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Pediatric Nephrology Unit
University Of Alexandria
• Excretion • Homeostasis • Osmoregulation • Regulation of salts in the body • Regulation of pH • Production of a hormone (EPO) .
4% of body weight vs 25% of cardiac output each minute • High metabolic demand – High oxygen consumption – High substrate delivery • High surface area – Glomerular basement membrane – Tubular microvilli .• 0.
Renal injury Results from • • • • Hemodynamic changes Direct injury to cells and tissue Inflammatory tissue injury Obstruction of renal excretion .
Acute renal failure Acute kidney injury Biochemical test Biomarkers .
Sudden causes affecting Renal Perfusion Called Pre-renal Parenchymal Structures Induce GFR Parenchymatous (intrinsic) Urine output Post-renal ARF .
. Thus “renal protection” is lost when “renal autoregulation” fails.• One of the most striking characteristics of the renal circulation is the ability of the kidney to maintain a constant renal blood flow (RBF) and glomerular filtration rate (GFR) as renal perfusion pressure is altered.
Tacrolimus ACE inhibitors NSAIDS Radiocontrast Amphotericin B Aminoglycosides Sepsis Small-vessel Renal Vascular Disease Vasculitis Atheroemboli Thrombotic Microangiopathies Transplant Rejection Hepatorenal Syndrome Ischemic Acute Kidney Injury .Conditions that Lead to Pre-renal Azotemia-Ischemic AKI Intravascular Volume Depletion Large-vessel Renal Vascular Disease Decreased Effective Circulating Volume CHF Cirrhosis Nephrosis Generalized or Localized Reduction in Renal Blood Flow Renal Artery Thrombosis Renal Artery Embolism Renal Artery Stenosis or Crossclamping Medications CYA.
Was admitted to the hospital for: Fever and vomiting. No information regarding diuresis before admittance was available. Two days before admittance. He was the third child. 2 months breast feeding and then artificial feeding with cow milk. Family history revealed young and apparently healthy parents. with normal gestational age. Based on an ultrasound examination.A 6-month old infant. . a suspicion of polycystic kidney was established. Birth weigh 3300g. the child was hospitalized in another pediatric department for bronchopneumonia being treated with association of antibiotics.
warm extremities.6g%. Biologic tests showed: Oligo-anuria was present during the entire evolution. severe pallor. Na=146→135→119mEq/l. uric acid=9.7mmol/l. enlarged abdomen. .5mEq/l. ph=7. U/S bilateral hydroureteronephrosis. Uroculture with E. urea=178mg%. Hb=6. creatinine=1.7mg%. no appetite. liver with inferior margin 2 cm below the right rib. BE=-19. Coli>100.000/ml.4mg%. albuminura..07.Clinical examination showed an infant with 3850g. leucocytouria. K=6. fever (T=390C). bad general state.
in the absence of therapy. The delayed diagnosis was determined by multiple factors: few clinical signs at the domicile. The case represents a diagnosis error. 2. ambiguous results at ultrasound examinations.• Conclusions: 1. and the rapid evolution of pyelonephritis . to acute renal failure. 3. Voiding urogram performed in due time would have been allow a timely diagnosis and a appropriate treatment .
In order to decrease the doses of intravenous vasoactive drugs.8 g/dL.• A 20-day-old male infant with a body weight of 2. urea 75 mg/dL. prescribing a dose of digoxin of 10 mcg/kg enterally. sodium 132 mmol/L. there was marked generalized edema. • On examination.6 mmol/L and chloride 96 mmol/L.5 mcg/kg/minute) and furosemide in a continuous infusion of 0. • On admission to the pediatric intensive care unit. the infant required mechanical ventilation. transferred from the neonatal unit on the ninth day after the surgical correction of Fallot's tetralogy and pulmonary atresia. dobutamine 10 mcg/kg/minute and milrinone 0. The patient had received treatment with vancomycin and amikacin up to 2 days earlier. potassium 4.5 kg. • It was decided to administer digitalis to the patient. . albumin 2. an infusion of vasoactive drugs (dopamine 6 mcg/kg/minute.5 mg/dL. The initial blood tests revealed a creatinine level of 0.4 mg/kg/hour.
