Dr.

Eslaban
April 19, 2023

Table Of Contents • We must also take note about Cockcroft and Gault
Chronic Kidney ............................................................. 1 formula because this is the one of the common
Dialysis .......................................................................... 7 formula that we use in computing the EGFR or
serum creatinine clearance.
• Green – Doc’s audio
• Blue – Upclass trans

CHRONIC KIDNEY
• Chronic kidney disease (CKD) encompasses a
spectrum of pathophysiologic processes
associated with abnormal kidney function and a
progressive decline in glomerular filtration rate
(GFR).
• The difference between AKI and CKD is the time
of onset. For the AKI it should be acute in onset
just within few hours or days or weeks. If we are
talking about CKD. What is the magic number? It Now a days, mas hapos na mag solve sini kay may
should be more than 3 months. app na nga available. But if wala ka app, what is
• The risk of CKD progression is closely linked to the most important here is the age and the weight
both the GFR and the amount of albuminuria. of the patient. Hapos lg sya tandaan. CKD-EPI is
• Progressive long-term reduction of nephron the one that is the most accurate
number and function (> 3 months) • The one that we usually use is and is more accurate
→ decrease in GFR in estimating the GFR of the patient is CKD-EPI
• Irreversible while AKI is reversible kidney function
→ According to our previous discussion in AKI, if KDIGO CLASSIFICAT ION
the px is managed accordingly, then there’s a
chance that the kidney function will go back to
normal
• Chronic Renal Failure
→ process of continuing irreversible reduction in
nephron number.
→ Typically corresponds to stages 3-5
→ It is already a permanent damage
→ When you talk about chronic renal failure it
means that you are already dealing with a stage
4 or 5 CKD. Before there was no staging of CKD.
• End stage renal disease
→ Stage 5
• If the patient is already in stage 5, the patient is
already a candidate for maintenance renal
replacement therapy by either dialysis or
transplantation
• The parameters used is GFR and Albumin. Usually,
RECOMMENDED EQUATION S FO R we don’t have the urine albumin results that is why
ESTIMATIO N OF GLOMER ULAR we use the GFR
FILTRATION RATE (GFR ) USING SERUM The stages of CKD is divided into the Albumin,
Albuminuria, and GFR. Most of the time we use the
GFR, but albumin or albuminuria level is also very
Group 15: Aludia, Jison, Limpiado, Tupaz Page 1 of 9
Assesor: Hiponia
 important especially in prognosticating the px. We
can get the albumin level using the urine albumin-
crea ratio. You can compute on the GFR using the
CKD-EPI.
Pls review the table, the color corresponds to the
risk. Green- Low risk; Yellow- low to moderate;
Orange- moderate to high; Red- Very high
STAGE S OF CKD
• Stages 1 and 2
→ asymptomatic
→ >60ml/min/1.73m2
→ Sometimes it is hard to tx this kind of patient
• Stages 3 and 4
→ clinical and laboratory complications appear
→ Patients will start to develop manifestations of
uremia
→ <60ml/min/1.73m2
• Normal annual decline in GFR starting age 20- 30
years of 1 ml/min/1.73m2
• Albuminuria
→ Important tool to monitor nephron injury or the
kidney function of the patient
• GFR depending on the age of the patient you have
to calculate/compute for a decreasing GFR as the
patient ages. The normal annual decline of GFR
starts from 20-30 years old. The normal GFR below
30 years old 120-125 ml/min/1.73m2
• But if you reach 30 years old, you have to expect
that there is a decline in the GFR of 1
ml/min/1.73m2 per year (normal decline)
→ Every year there is a decline in GFR as you age
• Base line is 120 and if you are 40 years old, minus
10 to the baseline, expected GFR of a 40- year-old
person is 110. At 60 years old, expected GFR is 80
ml/min/1.73m2
FIVE LEADING CATE GORIES OF CKD
• Diabetic Nephropathy
→ Now called ‘Diabetic Kidney Disease’
→ Diabetes is the most common cause of CKD
worldwide
→ Once the px mag kadto na sa ila
ophthalmologist and may diabetic retinopathy,
for sure may ckd na ang px
• Glomerulonephritis
• Hypertension-associated CKD (includes vascular
& ischemic disease & primary glomerular disease
with associated
→ Hypertensive nephrosclerosis
→ Hypertension - 2nd most common
• Autosomal dominant polycystic kidney disease
(ADPKD)
• Oher cystic & tubulointerstitial nephropathy
→ Chronic pyelonephritis
→ Stones
→ Chronic obstruction of kidney
• Right now
→ Diabetes and Hypertension - the leading cause
of both CKD and ESRD
• In elderly, hypertension is more common due to
Chronic Renal
→ Ischemia (Renovascular Disease)
→ Vascular system of an elderly patient is not that
good, there is already sclerosis due to
atherosclerosis. This patient will develop
chronic renal hypoperfusion, because of
atherosclerosis of BV, most of the time not only
found in kidney but also other parts of the body
→ Here in the PH, the most common cause of
uncontrolled diabetes is poor drug compliance
because of financial problem but there are also
financially able but don’t want to take meds.
