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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The intrarenal distribution of plasma flow was determined with a technique based on the analysis of the transit time of sodium o-[131I]- iodohippurate through the kidney in 43 patients with cirrhosis with near-normal total renal perfusion. 2. Twenty-five of the patients had an abnormal pattern of transit times, suggesting a redistribution of plasma flow from outer cortical to juxtamedullary nephrons. 3. Plasma renin activity ranged from below normal to six times normal and high values were found only in patients showing an abnormal pattern of transit times. The latter was also found to be related to sodium retention and a reduced renal capacity to excrete free water.
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PMID:Intrarenal distribution of plasma flow in cirrhosis as measured by transit renography: relationship with plasma renin activity, and sodium and water excretion. 86 40

Two patients with hepatorenal syndrome were treated by insertion of a peritoneovenous shunt. The renal deficit was corrected rapidly in both cases. A 62-year-old woman with a slow onset syndrome with urine output of 100 to 150 ml/day and urinary sodium excretion of 1 mEq/day responded with large volume urinary output and sodium excretion. She is alive with minimal ascites 18 months after shunt. A 53-year-old man with severe nutritional cirrhosis, alcoholic hepatitis, and eventual massive necrosis was treated for bleeding esophageal varices by portacaval shunt. Postoperative massive ascites progressed to acute hepatorenal syndrome. Insertion of a peritoneovenous shunt reversed the renal deficit. HE eventually exsanguinated due to a hemorrhagic diathesis caused by massive hepatic necrosis.
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PMID:Hepatorenal syndrome: reversal by peritoneovenous shunt. 88

1) Fluid retention and ascites are rarely seen in patients with primary biliary cirrhosis (PBC). In an attempt to clarify this clinical observation, renal handling of sodium, water and divalent ions was studied during extracellular volume expansion (ECVE) and maximal suppression of antidiuretic hormone (ADH) secretion in 5 patients with PBC and 9 normal subjects. 2) Mean fractional excretion of sodium, water, phosphate and calculated fractional distal delivery of sodium were significantly greater in patients with PBC as compared with normal controls. Fractional CH20 for given fractional urine flow was similar in patients with PBC and normals. 3) The data suggest that patients with PBC have a greater diminution of proximal tubular reabsorption of sodium in response to ECVE than controls. This augmented elimination of salt during ECVE in patients with PBC may explain the rarity of ascites and edema in this type of cirrhosis.
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PMID:Renal handling of sodium, water and divalent ions in patients with primary biliary cirrhosis. 89 21

Hepatic insufficiency is generally caused by active liver cirrhosis with portal hypertension. The final stage is the exogenous hepatic coma. Much rarer is the endogenous hepatic coma caused by fulminant acute hepatitis or severe intoxications. In the treatment of hepatic insufficiency it is first necessary to eliminate all exacerbating factors such as too high protein-intake, gastrointestinal bleedings, abuse of alcohol and diuretics. Because hepatic encephalopathy is mainly produced by toxic intestinal protein metabolites no protein should be adminstered at the beginining of the disease. The production of toxic protein metabolites in the gut can be diminished as well by enemas with sodium acetate buffer (pH 4, 5) as by neomycin (6-8 gm daily). Because long-term treatment with neomycin reduces also the physiological intestinal bacteria combination with lactulose (70-100 gm daily) is better. Treatment with lactulose reduces not only significantly hyperammoniemia but also increases serum phenols. The same effect have so-called ammonia reducing amino acids such as arginine, ornithine and glutamic acid. In endogenous hepatic coma blood exchange transfusions, liver perfusions and charcoal perfusions are necessary. Nevertheless, the prognosis of hepatic insufficiency caused by fulminant hepatitis is very poor in the final stage of the disease. Therefore early diagnosis and treatment in special departments with intensive care is necessary.
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PMID:[Therapy of hepatic insufficiency]. 91 52

The elimination of para-aminosalicylic acid (PAS) after the intravenous injection of 20 mg PAS sodium/kg was estimated in patients with liver disease, in uremic patients and in volunteers without damage of the liver or kidneys. The drug was estimated with a colorimetric and fluorometric method. In the volunteers, the half-lives obtained with the fluorometric method were significantly longer than those estimated with the colorimetric method. This is caused by the estimation of more PAS metabolites by the used fluorometric method. In the patients with renal insufficiency (dialysis patients) the elimination rate of unchanged PAS--estimated with the colorimetric method--was not altered, whereas the elimination of PAS and its metabolites extractable by ethyl acetate was markedly slowed in comparison with the results obtained with the volunteers. The clearance of the unchanged PAS was even increased in the uremic patients. The serum protein binding of PAS was lowered significantly in the serum of uremic patients. In patients with liver cirrhosis, acute virus hepatitis and cholangitis the elimination rate of the drug was not altered in comparison with the volunteers. The results show that the dose of PAS in patients with renal insufficiency may not be reduced. The therapeutic level of the drug cannot otherwise be reached in these patients.
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PMID:Elimination of para-aminosalicylic acid in patients with liver disease and renal insufficiency. 92 30