Instead of digoxin. The urinalysis was normal. • Subsequently. Intravenous sodium replacement was started according to the equation (135 . • Initially. • The medication chart was reviewed and the error was detected. which is 50 to 100 times higher than the therapeutic dose. . lactate 1.7 mg/dL and in urea to 89 mg/dL and a fall in sodium to 121 mmol/L. on persistence of the oliguria.• Four hours after the administration of the drug. to exclude hypovolemia. heart rate 140 bpm).121) × 0.4 to 1 mg/kg/hour.1 mmol/L. though no improvement in the diuresis was achieved.5 to 15 mcg/kg/minute in order to raise the mean blood pressure and improve renal perfusion. volume expansion was performed with 5% albumin (20 mL/kg). Blood tests revealed a rise in creatinine to 0.5 mL/kg/hour. the infusion of furosemide was increased from 0. indomethacin had been prescribed at a dose of 25 mg (10 mg/kg). There were no neurological clinical symptoms or alterations in the cerebral echography that suggested cerebral edema.6 × weight (kg) in 24 hours and the dose of dopamine was increased from 7. and with no change in the hemodynamic situation (blood pressure 65/40 mmHg. the child presented with progressive oliguria. with a fall in diuresis from 4 to 1.
• What are risk factors of this patient developing acute renal failure? • What are the possible preventable human errors? .
Decreased Effect Renal Blood Flow Sepsis Systemic inflammation Impaired cardiac output
Nephrotoxins Aminoglycosides Amphotericin Foscarnet Rhabdomyolysis Iodinated radiocontrast
Pre-renal Azotemia Nephrotoxic tubular injury
Ischemic tubular injury
Acute tubular necrosis
Tissue Hypoxia Inflammation
Multi Organ Failure
Resuscitation consistent with the new ACCM-PALS Guidelines resulted in 92% survival versus 62% survival among patients who did not receive resuscitation consistent with the new ACCM-PALS Guidelines. Han YY et al. Shock reversal resulted in 96% survival versus 63% survival among patients who remained in persistent shock state. Pediatrics 2003.Early reversal of pediatric-neonatal septic shock by community physicians is associated with improved outcome A. B. 112: 793-799 .
A positive cumulative fluid balance has been shown in several studies to independently predict hospital morbidity and mortality.A common adverse consequence of fluid resuscitation is ‘fluid overload’ and pulmonary oedema leading to a significant reduction in lung Organ preference function and oxygenation. Prefer the lung to the kidneys do not fill the kidneys A threshold may–exist beyond which the perceivedand flood the lungs benefit of additional fluid therapy after resuscitation may be detrimental. .
Follow-up of these patients is recommended. Sepsis increases the mortality of AKI AKI increases the mortality of sepsis More than half of children with septic AKI presents renal dysfunction at discharge and 1/3 develops abnormalities in the long term. Sepsis is a frequent cause of AKI in children. Genetic risk factors may be involved in the individual susceptibility to septic AKI .
351: 159-69 .Methods of Attenuating or Preventing Sepsis-Related Acute Renal Failure Arginine vasopressin Hydrocortisone Early directed resuscitation Maintenance of blood glucose < 145 mg/dl (8. NEJM 2004.0 mmol/l) Activated protein C Schrier RW et al.
• Early recognition and aggressive management of sepsis. • Avoid / minimize use of nephrotoxic drugs including radio contrast. • Early recognition and timely mangement of shock .• Ensure adequate renal perfusion.
• • • • Blood pressure Intravascular volume Cardiac output Other markers of perfusion .
No drug produces a single effect!!! .
0 to 2.0) 1. Journal of Pediatrics.1 to 2.Characteristic Age 0 to 3 years Male 1 to 4 additional meds 5 or more additional meds No clinic visit Odds Ratio (95 CI)* 1.0) 3.6 (1.5) 1.8 (1.7 (1.6) McPhillips et al.4 (1. 2005 .3 to 2.4) 1.4 (1.1 to 2.4 to 8.
Off-label medication use is common 3. Lack of guidelines regarding use of adult dosing regimens .1. Pediatric prescribing is complex 2. Lack of standardization of recommended doses 4.
Tacrolimus) Amphothericin B Chemotherapy .• Radiocontrast Agents • • • • • • • • Aminoglycosides Nonsteroidal Anti-Inflammatory Drugs (NAIDs) Angiotensin-Converting Enzyme Inhibitors (ACEIs) Lithium Crystal-Induced Acute Renal Failure Calcineurin inhibitors (Cyclosporine.
