Strategies to Extend Warm Ischemia Time During Laparoscopic Partial Nephrectomy- Part I

Author(s):
Thambi DoraiThambi Dorai1,*, Catherine MichelsCatherine Michels2, David S GoldfarbDavid S Goldfarb2, Michael GrassoMichael Grasso2
1Department of Urology, Saint Vincent Catholic Medical Centers, [email protected], USA
2Department of Urology, New York Medical College, Valhalla, USA
*Corresponding Author: Department of Urology, Saint Vincent Catholic Medical Centers, [email protected], USA. Tel: +212-604-1556. Fax: +212-604-2073. Email: [email protected]

Nephro-Urology Monthly:Vol. 1, issue 2; 79-93
Published online:Dec 31, 2009
Article type:Review Article
Received:Apr 25, 2009
Accepted:Jun 02, 2009
How to Cite:Dorai T, Michels C, Goldfarb D, Grasso M. Strategies to Extend Warm Ischemia Time During Laparoscopic Partial Nephrectomy- Part I. Nephro-Urol Mon. 2009;1(2):. doi:

Abstract

Laparoscopic partial nephrectomy (LPN) is being practiced at several noted medical institutions worldwide. But, it is yet to be accepted as the standard level of care for many renal cancer patients for whom it is indicated. Due to several technical issues that are unique to LPN, there is a tendency to prolong the warm ischemia time due to renal artery occlusion beyond 30 minutes. It has been determined by several clinicians that a warm ischemia time of more than 32 minutes severely compromises the renal function post-operatively. This is primarily due to the prolonged ischemic insult with serious consequences as a result of severe hypoxia and/or anoxia in the affected kidney. In this review, a molecular approach is taken to describe the events that occur due to severe hypoxia and anoxia and to evaluate the reversibility of the injuries that follow with particular reference to alternative modes of renal cell death. Analyses of these molecular mechanisms suggest that it is possible to "pre-condition" the kidney pre-operatively by several strategies which are nutritional, biochemical, pharmacological and environmental in nature. An attempt is made to arrive at a common denominator in all these approaches, i.e., the ischemic insult to the renal mitochondria during hypoxia and the endoplasmic reticulum stress (ER-stress) during anoxia. It is hypothesized that lending a helping hand to the ischemic mitochondria and the anoxic ER in the affected renal cells (by either hypoxic  and /or anoxic pre-conditioning) and empowering them by several ways may be the key to minimize the ischemic damage during LPN and thus may help enhance the warm ischemia time without compromising renal function.

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© 2009, Author(s). This open-access article is available under the Creative Commons Attribution 4.0 (CC BY 4.0) International License (https://creativecommons.org/licenses/by/4.0/), which allows for unrestricted use, distribution, and reproduction in any medium, provided that the original work is properly cited.

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