A 65-year-old man with diabetes and hypertension undergoes elective vascular surgery. Intraoperatively, he experiences prolonged hypotension (systolic BP 70–80 mmHg for 90 minutes) despite fluid resuscitation. On postoperative day 2, his serum creatinine rises from 1.2 to 2.1 mg/dL, urine output is 250 mL in 24 hours, and urinalysis shows muddy brown granular casts. A renal ultrasound shows swollen kidneys with a pale cortex and mottled, edematous medulla as marked **A** in the diagram. Which of the following BEST describes the primary pathophysiologic mechanism underlying the kidney injury in this patient?

Explanation

## Why "Ischemic acute tubular necrosis from prolonged renal hypoperfusion affecting the proximal tubule and thick ascending limb" is right The clinical presentation—prolonged intraoperative hypotension, rapid rise in creatinine, oliguria, and muddy brown granular casts—combined with the gross pathology shown at **A** (pale cortex with mottled, edematous medulla) is pathognomonic for acute tubular necrosis (ATN). The KDIGO guideline identifies ATN as the most common cause of intrinsic AKI in hospitalized patients (45% of cases). The pale cortex reflects vasoconstriction and shut-down of glomerular filtration; the congested dark medulla reflects vascular pooling and the medulla's inherent susceptibility to ischemia due to low baseline oxygen tension. Ischemic ATN follows prolonged prerenal hypoperfusion (as in this case with intraoperative hypotension), and characteristically injures the proximal tubule (S3 segment) and thick ascending limb. The muddy brown casts are sloughed tubular epithelial cells—the hallmark of ATN. This is intrinsic AKI, not prerenal, because the damage is structural and persistent. ## Why each distractor is wrong - **Nephrotoxic acute tubular necrosis from contrast-induced osmotic injury and vasoconstriction**: While contrast-induced ATN is a real entity, there is no mention of contrast administration in this case. The injury is purely from prolonged surgical hypotension, making ischemic ATN the correct answer. - **Prerenal acute kidney injury from volume depletion with intact tubular function**: Prerenal AKI would show FENa <1%, preserved urine osmolality >500 mOsm/kg, and absence of casts. The presence of muddy brown granular casts and the structural kidney changes visible on ultrasound indicate intrinsic (tubular) injury, not prerenal azotemia. - **Acute interstitial nephritis from surgical manipulation and inflammatory cytokine release**: AIN typically presents with fever, rash, eosinophiluria, and sterile pyuria. The muddy brown casts and pale cortex with mottled medulla are not consistent with AIN; this is ATN. **High-Yield:** ATN is the most common intrinsic AKI in hospitalized patients; ischemic ATN follows prolonged hypoperfusion and preferentially damages the proximal tubule and thick ascending limb; the medulla is most vulnerable due to low baseline oxygen tension. [cite: KDIGO Clinical Practice Guideline for Acute Kidney Injury 2012]