Microdialysis monitoring for evaluation of the influence exerted by pneumoperitoneum on the kidney: an experimental study.

Surg Endosc

Department for Clinical Science, Intervention and Technology (CLINTEC), Division of Transplantation Surgery, Karolinska Institute, Karolinska University Hospital, Huddinge, B56 141-86, Stockholm, Sweden.

Published: April 2008

AI Article Synopsis

  • Laparoscopic donor nephrectomy is favored for living kidney donations due to its benefits over open methods, and this study examines kidney tissue metabolism during pneumoperitoneum using microdialysis.
  • Eight pigs were used in the study, where catheters were implanted in the kidney to monitor metabolic markers during a 4-hour pneumoperitoneum at a pressure of 16-18 mmHg, followed by a quick decompression.
  • Results showed no ischemia indicators (glucose, lactate, pyruvate levels) during the procedure, but glycerol levels increased significantly in the kidney’s medulla after decompression, suggesting cell injury possibly due to hyperperfusion or mechanical stress rather than lack of blood flow.

Article Abstract

Background: Laparoscopic donor nephrectomy has become the first choice for living donor kidney transplantation, offering advantages over open donor nephrectomy. This study aimed to evaluate kidney tissue metabolism during and after pneumoperitoneum using a microdialysis technique.

Methods: Eight pigs underwent laparotomy and implantation of two microdialysis catheters: one in the cortex and one in the medulla of the left kidney. After laparotomy, the abdominal wall was closed, and pneumoperitoneum was induced with a constant standard pressure of 16 to 18 mmHg for 4 h, followed by rapid desufflation. In microdialysis samples collected from intrarenal catheters, markers of ischemia (glucose, lactate, pyruvate, and lactate-pyruvate ratio) and the marker of cell membrane injury (glycerol) were monitored.

Results: There were no changes in glucose, lactate, or pyruvate level before, during, or after pneumoperitoneum, either in the cortex or in the medulla. Additionally, the calculated lactate-pyruvate ratio did not show signs of ischemia during or after pneumoperitoneum. However, with regard to the marker of cell injury, glycerol increased in the medulla after decompression from 22.57 +/- 3.76 to 35.67 +/- 5.43 mmol/l (p < 0.01). This release of glycerol in the medulla was significantly higher than in the cortex (area under the curve [AUC], 22.18 +/- 4.87 vs 34.79 +/- 7.88 mmol/l; p < 0.01).

Conclusions: The pattern of metabolic changes monitored in the kidney during and after pneumoperitoneum indicates some kind of cell injury predominant in the medulla without any signs of kidney ischemia. This nonischemic injury could be related to hyperperfusion of the kidney after decompression or injury to cells attributable to mechanical cell expansion at the point of rapid decompression.

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http://dx.doi.org/10.1007/s00464-007-9525-0DOI Listing

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