Renal · Acute Tubular Necrosis
The facts most likely to be tested
Acute Tubular Necrosis (ATN) is the most common cause of intrinsic AKI and is characterized by muddy brown granular casts on urinalysis.
Fractional excretion of sodium (FeNa) greater than 2% indicates intrinsic renal damage rather than pre-renal azotemia.
Acute Interstitial Nephritis (AIN) classically presents with the triad of fever, rash, and eosinophiluria following exposure to medications like penicillins or NSAIDs.
Rhabdomyolysis causes intrinsic AKI through myoglobinuria, which manifests as a positive dipstick for blood but no red blood cells on microscopic examination.
Contrast-induced nephropathy typically presents as a transient rise in creatinine peaking within 3 to 5 days after exposure to iodinated contrast media.
Urinary osmolality in intrinsic AKI is typically isosthenuric (approximately 300 mOsm/kg) due to the kidney's inability to concentrate urine.
Proliferative glomerulonephritis presents with nephritic syndrome features, including hematuria, red blood cell casts, and hypertension.
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A 68-year-old male is hospitalized for a severe infection and receives a course of intravenous gentamicin. On day 5 of therapy, his serum creatinine rises from 0.9 mg/dL to 2.4 mg/dL. Urinalysis reveals muddy brown granular casts and a FeNa of 3%. The patient is currently oliguric and has no history of chronic kidney disease.
What is the most likely diagnosis?
Acute Tubular Necrosis (ATN)
The presence of muddy brown granular casts and a FeNa > 2% in the setting of nephrotoxic antibiotic exposure is pathognomonic for ATN, which is the most common form of intrinsic AKI.
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Etiology / Epidemiology
Most commonly caused by Acute Tubular Necrosis (ATN) from prolonged ischemia or nephrotoxins.
Clinical Manifestations
Presents with muddy brown casts and FENa > 2% indicating tubular damage.
Diagnosis
The renal biopsy is the gold standard, though clinical diagnosis often relies on FENa > 2% and BUN:Cr < 15:1.
Treatment
Management focuses on IV fluids for perfusion and avoiding nephrotoxins like NSAIDs.
Prognosis
Recovery depends on the underlying cause; oliguria lasting > 4 weeks suggests poor prognosis.
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Epidemiology & Etiology
Intrinsic AKI results from direct damage to the renal parenchyma, most frequently the tubules, interstitium, or glomeruli. Acute Tubular Necrosis (ATN) accounts for 85% of cases, often triggered by hypotension or sepsis. Other major causes include Acute Interstitial Nephritis (AIN) and Glomerulonephritis.
Pertinent Anatomy
Damage occurs within the nephron structures, specifically the proximal tubule or the interstitium. The glomerular basement membrane is the primary site of injury in nephritic syndromes. Disruption of these structures leads to the inability to concentrate urine or reabsorb electrolytes.
Pathophysiology
Ischemic or toxic injury causes tubular cell sloughing, leading to muddy brown casts that obstruct the tubular lumen. This obstruction increases intratubular pressure, decreasing the glomerular filtration rate (GFR). In AIN, a hypersensitivity reaction causes inflammatory cell infiltration of the interstitium, often triggered by medications.
Clinical Manifestations
Patients present with rapid rise in serum creatinine and azotemia. ATN is characterized by muddy brown granular casts on urinalysis. AIN may present with the classic triad of fever, rash, and arthralgias. Oliguria is a common red flag, though non-oliguric AKI occurs frequently.
Diagnosis
The renal biopsy is the definitive diagnostic test. Clinically, a FENa > 2% is the hallmark of intrinsic injury, reflecting the inability of damaged tubules to reabsorb sodium. BUN:Cr ratio < 15:1 helps distinguish intrinsic damage from prerenal azotemia.
Treatment
Discontinue all nephrotoxic agents immediately. IV isotonic saline is the first-line intervention to maintain renal perfusion. If AIN is suspected, corticosteroids may be indicated. Dialysis is reserved for refractory hyperkalemia, volume overload, or uremic encephalopathy.
Prognosis
Most patients with ATN recover within 1-3 weeks once the insult is removed. Chronic Kidney Disease (CKD) may develop if the injury is severe or prolonged. Monitor serum creatinine and potassium levels daily during the recovery phase.
Differential Diagnosis
Prerenal Azotemia: FENa < 1% and BUN:Cr > 20:1
Postrenal Obstruction: Hydronephrosis on renal ultrasound
Acute Interstitial Nephritis: Presence of eosinophiluria
Glomerulonephritis: Presence of dysmorphic RBCs and RBC casts
Contrast-induced Nephropathy: History of recent iodinated contrast exposure