Pathophysiology of hepatorenal syndrome

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What is the pathophysiology of hepatorenal syndrome?

Reduction in the effective arterial blood volume :

Hemodynamic changes of significant arterial vasodilatation occur in advanced cirrhosis, which preferentially localizes in the splanchnic circulation.

The pooling of blood in the splanchnic circulation, splanchnic steal syndrome , results in insufficient blood volume in other vascular compartments, including the systemic circulation, reducing the effective arterial blood volume .

Excess renal vasoconstriction :

The reduction in effective arterial blood volume activates the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system, and stimulates the nonosmostically induced release of vasopressin.

The vasoconstrictors decrease renal blood flow and, consequently, the glomerular filtration rate (GFR).

Abnormal renal autoregulation in advanced cirrhosis :

In cirrhosis, the renal autoregulation curve, which describes the relationship of mean arterial pressure and renal blood flow, is shifted to the right.

This means that for any given arterial pressure, there is less renal blood flow than in a healthy individual. The decreased renal blood flow may be due to excess sympathetic drive seen in cirrhosis. The decreased renal blood flow makes patients with advanced cirrhosis more susceptible to AKI.

Portal hypertension :

Independent of splanchnic vasodilatation and systemic hemodynamic changes, increased portal pressure reduces renal blood flow.

This is mediated by increased sympathetic nervous activity and is called the hepatorenal reflex. Insertion of a transjugular intrahepatic portosystemic shunt (TIPS) eliminates portal hypertension and increases renal blood flow.

Abnormal cardiac function in cirrhosis :

The presence of systemic arterial vasodilatation in advanced cirrhosis leads to a hyperdynamic circulation with tachycardia, high cardiac output, and low systemic vascular resistance.

The presence of cirrhotic cardiomyopathy, consisting of myocardial thickening, diastolic dysfunction at rest, and systolic dysfunction under conditions of stress, means that the heart is unable to further increase cardiac output in periods of stress (e.g., sepsis).

This lack of a cardiac reserve predisposes to the development of HRS.

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