Sodium Retention In Cirrhosis Research Articles

Renal sodium retention in cirrhosis: tubular site and relation to hepatic dysfunction.

Renal sodium handling, assessed by the response to acute saline loading, was investigated in 14 well-compensated, nonascitic alcoholic cirrhotics and six normal controls. Urinary sodium excretion in cirrhotic patients (199 +/- 141 mumoles per min) was significantly lower than in controls (387 +/- 104 mumoles per min; p less than 0.01) at 3 hr postinfusion. In contrast to controls, renal plasma flow and glomerular filtration rate did not increase in the cirrhotics in response to acute saline loading. Proximal fractional reabsorption of sodium was estimated by clearance techniques in the presence of a hypotonic diuresis. Cirrhotic subjects with impaired functional liver cell mass as assessed by antipyrine clearance were unable to decrease proximal fractional reabsorption of sodium significantly in response to saline loading. Assessment in the cirrhotics included measurement of hepatic vein pressure gradient, indocyanine green extraction ratio, indocyanine green clearance, and antipyrine clearance as indices of portal pressure, intrahepatic shunting, hepatic blood flow and functional hepatocellular mass, respectively. Urinary sodium excretion in the cirrhotics correlated strongly with antipyrine clearance (r = 0.839, p less than 0.0001) and weakly with portal pressure (r = 0.562, p = 0.037). No correlation was seen with the other indices of hepatic blood flow and shunting. The findings of this study suggest that alcoholic cirrhosis is associated with a decline in hepatocellular function which results in either a decreased clearance of a salt-retaining hormone or decreased synthesis of a natriuretic hormone.(ABSTRACT TRUNCATED AT 250 WORDS)

The sodium retention of cirrhosis: a reappraisal.

The sodium retention of cirrhosis: a reappraisal.

Renal and hemodynamic effects of the peritoneovenous shunt: II. Long-term effects

The long-term renal and hemodynamic effects of the peritoneovenous shunt for intractable ascites were studied in 11 patients to elucidate the mechanism of its persistent beneficial effect. Sodium balance studies were performed in 7 patients. All had patent shunts and no clinically detectable ascites. On a 20-mEq sodium diet, the mean sodium excretion was 17.2 ± 5.3 mEq/day which was increased over the preoperative mean of 2.4 ± 0.4 (p < 0.025) on the same diet. There was a 100% increase in creatinine clearance over the preoperative level (p < 0.0005). The mean plasma renin activity and serum aldosterone levels were within normal limits in most patients, and the sodium excretion correlated inversely with the levels of each. During 100-mEq sodium challenge diet, the sodium excretion ranged from 4 to 130 mEq/day with a mean of 56.1 ± 16.5 and with 6 of the 7 patients displaying sodium retention. On this diet the mean creatinine clearance was 104.3 ± 6.4 ml/min, and the mean plasma renin activity and serum aldosterone levels had decreased physiologically with the higher sodium intake. Again the sodium excretion correlated inversely with the serum aldosterone on the 100-mEq sodium diet. In 8 patients, the portal pressure, as reflected by the wedge hepatic vein pressure, had decreased by a mean of 37% (p < 0.0005). But, despite this, 2 of the 8 patients had major variceal hemorrhages postoperatively. There was a significant inverse correlation between the increase in sodium excretion and the fall in portal pressure in 4 patients. Thus, sodium retention in cirrhosis is multifactorial with the reninaldosterone system and, possibly, portal hypertension per se both playing a role. Peritoneovenous shunting in carefully selected patients partially reverses the sodium retention and renders patients more manageable over the long term.

Renal sodium retention in cirrhosis: relation to aldosterone and nephron site.

