Renal · Acute Kidney Injury
The facts most likely to be tested
Acute Tubular Necrosis is the most common cause of intrinsic acute kidney injury in hospitalized patients.
Urinalysis classically reveals muddy brown granular casts and renal tubular epithelial cells.
The fractional excretion of sodium (FeNa) is typically greater than 2% due to the inability of damaged tubules to reabsorb sodium.
Ischemic ATN is most frequently caused by prolonged hypotension or sepsis leading to hypoperfusion.
Nephrotoxic ATN is commonly associated with aminoglycosides, radiocontrast dye, or myoglobinuria from rhabdomyolysis.
The clinical course follows three distinct phases: the initiation phase, the maintenance phase (characterized by oliguria), and the recovery phase (characterized by polyuria).
Management is primarily supportive with fluid resuscitation and the avoidance of further nephrotoxic agents.
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A 68-year-old male is hospitalized for sepsis secondary to pyelonephritis and receives intravenous gentamicin. On hospital day 4, his serum creatinine rises from 0.9 mg/dL to 2.4 mg/dL. He is currently oliguric, and his urine output has decreased significantly. Urinalysis shows muddy brown granular casts and renal tubular epithelial cells. His FeNa is 3%.
What is the most likely diagnosis?
Acute Tubular Necrosis
The presence of muddy brown casts and an FeNa > 2% in the setting of nephrotoxic exposure (gentamicin) and sepsis is pathognomonic for ATN.
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Etiology / Epidemiology
Most common cause of intrinsic acute kidney injury; triggered by ischemia or nephrotoxins.
Clinical Manifestations
Sudden oliguria and rising creatinine; muddy brown casts are pathognomonic.
Diagnosis
Urinalysis showing muddy brown casts and FENa > 2%.
Treatment
Supportive care and IV fluids; avoid nephrotoxic agents.
Prognosis
Usually reversible; recovery phase marked by polyuria.
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Epidemiology & Etiology
ATN is the most frequent cause of hospital-acquired AKI. Primary etiologies include prolonged hypotension (ischemia) and exposure to aminoglycosides, radiocontrast dye, or myoglobinuria from rhabdomyolysis. It represents a direct injury to the renal tubular epithelial cells.
Pertinent Anatomy
The proximal tubule and the thick ascending limb of the loop of Henle are most susceptible to ischemic injury due to high metabolic demand. Damage here leads to loss of tubular integrity and impaired reabsorption.
Pathophysiology
Ischemia or toxins cause tubular cell necrosis and sloughing into the lumen. This creates tubular obstruction by casts, increasing intratubular pressure and decreasing glomerular filtration rate. Back-leak of filtrate through damaged epithelium further exacerbates the decline in renal function.
Clinical Manifestations
Patients present with rapid onset of azotemia and decreased urine output. The hallmark finding on microscopy is muddy brown granular casts. Hyperkalemia and metabolic acidosis are critical complications requiring immediate monitoring.
Diagnosis
The urinalysis is the diagnostic cornerstone, revealing muddy brown casts and renal tubular epithelial cells. A FENa > 2% indicates tubular damage preventing sodium reabsorption. BUN:Creatinine ratio < 15:1 helps distinguish ATN from prerenal azotemia.
Treatment
Management is primarily supportive care with careful fluid resuscitation to maintain perfusion. Discontinue all nephrotoxic medications immediately. If severe, hemodialysis is indicated for refractory hyperkalemia, volume overload, or uremic encephalopathy.
Prognosis
The recovery phase is characterized by a diuretic phase where tubular function slowly returns, often resulting in significant polyuria. Long-term prognosis is generally good, though patients remain at higher risk for future chronic kidney disease.
Differential Diagnosis
Prerenal Azotemia: FENa < 1% and BUN:Cr > 20:1
Acute Interstitial Nephritis: WBC casts and eosinophiluria
Glomerulonephritis: RBC casts and hematuria
Postrenal Obstruction: Hydronephrosis on ultrasound
Contrast Nephropathy: History of recent imaging with contrast