OBJECTIVE: Several studies have shown activation of the renin-angiotensin-aldosterone system (RAAS) in cirrhosis. Although the activated RAAS may have several determinants, the system is often considered a surrogate marker of effective hypovolaemia. In this study we investigated the activity of the RAAS and its potential determinants with special focus on the central and arterial blood volume (CBV). MATERIAL AND METHODS: Eighty-nine patients (Child class A/B/C: 19/41/29) and 32 controls were included in the study. All were given a haemodynamic examination with measurement of determinants of the RAAS, including the CBV. Circulating plasma renin concentrations were measured using an immunoradiometric assay. RESULTS: Arterial renin concentrations were significantly higher in the patients than in the controls (p < 0.003). Plasma renin correlated significantly with several indicators of liver dysfunction and splanchnic and systemic haemodynamics (r = - 0.56-0.55), but only weakly with CBV (r = - 0.25, p < 0.02). In a multivariate regression analysis, plasma renin was determined by serum sodium, alkaline phosphatases and systolic blood pressure (p < 0.04 to p < 0.001). CONCLUSIONS: CBV correlates weakly with circulating renin, and activation of the RAAS can therefore only partly be considered as an indicator of central hypovolaemia. Mechanisms other than central hypovolaemia relating to the liver disease and portal hypertension contribute significantly to the RAAS activation.
OBJECTIVE: Several studies have shown activation of the renin-angiotensin-aldosterone system (RAAS) in cirrhosis. Although the activated RAAS may have several determinants, the system is often considered a surrogate marker of effective hypovolaemia. In this study we investigated the activity of the RAAS and its potential determinants with special focus on the central and arterial blood volume (CBV). MATERIAL AND METHODS: Eighty-nine patients (Child class A/B/C: 19/41/29) and 32 controls were included in the study. All were given a haemodynamic examination with measurement of determinants of the RAAS, including the CBV. Circulating plasma renin concentrations were measured using an immunoradiometric assay. RESULTS: Arterial renin concentrations were significantly higher in the patients than in the controls (p < 0.003). Plasma renin correlated significantly with several indicators of liver dysfunction and splanchnic and systemic haemodynamics (r = - 0.56-0.55), but only weakly with CBV (r = - 0.25, p < 0.02). In a multivariate regression analysis, plasma renin was determined by serum sodium, alkaline phosphatases and systolic blood pressure (p < 0.04 to p < 0.001). CONCLUSIONS:CBV correlates weakly with circulating renin, and activation of the RAAS can therefore only partly be considered as an indicator of central hypovolaemia. Mechanisms other than central hypovolaemia relating to the liver disease and portal hypertension contribute significantly to the RAAS activation.
Authors: Damien du Cheyron; Bruno Bouchet; Brigitte Cauquelin; Damien Guillotin; Michel Ramakers; Cédric Daubin; Jean-Jacques Ballet; Pierre Charbonneau Journal: Intensive Care Med Date: 2007-09-29 Impact factor: 17.440