Pathogenetic background for treatment of ascites and hepatorenal syndrome

Abstract

Ascites and hepatorenal syndrome (HRS) are the major and challenging complications of cirrhosis and portal hypertension that significantly affect the course of the disease. Liver insufficiency, portal hypertension, arterial vasodilatation, and systemic cardiovascular dysfunction are major pathophysiological hallmarks. Modern treatment of ascites is based on this recognition and includes modest salt restriction and stepwise diuretic therapy with spironolactone and loop diuretics. Tense and refractory ascites should be treated with a large volume paracentesis, followed by volume expansion or transjugular intrahepatic portosystemic shunt. New treatment strategies include the use of vasopressin V(2)-receptor antagonists and vasoconstrictors. The HRS denotes a functional and reversible impairment of renal function in patients with severe cirrhosis with a poor prognosis. Attempts of treatment should seek to improve liver function, ameliorate arterial hypotension and central hypovolemia, and reduce renal vasoconstriction. Ample treatment of ascites and HRS is important to improve the quality of life and prevent further complications, but since treatment of fluid retention does not significantly improve survival, these patients should always be considered for liver transplantation.

Renal function and severity of bright liver. Relationship with insulin resistance, intrarenal resistive index, and glomerular filtration rate

“…Hepatorenal syndrome is the most common and more severe of different allied conditions, supervening along with acute and/or chronic liver failure [36,37]. Nonetheless, the observed close association of overweight-obesity with liver steatosis and, in different studies, with some degree of renal insufficiency, as assessed by GFR, suggests that a relationship can be present and, conceivably, some common pathophysiologic mechanism can be operating also in subjects without advanced liver and renal disease.…”

Relationship of Hepatic Functional Parameters with Changes of Functional Liver Volume Using Technetium-99m Galactosyl Serum Albumin Scintigraphy in Patients Undergoing Preoperative Portal Vein Embolization: A Follow-Up Report

“…[7,13,21,32,33] As expected, more correlated preoperative parameters could be observed in the present study: pre-PVE portal pressure, serum hyaluronic acid level, ICGR15, total bilirubin, albumin level and ALP level were correlated with decreased liver volume, and bilirubin level and platelet count were correlated with hypertrophic liver volume. Portal hypertension reflects impairment of the liver secondary to chronic hepatitis, and it increases operative risk [34,35]. In portal hypertension, there may already be impairment of the hepatocellular function or a decrease of functional liver cell mass resulting from chronic endothelial-cellular damage.…”

Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

“…However, the main features of liver decompensation in cirrhosis are ascites [85], hepatorenal syndrome [80,86] and hepatic encephalopathy [80]. Ascites and hepatorenal syndrome are the major challenging complications of cirrhosis and portal hypertension that significantly affect the course of the disease [87].…”

“…The three major factors involved in the pathogenesis of ascites are portal hypertension, arterial vasodilation and neurohormonal activation, all of them leading to sodium and water retention [87]. Arteriolar vasodilation causes underfilling of systemic arterial vascular space with a decrease in the effective arterial blood volume.…”

“…Arteriolar vasodilation causes underfilling of systemic arterial vascular space with a decrease in the effective arterial blood volume. Consequently, baroreceptor-mediated activation of reninangiotensin-aldosterone system, sympathetic and parasympathetic nervous systems and non-osmotic release of antidiuretic hormone occur to restore normal blood homeostasis [87,[89][90][91]. On the other hand, splanchnic vasodilation increases splanchnic lymph production exceeding the lymph transportation system capacity and leads to lymph leakage into the peritoneal cavity [92].…”