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  1. ACUTE RENAL FAILURE Academic Half Day February 9, 2012

  2. Objectives To review: • the etiologies of acute kidney injury (AKI) in the pediatric population • the work-up/diagnosis of AKI • the management of AKI • What is AKIs? “abrupt reduction in kidney function as measured by a rapid decline in GFR” • Previously known as Acute Renal Failure • Now failure represents one end of the spectrum • Etiology is variable • Definitions/classifications have varied in the literature…

  3. Classification - pRIFLE U/O <0.5cc/kg/h x 8h Risk Injury Failure Loss End-stage eCCl dec 25% eCCl dec 50% U/O <0.5cc/kg/h x 16h eCCl dec 75%/ < 35ml/min/1.73m2 <0.3cc/kg/h x 24h/ Anuric x 12h Persistent failure >4wks Failure > 3 months

  4. Leads to: • Impaired excretion of nitrogenous waste • Impaired water and electrolyte balancing • Impaired acid/base regulation • Impaired vascular tone regulation

  5. Burden of disease Incidence (US): 0.8/100 000; ~1/10 in ICU • Increasing Independent risk factor for ICU mortality Increases length of hospital stay May lead to chronic renal failure (40-50% ICU)

  6. Etiologies: a general approach Though likely multifactorial, can be divided into: Pre-renal Renal Post-renal

  7. Volume deplete: GI Vomiting Diarrhea Bleeding Trauma Surgery Diuresis Diabetes - DM, DI Drugs Kidney sees less volume: Sepsis CHF Cirrhosis Vascular - also consider in renal RAS Thrombus Takayasu, PAN, KD Drugs NSAIDs ACEi ARBs Pre-renal causes:Any cause which results from kidney seeing to little blood flow

  8. Renal causes Vascular: Microvasculature: • Sickle cell disease • HUS • Tumour lysis • rhabdomyolysis ?Syndromes • Hepatorenal • Cardiorenal • Pulmonary-renal • Glomerular: • Glomerulonephritis: • Post-infectious • membranoproliferative • SLE • HSP Tubulo/Interstitial:Acute tubular necrosis -secondary to nephrotoxic insults or poor perfusion Acute interstitial nephritis -drugs -infxn Cortical dysplasia -hypoxia/ischemia->infarct -toxins/severe HUS ?Sepsis inflamm, not all volume related

  9. Hemolytic UremicSyndrome History of Ecoli, Shigella, shiga-toxin… Atypical (non-diarrhea, non-shiga-toxin) Hemolytic anemia with fragmented RBCs Thrombocytopenia Renal injury CNS, liver, pancreas can also be affected

  10. Post-infectious glomerulonephritis Occurs in ages 5-12, post-GAS. Presentation can be asymptomatic to nephritis complete with gross hematuria, proteinuria, HTN, edema Labs: abnormal urinalysis, low complement Rx: supportive. Prognosis: most make complete recovery.

  11. HSP -Causes renal issues d/t IgA deposition. -A/W palpable purpura, arthritis, abdo pain. -Renal more likely to be an issue in older kids -Rx: if crescenteric, GN - steroids. -prognosis: often relapses. Can have late deterioration even if full recovery. 10-30% adults go on to have end-stage disease.

  12. Acute TubularNecrosis Describes an end effect of tubular damage… • Secondary to perfusion insults • Secondary to toxins Change in blood flow, obstruction and passive filtrate backflow into tubular cells can cause a cycle leading to further death…

  13. AIN Drugs (71%) - 1/3 antibiotics • Penicillins, cephalosporins, NSAIDs, sulfonamides, cipro, rifampin, PPIs, allopurinol… and more Infection (15%) • Strep, Legionella, leptospirosis, CMV, EBV… many Tubulointersitial nephritis and uveitis (5%) Autoimmune: SLE, Sjogren’s Sarcoidosis Idiopathic (8%)

  14. Nephrotoxins Vascular effect • ACEi, cyclosporine, tacrolimus Tubular effect • Proximal: aminoglycosides, amphotericin B, cisplatin, immunoglobulins, contrast • Distal: NSAIDs, ACEi, lithium, cyclophosphamide • Obstruction: sulfa, acylovir, methotrexate AIN

  15. Post-renal causes Two kidneys - distal or bilateral proximal obstruction Single kidney - obstruction anywhere • Posterior urethral valves • Ureteropelvic junction obstruction • Ureterovesicular junction obstruction • Ureterocele • Stones • Tumour • Hemorrhagic cystitis • Neurogenic bladder

  16. On history… ? pre-renal: • Vomiting, diarrhea, bleeding, sepsis, dec PO • Drug use - inc NSAIDs ? renal: • Bloody diarrhea? (HUS) Recent illness? (PSGN) Crush injury? • Drug use: aminoglycosides, antifungals, chemo • Associated lung/heart/liver symptoms? (dual organ) ? post-renal:

  17. On physical… Pre-renal: • Dehydration • Signs of heart failure/cirrhosis/sepsis Renal: • Edema (nephrotic syndrome) • Purpura (HSP Post-renal: palpable bladder?

