Effects of increased renal parenchymal pressure on renal function

Objective: Acute renal failure is seen with the acute abdominal compartment syndrome (AACS). The cause of acute renal failure in AACS is thought to be multifactorial, including increased renal venous pressure, renal parenchym al pressure (RPP), and decreased cardiac output. Previous studies have esta blished the role of renal venous pressure as an important mediator of this renal derangement. In this study, me evaluate the role of renal parenchymal compression on renal function. Methods: Two groups of swine (20-26 kg) were studied after left nephrectomy and placement of a renal artery flow probe and ureteral cannula, Two hours were allowed for equilibration. and an inulin infusion was begun to calcul ate inulin clearance as a measurement of glomerular filtration. In group 1 animals (n = 6), RPP was elevated by 30 mm Hg for 2 hours with renal parenc hymal compression, RPP then returned to baseline for 1 hour, In group 2 (n = 6, the RPP was not elevated, The cardiac index, preload, and mean arteria l pressure remained stable. Blood samples for plasma renin activity and pla sma aldosterone were taken at baseline and at hourly intervals. Results: Elevation of RPP in the experimental group showed no significant d ecrease in renal blood flow index: or glomerular filtration when compared w ith control animals. There were no significant elevations of plasma aldoste rone or plasma renin activity in the experimental animals when compared wit h control. Conclusion: Elevated renal compression alone did not create the pathophysio logic derangements seen in AACS, However, prior data from this laboratory f ound that renal vein compression alone caused a decreased renal blood flow and glomerular filtration and an increased plasma renin activity, plasma al dosterone, and urinary protein leak, These changes are partially or complet ely reversed by decreasing renal venous pressure as occurs with abdominal d ecompression for AACS, These data strengthen the proposal that renal vein c ompression, and not renal parenchymal compression, is the primary mediator of the renal derangements seen in AACS.