – 15% in adults 48. 3/27 adults .2 Prevention and treatment of osteoporosis Patients at highest risk of osteoporotic fractures are those with established osteoporosis.41. t score) may be diagnosed with dual energy X’ray absorptiometry (DEXA) at the time of renal transplant.50 10 .6.39.25 ug/day may reduce long term bone loss.5 SD below the young adult mean value.46 (Level D) The side effect is hypercalcaemia.45.40 (level B) This drug prevents bone resorption and may cause transient hypocalcaemia and hypophosphataemia. insulin dependent diabetes. 40 – 50% in adults 30 – 50% 30 – 40% De novo rate 5 – 10% Associated with hepatitis C Membranous GN Membranoproliferativ e GN Type I 20 – 30%.4: Recurrence of primary disease post renal transplant Type of GN Focal glomerulosclerosis 47 Recurrence rate 8/16 children.37. 80 – 100% in children < 15 years with ESRF within 3 years of FSGS.6 Osteoporosis (bone mineral density > 2.6. old age or who are post-menopausal.37. 80% recur in second graft (48. 50% in children < 5 years.54) 287 .30% 49. higher in children.5 mg/kg given at the time of renal transplant and one month later reduces bone loss.38.42 Calcium supplements (500 –1000 mg/day elemental calcium) and calcitriol 0. Oral alendronate and etidronate are alternatives.37 45.3 Recurrence of primary disease All reports are from observational studies.52.45.49.6.

53 10 – 50% From CSA toxicity – do not use CSA next renal transplant 40% 45.5 times that of cancer in the general population.53.4 Surveillance for malignancy The evidence is from retrospective case studies. typical HUS caused by diarrhoae does not recur. • short duration disease pre-ESRF. The incidence of cancer is 100 times that of the general population.56 50% but asymptomatic.58 It tends to be aggressive with mortality 4. • older age onset. The incidence is dependent on viral infections pre. increased in • atypical HUS.55 Recurrence correlates with disease activity and Tx only after activity subsides 12 months48 Delay transplant till circulating anti-GBM AB undetectable for 12 months. genetic 288 . It is dependent on the type and dose of immunosuppressants. Graft loss 10 – 20% < 10%.57. • use of living donors.54 50%. single centre series and registry data. sex of the patients. Transplant after activity subsides 12 months 16%.48. • autosomnal recessive HUS.and post-transplant. detection and therapy. usually > 5 years post renal transplant49.49. age.53.Type of GN Membranoproliferativ e GN Type II IgA nephropathy Recurrence rate 50 – 100%48. 75% graft survival at 5 years De novo rate Henoch-Schonlein purpura Anti-GBM antibody positive glomerulonephritis Rare Haemolytic uraemic syndrome Idiopathic crescentic glomerulophritis or Wegener’s or microscopic polyangitis Lupus nephritis 25 – 50%. stable ANCA and no symptoms transplant after 6 months. • cyclosporine47. policies for their prevention. increasing ANCA or active – do not transplant48 Low recurrence rate49.

factors and time after renal transplantation (incidence increases with time). The mean time of appearance is 69 months after renal transplantation. 45. In places with less sun exposure the incidence decreases. at multiple sites.1 Screening include: 289 . Cancer is found in body areas exposed to the sun and the incidence increases with time.2 relative risk. 80% of PTLD are in transplants with EBV +ve donor to EBV –ve recipients.4.1% versus 1. 45. marked decrease or cessation of immunosuppression b. acute rejection are observed before diagnosis of PTLD. more often for patients at risk. Premalignant lesions should be treated aggressively.5 Post transplant lymphoproliferative disorder (Level C) The incidence of post transplant lymphoproliferative disorder (PTLD) is more common in transplanted children compared to adults (10. 45.14 The incidence of dysplasia is 9%.14 (Level B) Self examination of the skin should be done monthly (Level B) and skin inspection by physician yearly14 (Level B).5. prostate.59 45. is aggressive and tends to recur after resection. The recommendations are for yearly pelvic examination and Pap smear in sexually active females > 18 years old.14 (Level A) 45. The incidence of breast cancer is decreased 25 – 30%.1 Treatment The treatment of PTLD consists of: a.60 Recommendations are to avoid and limit sun exposure. It occurs at younger age (30 years) compared to general population (60 years). However colon and breast cancers are common.6.2 Cancer of the cervix There is a 3 – 16 times increased risk with human papillomavirus infection having a 3. wearing sunscreen and protective clothing. In 30%. There is an association with human papillomavirus infection.6 Other cancers There is no increased incidence of lung. 45.1 Skin cancer There is increased incidence of squamous cell cancer but not basal cell cancer. The mortality rate is 5% compared to 2% in the general population.4.6. up to 40% incidence at 20 years with a 250 times increased risk.6. a small percentage (~ 2%) may require chemotherapy In children the outcome of PTLD is more favourable than adult in terms of patient and graft survival. colon and uterine cancer6.2%) especially in presence of vigorous immunosuppression.6.

