1. Approach to Acute Renal Failure Dr. Mercedeh Kiaii St. Pauls Hospital

2. Acute Renal Failure n Definition: Abrupt decrease in GFR sufficient to result in azotemia n Urine output can be low, normal or high –Anuric: < 100 ml/day –Oliguric: < 400 ml/day –Non-oliguric: > 400 ml/day

3. ARF: Approach n Assess severity and need for acute dialysis –Fluid overload –  k,  HC0 3 –Uremic encephalopathy –Uremic pericarditis

4. ARF: Approach n R/O chronic or acute on chronic RF –History: Fatigue, anorexia, nocturia, pruritis, restless legs –Lab: Anemia,  PO4,  Ca,  iPTH –U/S: Small (< 8 cm)  Chronic Normal ( ~9-12)  Acute or Chronic

5. ARF: Approach n Cause of ARF: –Pre-renal –Renal –Post-renal

6. Pre-renal ARF n Decrease in effective circulating volume (ECFV): –True decrease in intravascular volume Diarrhea, diuretic, hemorrhage etc –Relative decrease in volume 3rd spacing, poor cardiac output state

7. Pre-renal ARF: Approach n History n P/E n Lab: –Urine Na < 30 –FeNa < 1% (Una X Pcr) / (Pna X Ucr) –  BUN out of proportion to creat R/O other causes of increase in serum BUN

8. ARF: Post-renal n History: –Change in urine output –Pain –Phx of stones, or BPH, prostate or cervical ca n P/E: –Bladder distension –Prostate enlargement

9. ARF: Post-renal n U/S: Hydronephrosis, hydroureter unless: –Too early –Volume depletion –Retroperitoneal fibrosis n Diuresis renography or urography to rule out nonobstructive urinary tract dilatation

10. ARF: Post-renal Etiology n Intrarenal: –Stones –Papillary necrosis –Tumor, clot –Intratubular: uric acid, calcium oxalate, acyclovir, methotrexate n Extrarenal

11. ARF: Intrinsic renal n Vascular –Main renal artery and intra-renal arteries & arterioles n Glomerular n Interstitial n Tubular

12. ARF: Intrinsic Renal Vascular n Urinalysis: Bland n DDx: –Atheroembolic disease, Cholesterol emboli –TTP, PAN –Scleroderma, malignant hypertension –Drugs: Cyclosporine, tacrolimus NSAIDS Cocaine

13. ARF: Intrinsic Renal Glomerular n Nephritic  RBC +/- RBC casts, protein on urinalysis –RPGN n Nephrotic  3 g/d) n Mixed (Nephritic / Nephrotic): –MPGN

14. ARF: Glomerular Nephritic ( RPGN) RPGN Pauci-immune (IF negative) Immune complex Disease Linear Ig deposition Granular Ig deposition -Wegeners -Microscopic polyarteritis -Churgstraus -Polychondritis -SLE -PIGN -SBE -Anti-GBM -Goodpasteurs

15. ARF: Glomerular Nephrotic n Primary: –Membranous, FSGS, MCD n Secondary: –DM, MM, Amyloid n Usually superimposed acute insult in setting of nephrosis  ARF –ATN in MCD –RVT in Membranous –Papillary necrosis in DM –Intratubular obstruction in MM

16. ARF: Interstitial Nephritis n 30% have systemic manifestations n Urinalysis: WBC +/- WBC casts, eosinophils n Etiology: –Drugs: Abx: penicillins, cephalosporins, sulfonamides, and rifampin NSAIDS Diuretics (thiazides, furosemide)

17. ARF: Interstitial Nephritis n Etiology: –Infections: Pyelonephritis Systemic infection Immunologic disorders Sjogrens –Other Sarcoidosis Idiopathic

18. ARF: Acute tubular necrosis n Urinalysis: Brown granular casts +/- small amount of protein n Ischemic n Toxic: –Endogenous: Myoglobin, Hemoglobin, uric acid –Exogenous: AG, Amphotericin, contrast dye, acyclovir, indinovir

19. ARF Case presentation n 57 y/o male n Phx of CAD with CAGB, gout, borderline hypertension, gastritis n Presented to ER with hx of melena stool for 2 days n No active bleeding in ER, stable n Hgb 60, Creat 295

20. ARF Case Presentation: Approach n Severity of renal insufficiency? –Estimated CrCl: (140-57)(75 kg) / 295 X 1.2 = 25 ml/min –Determine need for hemodialysis?

21. ARF Case Presentation: Approach n Acute, chronic or acute on chronic? –Hgb not helpful, Po4 & Ca normal –U/S: Normal sized kidneys, symmetric n Etiology of ARF: –Prerenal, renal or postrenal? Intravascular volume depletion 2ndary to blood loss EF not known ( hx of cardiac disease) Recent NSAID use for gout

22. ARF Case Presentation: Approach n Investigations: –Una < 5 –U/S: no hydronephrosis –Urinalysis not available n Diagnosis: –ARF secondary to pre-renal state secondary to blood loss and NSAID use

23. ARF Case Presentation: Approach n Pt d/c’d home and adviced to increase po salt and fluid intake, and avoid NSAIDS, booked for outpt scope, and started on Iron therapy n F/U: –Hgb 68, scope shows H. pylori –Creat 255

24. ARF Case Presentation: Approach n Possible underlying chronic renal disease? –Risk factors: Hypertension Gout Renovascular disease n U/S normal size kidneys in CRF in: –DM, Amyloid, PCKD

25. ARF Case Presentation: Approach n DDx of ARF: –Vascular: ? TTP, ? PAN –Tubular: Ischemic ATN from volume depletion & hypoperfusion, and intrarenal v/c from NSAIDS Toxic ATN secondary to uric acid crystals –Interstitial nephritis secondary to NSAIDS –Glomerular

26. ARF Case Presentation: Approach n Urinalysis: –No blood, no WBC, > 5.0 g/l protein n 24 hour urine: 6 g/day protein

27. ARF Case Presentation: Approach n DDx (Nephrotic): –Minimal change disease 2 ndary to NSAIDS –Membranous 2 ndary to NSAIDS no known hx of Hep B –FSGS –Systemic causes ? Multiple myeloma, ? amyloid

28. ARF Case Presentation: Approach n UPEP: Suspicious for monoclonal protein, immunofixation pending n SPEP: Normal

29. ARF: Treatment Strategies n Treat obvious reversible factors: –Pre-renal state, obstruction –Remove possible nephrotoxins –Treat possible RPGN early n Dopamine and mannitol not effective n ANP in oliguric ATN n Urine alkalinization

30. ARF: Treatment Strategies n Avoid other nephrotoxins n Avoid ischemic episodes and volume depletion –Loss of autoregulation –Loss of tubular function

31. ARF: Treatment Strategies n Dialysis therapy: –Daily vs alternate days vs continuous –Bio-compatible dialyzer membranes