Pathogenesis of Renal Sodium Handling in Cirrhosis

Epstein, Murray

doi:10.1159/000166737

Cited by 33 publications

(24 citation statements)

References 49 publications

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“…1 Because glomerular filtration rate is normal or only slightly reduced, especially at an early stage of the disease, an enhanced tubular reabsorption of sodium must account for the renal sodium retention. 34,35 Traditionally, the increased distal tubular sodium retention has been attributed to an aldosterone effect. 1 Aldosterone concentrations are high in cirrhosis and their effect is successfully antagonized by aldosterone antagonists such as spironolactone in patients with cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of 11β-hydroxysteroid dehydrogenase by bile acids in rats with cirrhosis

et al. 1999

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Renal sodium retention and potassium loss occur early, in many instances in the preascitic state of cirrhosis, an observation that cannot be fully explained by increased aldosterone concentrations. We therefore hypothesize that 11␤-hydroxysteroid dehydrogenase 2 (11␤-HSD2), which protects mineralocorticoid receptors (MR) from glucocorticosteroids, is down-regulated in cirrhosis. Cirrhosis was induced by bile duct ligation in rats. The urinary ratio of (tetrahydrocorticosterone ؉ 5␣-tetrahydrocorticosterone)/ 11-dehydro-tetrahydrocorticosterone [(THB؉5␣-THB)/ THA] was measured by gas chromatography. Cortical collecting tubules (CCT) were isolated by microdissection and used for measurements of the activity of 11␤-HSD2 by assessing the conversion of corticosterone to dehydrocorticosterone. The mRNA content of 11␤-HSD2 was determined by reverse-transcription polymerase chain reaction (RT-PCR) in CCTs. The urinary ratio of (THB؉5␣-THB)/ THA increased concomitantly with the urinary excretion of bile acids following bile duct ligation. Chenodeoxycholic acid (CDCA) dose-dependently inhibited 11␤-HSD2 in CCT with a Ki of 19.9 mol/L. Four weeks after bile duct ligation, 11␤-HSD2 activity was decreased in CCT, an observation preceded by a reduced mRNA content at weeks 2 and 3. In cirrhosis, the MR-protecting effect by 11␤-HSD2 is diminished, and therefore, endogenous glucocorticoids can induce MR-mediated sodium retention and potassium loss. (HEPATOLOGY 1999;30:623-629.)Renal sodium retention and potassium loss are observed in patients suffering from cirrhosis. Traditionally, this abnormality was attributed to secondary hyperaldosteronism as a consequence of renal hypoperfusion related to intraabdominal fluid sequestration.

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Section: Discussionmentioning

confidence: 99%

Inhibition of 11β-hydroxysteroid dehydrogenase by bile acids in rats with cirrhosis

et al. 1999

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“…4). Numerous investigations had shown that water immersion can also be conveniently used in cirrhotic patients [84] to study volume regulation. ANF release after 1-h immersion has been found to be normal in cirrhotics without ascites, but reduced to about one-half in the presence of ascites [85] (Fig.…”

Section: Anf Releasementioning

confidence: 99%

Atrial natriuretic factor

1987

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“…The inability to measure and define this putative natriuretic hormone adequately, however, has impeded advances in investigating its role. 7 Recently, the atrial natriuretic factors have emerged as novel regulatory peptides with natriuretic, diuretic, and smooth-musclerelaxant properties. 8 " 11 We have demonstrated the occurrence of alpha-human atrial natriuretic factor -the authentic 28-amino acid-residue portion of the precursor hormone in human plasma 12 -and have observed elevated levels of atrial natriuretic factor in patients with hypertension 13 and patients with congestive heart failure (Arendt RM, et al: unpublished data).…”

Section: Special Articlementioning

confidence: 99%

Plasma Atrial Natriuretic Factor in Patients with Cirrhosis

1985

N Engl J Med

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Pathogenesis of Renal Sodium Handling in Cirrhosis

Cited by 33 publications

References 49 publications

Inhibition of 11β-hydroxysteroid dehydrogenase by bile acids in rats with cirrhosis

Inhibition of 11β-hydroxysteroid dehydrogenase by bile acids in rats with cirrhosis

Atrial natriuretic factor

Plasma Atrial Natriuretic Factor in Patients with Cirrhosis

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