title: Effects of increased renal parenchymal pressure on renal function.
abstract: 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 parenchymal pressure (RPP), and decreased cardiac output. Previous studies have established the role of renal venous pressure as an important mediator of this renal derangement. In this study, we 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 calculate 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 parenchymal 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 arterial pressure remained stable. Blood samples for plasma renin activity and plasma aldosterone were taken at baseline and at hourly intervals.
  
  
  RESULTS
  Elevation of RPP in the experimental group showed no significant decrease in renal blood flow index or glomerular filtration when compared with control animals. There were no significant elevations of plasma aldosterone or plasma renin activity in the experimental animals when compared with control.
  
  
  CONCLUSIONS
  Elevated renal compression alone did not create the pathophysiologic derangements seen in AACS. However, prior data from this laboratory found that renal vein compression alone caused a decreased renal blood flow and glomerular filtration and an increased plasma renin activity, plasma aldosterone, and urinary protein leak. These changes are partially or completely reversed by decreasing renal venous pressure as occurs with abdominal decompression for AACS. These data strengthen the proposal that renal vein compression, and not renal parenchymal compression, is the primary mediator of the renal derangements seen in AACS.
authors.affiliation: Department of Surgery, Medical College of Virginia of Virginia Commonwealth University, Richmond 23298-0519, USA.
authors.forename: J M
authors.initials: JM
authors.lastname: Doty
authors.forename: B H
authors.initials: BH
authors.lastname: Saggi
authors.forename: C R
authors.initials: CR
authors.lastname: Blocher
authors.forename: I
authors.initials: I
authors.lastname: Fakhry
authors.forename: T
authors.initials: T
authors.lastname: Gehr
authors.forename: D
authors.initials: D
authors.lastname: Sica
authors.forename: H J
authors.initials: HJ
authors.lastname: Sugerman
mesh_terms: D000005:Abdomen; D058186:Acute Kidney Injury / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology*; D000450:Aldosterone / Q000097:blood; D000818:Animals; D002302:Cardiac Output; D003161:Compartment Syndromes / Q000150:complications* / Q000601:surgery; D019299:Decompression, Surgical; D004195:Disease Models, Animal; D005919:Glomerular Filtration Rate; D012079:Renal Circulation; D012083:Renin / Q000097:blood; D012307:Risk Factors; D013552:Swine; D013997:Time Factors; D014690:Venous Pressure
chemical_list: D000450:Aldosterone; D012083:Renin