Relationship between Aldosterone and Sodium, Potassium, and Uric Acid Clearance in Cirrhosis with and without Ascites

Abstract

We have suggested that cirrhotic patients with high uric acid clearances had an increased effective vascular volume. This hypothesis was tested by studying the relationship between the excretion of uric acid, sodium, potassium, and aldosterone in cirrhosis. In 29 consecutive cirrhotic patients, of whom 17 had ascites, and in a control group, the logarithm of urinary sodium and aldosterone excretion highly correlated in control (r = – 0.79, p < 0.001) and cirrhotic patients without (r= – 0.72, p < O.Ol) and with (r= – 0.80, p < 0.001) ascites. The regression line significantly shifted to the left in the cirrhotic patients (p < 0.001). The urinary ratio K/K + Na also correlated with urinary aldosterone in controls (r= +0.66, p < 0.001) and in cirrhotic patients (r= +0.77, p < 0.001); this regression line shifted to the right in cirrhosis patients (p < 0.02). The fractional uric acid excretion significantly correlated with urinary aldosterone only in cirrhotic patients (r = – 0.76, p < 0.001). These data confirmed the existence of hypoaldosteronism in many cirrhotic patients and are consistent with tubular hypersensitivity to aldosterone and emphasize the major role of the effective vascular volume in the control of urid acid clearance in cirrhosis.

Bartter&rsquo;s Syndrome with a Salt Reabsorption Defect in the Cortical Part of Henle&rsquo;s Loop

“…Pa nel A of figure 2 shows a normal relationship between 24-hour urinary aldosterone and 24-hour natriuresis. Panel B demonstrates a correlation between urinary aldosterone excretion rate (log) and kaliuria studied by the urinary ratio U k/G k + ns comparable to that obtained formerly in our controls [24], The ANP level is in the low normal range at basal state (2.9 fmol/ml) and demon strates a slight increase during the water loading test (3.04 fmol/ml at 30 min. 3.15 at 60 min, 3.23 at 90 min.…”

“…The aldosterone secretion is, on the one hand, increased by the renin-angiotensin system, itself activated by the sodium chloride negative balance and by hypokalemia, and, on the other hand, inhibited by hypokalemia. In our patient, analysis of figure 2 panel A indicates that a nor mal relationship is maintained between urinary aldoste rone and sodium excretion [24]. Moreover, our patient, as 2 others studied in the same way [41], presents an appropriate relation between urinary aldosterone and the urinary ratio U k/U« + Na ( fig.…”

“…The glomerular filtration rate (GFR) was measured by endogenous creatinine clearance (Ccr). The study of the relationships in our patient between urinary aldosterone-18-glucuronide [22] and urinary sodium and urinary Uk/U k >Na ( fig-2) was made in comparison with the normal values of our laboratory [24]. We measured the plasma ANP (a-hANP) concentration by radioimmunoassay: the plasma was extracted on a Sep-Pak Cl 8 car tridge and eluted with methanol; the ANP standard was a-hANP (Bachem.…”

Sodium retention and ascites formation in a cholestatic mice model: Role of aldosterone and mineralocorticoid receptor?

“…23 To reconcile these findings, it has been proposed that aldosterone sensitivity was increased in cirrhosis. [24][25][26][27] This apparent high sensitivity to aldosterone might be accounted for in fact by the abnormal activation of MR by glucocorticoids. Supporting this hypothesis was the finding that 11␤ hydroxysteroid dehydrogenase type 2 (11␤ -HSD2) activity, which prevents access of glucocorticoids to MRs, 28 is decreased in cirrhosis.…”

Impaired 11β-hydroxysteroid dehydrogenase contributes to renal sodium avidity in cirrhosis: Hypothesis or fact?

“…Several independent groups of investigators demonstrated that for a given renal sodium excretion the values for aldosterone were too low in patients with cirrhosis and therefore hypothesized that these findings are explained by an increased renal tubular sensitivity to aldosterone. [10][11][12] Here, the evidence is given for another hypothetical mechanism, which might mimic the presumed increased renal tubular sensitivity to aldosterone, i.e., the presence of a MRactivating ligand other than aldosterone. This ligand is most likely cortisol.…”