Acute Renal Failure Pre(Renal (!Blood Flow) Hyaline Casts Acute Tubular Necrosis Muddy, Granular Brown Casts Eosinophils WBC casts Glomerulonephri6s Nephri6c RBC Casts Nephro6c Fa@y Casts Post(Renal Chronic Renal Failure Waxy or Broad Casts Allergic Inters66al Nephri6s WBC Cast( Acute Pyelonephri6s Granular Cast Typical HUS Waxy ESKD Fa@y MCD RBC Cast PSGN + obstruc*on, eg: endometrial cancer, stone BUN/Cr: >40 U Na+: <20 Uosm: >500 FeNa: <1% !GFR BUN/Cr: <20 U Na+: >40 Uosm: <300 FeNa: >1% HyperK + & acidosis ("anion gap) 4Azotemia 5 SMALL KIDNEYS 5 (5) SEDIMENT 5 ISOTHENURIA 5 PROTEIN <3.5 gm Oliguria Hematuria Proteinuria Intrinsic Normal BUN = 7-18 Normal BUN:Cr = 15 BUN and Cr at filtered at the tubule. BUN is reabsorbed, but Cr is not. When RAAS is ac;vated, sodium is reabsorbed, water and BUN follows !GFR, azotemia, oliguria. Back pressure can push BUN back into the blood. Tubular funcFon remains intact early on (FeNa <1%, Osm >500. With longstanding obstrucFon, the tubule will be damaged " intrinsic failure, inability to reabsorb BUN. Ischemic ATN(!Blood supply results in necrosis of tubule; o\en preceded by re(renal azotemia. Proximal tubular and medullary segment of thick ascending limb are par6cular vulnerable. Ischemia # coagula6ve necrosis (preserved architecture]. Nephrotoxic ATN( toxic agents may result in necrosis of tubules (proximal tubule is par6cularly suscep6ble). Toxic Agents include • Aminoglycosides • Heavy metals (lead) • Myoglobinuria (crush injury) • Ethylene glycol • Contrast dye • Urate (tumor lysis syndrome) Oliguria, fever, rash days to weeks a\er star6ng drug (NSAIDs, penicillin, diure6cs). HSR of inters66um and tubules. Inflammatory infiltrate between normal tubules. May progress to renal papillary necrosis, which presents as gross hematuria and flank pain; typically caused by chronic analgesic abuse, DM, Sickle Cell, severe, acute pyelonephri6s.