1. In a group of patients with cirrhosis who showed a wide range of values for the rate of renal sodium excretion, the latter was found to be inversely related to both the plasma concentration and rate of renal excretion of aldosterone. However, for a given sodium excretion the values for aldosterone were significantly lower in the patients than for a group of healthy control subjects. These findings suggest either an increased renal tubular sensitivity to aldosterone or the participation of other factors in the pathogenesis of the sodium retention. 2. Based on measurements of the rate of urine flow and the clearances of free water and inulin during a maximal water diuresis, the fractional reabsorption of sodium by the 'proximal', 'diluting segment' and 'distal' segments of the nephron was estimated. For patients retaining sodium the enhanced reabsorption occurred at both proximal and distal sites, the latter being quantitatively more important. There was no significantly enhanced sodium reabsorption in the diluting segment.

Renal function in dogs with acute selective hepatic venous outflow block.

ARTICLESRenal function in dogs with acute selective hepatic venous outflow blockM LevyM LevyPublished Online:01 Nov 1974https://doi.org/10.1152/ajplegacy.1974.227.5.1074MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByAfferent mechanisms of sodium retention in cirrhosis and hepatorenal syndromeKidney International, Vol. 77, No. 8Systemic hemodynamics, vasoactive systems, and plasma volume in patients with severe Budd-Chiari syndrome1 January 2005 | Hepatology, Vol. 43, No. 1Pathophysiology of Na and water retention in liver cirrhosis and its correction with vasoconstrictors and aquaretics22 December 2005 | Expert Opinion on Therapeutic Patents, Vol. 16, No. 1Ventilation and the KidneyThe Pathogenesis of Renal Sodium Retention and Ascites Formation in Laennec’s CirrhosisRenal water and sodium handling in compensated liver cirrhosis: mechanism of the impaired natriuresis after saline loadingEuropean Journal of Clinical Investigation, Vol. 15, No. 6Sympathetic nervous activity in cirrhosisJournal of Hepatology, Vol. 1, No. 1Salt and Water Balance in Liver Disease17 May 2016 | Hospital Practice, Vol. 19, No. 7SODIUM AND FLUID RETENTION IN HEPATIC CIRRHOSIS: A ROLE FOR CIRCULATING HORMONES?25 March 2008 | Australian and New Zealand Journal of Medicine, Vol. 14, No. 3Renal neural activity in hepatorenal syndromeKidney International, Vol. 25, No. 5Renal Handling of Sodium in Hepatic Diseases Other than CirrhosisDie Pathogenese des kardialen ÖdemsHepatic nephropathy, related to haemodynamics10 December 2008 | Liver, Vol. 3, No. 5Disturbed volume homeostasis in patients with cirrhosis of the liverKidney International, Vol. 23, No. 2Afferent and efferent neural roles in liver functionProgress in Neurobiology, Vol. 21, No. 4Body fluid homeostasis in congestive heart failure and cirrhosis with ascitesThe American Journal of Medicine, Vol. 72, No. 2A Comparison of Acute Reversible Pre- and Postsinusoidal Portal Hypertension on Salt and Water Retention in the Dog21 September 2007 | Hepatology, Vol. 2, No. 1Noradrenaline and adrenaline concentrations in various vascular beds in patients with cirrhosis Relation to haemodynamics.Clinical Physiology, Vol. 1, No. 3Hepatorenales SyndromKlinische Wochenschrift, Vol. 59, No. 9Effects of renal and hepatic venous congestion on renal function in the presence of low and normal cardiac output in dogs.Circulation Research, Vol. 47, No. 6Renal and Intrarenal Blood Flow in Patients with Cirrhosis before and after Portal-Systemic Shunt23 February 2010 | Scandinavian Journal of Gastroenterology, Vol. 15, No. 4Hepatic hemodynamics and the renin-angiotensin-aldosterone system in cirrhosisGastroenterology, Vol. 78, No. 1Plasma levels and hepatic extraction of renin and aldosterone in alcoholic liver diseaseThe American Journal of Medicine, Vol. 66, No. 5Deranged Sodium Homeostasis in CirrhosisGastroenterology, Vol. 76, No. 3Renal blood flow in cirrhosis: relation to systemic and portal haemodynamics and liver function8 July 2009 | Scandinavian Journal of Clinical and Laboratory Investigation, Vol. 37, No. 7Effect of portal-systemic anastomosis on renal haemodynamics in cirrhosis.Gut, Vol. 17, No. 11 More from this issue > Volume 227Issue 5November 1974Pages 1074-1083 Copyright & PermissionsCopyright © 1974 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1974.227.5.1074PubMed4374089History Published online 1 November 1974 Published in print 1 November 1974 Metrics

ARETAEUS ON THE DRY SKIN OF DROPSY.

