Hepatorenal Syndrome – causes, pathophysiology and mechanism

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“Hepatorenal syndrome is one of many potential causes of acute kidney injury in patients with acute or chronic liver disease including liver cirrhosis, severe alcoholic hepatitis and fulminant liver failure. In liver injury portal venous pressure increases resulting in portal hypertension. When this happens the portal vein tries to help by dilating the blood vessels to reduce the portal venous pressure. It does so by releasing Nitric oxide (NO) from the endothelium.

NO causes vasodilation of the arteries in the splanchnic circulation which decreases total peripheral resistance or the systemic vascular resistance. As hepatic disease becomes more severe the splanchnic arterial vasodilation and reduced systemic vascular resistance leads to reduced effective circulatory volume. Reduced effective circulatory volume means less blood is actually getting to the kidneys resulting in kidney injury and activation of the renin angiotensin aldoesterone sytem

Bacterial peritonitis or acute gastrointestinal bleeding (as a result of hepatic failure and portal hyeprtension) can trigger hepatorenal syndrome. Hepatorenal syndrome manifests as acute renal injury with reduced urine sodium in the setting a precipitating event in someone with liver failure.”

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