The Intrinsic Renal Compartment Syndrome: New Perspectives in Kidney Transplantation


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Abstract

Purpose.Inflammatory edema after ischemia-reperfusion may impair renal allograft function after kidney transplantation. This study examines the effect of edema-related pressure elevation on renal function and describes a simple method to relieve pressure within the renal compartment.Methods.Subcapsular pressure at 6, 12, 24, 48 hr, and 18 days after a 45 min warm ischemia was determined in a murine model of renal ischemia-reperfusion injury. Renal function was measured by 99mTc-MAG3 scintigraphy and laser Doppler perfusion. Structural damage was assessed by histologic analysis. As a therapeutic approach, parenchymal pressure was relieved by a standardized circular 0.3 mm incision at the lower pole of the kidney capsule.Results.Compared with baseline (0.9±0.3 mm Hg), prolonged ischemia was associated with a sevenfold increase in subcapsular pressure 6 hr after ischemia (7.0±1.0 mm Hg; P<0.001). Pressure levels remained significantly elevated for 24 hr. Without therapy, a significant decrease in functional parameters was found with considerably reduced tubular excretion rate (33±3.5%, P<0.001) and renal perfusion (64.5±6.8%, P<0.005). Histologically, severe tissue damage was found. Surgical pressure relief was able to significantly prevent loss of tubular excretion rate (62.5±6.8%, P<0.05) and renal blood flow (96.2±4.8%; P<0.05) and preserved the integrity of renal structures.Conclusions.Our data support the hypothesis of the existence of a renal compartment syndrome as a consequence of ischemia-reperfusion injury. Surgical pressure relief effectively prevented functional and structural renal impairment, and we speculate that this approach might be of value for improving graft function after renal transplantation.

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