→ In elderly, hypertension is more common due to
chronic renal ischemia brought about by
renovascular dse. And the most common cause
of renovascular dse is atherosclerosis.
• Genetics (ADPKD, diabetes, FSGS, essential
HPN, medullary cystic disease)
RISK FACT ORS
• Hypertension
• Diabetes Mellitus
• Autoimmune Disease
→ SLE - most common
• Old Age
• African Ancestry
• Family History of Renal Disease
• Previous episode of ARF
• Presence of proteinuria, abnormal urinary
sediment, or structural abnormality of urinary tract
→ Horseshoe kidney
→ Solitary kidneys
→ Double pelvis
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• Small for gestation birth weight and childhood
obesity
The most important to dx these px is to obtain a
good and thorough History and PE
PATHOPHYSIOLOGY
• 2 Mechanisms involved in the pathophysiology of
CKD:
→ Initiating mechanisms specific to the underlying
etiology (immune complex deposition and
inflammation in certain types of
glomerulonephritis, or toxin exposure.)
→ Always remember that CKD is just a
complication of other disease
→ Progressive mechanism involving hyperfiltration
and hypertrophy of remaining viable nephrons,
a common consequence of long-term reduction
of renal mass.
→ Why is there a hyper filtration and hypertrophy
of viable nephrons? This is to overcompensate.
Because there is already damage of some
nephrons so these remaining viable nephrons
would compensate by hyperfiltration and would
eventually hypertrophies which is helpful
initially, however in the long rung hyperfiltration
and hypertrophy would lead to nephrosclerosis.
• Underlying cause --- reduction of renal mass---
ESRD
• Azotemia - retention of waste products (BUN and
Creatinine) but without clinical symptoms
→ this is more of a laboratory diagnosis
• Uremia - Multiorgan system derangement
associated with clinical manifestations this is
already a clinical diagnosis. This has already a lot
of clinical manifestations that would make you
think that this patient has uremia. There is already
a multi-organ problem in cases of uremia. Uremia
may already be seen in Stages 3, more so in Stage
5.
CLINICAL MANIFE STATI O NS
ELECTROLYTE ABNORMAL IT IE S
• Hyperkalemia - most common
→ Because of the decrease in GFR, the K is also
affected, so that’s why there is accumulation of
K in the blood
→ Not all cases of CKD is hyper lang, but rather
Hypokalemia can also occur
→ Cardiac arrhythmia for both hyper and
hypokalemia
→ Hypokalemia may also cause paralysis
• Severe hypocalcemia may lead to seizure and
convulsion
• Hypo and hypernatremia
→ Common manifestation is obtundation
→ The patient’s sensorium is decreased and
sometimes end stage would lead to coma
• Hyperphosphatemia
• Patients with generalized edema, there is
dilutional hyponatremia. Not a true hyponatremia.