Current Opinion in Urol 2000. Vol 8 No 2 Silkensen J. UpToDate 2000. Vol 8 No 2. Parfrey P. NKF: Controlling the epidemic of CV disease in CRD: V. Zietse R et al. Parfrey P. Ischaemic heart disease after renal transplantation: how to assess and minimize the risk. Executive summary. NKF: Controlling the epidemic of CV disease in CRD: V. Vol 8 No 2. Roel J. and homocysteine. 11 : 1735 – 1743. 9. Jardine A. menopause. Roodnat J. Nephrol Dial Transplant 2000. 16. UpToDate 2000. Tobacco use. UpToDate 2000. UpToDate 2000. Colon: Faecal occult blood yearly and flexible sigmoidoscopy every 5 years in patients > 50 years old. NKF: Controlling the epidemic of CV disease in CRD: V. Cholesterol as an independent predictor of outcome after renal transplantation. 4. 3. Foley R. 69 : 1704 – 1710 Levey A. 13. Levey A. 2. Explained and unexplained ischemic heart disease risk after renal transplantation. UpToDate 2000. Sarnak M. 290 . 15 (2) : 269 – 277 Kasiske B. J Am Soc Nephrol 1998. Vol 8 No 2 Stewart G. 10 (2) : 81 – 86. Harmon W et al. Briggs J. Nephrol Dial Transplant 2000. JASN 2000. Mechanisms of hypertension after renal transplantation. 9 : S31 – S42. Breast: Mammography every 1 – 2 years at age 50 – 69 years. Kasiske B. Sunder-Plassmann G. NKF: Controlling the epidemic of CV disease in CRD: V. physical activity. 11 : S1 – S86 Murphy S. Foley R. Hyperlipidemia in patients with chronic renal disease. Meyer K. 7. NKF: Controlling the epidemic of CV disease in CRD: II. Long-term complications in renal transplantation. Ischaemic heart disease following renal transplantation. 9 : S16 – S23 Mailloux L. 10 : 87 – 94. 12. Floth A. J Am Soc Nephrol 2000. UpToDate 2000. Risk factors for cardiovascular disease in the renal transplant recipient. Levey A. Vol 8 No 2. Epidemiology of cardiac disease in chronic renal disease. 11. Nephrol Dial Transplant 1999. Part III. 5. 17. Part I. Vella J. Vol 8 No 2. Chekkera. 18. Sarnak M.a.14 (Level A) b. 11 : 582 – 588. 8. Harini A. Beto J. Part VI. Vol 8 No 2 Kasiske B. Controlling the epidemic of cardiovascular disease in chronic renal disease: report from the National Kidney Foundation task force on cardiovascular disease. 14. Rosenkrantz A. Part V. Clinical epidemiology of cardiovascular disease in chronic renal disease. Recommendations for the outpatient surveillance of renal transplant recipients. Current Opinion in Urology 2000. Hypertension in patients with chronic renal disease. Recommendations for the management of cardiovascular risk factors. Sayegh M. 10. I. Screening and treatment for cardiovascular disease in patients with CRD. NKF: Controlling the epidemic of CV disease in CRD: V. UpToDate 2000. J Am Soc Nephrol 2000. Hyperhomocysteinemia in organ transplantation. Part II. Bansal V.14 (Level A) References 1. J Am Soc Nephrol 1998.V. 15 (Suppl 5) : S58 – S154. Fodinger M. Mayer G. Mulder P. Foley R. 14 : 1075 – 1077. Parfrey P. 6. Wheeler D. 15. Transplantation 2000. Vazquez M.

