title: Recovery from acute renal failure predisposes hypertension and secondary renal disease in response to elevated sodium.
abstract: 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.
authors.affiliation: Dept. of Physiology, Medical College of Wisconsin, Milwaukee, USA.
authors.forename: Kimberly R
authors.initials: KR
authors.lastname: Spurgeon-Pechman
authors.forename: Deborah L
authors.initials: DL
authors.lastname: Donohoe
authors.forename: David L
authors.initials: DL
authors.lastname: Mattson
authors.forename: Hayley
authors.initials: H
authors.lastname: Lund
authors.forename: Leilani
authors.initials: L
authors.lastname: James
authors.forename: David P
authors.initials: DP
authors.lastname: Basile
mesh_terms: D058186:Acute Kidney Injury / Q000150:complications* / Q000503:physiopathology*; D000375:Aging / Q000502:physiology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002196:Capillaries / Q000502:physiology; D002395:Catecholamines / Q000494:pharmacology; D003404:Creatinine / Q000097:blood; D016572:Cyclosporine / Q000633:toxicity; D004032:Diet; D018450:Disease Progression; D006977:Hypertension, Renal / Q000209:etiology* / Q000503:physiopathology*; D007150:Immunohistochemistry; D007166:Immunosuppressive Agents / Q000633:toxicity; D007676:Kidney Failure, Chronic / Q000209:etiology / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000473:pathology; D007684:Kidney Tubules / Q000098:blood supply; D008297:Male; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D012079:Renal Circulation / Q000502:physiology; D012083:Renin / Q000097:blood; D012964:Sodium / Q000502:physiology*; D012982:Sodium, Dietary / Q000009:adverse effects
chemical_list: D002395:Catecholamines; D007166:Immunosuppressive Agents; D012982:Sodium, Dietary; D016572:Cyclosporine; D012964:Sodium; D003404:Creatinine; D012083:Renin