Studies on the activity of the renin-angiotensin-aldosterone system (RAAS) in patients with cirrhosis of the liver

Wernze, H.; Spech, H. J.; Müller, G

doi:10.1007/bf01477293

Cited by 80 publications

(32 citation statements)

References 53 publications

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“…Moreover, we have been able to confirm the direct relationship between portal venous pressure on one side and PRC and ALD on the other side, as first described by Bosch et al in 1980." This indicates to us that most often RAAS is activated during decompensation, suggesting an underfilling of the central vascular bed with activated volume and barorece~tors.…”

Section: Renin-angiotensin-aldosterone Systemsupporting

confidence: 77%

Pathogenesis of Ascites Formation and Hepatorenal Syndrome: Humoral and Hemodynamic Factors

Ring‐Larsen¹,

Henriksen²

1986

Semin Liver Dis

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Section: Renin-angiotensin-aldosterone Systemsupporting

confidence: 77%

Pathogenesis of Ascites Formation and Hepatorenal Syndrome: Humoral and Hemodynamic Factors

Ring‐Larsen¹,

Henriksen²

1986

Semin Liver Dis

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“…On the whole, urinary sodium excretion in these patients was significantly correlated with GFR values. It has been shown that about 40% of patients with "early" ascites have normal PRA and aldosterone plasma levels (43)(44)(45); we observed that 3 of 10 ascitic patients had PRA and aldosterone values within the normal range (data not shown).…”

Section: Discussioncontrasting

confidence: 63%

Loss of Tubuloglomerular Feedback in Decompensated Liver Cirrhosis: Physiopathological Implications

Sansoè

Silvano²,

Mengozzi

et al. 2005

Dig Dis Sci

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In healthy subjects, arterial pressure reduction or renal ischemia produces renal artery dilatation through autoregulation and tubuloglomerular feedback (TuGF). Patients with decompensated cirrhosis have reduced kidney perfusion pressure but show renal vasoconstriction instead of autoregulation-mediated vasodilation. This study investigates the consequences of kidney autoregulation loss on renal perfusion, glomerular filtration rate, and tubular handling of electrolytes in both compensated and ascitic nonazotemic cirrhotic patients. Forty-two consecutive patients with diuretic-free liver cirrhosis (32 with preascitic and 10 with ascitic disease) and 10 controls were submitted to the following determinations: (a) basal plasma renin activity and aldosterone levels; (b) endogenous dopaminergic activity measured as incremental aldosterone responses during metoclopramide administration; and (c) renal clearances of sodium, potassium, inulin, para-aminohippurate and lithium. Compared with the other groups, ascitic patients showed lower renal plasma flow (P < 0.01) and lithium clearance (P < 0.05), a higher filtration fraction (P < 0.01), and secondary aldosteronism. Controls and preascitic patients displayed tubuloglomerular feedback (the mechanism increasing the glomerular filtration rate when a reduced sodium load reaches the distal tubule), as demonstrated by negative correlations between fractional excretion of lithium (an expression of fractional delivery of sodium to the distal nephron) and glomerular filtration rate (respectively, r = -0.73, P < 0.03, and r = -0.48, P < 0.01). Conversely, patients with ascites showed a positive correlation between lithium fractional excretion and glomerular filtration rate (r = 0.64, P < 0.05). Reduction in renal perfusion, increased filtration fraction, and TuGF derangement, as found in decompensated patients, are indicative of prevalent postglomerular arteriolar vasoconstriction, with ensuing stimulation of proximal tubular sodium reabsorption.

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“…In our patients with liver cirrhosis, baseline urinary excretion of free aldosterone was not significantly higher in contrast to the previous observations [ 13]. In this con text, Bernardi et al [14] recently demonstrated that renin and plasma aldosterone were not elevated in cir rhotic patients.…”

Section: Discussioncontrasting

confidence: 55%

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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Studies on the activity of the renin-angiotensin-aldosterone system (RAAS) in patients with cirrhosis of the liver

Cited by 80 publications

References 53 publications

Pathogenesis of Ascites Formation and Hepatorenal Syndrome: Humoral and Hemodynamic Factors

Pathogenesis of Ascites Formation and Hepatorenal Syndrome: Humoral and Hemodynamic Factors

Loss of Tubuloglomerular Feedback in Decompensated Liver Cirrhosis: Physiopathological Implications

Role of Intestinal Bacteria in the Metabolism of Aldosterone in Man

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