Proximal convoluted tubule (s1/s2 segment) Aminoglycoside Cephaloridine Cadmium Cl K dichromate Glomeruli Interferon-α Gold Penicillamine Renal vessel NSAIDs ACE Inhibitor Cyclosporin A Interstitium Cephalosporin Pappillae Phenacetin Cadmium NSAIDs .
return to baseline. • Chronic renal injury (due to medication) Chronic tubulointerstitial inflammation.• • • • • Acute renal failure Chronic renal failure Nephrotic syndrome (Acute/Chronic) Fluid and Electrolyte disturbances Acid-base disorders • Most episodes of drug-induced renal disorders are reversible discontinue drug renal fn. pallillaly necrosis or prolonged proteinuria. .
NEBCIN ®] .Amikacin Gentamicin Neomicin Netilmicin Kanamicin Streptomycin Tobramycin [AMIKIN ®] [GARAMYCIN ®] [NETROMYCIN ®] [KANTREX ®] [TOBREX.
Lysosomal overload • Inhibition of intralysosomal phospholipase activity • Intralysosomal phospholipidosis • Altered phosholipase signalling mechanisms • PROXIMAL TUBULE NECROSIS .
•Recent previous AMG therapy Related to synergistic nephrotoxicity AMG combination with •Cyclosporin •Amphotericin B •Vancomycin •Diuretics Irreversible Damage! .Related to AMG dosing •Large total cumulative dose Related to Predisposing condition in the patient •Preexisting renal insufficiency •Increased age •Poor nutrition •Shock •Gram negative bactermia •Liver disease •Hypoalbuminemis •Obstructive jaundice •K+ or Mg++ deficiency •Prolong therapy •High peak or trough conc.
concomitant therapy with other nephrotoxic drugs •Limit total dose Management •Monitor Scr. renal fn and electrolytes •Discontinue AMG if changes are seen.Prevention •Switching to alternative antibiotics •Avoid volume depletion. •Decreasing the frequency of AMG dosing to at least daily (as direct by renal clearance) . concentration.
1. Fever is a symptom not a disease .
A child can have meningitis with a low fever or a viral URTI with a high fever .1. Fever is a symptom not a disease 2.
2. Fever is a symptom not a disease A child can have meningitis with a low fever or a viral upper respiratory tract infection with a high fever 3. The difference is in how sick the child is!! .1.
2. 3. Fever is a symptom not a disease A child can have meningitis with a low fever or a viral upper respiratory tract infection with a high fever The difference is in how sick the child is!! 4. FLUIDS .1. MINIMAL CLOTHES & COOL ENVIRONMENT 5.
Hypertension .Induced ARF • Acute Interstitial Nephropathy + Proteinuria • Papillary necrosis and chronic renal failure (Analgesic nephropathy) • Salt and water retention.Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) • Hemodynamically. Hyperkalemia.
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) • Papillary necrosis .
Cirrhosis. diuretics) . Volume depletion (vomiting. diarrhea.lupus). Congestive Heart Failure. Hypercalcemia.Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) Patients at risk: Preexisting renal disease (glomerular disease nephrotic syndrome .
antimetabolite) • Sulfonamide antibiotics • Triamterene . protease inhibitor) • Methotrexate (antineoplastic agent.• Acyclovir (antiviral agent ) • Indinavir (antiretroviral agent.
Ann Intern Med 128-321 . 1998.Sulfonamide crystals Indinavir sulfate urinary crystals Gagnon et al.
. • Use the lowest dose and shortest course of therapy that is efficacious. • Consider alternative diagnostic and therapeutic approaches. • Compare the potential risks and expected benefits for each course of treatment. • Monitor therapy if toxicity is occurs. • Monitor appropriately for potential toxicity.• Know the potential nephrotoxicity of drug and therapeutic pharmacologic agents.
3. perfusion pressure and GFR . Recognise and assess the patient at risk Avoid nephrotoxic agents Maintain effective circulatory volume Recognise and treat hypoxia Early recognition of rising BUN and Cr. Treat infection. 6. 4. 7. 2. 5. avoid nosocomial infection Pharmacological manipulation to maintain RBF.1.
Timely referral to a pediatric nephrologist in cases with suspected renal disease or insult . 9.8. Spread of health education information to parents as regards what is normal and what is abnormal concerning their children's renal system. 10. Awareness of signs and symptoms of different renal diseases for early detection and timely referral.
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