Summary
Highlights
Acute renal failure is a rapid, severe decrease in kidney function, characterized by azotemia (increased nitrogenous waste in blood, measured as BUN and creatinine) and often oliguria (low urine production). The causes are classified as pre-renal, post-renal, or intra-renal.
Pre-renal azotemia is caused by decreased blood flow to the kidneys, leading to reduced GFR, azotemia, and oliguria. It's diagnosed by a BUN to creatinine ratio greater than 15, FeNa less than 1%, and urine osmolality greater than 500 mOsm/kg, reflecting intact tubular function and increased water reabsorption due to activated renin-angiotensin-aldosterone system.
Post-renal azotemia results from obstruction of the urinary tract, causing back pressure, decreased GFR, azotemia, and oliguria. Early stages show a BUN to creatinine ratio greater than 15, FeNa less than 1%, and urine osmolality greater than 500 mOsm/kg, similar to pre-renal, due to intact tubular function. Long-standing obstruction, however, damages tubules, leading to a BUN to creatinine ratio less than 15, FeNa greater than 2%, and urine osmolality less than 500 mOsm/kg.
ATN is the most common cause of acute renal failure, involving injury and necrosis of tubular epithelial cells. These necrotic cells slough off, plugging tubules, which reduces GFR. Hallmarks include dirty brown granular casts in urine, a BUN to creatinine ratio less than 15, FeNa greater than 2%, and urine osmolality less than 500 mOsm/kg, indicating dysfunctional tubules.
ATN can be ischemic or nephrotoxic. Ischemic ATN results from prolonged decreased blood supply, often following pre-renal azotemia, affecting ATP-dependent tubules. Nephrotoxic ATN is caused by toxic agents such as aminoglycosides, heavy metals, myoglobinuria (from crush injury), ethylene glycol (antifreeze), radiocontrast dye, and urate (e.g., in tumor lysis syndrome). Prophylaxis for tumor lysis syndrome includes hydration and allopurinol.
Clinically, ATN presents with oliguria, brown granular casts, rising BUN and creatinine, hyperkalemia, and a metabolic acidosis with an increased anion gap. ATN is generally reversible as tubular cells can regenerate, but it often requires supportive dialysis due to severe electrolyte imbalances. Oliguria may persist for 2-3 weeks because tubular cells are stable and take time to re-enter the cell cycle and regenerate.
AIN is a drug-induced hypersensitivity reaction of the kidney interstitium, often involving tubules. Common causes include NSAIDs, penicillin, and diuretics. Presentation includes oliguria, fever, and rash days to weeks after starting the drug, with eosinophils in the urine being a hallmark. It resolves with drug cessation but can progress to renal papillary necrosis.
Renal papillary necrosis involves necrosis of the renal papillae, presenting with gross hematuria and flank pain. Causes include chronic analgesic abuse (e.g., phenacetin, aspirin), diabetes mellitus, sickle cell disease or trait, and severe acute pyelonephritis.