Aldosterone related blood volume expansion in cirrhosis before and during the early phase of ascites formation.

Bernardi, Mauro; Trevisani, Franco; Santini, Costanza; Palma, Rossana De; Gasbarrini, Giovanni

doi:10.1136/gut.24.8.761

Cited by 102 publications

(48 citation statements)

References 19 publications

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“…Aldosterone is considered an important hormone in the sodium retention of cirrhotic patients [1], In cirrhotics without fluid retention, plasma aldosterone concentra tion and urine aldosterone excretion, expressed as a function of urine sodium excretion, are reduced [2][3][4]. Moreover, only one third of the patients with ascites and without renal failure have an activated renin-angiotensin-aldosterone system [3].…”

Section: Introductionmentioning

confidence: 99%

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

Decaux¹,

Hanson²,

Cauchie³

et al. 1986

Nephron

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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.

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Section: Introductionmentioning

confidence: 99%

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

Decaux¹,

Hanson²,

Cauchie³

et al. 1986

Nephron

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“…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.…”

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confidence: 99%

Sodium retention and ascites formation in a cholestatic mice model

et al. 2007

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Renal sodium retention in experimental liver cirrhosis originates from the distal nephron sensitive to aldosterone. The aims of this study were to (1) determine the exact site of sodium retention along the aldosterone-sensitive distal nephron, and (2) to evaluate the role of aldosterone and mineralocorticoid receptor activation in this process. Liver cirrhosis was induced by bile duct ligation in either adrenalintact or corticosteroid-clamped mice. Corticosteroid-clamp was achieved through adrenalectomy and corticosteroid supplementation with aldosterone and dexamethasone via osmotic minipumps. 24-hours renal sodium balance was evaluated in metabolic cages. Activity and expression of sodiumand potassium-dependent adenosine triphosphatase were determined in microdissected segments of nephron. Within 4-5 weeks, cirrhosis induced sodium retention in adrenal-intact mice and formation of ascites in 50% of mice. At that time, sodium-and potassium-dependent adenosine triphosphatase activity increased specifically in cortical collecting ducts. Hyperaldosteronemia was indicated by increases in urinary aldosterone excretion and in sgk1 (serum-and glucocorticoid-regulated kinase 1) mRNA expression in collecting ducts. Corticosteroid-clamp prevented induction of sgk1 but not cirrhosis-induced sodium retention, formation of ascites and stimulation of sodium-and potassiumdependent adenosine triphosphatase activity and expression (mRNA and protein) in collecting duct. These findings demonstrate that sodium retention in cirrhosis is independent of hyperaldosteronemia and of the activation of mineralocorticoid receptor. Conclusion: Bile duct ligation in mice induces cirrhosis which, within 4-5 weeks, leads to the induction of sodium-and potassium-dependent adenosine triphosphatase in cortical collecting ducts, to renal sodium retention and to the formation of ascites. Sodium retention, ascites formation and induction of sodium-and potassium-dependent adenosine triphosphatase are independent of the activation of mineralocorticoid receptors by either aldosterone or glucocorticoids. (HEPATOLOGY 2007;46:173-179.) See Editorial on Page 9 P atients with liver cirrhosis and portal hypertension develop renal sodium retention which promotes formation of ascites and peripheral edema. The "underfill theory" initially attributed sodium retention to secondary hyperaldosteronism accounted for by renal hypoperfusion brought about by intraabdominal fluid sequestration. 1 However, the underfill theory cannot explain the early phase of cirrhosis as sodium retention may precedes formation of ascites. 2-7 Thus, the "overflow theory" postulated that edema and ascites formation resulted from primary renal sodium retention promoting plasma volume expansion. 8 This theory is supported by the fact that abolishing portal hypertension in cirrhotic dogs by sideto-side portocaval shunt prevented ascites formation but not sodium retention. 5,6 Later, the "revised underfill theory" proposed that peripheral arterial vasodilatation leading to decreased effec...

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“…In this con text, Bernardi et al [14] recently demonstrated that renin and plasma aldosterone were not elevated in cir rhotic patients. Studies by Sellars et al [15] showed that the renin-aldosterone system is not activated in un treated, decompensated cirrhosis with established as cites.…”

Section: Discussionmentioning

confidence: 99%

Role of Intestinal Bacteria in the Metabolism of Aldosterone in Man

et al. 1988

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Urinary aldosterone metabolites were measured before and after the administration of 1 g/day of kanamycin, a nonabsorbable antibiotic, for 7 days, in 6 normal volunteers and in 11 patients with liver cirrhosis. Urinary excretion of 21-deoxytetrahydroaldosterone (21-deoxy-THAldo) decreased by 40 and 86% from the control values in normal volunteers and in patients, respectively (p < 0.05), after kanamycin administration. Urinary excretion of 21-deoxyaldosterone (21-deoxy-Aldo) also fell by 48 and 89% in normal subjects and in patients, respectively, but the decrease was significant only in the normal subjects (p < 0.05). In normal volunteers, urinary free aldosterone and THAldo remained constant, whereas the ratio of 21-deoxy-Aldo to aldosterone and 21-deoxy-THAldo to THAldo decreased from 10.2 to 3.7 and 2.1 to 0.3, respectively (p < 0.01). These results indicate that intestinal bacteria participate in the metabolism of aldosterone during enterohepatic circulation in man.

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Aldosterone related blood volume expansion in cirrhosis before and during the early phase of ascites formation.

Cited by 102 publications

References 19 publications

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

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

Sodium retention and ascites formation in a cholestatic mice model

Role of Intestinal Bacteria in the Metabolism of Aldosterone in Man

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