Effects of amiloride on renal lithium handling in nonazotemic ascitic cirrhotic patients with avid sodium retention

Angeli, Paolo; Bei, E. De; Pria, M. Dalla; Caregaro, L.; Ceolotto, Giulio; Albino, G.; Gatta, Angelo

doi:10.1002/hep.1840150416

Cited by 20 publications

(13 citation statements)

References 18 publications

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“…However, in a study by Angeli et al 31 of patients with cirrhosis with ascites and avid sodium retention, no reabsorption in the distal tubule was found. 31 A negative C H2O value in the treatment groups represents hypertonic urine, in contrast to the urine in the placebo group, which becomes more hypotonic. The mean value of C H2O in the P group in the 3 baseline clearance periods was higher (Fig.…”

Section: Discussionmentioning

confidence: 90%

Terlipressin improves renal function in patients with cirrhosis and ascites without hepatorenal syndrome

et al. 2007

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Patients with advanced cirrhosis and ascites are characterized by circulatory dysfunction with splanchnic vasodilatation and renal vasoconstriction, which often lead to ascites. The vasoconstrictor terlipressin improves renal function in hepatorenal syndrome (HRS). The aim of this study was to evaluate if terlipressin also improves renal function in patients with ascites without HRS. Twenty-three patients with cirrhosis participated; 15 with nonrefractory ascites were randomized to either terlipressin (N group, n ‫؍‬ 11) or a placebo (P group, n ‫؍‬ 4), and 8 had refractory ascites and received terlipressin (R group). The glomerular filtration rate (GFR), sodium clearance (C Na ), lithium clearance (C Li ), osmolal clearance (C Osm ), and urine sodium concentration (U Na ) were assessed before and after the injection of 2 mg of terlipressin or the placebo. GFR increased in the N group (69 ؎ 19 versus 92 ؎ 25 mL/min, P < 0.005) and in the R group (31 ؎ 19 versus 41 ؎ 31 mL/min, P < 0.05) after terlipressin. In the N group, terlipressin induced an increase in C Na (0.89 ؎ 0.21 versus 1.52 ؎ 1.45 mL/min, P < 0.05), C Li (17.3 ؎ 8.9 versus 21.5 ؎ 11.6 mL/min, P < 0.05), and C Osm (2.10 ؎ 0.81 versus 3.06 ؎ 2.0 mL/min, P < 0.05). In the R group, terlipressin induced an increase in C Na (0.11 ؎ 0.18 versus 0.35 ؎ 0.40 mL/min, P < 0.05) and C Li (5.5 ؎ 4.2 versus 9.5 ؎ 8.55 mL/min, P < 0.05). U Na increased in both groups after terlipressin (P < 0.005). Plasma norepinephrine (P < 0.05) and renin (P < 0.05) decreased after terlipressin. All parameters remained unchanged after the placebo. A scites is a serious complication of cirrhosis, occurring in about 50% of patients within 10 years after diagnosis, and it is associated with 50% mortality in 2 years. 1,2 Patients with ascites have hyperdynamic circulation, which is characterized by peripheral and splanchnic arterial vasodilatation and reduced arterial blood pressure and systemic vascular resistance. 3 Portal hypertension and splanchnic vasodilatation are major factors in the development of ascites. 4,5 Secondary to vasodilatation, vasoactive hormones, such as the reninangiotensin-aldosterone system and the sympathetic nervous system, are activated. This leads to renal vasoconstriction and reduced renal perfusion and filtration pressure. The current standard treatment of ascites involves diuretics and paracentesis, which are not designed to improve the underlying pathophysiology. The changes in the renal handling of water and salt seem to develop stepwise from a stage that can be controlled by diuretics to a stage refractory to diuretics and finally to full-blown renal failure, which is known as hepatorenal syndrome (HRS) type 1. 6 Several clinical studies have evaluated the efficacy of the long-term administration of terlipressin [a vasopressin 1 (V1) receptor agonist] in patients with HRS, [7][8][9][10][11][12][13] and there is evidence that terlipressin may improve renal

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Section: Discussionmentioning

confidence: 90%

Terlipressin improves renal function in patients with cirrhosis and ascites without hepatorenal syndrome

et al. 2007

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“…This limitation holds specifically for studies aiming to measure absolute\fractional reabsorption, as well as the fractional excretion of fluid and sodium by means of the lithium clearance technique [48][49][50]. In effect, our protocol has unmasked a marked overestimation not only of GFR and filtered sodium load, but also of the proximal and total tubular reabsorption of sodium (Table 2).…”

Section: Discussionmentioning

confidence: 95%

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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“…Lithium clearance is used as a marker of proximal tubule sodium reabsorption, based on the assumptions that lithium is filtered freely across the glomerulus, that lithium is reabsorbed in proportion to sodium and water in the proximal tubules, and that no reabsorption or secretion of lithium takes place in the distal tubules. 23,24 Fractional excretion (FE) is calculated as: FE x ϭ C x /GFR and, finally, free water clearance (C H2O ) is:…”

Section: Patientsmentioning

confidence: 99%

Effects of a long-acting formulation of octreotide on renal function and renal sodium handling in cirrhotic patients with portal hypertension: A randomized, double-blind, controlled trial

et al. 2001

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Octreotide has been widely used for controlling acute variceal bleeding in cirrhotic patients. The exact mechanisms of the hemodynamic changes in response to octreotide are partly unknown, 1 and only a transient or no effect on hepatic venous pressure gradient (HVPG) has been demonstrated. [2][3][4][5][6] Lately, a marked increase of lower esophageal sphincter pressure has been described in response to intravenous octreotide in portal hypertensive patients in addition to a sustained suppression of postprandial splanchnic hyperemia. 3,7-9 These effects coincide with a reduction of plasma glucagon, 8,9 and this mechanism has been thought to be responsible for the suppression of splanchnic hyperemia. However,

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Effects of amiloride on renal lithium handling in nonazotemic ascitic cirrhotic patients with avid sodium retention

Cited by 20 publications

References 18 publications

Terlipressin improves renal function in patients with cirrhosis and ascites without hepatorenal syndrome

Terlipressin improves renal function in patients with cirrhosis and ascites without hepatorenal syndrome

Cimetidine administration and tubular creatinine secretion in patients with compensated cirrhosis

Effects of a long-acting formulation of octreotide on renal function and renal sodium handling in cirrhotic patients with portal hypertension: A randomized, double-blind, controlled trial

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