PMID: 8461632Feb 1, 1993Paper

New clues to the pathophysiology of hepatorenal failure

The Clinical Investigator
F LangD Häussinger

Abstract

In patients with advanced liver disease, decreases in renal blood flow, glomerular filtration rate, and urinary output are frequently observed. The deterioration in renal function is usually not due to a unique cause but is the result of the concerted action of several mechanisms operating in parallel; decreased plasma protein formation and increased intrahepatic vascular resistance lead to sequestration of blood volume, favoring hypovolemia and reduction in cardiac output. At the same time enhanced formation of nitroxide leads to peripheral vasodilation; bacterial endotoxin escaping clearance by the diseased liver stimulates the expression of a long-acting nitroxide synthase. Furthermore, vasodilating intestinal mediators such as substance P escape inactivation by the liver. In the face of peripheral vasodilation the maintenance of blood pressure requires an increase in cardiac output, which is achieved by activation of sympathetic nervous tone, renal vasoconstriction, enhanced release of renin, angiotensin, aldosterone, and antidiuretic hormone, leading to renal retention of sodium and water. Renal vasoconstriction is opposed by vasodilatatory prostaglandins, and renal failure may be triggered by inhibition of prostaglandin f...Continue Reading

Citations

Feb 7, 2001·Gastroenterology Clinics of North America·M S Cappell, M Abdullah
Mar 12, 2003·Prostaglandins, Leukotrienes, and Essential Fatty Acids·G L Capella
Jan 13, 1998·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·M GuevaraJ Rodés
Nov 1, 1994·Prostaglandins, Leukotrienes, and Essential Fatty Acids·S PostM D Menger
Jun 11, 2002·Critical Care Clinics·Andrew E Briglia, Frank A Anania
Mar 27, 2004·Pediatrics International : Official Journal of the Japan Pediatric Society·Sema AydogduRasit Yagci
Jul 14, 2012·American Journal of Physiology. Renal Physiology·S SeidelA Paliege

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