Hepatorenal syndrome is quite common in the cirrhotic population and is found in approximately 10% of individuals admitted to the hospital with ascites.
It is characterized by azotemia, oliguria (500mL per day), low urinary sodium excretion (10mEq per liter), and increased urine-plasma osmolality ratio (U:P 1.0) in the absence of urinary sedimentation.
Histology of renal tissue from patients with hepatorenal syndrome is normal.
Hepatorenal syndrome occurs in patients with pre-existing parenchymal liver disease after a precipitating event such as surgery or a hypotensive episode (e.g., GI bleed, dialysis, sepsis).
The etiology of hepatorenal syndrome is not completely understood but appears to involve vasodilation, decreased effective arterial volume, and further reduction of glomerular filtration by the reninangiotensin- aldosterone system.
Hepatorenal syndrome progress over days to weeks after the precipitating event. While initially partly responsive to volume expansion, it is ultimately refractory to all interventions except liver transplantation.
rroyo, V, Guevara M, Gin`es P, et al. (2002) Hepatorenal syndrome in cirrhosis: pathogenesis and treatment. Gastroenterology 122 (6), 1658–76.
Mulholland MW, Lillemoe KD, Doherty G et al. (2010) Greenfield’s Surgery: Scientific Principles and Practice, Lippincott Williams & Wilkins, Philadelphia, PA.
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