Previous reports have suggested that the ischemic kidney develops a compression syndrome due to intracapsular edema and that decapsulation may improve function. This report evaluates renal function in ischemic kidneys with and without decapsulation. Thirteen dogs underwent creation of a split urinary bladder and the formation of bilateral cystocutaneous fistulas for measurement of split renal function. After systemic heparinization the suprarenal aorta was crossclamped for 1 1 2 hr. One kidney underwent removal of the anterior aspect of the capsule and the other intact kidney served as the control. The animals received 1000 ml/24 hr, 0.15 N NaCl solution IV postoperatively. Urine volume, osmolarity, creatinine, and sodium were quantitated during three consecutive 24-hr periods. Seventy-two hours following the ischemic injury, the dogs were reexplored. Renal interstitial pressures were measured and renal biopsies and an intravenous pyelogram performed prior to sacrifice. Significantly greater urine volume was produced by the decapsulated kidney (302 ± 35 ml/24 hr) than by the nondecapsulated kidney (173 ± 39 ml/24 hr). Urine sodium excretion/24 hr was consistently greater from the decapsulated kidney than from the intact kidney while urine osmolarity at 72 hr from the decapsulated kidney was 584 ± 76 and from the intact kidney was 325 ± 76 mosmole/liter (P < 0.05). Renal interstitial pressures were significantly greater in the intact kidney than in the decapsulated kidney. These data suggest that release of intercapsular compression can improve renal function in the ischemic canine kidney.
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