Renal Decapsulation in the Prevention of Post-ischemic Oliguria

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Abstract
The delayed onset of anuria/oliguria in acute tubular necrosis was theorized to represent a complicating compartment syndrome, i.e., parenchymal swelling within an unyielding capsule. To test this proposition, 12 monkeys had suprarenal aortic cross-clamping, followed by unilateral renal decapsulation to create an experimental and a control kidney unit in the same animal. Histologic examination uniformly confirmed tubular necrosis at death or sacrifice. Subsequent split renal function studies (creatinine, urea and free water clearances) indicated significantly greater maintenance of renal function by the decapsulated kidney than by its paired control. Clinical evaluation in 21 hemorrhagic shock patients, with the capsule of 1 kidney stripped, revealed on follow-up that 15 developed a renal failure consistent with acute tubular necrosis. Although 3 patients with polyuric failure died before split studies could be run and 2 others were too recent for computer analysis to be completed, 9 of the remaining 10 had significantly greater renal plasma flows and significantly greater urine flows on the decapsulated side than on the control, as determined by differential renal scans. No significant difference in these same lateralized renal functions was noted in the 10th patient with renal failure and in the 6 survivors without renal failure. Renal decapsulation as prophylaxis reduced the anticipated incidence of oliguria/anuria from an expected 75% to 7% (P < .01) in these 21 shock patients. Delayed renal ischemia, possibly based on a compartment syndrome, may be the cause for a progression of acute tubular necrosis from polyuria to oliguria, then to anuria.