280 (7) : 605 . Journal of Clinical Pharmacy & Therapeutics 1999. Wanner C. 32. JAMA 1998. deMattos A. Osteoporosis after transplantation. 23. Ford I et al. 57 : 684 – 690. Grady D. Fellstrom B. Holdaas H. Weingartner K. Olyaei A. 291 . Academy of Medicine Malaysia. Castro R. N Eng J Med 1998. Lancet 2003. 30. Fonseca J et al. 21. Current Opinion in Urology 2000. 104 (5) : 459 – 469. Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. Rodino M. Jardine H. Wald N. Queiros I. Treatment of hyperlipidemia in renal transplant recipients. Rosenblatt M. Effect of fluvaswtatin on cardiac outcomes in renal transplant recipients: a multicentre. Hypertension after renal transplantation. Bennett W. placebo-controlled trial. 7 (5) : 579 – 584 33. Clearfield M. A practical guide to the management of hypertension in renal transplant recipients. Sacks F. Am J Med 1998. 39. Quaschning T. Weis S. Ministry of Health Malaysia. Parathyroid and mineral metabolism after renal transplantation. 1998. Transplantation 1997. An evidence-based assessment of the NCEP adult treatment panel II guidelines. 361 :2024 – 2031 31. Br Med J 1994. 279 (2) : 1615 – 1622. 34. Berg A. 80 (3) : 257 – 268 22. Cobbe S. 38. Ball E et al. 26. Almond M. JAMA 1999. 344 : 1383 – 1389. By how much and how quickly does reduction in serum cholesterol concentration lower risk of ischaemic heart disease. Kid Int 2000. Impact of dyslipidaemia in renal transplant recipients. 25. Sayegh M. 27. 63 : 339 – 345. Vol 8 No 2. Holdaas H. Lancet 1994. Mandelbaum A. Ansell B. Current Opinion in Nephrology & Hypertension 1998. UpToDate 2000. 333 (20) : 1301 – 1307. Thompson S. Bush T et al. The long-term intervention with pravastatin in ischaemic disease (LIPID) study group. Rosen H. Watson K. Jardine AG. 24 (6) : 397 – 408. Fluvastatin in combination with cyclosporin in renal transplant recipients: a review of clinical and safety experience. Pfeffer M.613. Quarles L. Butterly D. Ritz E. Scandinavian simvastatin survival study group. Zeier M. JAMA 1998. Downs J. Vol 8 No 2. randomised. Nephron 1998. Moye L et al. N Eng J Med 1995. Hulley S. 10 : 77 – 80. Vella J. 20. 35. Fan S. Vol 8 No 2. Drugs 1999. 282 (21) : 2051 – 2057. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. N Eng J Med 1996. Fogelman A. 37. 12 : 2140 – 2143 36. UpToDate 2000. Holme I et al. Pamidronate therapy as prevention of bone loss following renal transplantation. Statins and the kidney. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. Therapy of post-transplant hyperlipidaemia: comparative study with simvastatin and fish oil. 339 (19) : 1349 – 1357. 335 (14) : 1001 – 1009 24. 29. Osteoporosis after organ transplantation. Wheeler D. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival study (4S). Law M. Hypertension in the transplanted patient. Shane E. 58 (6) : 1011 – 1027. 40. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: results of AFCAPS / TexCAPS.19. Nephrol Dials Transplant 1997. Arnadottir M. Sheperd J. Second consensus statement on management of hyperlipidemia. Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. UpToDate 2000. 308 : 367 – 372 28.

