Characterization of the renin-aldosterone system in decompensated cirrhosis.

Epstein, Murray; Levinson, R. Saul; Sancho, José; Haber, Edgar; Ré, Richard N.

doi:10.1161/01.res.41.6.818

Cited by 161 publications

(54 citation statements)

References 24 publications

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“…Although normal values for PRA and plasma renin concentration have been reported in some patients with ascites, 14 -" the abnormally low values, as found in our patients without ascites (Group A) and in some of those accumulating ascites (Group B), have not been reported. Hepatic synthesis of renin substrate is often presumed to be reduced in cirrhosis and might low values for the latter were found in only five.…”

Section: Discussioncontrasting

confidence: 67%

Changes in plasma renin activity in cirrhosis: a reappraisal based on studies in 67 patients and "low-renin" cirrhosis.

Wilkinson¹,

Smith²,

Williams³

1979

Hypertension

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Section: Discussioncontrasting

confidence: 67%

Changes in plasma renin activity in cirrhosis: a reappraisal based on studies in 67 patients and "low-renin" cirrhosis.

Wilkinson¹,

Smith²,

Williams³

1979

Hypertension

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“…We therefore speculated that altered protein abundance and/or apical membrane targeting of ENaC subunits (␣, ␤, and ␥) may account for the increased sodium reabsorption in the collecting duct and sodium retention in liver cirrhosis. However, other investigators have demonstrated that plasma aldosterone levels were normal in patients who had cirrhosis and presented ascites and that sodium retention persisted despite the maintenance of plasma aldosterone levels within normal limits (9,15). Thus, it would also be possible that the increased sodium reabsorption in the distal nephron and collecting duct could be mediated by other regulatory mechanisms.…”

mentioning

confidence: 99%

Increased Apical Targeting of Renal Epithelial Sodium Channel Subunits and Decreased Expression of Type 2 11β-Hydroxysteroid Dehydrogenase in Rats with CCl4-Induced Decompensated Liver Cirrhosis

Kim¹,

Schou²,

Peters³

et al. 2005

Journal of the American Society of Nephrology

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It was hypothesized that dysregulation of renal epithelial sodium channel (ENaC) subunits and/or 11␤-hydroxysteroid dehydrogenase (11␤HSD2) may play a role in the increased sodium retention in liver cirrhosis (LC). Experimental LC was induced in rats by CCl 4 (1 ml/kg, intraperitoneally, twice a week) for 12 wk (protocol 1) or for 11 wk (protocol 2). In both protocols, one group of rats with cirrhosis showed significantly decreased urinary sodium excretion and urinary Na/K ratio (group A), whereas a second group exhibited normal urinary sodium excretion (group B) compared with controls, even though extensive ascites was seen in both groups of rats with cirrhosis. In group A, protein abundance of ␣-ENaC was unchanged, whereas ␤-ENaC abundance was decreased in the cortex/outer stripe of outer medulla compared with controls. The ␥-ENaC underwent a complex change associated with increased abundance of the 70-kD band with a concomitant decrease in the main 85-kD band, corresponding to an aldosterone effect. In contrast, no changes in the abundance of ENaC subunit were observed in group B. Immunoperoxidase microscopy revealed an increased apical targeting of ␣-, ␤-, and ␥-ENaC subunits in distal convoluted tubule (DCT2), connecting tubule (CNT), and cortical and medullary collecting duct segments in group A but not in group B. Immunolabeling intensity of 11␤HSD2 in the DCT2, CNT, and cortical collecting duct was significantly reduced in group A but not in group B, and this was confirmed by immunoblotting. In conclusion, increased apical targeting of ENaC subunits combined with diminished abundance of 11␤HSD2 in the DCT2, CNT, and cortical collecting duct is likely to play a role in the sodium retaining stage of liver cirrhosis.

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“…9 Epstein and associates observed that head-out water immersion suppressed aldosterone levels in all patients, but that some of these patients failed to have a natriuresis. 19 These authors concluded that aldosterone was not important in renal sodium retention in these patients. However, it must be remembered that the effect of changes in aldosterone concentration on tubular sodium absorption requires hours and thus may not appear during a short immersion study.2'…”

mentioning

confidence: 95%

“…Epstein and co-workers found similarly that the patients with the highest renin and aldosterone levels (and thus the lowest effective arterial volume) did not respond to water immersion with diuresis. 19 In summary, patients with cirrhosis, ascites and renal salt retention have a decreased effective arterial volume, which is due to ascites formation and arteriovenous fistulae. These patients should therefore always be diuresed or paracentesed with caution.…”

mentioning

confidence: 99%

Renal Sodium Retention in Liver Disease

Epstein¹

1995

Hospital Practice

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Characterization of the renin-aldosterone system in decompensated cirrhosis.

Cited by 161 publications

References 24 publications

Changes in plasma renin activity in cirrhosis: a reappraisal based on studies in 67 patients and "low-renin" cirrhosis.

Changes in plasma renin activity in cirrhosis: a reappraisal based on studies in 67 patients and "low-renin" cirrhosis.

Increased Apical Targeting of Renal Epithelial Sodium Channel Subunits and Decreased Expression of Type 2 11β-Hydroxysteroid Dehydrogenase in Rats with CCl4-Induced Decompensated Liver Cirrhosis

Renal Sodium Retention in Liver Disease

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