Resistance to Acute Renal Failure Afforded by Prior Renal Failure: Examination of the Role of Renal Renin Content

Abstract

In this study, rats recovering from glycerol-induced acute renal failure were found to be protected from mercury-induced nephropathy, and HgCl₂ poisoning protected rats from developing myohemoglobinuric renal failure. In view of the widely disparate nature of the renal failure models used, refractoriness appears to relate to an altered sensitivity of the organism itself rather than reflecting resistance to a particular nephropathic challenge. Renal renin content of the rats at the time of rechallenge was normal or high, a finding which contrasts sharply with that of chronically saline-loaded animals which also are refractory to ARF but have a maximally suppressed renal renin content. Renal renin depletion is not essential to the prevention of acute renal failure in the rat.

Chronic Kidney Disease

“…Others have found less nephrotoxicity from uranium during second exposure to the agent and in animals with a previous renal injury such as nephritis. Similar findings were observed on repeated exposure to glycerol and protection against mercuric chloride in animals with prior glycerol nephrotoxicity (48,49). This form of "preconditioning" has been observed in other organs as well, particularly in response to recurring ischemic insults (44,23).…”

Molecular mechanisms of enhanced renal cell division in protection againstS-1,2-dichlorovinyl-l-cysteine-induced acute renal failure and death

“…The possibility of protection against subsequent lethal injury by prior injury or preconditioning maneuvers has been an area of increasing interest (5,8,26,33,34,59,64). Although autoprotection has not been demonstrated in the kidney using survival as the end point until recently (64), literature suggesting the existence of such a phenomenon for renal toxicants is available (41,57). Some of the candidate mediators of preconditioning are heat shock protein molecular chaperones (9), activation of the nitric oxide synthase pathways (42), stimulation of PPAR receptors (47), induction of endoplasmic reticulum and stress proteins (24), activation of ERK 1/2 (43), and activation of a phosphatidylinosital 3-kinase Akt/PKB pathway (2).…”

Protection Against Acute Renal Failure by Prior Acute Renal Failure: Differences between Myohemoglobinuric and Ischemic Models

“…Protection against acute renal failure has been well documented with repeated exposure to the same insult [6,19] or with the sequential challenge with different insults [8,9]. Repeated injections of uranium nitrate [19], glycerol [8], gentamicin [6] or sequential ischemic insults [7] re sulted in reduced impairment of renal function when an identical insult was delivered on subsequent occasions.…”

“…In the case of acute renal failure, or acute tubular necrosis, two maneuvers have been espe cially effective in reducing the frequency and severity of the acute azotemia: the first is the protection conferred by the ingestion of sodium chloride [1][2][3][4], the second is protection conferred by prior acute renal failure [5][6][7][8][9], Recent studies indicate that the administration of sodium chloride protects against many forms of renal insult in cluding injury induced by nephrotoxins and myohemoglobinuria [10]. Cross-protection also exists between my ohemoglobinuric (induced by glycerol injection) and nephrotoxic acute renal failure, independently of which agent is administered first or second [8], Although is chemia-induced renal injury is a well-described model of acute renal failure [11,12], protection conferred by a prior, unrelated type of renal injury against a subsequent, is chemia-induced acute renal failure has not been studied. These experiments were performed to determine whether prior acute renal failure protects against ischemia-in duced injury and whether ischemia-induced acute renal failure protects against subsequent injury.…”