A 54-year-old man hospitalized with an acute myocardial infarction goes into cardiac arrest. The patient is resuscitated successfully and transferred to the cardiac intensive care unit where he remains hemodynamically stable. However, on the second day of hospitalization, his urine flow diminishes to 400 mL/day. Blood pressure is 115/68 mm Hg and pulse is 78/min. Laboratory results are as follows:
| Day 1 | Day 2 | |
| Sodium | 134 mEq/L | 133 mEq/L |
| Potassium | 4.2 mEq/L | 4.0 mEq/L |
| Chloride | 96 mEq/L | 94 mEq/L |
| Bicarbonate | 26 mEq/L | 22 mEq/L |
| Blood urea nitrogen | 16 mg/dL | 26 mg/dL |
| Creatinine | 1.1 mg/dL | 2.4 mg/dL |
Urine sediment microscopy reveals muddy brown casts. Which of the following renal structures are most likely to demonstrate signs of ischemic injury?
This patient most likely has acute tubular necrosis (ATN) due to decreased renal perfusion during cardiac arrest (cardiogenic shock). Ischemic kidney injury predominantly affects the renal medulla, which has low blood supply even under normal conditions. The most metabolically active segments of the nephron are particularly vulnerable, including the proximal tubule and thick ascending limb of the loop of Henle.
ATN is characterized histologically by flattening of the tubular epithelial cells with loss of the brush border and subsequent cell necrosis and denudation of the tubular basement membrane. Muddy brown casts consisting of sloughed and degenerated tubule cells are pathognomonic for ATN. Patients frequently have increased serum creatinine, a blood urea nitrogen/serum creatinine ratio <20 (indicating intrinsic renal pathology), and oliguria.
(Choices A and B) The distal tubules are located in the renal cortex, and the collecting ducts are in the cortex and medulla. They are less likely to show signs of ischemic injury because they are less metabolically active than the proximal tubules or the thick ascending limb of the loop of Henle.
(Choice C) The increased distal sodium delivery caused by tubular dysfunction in ATN leads to afferent arteriolar constriction via the tubuloglomerular feedback mechanism. This can further reduce medullary blood flow and worsen tubular ischemic damage. However, the glomeruli themselves are less susceptible to ischemic injury because of their low metabolic activity.
(Choice E) Renal papillary blood supply may be interrupted by urinary tract obstruction/infection, interstitial nephritis due to analgesic ingestion, or microvascular disease (eg, diabetes mellitus, sickle cell disease). However, renal papillary necrosis typically presents with gross hematuria and flank pain.
Educational objective:
Acute tubular necrosis can be caused by renal ischemia and is characterized by oliguria, increased serum creatinine, and muddy brown casts. Ischemic injury predominantly affects the renal medulla, which has a relatively low blood supply. The proximal tubules and the thick ascending limb of the loop of Henle are the most commonly involved portions of the nephron.