You don’t need to treat it, what you do is give
diuretic agents to the patient
ACID -BASE ABNORMALIT IES
• Metabolic acidosis
FLUID OVERLOAD
• Anemic patient
HYPERTE NSION
• Most common complication of CKD & ESRD
→ Major cause of uremia is volume overload
• Goals of Treatment:
→ To slow the progression of CKD
→ To prevent extra-renal complication of HPN –
most common complication is
cardiovascular/cardiac.
• Patients who are already have prior hypertension
that develop CKD will have further deterioration of
their kidney function, the blood pressure will be
higher and eventually become resistant to
treatment.
CARDIAC ABNORMALIT IE S
• It is the leading cause of morbidity and mortality.
• Pericarditis, arrhythmia, accelerated
atherosclerosis, CHF and ischemic CVD.
• Cardiovascular complications risk 10-200-fold
depending on the stage of CKD, other risk factors
and comorbid conditions.
• Pericarditis is due to retained metabolic toxins
(absolute indication of urgent initiation of dialysis
or intensification of dialysis prescription) – patient
usually has friction rub on auscultation. If you hear
this in a patient with very high creatinine, then px
needs to start dialysis immediately.
• Accelerated atherosclerosis is due to HPN,
hyperlipidemia, glucose intolerance, chronic
increase of Cardiac output, metabolic vascular &
myocardial calcification (Lifetime Statin Therapy)
• Ischemic cardiovascular disease is due to
occlusive coronary heart, cerebrovascular &
peripheral vascular disease
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• Actually, all organs of the body are affected by
uremia. Because this nitrogenous waste product
would accumulate in the blood and all organs in
the body.
HEMATOLOGIC ABNORMAL ITIES
• Anemia - usually normochromic, normocytic.
Causes of Anemia:
→ Decrease EPO production (main reason)
→ Diminished RBC survival - (Normal is 120
→ days)
→ GI bleed & other bleeding diathesis due to
prolonged BT, decreased PC, abnormal platelet
aggregation & adhesiveness, impaired
prothrombin consumption
→ Iron deficiency - patient have poor appetite
→ Hyperparathyroidism / bone marrow fibrosis
→ Chronic inflammation - (inc CRP)
→ Folate or Vitamin B12 deficiency
→ Hemoglobinopathy
→ Comorbid conditions
• Changes in leukocyte formation & function,
susceptible to infection (due to acidosis,
hyperglycemia, CHON-calorie malnutrition,
serum/tissue hyperosmolarity due to azotemia)
NEUROMUSCULAR ABNORM ALIT IES
• Peripheral neuropathy – firm indication to
initiate RRT (renal replacement therapy)
→ Once the patients develop peripheral
neuropathy, you really need to convince the
patient to initiate RRT as soon as possible just
like pericarditis. Although peripheral
neuropathy is not as urgent as pericarditis, but
yet it is already a firm indication to start renal
therapy
→ Late manifestation of uremia. Usually stage 4-5
• Impaired sensorium
→ Sometimes it will start as insomnia. Ask the
patient how was his/her sleep. The first
neurologic abnormality is usually insomnia
→ Later on, as the disease progresses then the
sensorium impaired, they would become
lethargic until such time that in the terminal
stages will develop into coma
• Coma in terminal stages
Dialysis complications:
• Dialysis dementia
→ This is usually found who is already on chronic
dialysis for a year
→ Chronic dialysis complication
→ Aluminum intoxication – a major contributor
▪ Before, some of the phosphate binders that
were used contains aluminum. But now, this
is seldom seen because we are no longer
using this aluminum compound
• Dialysis disequilibrium syndrome
→ Noted on 1st few dialysis
→ Associated with rapid decrease in BUN
→ We usually prescribe dialysis in a gentle way
during the 1st few sessions even the blood flow
rate is low
GASTRO INTE STINAL ABN ORMAL ITIE S
• Nausea and vomiting, anorexia, hiccups
• Uremic fetor – uriniferous odor of the breath
associated with unpleasant taste (breakdown of
urea in saliva to NH3)
→ Because the patient has already a lot of urea in
the body
→ Remember that urea is nitrogenous waste
products and they are accumulated inside the
body even in saliva
→ The patient will usually complain having a bad
breath even though their oral hygiene is good
→ Bad breath can only be improved by starting
dialysis
• Uremic gastroenteritis (mucosal ulcerations
