Acute Renal Failure (ARF) PDF

# ACUTE RENAL FAILURE (ARF) ## I. BASIC PRINCIPLES - Acute, severe decrease in renal function (develops within days) - Hallmark is azotemia (increased BUN and creatinine [Cr]), often with oliguria. ## II. PRERENAL AZOTEMIA - Due to decreased blood flow to kidneys (e.g., cardiac failure); common...

# ACUTE RENAL FAILURE (ARF) ## I. BASIC PRINCIPLES - Acute, severe decrease in renal function (develops within days) - Hallmark is azotemia (increased BUN and creatinine [Cr]), often with oliguria. ## II. PRERENAL AZOTEMIA - Due to decreased blood flow to kidneys (e.g., cardiac failure); common cause of ARF - Decreased blood flow results in ↓ GFR, azotemia, and oliguria. - Reabsorption of fluid and BUN ensues (serum BUN:Cr ratio > 15); tubular function remains intact (fractional excretion of sodium [FENa] < 1% and urine osmolality [osm] > 500 mOsm/kg). ## III. POSTRENAL AZOTEMIA - Due to obstruction of urinary tract downstream from the kidney (e.g., ureters) - Decreased outflow results in ↓ GFR, azotemia, and oliguria. - During early stage of obstruction, increased tubular pressure "forces" BUN into the blood (serum BUN:Cr ratio > 15); tubular function remains intact (FENa < 1% and urine osm > 500 mOsm/kg). - With long-standing obstruction, tubular damage ensues, resulting in decreased reabsorption of BUN (serum BUN:Cr ratio < 15), decreased reabsorption of sodium (FENa > 2%), and inability to concentrate urine (urine osm < 500 mOsm/kg). ## IV. ACUTE TUBULAR NECROSIS - Injury and necrosis of tubular epithelial cells (Fig. 12.5); most common cause of acute renal failure (intrarenal azotemia) - Necrotic cells plug tubules; obstruction decreases GFR. - Brown, granular casts are seen in the urine. - Dysfunctional tubular epithelium results in decreased reabsorption of BUN (serum BUN:Cr ratio < 15), decreased reabsorption of sodium (FENa > 2%), and inability to concentrate urine (urine osm < 500 mOsm/kg). - Etiology may be ischemic or nephrotoxic. - **Ischemia** - Decreased blood supply results in necrosis of tubules. - Often preceded by prerenal azotemia - Proximal tubule and medullary segment of the thick ascending limb are particularly susceptible to ischemic damage. - **Nephrotoxic** - Toxic agents result in necrosis of tubules. - Proximal tubule is particularly susceptible. - Causes include aminoglycosides (most common), heavy metals (e.g., lead), myoglobinuria (e.g., from crush injury to muscle), ethylene glycol (associated with oxalate crystals in urine), radiocontrast dye, and urate (e.g., tumor lysis syndrome). - Hydration and allopurinol are used prior to initiation of chemotherapy to decrease risk of urate-induced ATN. - **Clinical features** - Oliguria with brown, granular casts - Elevated BUN and creatinine - Hyperkalemia (due to decreased renal excretion) with metabolic acidosis - **Reversible, but often requires supportive dialysis since electrolyte imbalances can be fatal** - Oliguria can persist for 2-3 weeks before recovery; tubular cells (stable cells) take time to reenter the cell cycle and regenerate. ## V. ACUTE INTERSTITIAL NEPHRITIS - Drug-induced hypersensitivity involving the interstitium and tubules (Fig. 12.6); results in acute renal failure (intrarenal azotemia) - Causes include NSAIDs, penicillin, and diuretics. - Presents as oliguria, fever, and rash days to weeks after starting a drug; eosinophils may be seen in urine. - Resolves with cessation of drug - May progress to renal papillary necrosis ## VI. RENAL PAPILLARY NECROSIS - Necrosis of renal papillae - Presents with gross hematuria and flank pain - Causes include - Chronic analgesic abuse (e.g., long-term phenacetin or aspirin use) - Diabetes mellitus - Sickle cell trait or disease - Severe acute pyelonephritis