Vol. 48. 58. Walker R.463. 47. AntiGBM antibody disease: recurrence after transplantation. Saag K. 59. Niaudet P. 8 No. Vol 8 No 2. 35 (20):227-236 44. UpToDate 2000. 45. Focal glomerulosclerosis: recurrence after transplantation. Sayegh M. Intermittent etidronate therapy to prevent corticosteroid-induced osteoporosis. Barbagallo S et al. outcome and risk factors. Adachi J. Kelly P et al. UpToDate 2000. 60. Transplantation 1997. Arthritis & Rheumatism 1997. UpToDate 2000.2. The EBPG Expert Group on Renal Transplantation.25-dihydroxyvitamin D3 and calcium carbonate on bone loss associated with long-term renal transplantation. 13 (3) : 195 – 199 54. UpToDate 2000. Sayegh M. Nephrol Dial Transplant 2000. 63 (8) : 1045 – 1052. Complications of renal transplantation in children. European best practice guidelines for renal transplantation (part 1). 52. 98 (5) : 459 . Kaplan A. 55. 50 (3) : 144 – 153. Vol 8 No 2. Membranous nephropathy and renal transplantation. Kotanko P. Pusey C. 42. Konel S. Sayegh M.41. 56. 40 : S136. Freemont A. Felson D. (Abstract). Becker G. Diamond T. Simms W. J Am Soc Nephrol 2000. Effect of 1. UpToDate 2000. UpToDate 2000. Development of malignancy following solid organ transplantation. 68 (10) : 1597 – 1619. calcitriol and calcitonin. Patterns of malignancies following renal transplantation. Sayegh M. Bensen W. Recurrent glomerulonephritis following renal transplantation. Arthritis & Rheumatism 1997. 57. Cyclical etidronate plus ergocalciferol prevents glucocorticoid-induced bone loss in post-menopausal women. 43. Emkey R. Alendronate for the management of glucocorticoid-induced osteoporosis: results of the multicenter US study. (Abstract). IgA nephropathy: recurrence after transplantation. Sambrook P. Brown J et al. Vol 8 No 2. UpToDate 2000. Impact of acute rejection therapy on infections and malignancies in renal transplant recipients. 337 : 382 – 387. Transplantation 1999. Cueto-Manzano A. 46. Vol 8 No 2. Recurrent and de novo diseases after renal transplantation. Sayegh M. A meta-analysis evaluating the efficacy of calcium and vitamin D for corticosteroid-induced osteoporosis. Nicholls K. Gruber B et al. Amin S. 328 : 1747 – 1752. Hariharan S. Membranoproliferative glomerulonephritis: recurrence after transplantation. 51. Seminars in Dialysis 2000. Sheil R. Cosyns J. UpToDate 2000. 49. 50. N Eng J Med 1997. Sayegh M. Vol 8 No 2. Pouteil-Noble C et al. Vol 8 No 2. Vol 8 No 2. Jamil B. McGuigan L. Transplant Proc 1999. Clin Nephrol 1998. Couchoud C. Sayegh M. Prevention of corticosteroid osteoporosis – a comparison of calcium. 40 : S136. Birmingham J. et al. N Eng J Med 1993. Recurrence of membranous nephropathy after renal transplantation: probability. 15 Suppl 7.TTP-HUS: recurrence after transplantation. 53. Am J Medicine 1995. Levy J. 31 (12) : 1263 – 1265 292 .

2.46.1.1. Table 46.1: Graft survival with respect to donor age Donor age 1 yr graft survival 5 yr graft survival < 2 years 2 – 5 years en bloc single kidney 6 – 15 years > 16 years 20% 82% 64% 70% comparable to adult kidneys 70% 40% comparable to adult kidneys a.2 Immunisation As information about the use of live virus vaccines after solid organ transplantation is limited. Long-term results with single paediatric donor (< 6 year) kidney transplants into adult recipients: • increase incidence in requirement for early dialysis (45% vs 24%) • higher incidence of proteinuria > 0.1 Cadaveric kidneys from young donors Cadaveric kidneys from young donors yield poorer graft survival and should be used with caution. Children who are scheduled for transplant should have their immunisation completed at least one month prior to transplantation.1 Pretransplant Work-up Obstructive uropathy accounts for approximately 20% ESRF and needs to be fully evaluated before transplantation. it is advisable to avoid live vaccines post transplantation.8 g/24 hr (67% vs 48%) • higher incidence of rejection within 6 months (80% vs 60%) Recommendations (Level C): • Kidneys < 6 cm employ en-bloc transplantation • Lighter patients generally given preference for receiving paediatric kidneys 46. 293 .1. Donors < 2 years should not be routinely used en bloc or singly. PAEDIATRIC RENAL TRANSPLANTATION 46. Outcome of transplant in patients with obstructive uropathy is not significantly different from others though there may be an increased incidence of post-transplantation urological complications and urinary tract infection.3 (Level C) 46.

