INTERRELATIONSHIPS BETWEEN SYSTEMIC HEMODYNAMICS, URINARY SODIUM-EXCRETION, AND RENIN-ANGIOTENSIN SYSTEM IN CIRRHOSIS

Citation
L. Aliaga et al., INTERRELATIONSHIPS BETWEEN SYSTEMIC HEMODYNAMICS, URINARY SODIUM-EXCRETION, AND RENIN-ANGIOTENSIN SYSTEM IN CIRRHOSIS, Acta Gastro-Enterologica Belgica, 58(2), 1995, pp. 213-221
Citations number
NO
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
00015644
Volume
58
Issue
2
Year of publication
1995
Pages
213 - 221
Database
ISI
SICI code
0001-5644(1995)58:2<213:IBSHUS>2.0.ZU;2-T
Abstract
We studied the interrelationships between systemic hemodynamics, sodiu m excretion and the renin-angiotensin system in 28 nonazotemic cirrhot ic patients on a sodium restricted diet. renal hemodynamics were also assessed. The patients were divided into three groups. Group A compris ed 9 patients without ascites or edema; group B comprised 8 patients w ith ascites and relatively high sodium excretion (41.9 +/- 12.9 mmol/d ay); and group C comprised 11 patients with ascites and very low sodiu m excretion (4.8 +/- 12.9 mmol/day). There were no significant differe nces in urine flow, glomerular filtration rate or effective renal plas ma flow between the three groups of patients, although renin and aldos terone levels were significantly increased in group C. Groups A and B did not differ in hemodynamic parameters and no differences were found between the three groups in heart rate or in plasma volume. Group C, however, showed significantly higher cardiac index and lower arterial pressure and systemic vascular resistance. Plasma volume was inversely related to systemic vascular resistance, and natriuresis correlated s ignificantly with both cardiac index (directly). In addition, renin an d aldosterone levels were inversely correlated with both mean arterial pressure and systemic vascular resistance. The systemic hemodynamic d isturbances in nonazotemic cirrhotics is paralleled by the impairment in sodium homeostasis, suggesting that the decrease in systemic vascul ar resistance is the primary event leading to hypotension, high cardia c output and the activation of the renin-angiotensin system in these p atients.