Mechanisms of protection in acute renal failure.
It has been generally accepted that renal ischemia, tubular obstruction, and the back-leak of glomerular filtrate are major factors involved in the pathogenesis of acute renal failure (ARF). Experimental studies have been conducted using various therapeutic measures to eliminate the adverse effects of these factors and thereby preserve renal function. These therapeutic measures include the use of pharmacologic agents such as vasodilators, diuretics, and calcium channel blockers, and saline or Ringer's volume expansion. Though experimental results appear encouraging, attempts to prevent ARF in humans have been generally unsuccessful. The administration of furosemide, however, has resulted in the conversion of oliguric ARF to nonoliguric ARF in some patients. With the development of experimental ARF models in which renal function is preserved, such as our splenectomized model, the mechanism(s) involved in the pathogenesis of ARF can be further delineated. Thus, more effective therapeutic interventions may be available for the treatment and prevention of human ARF.
D058186:Acute Kidney Injury / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D000818:Animals; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D004195:Disease Models, Animal; D004232:Diuretics / Q000627:therapeutic use; D006801:Humans; D012084:Renin-Angiotensin System; D013156:Splenectomy; D014665:Vasodilator Agents / Q000627:therapeutic use
D002121:Calcium Channel Blockers; D004232:Diuretics; D014665:Vasodilator Agents