A 58-year-old man with diabetes mellitus type 2 undergoes elective coronary angiography for stable angina. Six hours post-procedure, he develops oliguria (urine output 200 mL/24 h). Serum creatinine rises from 1.2 mg/dL (baseline) to 3.8 mg/dL within 48 hours. Urinalysis shows muddy brown casts and epithelial cell casts. Urine sodium is 60 mEq/L and fractional excretion of sodium (FENa) is 3.2%. Which of the following is the most likely diagnosis?
A. Acute interstitial nephritis
B. Prerenal azotemia
C. Acute tubular necrosis
D. Contrast-induced glomerulonephritis
Explanation
Clinical Presentation & Key Findings
This patient presents with acute kidney injury (AKI) in the setting of contrast exposure during coronary angiography. The clinical and laboratory features are diagnostic of acute tubular necrosis (ATN).
Diagnostic Criteria for ATN
Key Point
ATN is characterized by damage to the tubular epithelium, leading to loss of tubular integrity and function.
Table
Feature
ATN
Prerenal
AIN
CIGN
FENa
>2%
<1%
Variable
<1%
Urine casts
Muddy brown, epithelial
Hyaline
WBC, RBC
RBC, RBC casts
Urinary sodium
>40 mEq/L
<20 mEq/L
>20 mEq/L
Variable
Urine osmolality
<350 mOsm/kg
>500 mOsm/kg
>500 mOsm/kg
Variable
Mechanism
Tubular injury
Hypoperfusion
Drug/immune
Immune complex
High-YieldNEET PG
In this case:
FENa 3.2% (>2%) → intrinsic renal disease, rules out prerenal
Muddy brown casts → pathognomonic for ATN (represent sloughed tubular epithelial cells mixed with Tamm-Horsfall protein)
Epithelial cell casts → direct evidence of tubular damage
Urine sodium 60 mEq/L (>40) → confirms tubular dysfunction and inability to reabsorb sodium
Rapid rise in creatinine post-contrast → contrast-induced nephropathy causing ATN
Pathophysiology of Contrast-Induced ATN
1.
Direct tubular toxicity — contrast agent causes oxidative stress and mitochondrial dysfunction in proximal tubule cells
2.
Renal vasoconstriction — leads to hypoxic injury, particularly in the outer medulla
3.
Tubular obstruction — precipitation of contrast and cellular debris
4.
Loss of tubular integrity → leak of glomerular filtrate back into interstitium
Clinical Pearl
Muddy brown casts are virtually diagnostic of ATN; they are rarely seen in other forms of AKI and represent the hallmark histological finding of tubular epithelial necrosis.
Why This Is ATN and Not Other Causes
Not prerenal: FENa >2% excludes prerenal azotemia (which would have FENa <1%)
Not AIN: No mention of fever, rash, or eosinophiluria; muddy brown casts are not typical of AIN
Not CIGN: Glomerulonephritis would present with hematuria and RBC casts, not epithelial casts; also, contrast itself does not cause immune-mediated glomerulonephritis
Mnemonic: MUDDY BROWN = ATN
Muddy brown casts
Urinary sodium >40 mEq/L
Damaged tubular epithelium
Diabetic/elderly patients at risk
Y (why?) = Loss of tubular integrity
Blood urea rises disproportionately to creatinine
Renal failure with intrinsic disease (FENa >2%)
Oliguria common
Wide cast spectrum (epithelial, muddy brown)
Nephrotoxic insult (contrast, drugs, sepsis)
Management Principles
1.
Supportive care — fluid management, electrolyte correction, avoid further nephrotoxins
2.
Monitor urine output — oliguria vs. non-oliguric ATN (non-oliguric has better prognosis)
3.
Renal replacement therapy — if severe hyperkalemia, pulmonary edema, or uremia develops
4.
Recovery — ATN is potentially reversible; tubular epithelium regenerates over 1–3 weeks
Key Point
ATN is the most common cause of intrinsic AKI in hospitalized patients and is potentially reversible if the inciting agent is removed and supportive care is provided.
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