Eicosanoids and Acute Renal Failure

  • A. Schieppati
  • G. Remuzzi
Part of the Current Concepts in Critical Care book series (CRITICAL CARE)

Abstract

Many theories have been proposed over the last decades to explain the reduced glomerular filtration rate (GFR) in acute renal failure (ARF). However, the precise pathogenetic mechanisms of this syndrome are still largely undefined. Several animal models of ARF have been employed over the years and different experimental conditions in the same animal model have been studied, in the attempt to dissect the components of the pathogenetic mechanisms. Traditionally, the causes of ARF can be divided in the two broad categories of ischaemic and nephrotoxic type. Ischaemic injury to the kidney may occur in the clinical setting as a consequence of volume depletion, septic shock, cardiovascular failure, major trauma. A particular and interesting condition of postischaemic ARF is represented by cadaver renal transplantation, which occurs when the warm or the cold ischaemia are too prolonged. Experimental models of ischaemic injury are obtained by glycerol injection, intrarenal infusion of vascoconstrictor agents, such as noradrenaline, and vascular clamp of the renal arteries. Nephrotoxic ARF is today largely due to iatrogenic causes, in association with aminoglycoside antibiotics, X-ray contrast media, non-steroidal anti-inflammatory drugs, cis-platinum, and, more recently, the novel immunosuppressive agent cyclosporin A. All these agents have been used in laboratory animals to reproduce the ARF, in addition to the traditional models of nephrotoxic ARF (mercuric chloride, uranyl nitrate).

Keywords

Lipase Pancreatitis Angiotensin Noradrenaline Cyclosporin 

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© Springer-Verlag Berlin Heidelberg 1990

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  • A. Schieppati
  • G. Remuzzi

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