title: The intrinsic renal compartment syndrome: new perspectives in kidney transplantation.
abstract: OBJECTIVE
  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 Tc-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.
authors.affiliation: Department of Surgery, Experimental Medicine, University of Munich, Munich, Germany. tanja.herrler@med.uni-muenchen.de
authors.forename: Tanja
authors.initials: T
authors.lastname: Herrler
authors.forename: Anne
authors.initials: A
authors.lastname: Tischer
authors.forename: Andreas
authors.initials: A
authors.lastname: Meyer
authors.forename: Sergej
authors.initials: S
authors.lastname: Feiler
authors.forename: Markus
authors.initials: M
authors.lastname: Guba
authors.forename: Sebastian
authors.initials: S
authors.lastname: Nowak
authors.forename: Markus
authors.initials: M
authors.lastname: Rentsch
authors.forename: Peter
authors.initials: P
authors.lastname: Bartenstein
authors.forename: Marcus
authors.initials: M
authors.lastname: Hacker
authors.forename: Karl-Walter
authors.initials: KW
authors.lastname: Jauch
mesh_terms: D000818:Animals; D003161:Compartment Syndromes / Q000453:epidemiology* / Q000209:etiology; D007668:Kidney / Q000000981:diagnostic imaging; D007674:Kidney Diseases / Q000000981:diagnostic imaging / Q000473:pathology; D016030:Kidney Transplantation / Q000009:adverse effects / Q000502:physiology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D011877:Radionuclide Imaging; D015427:Reperfusion Injury / Q000000981:diagnostic imaging / Q000473:pathology; D017263:Technetium Tc 99m Mertiatide
chemical_list: D017263:Technetium Tc 99m Mertiatide