brought about by waste products) – the one that
causes occult bleeding in uremic patients
NUTRITIO NAL ABNORMAL ITIES
• Protein-energy malnutrition is a consequence of
low protein and caloric intake in CKD patients
→ Common manifestation of uremia is anorexia
→ Most of the time they would not eat, because if
they eat, they would have nausea or vomit
• Indication for initiation of RRT
ENDOCRINE
• Secondary to hyperparathyroidism (due to
increased calcium impaired Vit. D3)
• Abnormal glucose intolerance
• Insulin metabolism
• Nutritional abnormality
→ FEMALE: decrease estrogen, amenorrhea,
abortions
→ MALE: impotence, oligospermia, decrease
testosterone
→ ADOLESCENTS: impaired sexual maturation
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 DERMATOLOGIC ABNORMA LITIE S
• Uremic frost – fine white powder found on skin
surface (evaporation of urea in sweat)
→ Uremic frost and uremic fetor – you can see this
when the patient is ABOUT to start dialysis
• Uremic pruritus – give phosphate binders
→ Because of the accumulation of phosphorous
beneath the skin
• Hemochromatosis– slate - gray - bronze
discoloration of skin
→ Very common in those who receive multiple
blood transfusions
• Nephrogenic fibrosing dermopathy – → Favored approach
progressive subcutaneous induration prominently
seen in the arms and legs
→ Gray nodule-like, very common among patients
who are under dialyzed, mga permi ga absent,
those who have financial problem
BONE MANIFESTAT IONS
• Classified into:
High bone turnover with elevated PTH level
• Osteitis fibrosa cystica – classic lesion of
secondary hyperparathyroidism; because of the
hypocalcemia, so body compensates by
increasing thyroid function.
Low bone turnover with low or normal PTH levels
• Adynamic bone disease and Osteomalacia
DIAGNOSIS
• History and PE
• Laboratory Tests
→ CBC
→ Serum electrolytes
→ ABG
→ Uric Acid
→ Creatinine
→ BUN
→ Imaging studies (The most useful imaging study
is renal ultrasound); as much as possible avoid
diagnostics that use contrast
→ Renal biopsy
▪ Renal biopsy reserved for patients with near
normal kidney size and possibility of
reversibility is tenable, and clarification of
underlying disease may alter medication –
only for patients who develop AKI on top of
CKD, so when AKI is managed the CKD is
stable.
▪ Not advised in a patient with bilateral small
kidneys because:
o It is technically difficult and has a greater
likelihood of causing bleeding and
other adverse consequences – kidney is
a highly vascular organ
o There is usually so much scarring that
the underlying disease may not be
apparent
o The window of opportunity to render
disease-specific therapy has passed.
• Ultrasound-guided percutaneous biopsy
Indications for Kidney biopsy
→ Suspicion of concomitant or superimposed
active process such as interstitial nephritis
→ Accelerated loss of GFR
→ Bleeding time should be measured and
desmopressin administered if kidney biopsy is
indicated in a CKD patient
→ Brief run of hemodialysis without heparin may
also be considered prior to renal biopsy to
normalize bleeding time
Contraindications of Kidney Biopsy
• Bilateral small kidneys
• PKD (polycystic kidney disease)
→ induce hemorrhage
• Uncontrolled HPN
• Urinary tract or perinephric infection
• Bleeding diathesis
• Respiratory distress
• Morbid obesity
• Establishing the Diagnosis and Etiology of CKD
→ Most important initial diagnostic step in the
evaluation of a patient presenting with elevated
serum creatinine is to distinguish newly
diagnosed CKD from acute or subacute renal
failure
• Acute
→ If normal values from recent months and even
years
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 → If history suggests multiple systemic → 125/75 mmHg target blood pressure in
manifestations of recent onset (e.g., fever, proteinuric CKD patients
polyarthritis, and rash) → ACE inhibitors and ARBs
• Chronic → Calcium channel blockers
→ Elevated serum creatinine concentration in the → Diltiazem
past
→ Evidence of metabolic bone disease with SLOWING PROG RE SSION OF DIABETIC
hyperphosphatemia, hypocalcemia, and RENAL DISEA SE
elevated PTH • Diabetic nephropathy is now the leading cause of
→ Elevated bone alkali phosphatase CKD requiring renal replacement therapy in many
→ Normochromic, normocytic anemia parts of the world.
