Hepatorenal syndrome and its treatment today

The pathogenesis of ascites, a severe and the most frequent complication du ring cirrhosis, is still not completely understood, but present evidence in dicates that portal hypertension principally triggers renal sodium and wate r retention. Ascites is associated with profound disturbances of splanchnic and systemic haemodynamics, which in turn may influence renal function, Wi thin the kidney the balance between vasoconstricting and vasodilating facto rs is critical for the maintenance of renal function. As the disease progre sses, vasoconstricting factors (mainly angiotensin II, catecholamines, thro mboxane, leucotrienes and endothelins) prevail, probably due to the exhaust ion of the vasodilating renal autacoid system (mainly prostaglandins). In t his setting, vasoconstriction of the intrarenal vascular system induces mar ked and often irreversible sodium and water retention, leading to refractor y ascites, a progressive rise in plasma creatinine levels and reduction of renal clearances (hepatorenal syndrome, MRS). This persistent renal hypoxia may also favour the occurrence of tubular damage due to several causes. A careful therapeutic approach is first based on sequential diuretic treatmen t land the addition of adequate plasma expansion with human albumin for pat ients with diuretic resistant ascites), which may lead to control of ascite s for years. However, when HRS occurs, all the proposed treatments (such as paracentesis, administration of renal vasodilators, systemic vasoconstrict ors, calcium channel antagonists, TIPS, surgical portosystemic shunts) have been shown to moderately or temporarily improve renal function only, leavi ng liver transplantation as the only choice of treatment for patients, fur J Gastroenterol Hepatol 11:1061-1065 (C) 1999 Lippincott Williams & Wilkins .