Hepatorenal Syndrome or Hepatocardiorenal Syndrome: Revisiting Basic Concepts in View of Emerging Data

Abstract

Background: Accumulating evidence on the pathophysiology of hepatorenal syndrome has challenged the conventional model of liver-kidney connection. While liver cirrhosis is traditionally considered the origin of a cascade of pathophysiologic mechanisms directly affecting other organs such as the kidney, emerging data point to the heart as the potential mediator of the untoward renal effects. Summary: Herein, we briefly review the often-overlooked contribution of the heart to circulatory dysfunction in hepatorenal syndrome and put forward evidence arguing for the involvement of systemic inflammation and endothelial dysfunction in this setting. The temporality of cardiorenal interactions in hepatorenal syndrome and the observed beneficial effects of portosystemic shunting on these pathways lend further support to the notion that cardiac involvement plays a key role in the development of renal dysfunction in severe cirrhosis. Key Messages: The disturbances traditionally bundled within hepatorenal syndrome could represent a hepatic form of cardiorenal syndrome whereby the liver affects the kidney in part through cardiorenal pathways. This new model has practical implications and calls for a shift in the focus of diagnostic and therapeutic approaches to renal dysfunction in advanced cirrhosis.

Acute kidney injury spectrum in patients with chronic liver disease: Where do we stand?

“…Decreased cardiac output and increased right atrial pressure cause renal tissue hypoxia and venous congestion, respectively, leading to kidney injury and lower glomerular filtration rate[37]. Accordingly, cardiac dysfunction in advanced chronic liver disease deteriorates renal function in HRS through a liver–heart–kidney connection, which is possibly related to a new model of therapeutic approaches to HRS[38].…”

Prevalence and short-term outcome of hepatorenal syndrome: A 9-year experience in a high-complexity hospital in Colombia

“…It is part of the complications of cirrhosis and advanced liver failure [1]. This syndrome is characterized by a severe renal failure in cirrhotic patients caused by splanchnic vasodilatation, decreasing the effective circulating volume; this produces renal vasoconstriction, reducing glomerular filtration [2]. Its reported prevalence is variable, (7-45%) [3][4][5].…”

Transition to decompensation and acute-on-chronic liver failure: Role of predisposing factors and precipitating events

“…62 Thirdly, as portal hypertension progresses, impaired cardiac function (socalled cirrhotic cardiomyopathy) and hyperdynamic or hypodynamic circulation increasingly take effect, which not only compromises basal effective circulating volume but also predisposes to an incompetent cardio-haemodynamic compensatory system in response to potential additional deleterious precipitants, expediting end-organ dysfunction. 63,64 Fourthly, clinical manifestations of portal hypertension are aggravated by its progression and, therefore, impact on end-organ function (e.g. the brain in cases of hepatic encephalopathy, the kidney in cases of refractory ascites)…”