The hepatorenal syndrome is characterized by renal vasoconstriction and a reduction in renal blood flow, glomerular filtration rate, and urine output in the presence of normal renal histology. While it is important to maintain normovolemia and adequate renal perfusion pressure, since this will facilitate renal blood flow and may delay the deterioration in renal function, this may be impossible to achieve in patients with cerebral edema. In this circumstance renal protection takes secondary importance to cerebral protection. The hepatorenal syndrome may be mediated by catecholamines, endothelins, and the renin-angiotensin-aldosterone axis, and may be exacerbated by jaundice, infection, or nephrotoxic agents such as radiocontrast dyes or excessive diuretic therapy ( Lerman...efMa/ 1991). Spontaneous recovery without hepatic transplantation is rare. Acute tubular necrosis secondary to cardiovascular failure or sepsis may also contribute to, or cause, renal failure during the pretransplant phase.
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