RETA1/;t;S, tile Cappadocian, in tile second century A.D. was clearly conversant with many kinds of liver disease. In On the Causes and Symptoms of Chrouic Diseases, Book I, he refers to the "dropsy" of certain chronic hepatic afflictions, noting what is still true today, that "the best tiling is for it (tile accunmlated water) to be discharged by the urine; for the passage by it (the urine) is safer and less troublesome .... " Later, Aretaeus observes, "Sweating, if copious, carries off the disease . . . for dropsical persons generally have not a moist skin." The relationship between edematous states ("dropsy") and sweating is not entirely clear and requires further investigation, but it is probable that Aretaeus was right. Streeten et al. a have demonstrated that a metabolically provoked increase in aldosterone secretion in normal men is accompanied by a marked fall in the sodium excretion of the sweat glands. Berger and Steele e have also found, in a few patients, reduced sodium loss through perspiration in congestive heart failure and cirrhosis of the liver, but in a large number of children with congestive heart failure, Morgan and Nadas a showed that perspiration, grossly, and sweat sodinm loss, quantitatively, were considerably augmented. However, the factors responsible for sodium retention in cirrhosis and in heart failure are probably not identical, as is so commonly suggested by the efficacy of mercurial diuretics in the latter but not in the former. Moreover, the sympathetic nervous stimulation of heart failure, while variable, may be very strong, and whether neurogenic evocation of sweating or its endocrine suppression prevailed in a given case might well depend upon several independent variables. All things considered, incomplete evidence suggests that the Cappadocian's observation of dry skin in hepatic anasarca was accurate and significant. His empirical conclusion was shared by a patient of mine, a physician, whose duodenal ulcer had been effectively treated by subtotal gastrectomy. The doctor thereafter noted profuse generalized diaphoresis if he ate hastily or drank a malted milk. This manifestation of the "dumping

Local Factors in Ascites Formation during Sodium Retention in Cirrhosis

PREVIOUS studies have indicated that in patients with cirrhosis the presence or absence of ascites can be explained by a consideration of hydrostatic and osmotic forces, and a similar analysis can be used to explain the responses to various forms of treatment.1 , 2 It is well established that, in cirrhosis, an increased intake of sodium causes an increased rate of ascites formation,3 but the precise local forces leading to the transfer of fluid across the peritoneal membrane under these conditions have not been defined. The present study was undertaken to provide such information. Patients and Methods Four patients with portal cirrhosis . . .

The mechanism of sodium retention in cirrhosis of the liver with ascites: the effect of acetazolamide (diamox) on urinary electrolytes.

SummaryAcetazolamide is shown to increase the urinary excretion of sodium and the sodium to potassium ratio in seven normal subjects and five cirrhotic patients without ascites. In seven cirrhotic patients with ascites the urinary output of sodium and the sodium to potassium ratio were low initially, and were unchanged by acetazolamide.The subjects with ascites had no evidence of renal disease, and the failure to excrete sodium must be attributed to an extrarenal factor. These observations are compatible with the hypothesis that there is an excessive secretion of aldosterone, though they do not indicate the cause. It is not necessarily lowering of plasma sodium level, as the abnormality of sodium and potassium excretion was also noted in one subject with a high normal plasma level. Liver disease also is not essential, as similar sodium retention occurred in one subject whose ascites was due to extrahepatic portal hypertension.Acetazolamide is found not to be a good diuretic in patients suffering from liver disease.