Acute Renal Failure: Pathophysiology, Prevention, and by Vittorio E. Andreucci (auth.), Vittorio E. Andreucci (eds.)

By Vittorio E. Andreucci (auth.), Vittorio E. Andreucci (eds.)

`No doubt than it good merits its position within the library of the younger and not more younger nephrologists either almost always within the medical perform or in research.'
Nephron (1986)
`The ebook is an up to date and beneficial compendium of present wisdom within the scientific administration of acute renal failure.'
Journal of the Royal Society of drugs, seventy eight (1985)

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Extra resources for Acute Renal Failure: Pathophysiology, Prevention, and Treatment

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On the other hand, not only the increased distal delivery of salt (or solutes) but also the salt depletion-that may result from the initially high urine output and salt excretion both in ischemic and nephrotoxic models of ARF, as testified by the body weight loss observed after ischemia {l23}, uranyl nitrate {22}, or HgCl 2 administration {41, 49}-may stimulate the RAS. , by the increased urinary excretion of salt in a condition of reduced intake). Thus, both renal vasoconstriction and reduction in Kf observed in ischemic and toxic models of ARF may be attributed to All and may well account for the initiation of ARF, when no morphological lesions can be detected as yet throughout the nephrons.

The increased solute excretion induced in rats by pretreatment with diuretics clearly protected the animals against HgClrinduced ARF, although no change in renal renin content had occurred [233}. Pretreatment with beta-blocking agents prevented the rise in plasma and renal cortical renin activities in HgClrinjected rats; yet ARF occurred in all animals even though in attenuated form [32}. These observations, therefore, argue against an important role of both intrarenal renin and TGF either in inducing or influencing the severity of ischemic or nephrotoxic ARF: renin suppression confers, in fact, no protection against experimental ARF [127}.

Plasma infusion, in fact, has been shown to significantly increase cardiac output and restore RBF [162}. Thus, the initiation stage of glycerol-induced ARF, which is partially reversible by ECV or plasma-volume expansion, appears as a "functional" ARF, with a marked reduction in plasma volume, {l62} and in RBF. FENa has been found, in fact, far less than 1% [166}, which is consistent with a "functional" phase of ARF (prerenal ARF). The primary role of intrarenal hemodynamic changes in the pathogenesis of glycerol-induced ARF is further supported by the observation that recent (48 hours) uninephrectomy partially protects the rats against ARF [163, 170}.

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