Varicella vaccination Varicella vaccine for those patients who are seronegative. Vaccinees whose serum anti-HBsAb is < 10 mIU/ml after a primary vaccine series should be revaccinated.2.a. a. Maintain central venous pressure at 10 – 14 cm H2O c. Those who remain anti-HBs negative after a revaccination series of 3 doses are unlikely to respond to additional doses of vaccine. Urine output must be replaced to prevent hypovolaemia. Table 46.0g/kg) may be given during the creation of the vascular anastomosis to facilitate urine output. b. Hepatitis B vaccination Potential recipients who are seronegative for Hepatitis B should be vaccinated with double the recommended dose of Hepatitis B vaccination at month 0.5-1. Maintain mean arterial pressure above 70 mmHg before vascular clamps are removed.2: Dosing for varicella vaccine Age Dose of vaccine 12 months to 13th birthday one dose of varicella vaccine Adolescents and adults two doses of vaccine 4 to 8 weeks apart b.2 Peritransplant management issues in children3 46. Administer estimated amount of blood sequestered by an adult kidney of isotonic crystalloid or colloid solutions before renal vessels are unclamped. 46. d. 46. Check the antibody response after one month on completing the immunisation. 2. and 6. Frusemide (0.5-1mg/kg) and mannitol (0. 1.2.1 Intraoperative Fluid Management (Level D) Precise intraoperative fluid management and maintenance of adequate vascular volume are essential to minimise post-transplant delayed graft function particularly when placing an adult kidney in a relatively small child. Maintain central venous pressure in the range of 6 – 10 cm H2O and mean arterial pressure above 70 mmHg 294 .2 Postoperative fluid management (Level D) a.1.3 Immunosuppression Immunosuppressive protocol for paediatric kidney transplantation at Paediatric Nephrology Hospital Kuala Lumpur (Refer to chapter 41) 46. Revaccination consists of three doses.

CMV infection may manifest as only modest fever and a minimal rise in serum creatinine level in situations where aggressive antiCMV prophylactic therapies are employed 46. Catch-up growth occurs in only 30 – 50 % of children after transplantation. a. urinary tract infections in young children can be clinically indistinguishable from acute rejection c.2.3 Acute allograft dysfunction in children (Level C) The differential diagnosis of an algorithm for working-up acute graft dysfunction in children is generally similar to that of adult.3. • Cytomegalovirus4. Many young children have not yet been exposed to these viruses and because they lack protective immunity. herpesvirus. (refer to chapter 41) Particular emphasis however should be made in the following circumstances: a. the greater is the potential for serious infection when a CMV positive donor kidney is transplanted.3. Insensible fluid losses (400 ml/m2) should be administered as 0. small rise or no recognisable rise in serum creatinine can occur in acute rejection especially in small children who receive large kidneys b. Urine output should be replaced “ml for ml” with 0. Efforts should focus on the normalisation of height before transplantation or before the onset of puberty.1 Infections a.2 Growth (Level C) Growth retardation remains a major concern in children with chronic renal failure. their predisposition for serious primary infection is high.18% dextrose saline c. 46. (Refer to chapter 42) • Herpes Simplex The typical perioral herpetic ulcerations are common in immunosuppressed children and will usually respond to oral acyclovir therapy (dose 200 mg 5x/day).b. Viral Infections The herpes group viruses (CMV. The target urine output should be more than 1ml/kg/hr 46. varicella-zoster virus and EBV) pose a special problem in view of their common occurrence in children.45% saline.5 (Level B) The younger the child. often in children less than 6 years old.3 Problems encountered in children post transplant 46. Determinants of post-transplant growth : Age at transplant 295 .