→ Reduced kidney size (<8.5cm) Control of Blood Glucose
• Renal biopsy
• Target pre-prandial glucose: 5.0—7.2 mmol/L (90-
→ can be performed in early CKD (Stages 1-3)
130 mg/dl)
• Ischemic Nephropathy
• Target HbA1c: <7%
→ Presence of long-standing hypertension Control of Blood Pressure and Proteinuria
→ Evidence of ischemic disease (cardiac or
• Microalbuminuria precedes the decline in GFR
peripheral vascular disease)
and heralds renal and cardiovascular
▪ Finding of non-nephrotic proteinuria in the
complications
absence of urinary blood or red cell casts
• Testing for microalbumin is recommended in all
diabetic patients
TREATMENT
• Antihypertensive agents reduce albuminuria and
• Treat the underlying cause diminishes its progression even in normotensive
• Diet Modification diabetic patients
→ Protein Restriction ~0.6 g/Kg/day; may retard Protein Restriction
progression of renal disease if initiated early –
• Slows the rate of renal decline at earlier stages of
only for those who are not undergoing dialysis
renal disease → protein-mediated hyperfiltration
yet.
contributes to ongoing decline in renal function in
→ Energy Req. is 35 Kcal/Kg/day many different forms of renal disease
→ Low Sodium, Low Purine, Low Potassium (if • Daily protein intake of between 0.60 and 0.75 g/kg
hyperkalemic), Low Phosphorus per ay
• Treat anemia – ESA (erythropoietin stimulating • At least 50% of the protein intake be of high
agent) biologic value
→ target is hemoglobin of 100-115 g/L • 0.9 g/kg per day might be recommended
• Hypertension control • Sufficient energy intake to prevent protein-calorie
• Correction of electrolytes and acid-base disorders malnutrition
(start sodium bicarbonate when bicarbonate level • 35kcal/kg is recommended
falls below 20-23 mmol/L
• Renal Replacement Therapy
CRIT ER IA FOR INIT IAT ING PAT IE NTS ON
→ dialysis/transplant
MAINTENA NC E DIALYSIS
• Uremia
SLOWING THE PROG RE SS ION O F CKD
• Intractable Hyperkalemia
• Following interventions should be considered in
• Persistent ECF volume expansion despite diuretic
an effort to stabilize or slow the decline of renal
therapy
function
• Acidosis refractory to medical therapy
• Reducing intraglomerular hypertension and
• Bleeding Diathesis
proteinuria
• Creatinine Clearance or GFR <10 ml/min/1.72m 2
•
TREATMENT FOR SLOW IN G TH E
PROGRESSION OF CKD
• Antihypertensive therapy

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 DIALYSIS
DIALYSIS
• Indicated for both ARF & CKD
• Hemodialysis / peritoneal dialysis / CRRT / Slow
Low-Efficiency Dialysis
• CRRT & SLED are specific for the management of
AKI
• CRRT is done continuously
• SLED is done for over 6-12 hours
• Hemodialysis is done for 3-4 hours
• Peritoneal dialysis (CAPD or CCPD)
• The decision to initiate dialysis usually depends on
a combination of the PX’s symptoms, comorbid
conditions, and laboratory parameters.
• Unless a living donor is identified, transplantation
is deferred by necessity, due to the scarcity of
cadaveric donor organs (median waiting time, 3–6
years at most transplant centers).
