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Am J Physiol Renal Physiol 293: F269-F278, 2007. First published May 16, 2007; doi:10.1152/ajprenal.00279.2006
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Recovery from acute renal failure predisposes hypertension and secondary renal disease in response to elevated sodium

Kimberly R. Spurgeon-Pechman,1 Deborah L. Donohoe,1 David L. Mattson,1 Hayley Lund,1 Leilani James,1 and David P. Basile2

1Department of Physiology, Medical College of Wisconsin, Milwaukee Wisconsin, and 2Department of Cellular and Integrative Physiology, Indiana University, Indianapolis, Indiana

Submitted 21 July 2006 ; accepted in final form 13 May 2007

Recovery of renal function is a well-characterized feature of models of acute renal failure; however, more recent studies have reported a predisposition to chronic renal disease. This study sought to determine the susceptibility to sodium-dependent hypertension following recovery from ischemic acute renal failure. Following ischemia-reperfusion (I/R) injury, rats were allowed to recover for 35 days on a 0.4% salt diet, then were switched to 4.0% salt diet for an additional 28 days. Blood pressure was significantly increased in postischemic rats switched to high-sodium diet at day 35 (19 ± 9 mmHg) compared with postischemic rats maintained on low-sodium diet. Plasma renin activity and creatinine clearance were not affected by I/R injury. The ischemic injury combined with transfer to 4.0% salt diet resulted in marked renal hypertrophy characterized by interstitial cellular deposition, tubular dilation, and enhanced rates of albumin excretion. Glomerular structure was altered in post-I/R rats switched to high-sodium diet but not in those maintained on low-sodium diets. When rats were acclimated to high-sodium diet before I/R injury, the early injury was similar to that observed in animals acclimated to low-sodium diet, and these animals progressed rapidly toward chronic kidney disease, as evidenced by advancement of albuminuria. These data suggest that the recovery from acute I/R injury is not complete, compromises Na homeostasis, and predisposes hypertension and secondary renal disease.

ischemia; blood pressure; sodium sensitivity


Address for reprint requests and other correspondence: D. P. Basile, Dept. of Cellular and Integrative Physiology, Indiana Univ. School of Medicine, 635 Barnhill Dr., MS 334, Indianapolis, IN 46202 (e-mail: dpbasile{at}iupui.edu)




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