3.10 a. Dietary measures to reduce hyperlipidaemia are advocated. b. Non-compliance should be suspected when any of the following are observed • diminution in cushingnoid features • sudden unexplained weight loss and • unexplained swings in the patient’s kidney function or cyclosporin trough blood level b. 296 . Hypertension has been shown to be associated with poorer graft function.9.3 Hypertension and cardiovascular disease Persistent post-transplant hypertension is seen in 50% of living related transplant and 70% of cadaveric transplant.7. 46. (Level C) The incidence of post-transplant hyperlipidemia is high (approximately 50%) in long-term paediatric graft recipients. • Prospective introduction of behaviour modification programs. Strategies for improving growth include: • Using low dose steroids • Maintain good graft function • Using human recombinant growth hormone6.3: Height gained post renal transplant in relationship to age of transplant Age at Tx Height gained 1 – 2 yrs post-transplant < 6 yrs + 1. Early transplantation allows less time for growth failure on dialysis and therefore less requirement for catch-up growth.Table 46.1 SDS > 13 yrs may be no mean increase The fact that younger children benefit the most in statural growth from early transplantation provides a strong argument for expedited transplantation in an attempt to optimise and perhaps normalise stature. There is currently no consensus to make firm recommendations for the use of pharmacologic measures in children. • Modified medication by using medications with less cosmetic side effect and daily dosing regime. (Level C) 46. Management of non-compliance • Ongoing counseling should be undertaken in high-risk patients pre-transplant.3.4 Non compliance Non-compliance has been estimated to be the principal cause of graft loss in 10 – 15% of all paediatric kidney transplants.0 SDS 6 – 12 yrs + 0.8.

60% were PTLDs and lymphoma.3 46.14 subsequent year).48 first year.1 Special problems pertaining to infants and young children a.1 Advantages of preemptive transplantation a. vascular thrombosis (23%) b. infants with end stage renal disease are the most challenging subgroup of patients undergoing renal transplantation.18 second year. • the highest risk for early graft loss • a higher mortality rate.5. high incidence of obstructive uropathy and other anomalies of the genitourinary system that pose challenging anatomical and 297 . technical error d.12.46. various inherited and sporadic syndromes with multiorgan involvement f. Preemptive transplantation eliminates complications and inconvenience of dialysis as well as transfusion requirements and its associated morbidity. 46. 0. however exhibited the best long-term graft survival with graft half-life of 18 years compared with adults (11 years) and adolescents (7 years).5 Transplantation in infants and young children1. b. there is even higher mortality rate (14% at 1 year and 25% at 2 years) with • accompanying co-morbid factors • difficulty maintaining long-term dialysis access. With dialysis and without transplantation.13 (Level C) Compared with adults and larger paediatric patients.11. 0.4. irreversible acute rejection e. Preemptive transplantation demonstrated longer graft survival compared to conventional transplantation (rate ratio of allograft failure 0. however. Recipients who survived the first year with good renal allograft function.3.4%. Of these.5 Malignancy The incidence of post-transplant malignancy in children has been reported to be 1. primary non-function (delayed graft function: 12%) c. 46.4 Preemptive transplantation (Level C) Pre-emptive transplantation should be considered if • creatinine clearance reduced to 10 – 20 ml/min or • severe growth failure 46.

Danovitch . Paedr Nephrol 1997. Transplantation of adult living donor kidneys into infants and small children. 14: 469-472 11.2 Special precautions in transplants involving infants a. Paedr Nephrol 1999. Dominique Simon. Arch Surg. CMV infections following renal transplantation – effects of antiviral prophylaxis: a report of NAPRTCS. The 1995 Annual Report of the North Paediatric Renal Transplant Cooperative Study. aggressive fluid management d. A report of the NAPRTCS. 14: 679-681 8. Renal transplantation in children under 5 years of age. 13: 730-736 298 . Non-compliance and transfer from paediatric to adult transplant unit. chronic dialysis and chronic renal insufficiency in children and adolescents. Paedr Nephrol 1998. Paedr Nephrol 2000. Arch Surg. careful integration of urologic and transplant surgery References 1. Alan R. Kan. Robert B. 11: 49-64 3. dedicated paediatric urological team b. Ettenger. Scott J. 13: 373-378 5. 13: 723-729 9. 46. Richard Fine. Paedr Nephrol 1997. The impact of recombinant human growth hormone treatment on final adult height. Paediatric renal transplantation without steroids. Renal Transplantation. Millan et al. Samhar I. Center volume effects in paediatric renal transplantation. Watson. Paedr Nephrol 1999.Handbook on Renal Transplantation 4. Douglas M.1997. Jameela A. 2000. 2000. Paedr Nephrol. tight immunosuppressive management c. Sven Arvid Birkeland. 5: 537-41 12. Post-graft development of short children treated with growth hormone before kidney graft.functional problems and require special approaches in preparation for transplant. Silverstein. Paedr Nephrol 1999. 11: 665-667 6.12: 87-92 7. Mahmoud A. Schurmann. Haeley et al. 135(9): 1035-1041 13. 135(9): 1063-1068 2. Paedr Nephrol 2000. Al-Akash .5. 14:105-110 10. Outcome of preemptive renal transplant and pre-transplant dialysis in children. Risk factors for hyperlipidemia in longterm paediatric renal transplant recipients. Paedr Nephrol 2000. Kidney transplantation in children. A 100% 2-year graft survival can be attained in high risk 15 kg or smaller infant recipients of kidney allografts.

