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1 Physiology, Medical College of Wisconsin, Miwaukee, Wisconsin, United States
2 Cellular & Integrative Physiology, Indiana University, Indianapolis, Indiana, United States
* To whom correspondence should be addressed. E-mail: dpbasile{at}iupui.edu.
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 I/R injury rats were allowed to recover for 35 days on a 0.4% sodium diet, and switched to high sodium diet, 4.0%, for an additional 28 days. Blood pressure was significantly increased in post-ischemic rats switched to high sodium diet at day 35 (19 ± 9 mmHg) compared with post-ischemic rats maintained on 0.4% sodium diet. Plasma renin activity (PRA) and creatinine clearance were not affected by I/R injury. The ischemic injury combined with transfer to 4% sodium 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 0.4%-salt diets. When rats were acclimated to 4.0% salt diet prior to I/R injury, the early injury was similar to that observed when animals acclimated to 0.4% salt 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 and alters Na homeostasis, thereby predisposing hypertension and secondary renal disease.
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