• Dialytic options include hemodialysis and
peritoneal dialysis (PD)
HEMODIALYSIS
• Employs a process of diffusion across a
semipermeable membrane to remove unwanted
substances from the blood while adding desirable
components
• (-) hydrostatic pressure on the dialysis side for fluid
removal (ultrafiltration)
• Most patients require 9-12 hours/week
• BFR ranges from 250-500 ml/minute- vol of
heparinized blood filtered in dialyzer per unit of
time.
• Dialysate flows in an opposite counter-current
direction at 500–800 mL/min
• Hemodialysis requires direct access to the
circulation, either via a native arteriovenous fistula
(the preferred method of vascular access), usually
at the wrist (a “Brescia-Cimino” fistula); an
arteriovenous graft, usually made
polytetrafluoroethylene; a large-bore intravenous
catheter; or a subcutaneous device attached to
intravascular catheters.
• Blood is pumped though hollow fibers of an
artificial kidney (the “dialyzer”) and bathed with a
solution of favorable chemical composition
(isotonic, free of urea and other nitrogenous
compounds, and generally low in potassium).
THREE E SSENT IAL COMP ONENT S TO
HEMODIALYSIS
Dialyzer
• Is a plastic chamber with the ability to perfuse
blood and dialysate compartments
simultaneously at very high flow rates
Dialysate
• The potassium concentration of dialysate may be
varied from 0 to 4 mmol/L depending on the
predialysis serum potassium concentration.
• The usual dialysate calcium concentration is 1.25
mmol/L (2.5 mEq/L).
• The usual dialysate sodium concentration is 136–
140 mmol/L.
Blood Delivery System
• Composed of the extracorporeal circuit and the
dialysis access.
• Most patients undergo dialysis thrice weekly,
usually for 3–4h.
• The efficiency of dialysis is largely dependent on:
→ Duration of dialysis,
→ Blood flow rate,
→ Dialysate flow rate, and;
→ Surface area of the dialyzer
DIALYSIS AC CE SS: FIS TULA, GR AFT,
CATHETE R
• FISTULAS have the highest long-term patency
rate (Permanent access)
• GRAFTS & CATHETERS are used among persons
with smaller caliber veins
• Urea Clearance Rate ranges from 200-350
ml/minute
• Dose of hemodialysis depends on:
→ Patient size
→ Residual renal function
→ Dietary protein intake
o Inc in CHON intake = Inc. Creatinine
of
→ Degree of anabolism or catabolism
→ Presence of comorbid conditions
*The dialysis prescription is not uniform for all
patients, so you have to individualize your patients.
• Hemodialysis adequacy is based on decreased
BUN concentration during dialysis treatment
→ Urea Reduction Ratio (URR)
▪ 1- (post/pre-dialysis plasma urea level ratio)
→ KT/V
▪ Where:
o K = urea clearance rate
o T = time spent on dialysis
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 o V = size of urea pool presented by urea
distribution volume which is roughly
equal to total body water
• Minimal standards:
→ → URR = 65%
→ → KT/V = 1.2
*Most of the time we use KT/V. Before we really
need to compute for KT/V. RIght now, medyo
hightech na ang mga machines ta right now so
they can already check for the KT/V of the patient.
Once the KT/V is below 1.2 then you have to adjust
because that means that your patient is under-
dialysed. The adequacy of your patient is not that
good. So you have to check and review your
dialysis prescription.
• Hemodialysis removes both low and high
molecular weight solutes.
COMPLICATIONS OF HEMODIALYSI S
Hypotension - most common especially among
diabetic patients
→ Causes:
▪ Excessive ultrafiltration with inadequate
compensatory vascular filling (most
common)
o If you noticed that your patient
develops every time that they undergo
hemodialysis, try to check the
ultrafiltration prescription that you give
to the patient, then you have to
decrease.
▪ Impaired vasoactive or autonomic responses
▪ Osmolar shifts
o During hemodialysis, urea and other
toxins are also moving which would
cause sudden shift of the fluids between
cells.
▪ Overzealous use of antihypertensive agents
o Patients undergoing hemodialysis are
advised not to take their
antihypertensive medications BEFORE
undergoing the procedure. We just
advise them to bring their
antihypertensive meds during dialysis
to the dialysis unit so that if incase the
BP would increase, then we can advise
them to take their medicine at that
particular time.