Glossary HLA Ab ACE ACEI AHG AII ALG ALT ANCA Anti IL-II APKD APTT ATG ATN BAL BMI BP C&S Ca2+ CAPD CDC CMV Cr EDTA CrCl CRF CRP CSA CT CVP CXR DEAFF DNA DTPA DTT EBV ECG EDTA ELISA ENT Human leucocyte antigen Antibody Angiotensin converting enzyme ACE inhibitor Anti human globulin Angiotensin 2 Anti-lymphocyte globulin Alanine transaminase Anti-neutrophil cytoplasmic antibody Anti-interleukin 2 Adult polycystic kidney disease Activated partial thromboplastin time Anti-thymocyte globulin Acute tubular necrosis Broncho-alveolar lavage Body mass index Blood pressure Culture and sensitivity Calcium Continuous ambulatory peritoneal dialysis Complement-dependent cytotoxicity Cytomegalovirus Chromium EDTA Creatinine clearance Chronic renal failure C reactive peptide Cyclosporin Computer axial tomography Central venous pressure Chest X’ray Direct early antigen fluorescent foci Deoxyribonucleic acid Diethylenetriaminepentaacetic acid Dithiothreitol Epstein Barr virus Electrocardiogram Ethylene diamine tetraacetic acid Enzyme linked immunosorbent assay Ear nose throat 299 .

pyrazinamide Extended spectrum beta lactamase End stage renal failure Full blood count Fasting blood sugar Focal segmental glomerulosclerosis Glucose-6-phosphate deficiency Glomerular basement membrane Glomerular filtration rate Gastrointestinal Glomerulonephritis Water Haemoglobin A1C Hepatitis B e antigen Hepatitis B surface antibody Hepatitis B surface antigen Hepatitis C Haemodialysis High density lipoprotein Human immunodeficiency virus Hospital Kuala Lumpur 3-hydroxy-3-methyl-glutaryl coenzyme A Hypertension Haemolytic uraemic syndrome Intensive care unit Interferon Immunoglobulin A Immunoglobulin G Immunoglobulin M Ischaemic heart disease Intact parathyroidhormone Intravenous pyelogram Kidney ureter bladder Low density lipoprotein Liver function test Living related donor renal transplant Magnesium Myocardial infarction Mycophenolate mofetil Millimetres of mercury Malaysian organ sharing system Magnetic resonance angiography 300 . rifampicin.ERZ ESBL ESRF FBC FBS FSGS G6PD GBM GFR GI GN H20 HbA1c HBeAg HBsAb HBsAg HCV HD HDL HIV HKL HMG CoA HT HUS ICU IFN IgA IgG IgM IHD iPTH IVP KUB LDL LFT LRRT Mg2+ MI MMF mmHg MOSS MRA Ethambutol.

aureus Methicillin resistant staph. aureus Mid stream urine Operating theatre Polymerase chain reaction Packed cell volume Phosphate Panel reactive antibodies Prostatic specific antigen Prothrombin time Post transplant diabetes mellitus Post transplant lymphoproliferative disorder Random blood sugar Ribonucleic acid Standard CDC Save our souls Tuberculosis Triglyceride Transplant Upper respiratory tract infection Ultrasound Urinary tract infection 301 .MRSA MRSE MSSA MSU OT PCR PCV PO4 PRA PSA PT PTDM PTLD RBS RNA SCDC SOS TB TG Tx URTI US UTI Methicillin resistant staph. epidermidis Methicillin sensitive staph.

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