Circulatory function and hepatorenal syndrome in cirrhosis (original) (raw)

A Review of Hepatorenal Syndrome

Renal dysfunctions are not uncommon occurrences in liver cirrhosis and hepatorenal syndrome (HRS) is a major one with a very high morbidity and mortality. The major pathophysiological mechanisms have been mostly unravelled, consisting of splanchnic vasodilation and renal cortical vasoconstriction. These vascular anomalies stem from endogenous release of vasodilatory biomolecules such as nitric oxide in the face of high hepatic sinusoidal pressure and portal hypertension. The vasodilatation leads to ineffective tissue perfusion and subsequently triggering the release of vasoconstrcting substances via the rennin-angiotensin-aldosterone system, thus leading to a vicious cycle. Therapeutic intervention is anchored on the reversal of the splanchnic vasodilation and renal ischaemia. Measures that have shown promise include the use of vasopressin analogues like terlipressin or ornipressin, and alpha adrenergic agonists like midodrine and norepinephrine. The use of these vasoactive substanc...

Update on peripheral arterial vasodilation, ascites and hepatorenal syndrome in cirrhosis

Canadian journal of gastroenterology = Journal canadien de gastroenterologie, 2000

In cirrhosis of the liver, according to the peripheral arterial vasodilation hypothesis, relative underfilling of the arterial tree triggers a neurohumoral response (activation of renin-angiotensin-aldosterone system, sympathetic nervous system, nonosmotic release of vasopressin) aimed at restoring circulatory integrity by promoting renal sodium and water retention. Evidence has accumulated for a major role of increased vascular production of nitric oxide as the primary cause of arterial vasodilation in cirrhosis. Ascites is a common complication in cirrhosis. Treatment of ascites consists of a low salt diet with diuretics, and paracentesis together with plasma volume expanders in diuretic-resistant patients. Progression of cirrhosis may result in hepatorenal syndrome, a state of functional renal failure that carries an ominous prognosis. Orthotopic liver transplantation has remained the only curative treatment for patients with advanced liver disease; other modalities such as trans...

Hepatorenal syndrome: pathogenesis and novel pharmacological targets

Current Opinion in Pharmacology, 2004

Hepatorenal syndrome is functional, reversible renal failure that occurs in patients with advanced liver cirrhosis or acute hepatic failure. The fundamental problem in hepatorenal syndrome is renal ischemia secondary to hypotension and profound renal cortical vasoconstriction. Sinusoidal hypertension and its associated splanchnic arterial vasodilatation initiate a cascade of events leading to activation of systemic and local vasoconstrictors and depletion of local renal vasodilators. Therapy with vasopressin V 1 receptor and a-adrenergic agonists, and plasma expanders, reverses type I and type II hepatorenal syndrome and improves survival. Large randomized, controlled, multicenter trials are needed to determine which drug is most effective, as well as the optimal dose and duration of treatment. Abbreviations AVP arginine vasopressin CI cardiac index GFR glomerular filtration rate HRS hepatorenal syndrome IHVR intrahepatic vascular resistance MAP mean arterial pressure NO nitric oxide PRA plasma renin activity RAAS renin angiotensin aldosterone system RBF renal blood flow RI resistive index RPF renal plasma flow SBP spontaneous bacterial peritonitis SNS sympathetic nervous system SVR systemic vascular resistance TNF-a tumour necrosis factor-a Pathogenesis of hepatorenal syndrome The occurrence of HRS is better predicted by the presence of circulatory dysfunction, renal function abnormalities www.sciencedirect.com

Hepatorenal Syndrome: Aetiology, Diagnosis, and Treatment

Gastroenterology Research and Practice, 2015

Acute renal impairment is common in patients with chronic liver disease, occurring in approximately 19% of hospitalised patients with cirrhosis. A variety of types of renal impairment are recognised. The most important of these is the hepatorenal syndrome, a functional renal impairment due to circulatory and neurohormonal abnormalities that underpin cirrhosis. It is one of the most severe complications of cirrhosis with survival often measured in weeks to months. A variety of treatment options exist with early diagnosis and appropriate treatment providing the best hope for cure. This paper provides a comprehensive and up-to-date review of hepatorenal syndrome and lays out the topic according to the following sections: pathophysiology, historical developments, diagnostic criteria and limitations, epidemiology, precipitating factors, predictors, clinical and laboratory findings, prognosis, treatment options, prophylaxis, and conclusion.

Pathogenesis and pathophysiology of hepatorenal syndrome - is there scope for prevention?

Alimentary Pharmacology and Therapeutics, 2004

The hepatorenal syndrome (HRS) is a functional impairment of the kidneys in chronic liver disease caused by a circulatory failure. The prognosis is poor, particularly with type 1 HRS, but also type 2, and only liver transplantation is of lasting benefit. However, recent research into the pathophysiology of ascites and HRS has stimulated new enthusiasm in their prevention and treatment. Patients with HRS have hyperdynamic circulatory dysfunction with reduced arterial blood pressure and reduced central blood volume, owing to preferential splanchnic arterial vasodilatation. Activation of potent vasoconstricting systems, including the sympathetic nervous and renin-angiotensin-aldosterone systems, counteracts the arterial vasodilatation and leads to a pronounced renal vasoconstriction with renal hypoperfusion, a reduced glomerular filtration rate, and intense sodium-water retention. Thus prevention of HRS should seek to improve liver function, limit arterial hypotension and central hypovolaemia, and reduce renal vasoconstriction and the renal and interstitial pressures. Portal pressure can be reduced with b-adrenergic blockers and transjugular intrahepatic portosystemic shunt (TIPS). Precipitating events, like infections, bleeding, and postparacentesis circulatory syndrome, should be treated to avoid further circulatory failure. Improvement in arterial blood pressure and central hypovolaemia can be achieved with vasoconstrictors, such as terlipressin (Glypressin Ò), and plasma expanders such as human albumin. In the future endothelins, adenosine antagonists, long-acting vasoconstrictors, and antileukotriene drugs may play a role in preventing and treating HRS.