  18. What to order? BUN, Cr, lytes, fractional excretion of sodium Urinalysis

  19. NORMAL: -pre-renal (may be concentrated) -post-renal -ATN ABNORMAL: -brown granular/epithelial casts = ATN -red cell casts = glomerulonephritis -proteinuria = glomerular -pyuria, white cell casts = UTI or glomerulonephritis (post- infxn) -hematuria = AIN, vasculitis, infarction, obstruction On labs… Everyone gets a urinalysis…

  20. And even more information from urine… Urine osmolality: • Typically low in ATN (<350 mosmol/kg) • Typically high in pre-renal disease (>500) Urine volume: Often low, especially given criteria for AKI. However, some ATN is non-oliguric Urine eosinophils Urine sodium…

  21. Sodium excretion Why? Helps distinguish pre-renal vs ATN… • >30-40 mEq/L = ATN • <10 mEq/L = effective volume depletion(20-30 in infants) • BUT what if there is a large urine output?

  22. Fractional Excretion of Sodium FENa compensates for the urine output… UNa x PCr PNa x UCr …can also be thought of as UNa/PNa UCr/PCr <1% --> pre-renal disease 1-2% --> ?? >2% --> ATN

  23. Bloodwork… CBC: look for MAHA, thrombocytopenia Extended lytes. Renal injury can result in: • Hyperkalemia • Hyperphosphatemia • Hypocalcemia • Metabolic acidosis Other options, depending on history: ANCA, ANA, ASOT, complement, drug levels…

  24. And of course, creatinine Creatinine is usually elevated • Normal Cr varies by age • Note Cr can NOT be used to estimate GFR in acute kidney injury… • This is why the search is on for a “troponin of the kidneys”

  25. Troponin of the kidneys? Unfortunately, not yet… Some ideas: • Urinary neutrophil gelatinase-associated lipocalin (NGAL) • Increased 50-fold, and 24h before serum Cr • Has been shown to predict AKI severity in SLE, HUS, renal transplant patients • Kidney injury molecule - 1 (KIM-1) • IL-18

  26. Imaging Ultrasound - in all children if etiology unclear • # of kidneys • Size of kidneys • Obvious parenchymal damage • Obstruction • Thrombus/vessel occlusion

  27. Renal biopsy Only when diagnosis remains unknown, or there is a failure to respond to treatment

  28. Approach summary:

  29. Treatment Principles: • FEN • Avoid complications • Treat underlying cause Generally pediatric nephrology will be involved.

  30. Child can be hypo-, eu- or hypervolemic. FEN - fluids HTN can occur and is usually secondary to volume overload. Treatment based on diuretic response, severity.

  31. FEN - electrolytes Hyperkalemia - if severe (>7) - C BIG K Die… • Don’t give K (IVs, low K diet) • stabilize the cardiac membrane - IV calcium gluconate • Move K ECF -> ICF by: • Insulin (with glucose) • Sodium bicarb • Beta agonists • Remove K from the body - kayexalate • Can try diuretics - unlikely to do enough • RRT if the above doesn’t work

  32. FEN - electrolytes Acidosis • Respiratory compensation can be enough • Sodium bicarb ONLY if life-threatening and/or contributing to hyperkalemia • Def not if pH >7.2 or bicarb >14mEq/L • Can decrease Ca further -> seizures • Can increase intravascular volume • If refractory volume overload, hypernatremia -> RRT

  33. FEN - electrolytes Hyperphosphatemia: • Low phosphate diet • Binders Hypocalcemia: • Calcium gluconate • Can pre-empt if sodium bicarb being given

  34. FEN - Nutrition AKI is a catabolic state Ensure adequate calories - 120kcal/kg/d in infants - usual maintenance for children PO -> enteral -> TPN If fluid balance off with adequate nutrition: RRT

  35. Avoid complications Including making things worse…so no: Aminoglycosides NSAIDs Antifungals Immunosuppressive drugs Contrast media

  36. Renal Replacement Therapy (RRT) Indications: • Uremia s/s - pericarditis, neuropathy, decline • Azotemia - BUN >36 • Refractory fluid overload - HTN, pulm edema, CHF • Refractory hyperK, hypo/hyperNa, acidosis • Nutritional support with fluid balance issues

  37. RRT Options: Continuous renal replacement therapy Peritoneal dialysis Hemodialysis

  38. Prognosis Mortality: 60% (critically ill) 20-25% go on to have some degree of chronic renal issues

  39. Take home points Etiology: Best divided into pre-, renal and post-renal Work-up: Urinalysis, ultrasound, bloodwork… Treatment: Fluids - close balance Electrolytes - esp K, PO4, Ca Acidosis Nutrition Dialysis - talk later today

  40. References Akcan-Arikan A, Zappitelli M, Loftis L, Washburn K, Jerrerson L, and Goldstein S. Modified RIFLE criteria in critically ill children with acute kidney injury. Kidney International; 2007: 71: 1028-35. Basu R, Devarajan P, Wong H, and Wheeler S. An update and review of acute kidney injury in pediatrics. Pediatric Critical Care Medicine; 2011: 12(3): 339-47. Imam A. Clinical presentation, evaluation, and diagnosis of acute kidney injury (acute renal failure) in children. Uptodate. Accessed Feb 8, 2012 at Imam A. Prevention and management of acute kidney injury (acute renal failure) in children. Uptodate. Accessed Feb 8, 2012 at Kliegman R, Stanton B, Geme J, Schor N, and Behrman R. Nelson Textbook of Pediatrics 19th e. Elsevier; 2011: 1814-22.