▪ Reduced cardiac reserve
o Especially in patients that have poor
cardiac function where the ejection
fraction is very low.
• Rapid change in electrolytes leading to arrhythmia
▪ Usually due to hypokalemia during
hemodialysis; really needs to be checked
because it can cause cardiac arrest
• Disequilibrium syndrome
• Dementia
• Use of heparin
→ We use anticoagulants to avoid clotting of
blood during hemodialysis. This use of heparin
may lead to some form of hemorrhage,
especially when your patient would develop a
sudden drop in the hemoglobin. So, if the
hemoglobin is stable with those of the
erythropoietin that you are giving to them and
suddenly there is a significant drop in the
hemoglobin, then you have to look for some
form of bleeding anywhere in the body.
→ May lead to subdural hematoma,
retroperitoneal, GI, pericardial & pleural
hemorrhages
• Malnutrition
→ HD may affect and increase catabolism & allow
amino acid loss through the membrane.
ADVANTAGES OF HEMODI ALYSIS
• Short treatment time
→ The patient will just sit there for 4 hours, and
after 4 hours, the dialysis is finished. The patient
may go home after that.
• Minimal interruption of lifestyle between
treatment
• Rapid clearance rate
→ For those patients with very severe volume
overload, like patients with pulmonary edema
(they already have difficulty of breathing &
hypoxemia), then you need to do HD because it
has a rapid clearance rate of fluid compared to
peritoneal dialysis.
PER ITONEAL DIALYSIS
• Infusion of dextrose containing solution (1.5 - 3L)
into the peritoneal cavity and allowed to dwell for
a period of time (2-4 hours)
→ We have the continuous ambulatory peritoneal
dialysis (CAPD), and we do exchanges for
approximately 4-5 times a day, so that’s why it’s
more tiring to do than HD.
• Involves the process of diffusion through a
semipermeable membrane (peritoneum); the
peritoneum is the dialyzer
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 ADVANTAGES OF PERITO NEAL DIALYSIS • Deaths are due mainly to cardiovascular diseases
• Avoidance of heparinization (~40%) and infections (~10%)
→ If the patient has a bleeding problem, then you • Important predictors of death:
can do PD because there is no need for you to → Older age
use heparin. → Male sex
• Avoidance of vascular surgery → Non-black race
• Slower clearance rate → Diabetes mellitus
• More amenable to self-treatment → Malnutrition
→ More advantageous to those patients who are → Underlying heart disease
living far from a place with a hemodialysis
center.

DISADVANTAGES OF PE R ITONE AL Reference:

DIALYSIS • Lecturer’s ppt and discussion
• Longer treatment time • Upclass’ Trans
• Should not be used in patients with severe
pulmonary disease
→ Because you are infusing 1.5-3L of fluid into the
peritoneal cavity. This would increase the
intraperitoneal pressure, and would further
increase the pulmonary pressure.
• Should not be used in patients with extensive
abdominal adhesions due to surgery
• Inadequate clearance in patients with
scleroderma, vasculitis, malignant hypertension,
peritoneal fibrosis, or in heavy patients (70 kg) with
no residual renal functions

COMPLICATIONS OF PER ITO NE AL

DIALYSIS
• Peritonitis
→ Elevated PF leukocyte count = 100/µL (50%
PMN)
→ This particular complication also depends on
the hygiene of the patient.
• The most common culprit organisms in peritonitis
are Gram (+) cocci (Staphylococci)
• Catheter-associated nonperitonitis infections
(Tunnel Infection)
• Weight gain & other metabolic disturbances
→ Fluid that is infused to the patient contains
glucose, so that’s why the patient would gain
weight. If the patient is diabetic, you need to
monitor the sugar frequently.
• Residual Uremia (patients with no residual kidney
function)
→ Clearance is usually very slow. If the patient
develops residual uremia, you need to advise
them to shift to HD.
PROGNO SIS
• 5-year survival rate of patients on both kinds of
dialysis (USA) is ~35-40%

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