Endogenous dopaminergic activity in Child–Pugh A cirrhosis: potential role in renal sodium handling and in the maintenance of clinical compensation

Sansoè,; Ferrari, Paolo; Baraldi,; Grisolia,; Santis, De; Villa, Erica; Manenti,

doi:10.1046/j.1365-2362.1998.00252.x

Cited by 8 publications

(5 citation statements)

References 38 publications

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“…5 (May 2005) sensitive marker of expanded central fluid volume. This is supported by the previous observations that plasma dopamine (DA) increases after saline infusion or head-out water immersion in normal men (39,40) and that an inverse correlation between dopaminergic function and circulating active renin does exist in liver cirrhosis (27,41). Our preascitic patients showed slightly lower fractional excretion of lithium and significantly increased values of fractional distal tubular sodium reabsorption (DFRNa) compared to controls (Table 3), in agreement with other reports (27).…”

Section: Discussionsupporting

confidence: 92%

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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Section: Discussionsupporting

confidence: 92%

Loss of Tubuloglomerular Feedback in Decompensated Liver Cirrhosis: Physiopathological Implications

Sansoè

Silvano²,

Mengozzi

et al. 2005

Dig Dis Sci

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“…The presence of an expanded extracellular and\or central fluid volume in patients with compensated cirrhosis has been documented several times, by means of various experimental observations : increased distribution volume of "$"I-labelled albumin and of &"Cr-labelled erythrocytes [4], increased central blood volume measured by radionuclide angiography [7], increased end-diastolic and endsystolic left ventricular diameters [46], depression of the renin-angiotensin-aldosterone axis [8][9][10], high plasma atrial natriuretic factor concentrations [6], and hypertone of endogenous dopaminergic activity [47].…”

Section: Discussionmentioning

confidence: 99%

Cimetidine administration and tubular creatinine secretion in patients with compensated cirrhosis

et al. 2001

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Cimetidine inhibits the tubular secretion of creatinine, without altering the glomerular filtration rate (GFR). During cimetidine administration the creatinine/inulin clearance ratio approaches unity in patients with renal failure. We determined the clearance of lithium (an index of fluid delivery to the distal nephron), inulin (a measure of the actual GFR) and creatinine during cimetidine administration to investigate the occurrence of tubular creatinine secretion in patients with compensated cirrhosis. A total of 12 patients with Child-Pugh A cirrhosis were studied initially. The subjects consumed a stable diet containing 100 mmol of sodium. On successive days, 9 h creatinine clearances were measured, first without and then with the oral administration of cimetidine (400 mg as a priming dose, followed by 200 mg every 3 h). During the first study day, 4 h renal lithium clearance was also calculated. A further group of five patients with fully compensated cirrhosis underwent the measurement (on successive days) of plasma inulin clearance, first without and then with the oral administration of cimetidine (same schedule of drug administration). Cimetidine administration unmasked a marked overestimation of GFR when calculated as creatinine clearance (baseline, 138+/-20 ml/min; +cimetidine, 89+/-13 ml/min; P<0.01). Consequently, during cimetidine administration the calculated lithium fractional excretion (a measure of the fraction of filtered sodium load that is delivered to the loop of Henle) rose from 21.4+/-13.2% to 32.3+/-18.9% (P<0.05), and the ratio between absolute distal tubular sodium reabsorption and filtered sodium load rose from 20.6+/-13.1% to 31.6+/-19.3% (P<0.01). Cimetidine caused no significant decrease in the actual GFR (i.e. inulin clearance) when administered to the second group of patients with compensated cirrhosis. Our data demonstrate significant tubular secretion of creatinine in patients with compensated cirrhosis and, consequently, a marked overestimation of GFR and filtered sodium load and an underestimation of the fractional distal tubular sodium reabsorption when these parameters are calculated by means of the traditional creatinine and lithium clearance computation. The true GFR (measured as inulin clearance) is unaffected by cimetidine administration.

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“…This has been shown by several experimental observations: increased distribution volume of 131 I-labelled albumin and 51 Cr-labelled erythrocytes4; increased central blood volume measured by radionuclide angiography5; increased end diastolic and end systolic left ventricular diameters6; suppression of the renin-angiotensin-aldosterone axis7-9; high plasma atrial natriuretic factor concentrations10; increased endogenous dopaminergic activity 11…”

mentioning

confidence: 88%

Renal distal tubular handling of sodium in central fluid volume homoeostasis in preascitic cirrhosis

Sansoè

Ferrari

Baraldi

et al. 1999

Gut

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Background/Aims-Patients with preascitic liver cirrhosis have an increased central plasma volume, and, for any given plasma aldosterone concentration, they excrete less sodium than healthy controls. A detailed study of the distribution of sodium reabsorption along the segments of the renal tubule, especially the distal one, is still lacking in preascitic cirrhosis. Conclusions-These data suggest that in preascitic cirrhosis the distal fractional tubular reabsorption of sodium is increased and critical in regulating both central fluid volume and sodium excretion. (Gut 1999;45:750-755) Methods-Twelve

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Endogenous dopaminergic activity in Child–Pugh A cirrhosis: potential role in renal sodium handling and in the maintenance of clinical compensation

Cited by 8 publications

References 38 publications

Loss of Tubuloglomerular Feedback in Decompensated Liver Cirrhosis: Physiopathological Implications

Loss of Tubuloglomerular Feedback in Decompensated Liver Cirrhosis: Physiopathological Implications

Cimetidine administration and tubular creatinine secretion in patients with compensated cirrhosis

Renal distal tubular handling of sodium in central fluid volume homoeostasis in preascitic cirrhosis

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