| Autor: |
Gullo, Antonino, Lumb, Philip D., Besso, J., Pru, C., Padron, J., Plaz, J. |
| Zdroj: |
Intensive & Critical Care Medicine; 2005, p9-26, 18p |
| Abstrakt: |
Initial reports by Frerichs (1861) and Flint (1863) [1], who had noted an association between advanced liver disease with ascites and acute oliguric renal failure in the absence of significant histological changes in the kidneys, led Heyd [2], and later Helwig and Schutz [3], to introduce the concept of the hepatorenal syndrome (HRS) to explain the increased frequency of acute renal failure after biliary surgery. However, because HRS could not be reproduced in animal models, pathophysiological concepts remained speculative and its clinical entity was not generally accepted. During the 1950s, HRS was more specifically characterised as a functional renal failure in patients with advanced liver disease, electrolyte disturbances and low urinary sodium concentrations [4]. Hecker and Sherlock [5] showed its temporal reversibility by norepinephrine administration. Over the next few decades, haemodynamic and perfusion studies by Epstein and other investigators [6] identified splanchnic and systemic vasodilatation and active renal vasoconstriction as the pathophysiological hallmarks of HRS. Improved models of ascites and circulatory dysfunction contributed to therapeutic advances, including the introduction of large-volume paracentesis, vasopressin analogues, and transjugular intrahepatic stent-shunt (TIPS), which in turn have led to an improved pathophysiological understanding of HRS [7]. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Supplemental Index |
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