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Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,6
Online ISSN 1827-1898
Pasqualetti P., Casale R.*
From the Department of Internal Medicine and Public Health Faculty of Medicine and Surgery, University of L’Aquila and the Division of 1st Internal Medicine, “S. Salvatore” General Hospital of Coppito, ASL 04, L’Aquila, Italy
Background. The etiology of hepatorenal syndrome is still incompletely understood, but the non-osmotic release of arginine vasopressin (AVP) seems to have an important role in its pathogenesis. The aim of the study was to investigate the circulating plasma concentrations of AVP in patients with hepa-torenal syndrome, compared with healthy controls, in relation with plasma osmolality.
Methods. Venous blood samples were drawn in 20 healthy subjects and in 20 patients with HRS for the determination of the plasma levels of AVP by radio-immunoassay and of plasma osmolality. The comparison between the two groups was carried out by the Student “t”-test for unpaired data; the plasma AVP levels were correlated with the values of plasma osmolality by linear regression analysis.
Results. The patients presented significantly (p<0.001) higher plasma AVP levels in respect to controls; on the contrary, plasma osmolality was significantly lower in patients than in controls (p<0.005). Whereas a significant (r=0.83; p<0.001) relationship was demonstrated between plasma AVP and osmolality in controls, no significant (r=0.23; p>0.05) correlation was found in patients.
Conclusions. These results confirm the existence of an activation in the release of AVP in hepatorenal syndrome, due to the activation of the sympathetic adrenal system and to hyponatriemia. The contraction of diuresis in hepatorenal syndrome, on the other hand, is not due to a deficiency in plasma AVP. AVP release occurs despite low plasma osmolality, which normally inhibits its secretion. This great upset in functional organization, together with that of the atriopeptin-renin-angiotensin-aldosterone system, could play an important role in promoting and/or in the maintenance of the hydro-electrolyte imbalance that characterizes the syndrome.