Hepatorenal syndrome

A Gattoni, F Marotta, B Vangieri, G Pisani, F Cristiano
La Clinica Terapeutica 2004, 155 (9): 375-89

PURPOSE: Discuss exhaustively the clinical aspects of hepatorenal syndrome (HRS), laboratory data, the progress made in understanding the pathogenesis, and treatment.

DESIGN: The work is a result of the research conducted in the framework of the most important studies on HRS.

RESULTS AND CONCLUSIONS: Functional renal failure (FRF) is the most severe manifestation of hepatorenal syndrome, and becomes manifest with a decreased renal perfusion along with oliguresis, reduced excretion of sodium, high urinary osmolarity, azotemia and creatinemia. Liver transplantation restores normal renal function in patients affected by HRS; this suggests the functional origin of the disease. Portal hypertension determines systemic arterial vasodilatation (peripheral vasodilatation theory), with non absolute but effective hypovolemia in terms of its ability to release high circulating levels of vasoactive substances (PG vasodilators, endotoxins, nitric oxide, calcitonin-GPP, glucagon and PAF). Following vasodilatation, a number of systems are triggered to restore peripheral resistance, such as the renin-angiotensin-aldosterone system, the sympathetic systems and the antidiuretic hormone. In some subjects, the activation of these hormones is sufficient to restore resistance and fill the dilated vascular bed, with the subsequent inactivation of the systems themselves. Conversely, in a subgroup of cirrhosis patients with severe portal hypertension, the activation of water retention and vasoconstrictive systems is not sufficient to restore an effective volemia. These subjects present hypotension, effective hypovolemia, high renin levels, high norepinephrine levels and high antidiuretic hormone levels. These substances cause in a sequence, at the renal level, water and sodium retention, progressive vasoconstriction, reduction of plasma flow and GF, initially countered by intrarenal defense mechanisms such as PG, prostacyclins and callicreins. The FRF also sets in because the kidney, in its context, produces determinant endogenous ischemia-inducing substances like tromboxanes, endothelines and leukotrienes. Kidney transplantation is the only treatment.

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