Can ischemic preconditioning ameliorate renal ischemia-reperfusion injury in a single-kidney porcine model?

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Abstract

Ischemic preconditioning (IP) refers to the phenomenon of a brief ischemia-reperfusion event providing resistance to injury from subsequent ischemic periods. We sought to determine the effect of a specific preconditioning regimen on ischemia-reperfusion renal injury in a single-kidney porcine model.

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Most cited references 22

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Visualization of an Oxygen-deficient Bottom Water Circulation in Osaka Bay, Japan

Y Hosokawa, K Furukawa, H. Yoshimura … (2000)

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Reoxygenation-specific activation of the antioxidant transcription factor Nrf2 mediates cytoprotective gene expression in ischemia-reperfusion injury.

E Kieran, Katherine Howell, Saravanakumar Dhakshinamoorthy … (2006)

Tissue reoxygenation following hypoxia is associated with ischemia-reperfusion injury (IRI) and may signal the development of ischemic preconditioning, an adaptive state that is protective against subsequent IRI. Here we used microarray RNA analysis of in vivo and in vitro models of IRI to delineate the underlying molecular mechanisms. Microarray analysis of renal tissue after ischemia-reperfusion revealed a number of highly up-regulated antioxidant genes including aldehyde dehydrogenases (ALDH1A1 and ALDH1A7), glutathione S-transferases (GSTM5, GSTA2 and GSTP1), and NAD(P)H quinone oxidoreductase (NQO1). The transcription factor NF-E2-related factor-2 (Nrf2), a master regulator of this antioxidant response, is also elevated in IRI. Furthermore, microarray analysis of renal epithelial cells exposed to hypoxia/reoxygenation identified Nrf2 to be up-regulated on reoxygenation. We also reveal a reoxygenation-specific nuclear accumulation of Nrf2 protein and subsequent activation of a NQO1 promoter reporter construct. Attenuating reactive oxygen species (ROS) in reoxygenation using the antioxidant N-acetyl cysteine results in inhibition of Nrf-2 activation. mRNA levels for Nrf2-dependent genes were detected in human liver biopsy 1 h after transplantation. These results indicate that reoxygenation-dependent Nrf-2 activity facilitates ischemic preconditioning through the induction of antioxidant gene expression and that ROS may be critical in signaling this event.

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Predictors of ARF after cardiac surgical procedures.

Katherine Tuttle, Neil Worrall, Lynn R Dahlstrom … (2003)

In a pilot study, a low preoperative serum ferritin level predicted increased risk for acute renal failure (ARF) after cardiopulmonary bypass. It was hypothesized that this may reflect a decreased ability to bind free iron and defend against oxidative stress. However, the pilot study was performed in a small number of patients (n = 30) operated on by a single surgeon. The purpose of this study was to validate whether the serum ferritin level predicts ARF in a larger sample. The present study evaluated 120 patients who underwent procedures performed by eight surgeons at another tertiary referral center. Data were collected prospectively and included patient characteristics, laboratory studies, procedure types, and postoperative course. ARF was defined as a 25% or greater increase in creatinine level 48 hours after surgery. The frequency of ARF was 42%, but no patient required dialysis therapy. Preoperative serum ferritin levels did not differ in the groups with and without ARF (158 +/- 119 and 163 +/- 125 ng/mL, respectively), and rates of ARF did not differ when examined by ferritin quartiles. ARF was more frequent in those who underwent valve surgery (54% versus 35% in patients who did not undergo valve procedures; P = 0.044). The odds ratio for ARF after valve surgery was 2.58 (95% confidence interval, 1.06 to 6.29; P = 0.037), adjusted for longer times of surgery and aortic cross-clamp. Most excess ARF occurred in those who underwent aortic valve replacement (AVR; 62%; P = 0.014 versus nonvalve procedures). Low preoperative serum ferritin level was not confirmed to predict ARF after cardiac surgery. Valve procedures, particularly AVR, increased the risk for ARF. Copyright 2003 by the National Kidney Foundation, Inc.