1-Sar-8-ala angiotensin II (saralasin) was infused intravenously in graded doses of from 0.1 to 10 mug/kg/min to five patients with cirrhosis and ascites after three days of restricted sodium intake. In each patient blockade of AII by saralasin produced a marked fall in blood pressure, a rise in plasma renin activity (PRA) and plasma renin concentration (PRC) and, in four of the five, a fall in plasma aldosterone (PA). The rise in PRA and PRC correlated poorly with changes in blood pressure. The effects of saralasin rapidly reversed after cessation of the infusion. Plasma volume was normal or high in each case. Three patients were mildly hypotensive in the control state, and all five were resistant to the pressor effect of infused AII. After three days of salt loading, the above effects of saralasin were diminished but not abolished. In four normal subjects, after salt depletion, saralasin infusion induced qualitatively similar but much smaller changes in blood pressure, PRA and PRC. In two cirrhotic patients without ascites, after salt depletion, saralasin infusion caused a rise in blood pressure with no significant changes in PRA, PRC or PA. These results provide evidence that in patients with cirrhosis and ascites circulating AII is active in support of blood pressure, in direct suppression of renal renin release, and in stimulation of aldosterone release.
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PMID:Effect of blockade of angiotensin II on blood pressure, renin and aldosterone in cirrhosis. 94 Feb 84

The renal regulation of sodium is intertwined with the extracellular fluid volume (ECFV). Most adjustments in sodium elimination in man are accomplished via alterations in tubular reabsorption. The latter is sensitive to change in ECFV. An expanded ECFV results in less reabsorption and more excretion of sodium, and a contracted ECFV has the converse effect. There are direct and indirect mechanisms whereby ECFV influences sodium reabsorption. Patients with nephrotic syndrome, heart failure, and cirrhosis "behave" physiologically as normal individuals with a contracted ECFV. Water balance is normally determined by intake and losses in sweat which is always hypoosmotic to plasma, by evaporation from skin and lungs, and through renal excretion. The major factors that determine the ability to concentrate the urine are (1) the establishment of a concentrated environment around the collecting ducts, and (2) the elaboration and effects on the kidney of antidiuretic hormone. The evaluation of a patient with abnormalities of sodium and water rests initially and largely on clinical information. The clinical setting provides clues to anticipating, preventing, and interpreting distortions of body sodium and water. The laboratory can detect an abnormality, confirm or refute clinical assessment, and assist in the quantitative aspects of treatment and its efficacy.
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PMID:Sodium and water: an overview. 96 14

Glomerular filtration rate and renal plasma flow may be normal, reduced or increased in cirrhosis. The mechanism of departures from normal is not known. Other renal functional changes in cirrhosis include avid sodium reabsorption, impaired concentrating and diluting abilities, and partial renal tubular acidosis. Fluid and electrolyte disorders are common. Sodium retention with edema and ascites should generally be treated conservatively because they tend to disappear as the liver heals and because forced diuresis has hazards. The indications for diuretics are (1) incipient or overt atelectasis; (2) abdominal distress; and (3) possibility of skin breakdown. Hyponatremia is common and its mechanism and treatment must be assessed in each patient. Hypokalemia occurs and requires treatment. Respiratory alkalosis and renal tubular acidosis seldom need therapy. The hepatorenal syndrome is defined as functional renal failure in the absence of other known causes of renal functional impairment. The prognosis is terrible and therapy is unsatisfactory. The best approach is not to equate the occurrence of renal failure in cirrhosis with the hepatorenal syndrome. Rather the physician should first explore all treatable causes of renal failure, eg, dehydration, obstruction, infection, heart failure, potassium depletion, and others.
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PMID:Fluid and electrolyte disturbances in cirrhosis. 96 15

The net ionic flux through the gastric wall was determined in eleven patients with hepatic cirrhosis and five normal controls. The back-diffusion of C1- and H+ was significantly increased in the cirrhotic group. In nine patients of this group the H+ loss was above the upper limits of normal. The Na+ flux was positive in both the control and the cirrhotic group. The Na+ flux towards the gastric cavity in the cirrhotic patients was not proportional to the loss of H+. Vasodilatation and edema of the lamina propria was always present as judged by gastric biopsy; in five cases mucosal hemorrhage was observed, in three superficial epithelial desquamation and in one melaena due to hemorrhagic gastritis. One the basis of the increase in H+ loss and the histological findings, we suspect an alteration in the gastric mucosal barrier in the patients with hepatic cirrhosis.
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PMID:Functional study of the gastric mucosal barrier in hepatic cirrhosis. 98 63

Thanks to diuretics, adequate diet, and other measures, the treatment of cirrhotic ascites in recent years has brought better results. Nonetheless, a certain number of patients do not respond to the above mentioned treatment. Such patients are afflicted with so called Refractory Ascites on which diuretics have no effect. In recent years the concentrated continuous reinjection methods has been accepted. During a nine month period, we have treated and analyzed thirty patients with severe Hepatic Ascitogenic Cirrhosis. The results have shown: 8 patients with satisfactory improvement with one reinjection, in 2 patients Ascites did not reoccur; 6 patients died; 6 patients failed to return for a control reexamination; in 2 patients, ascites persisted even after repeated reinjections. The patients were given diuretics the third week following the reinjection, and were put on a low salt diet. Ascites reoccurred, and to a greater degree during the second third, and fourth month. A reduced sodium level was corrected by the reinjection and by the administration of NaCl during the reinjection. K and Cl levels did not change significantly. Urea levels, which were elevated in many cases were normalized. Ammoniums and Phenols also tended to normalize following reinjection. Bilirubin values were highly variable especially in two patients. One of whom had a severely damaged liver (direct bilirubin), the other of whom had bleeding varicoses of the esophagus (indirect bilirubin). Both of these patients died. In such cases reinjection should not be performed until the bilirubin values fall below 5 mgr %. Of the six patients who died, four died of unforeseen esophageal hemorrhaging. A larger number of patients grew more tolerant of diuretics. Preparation for a Portocaval Shunt with the reinjection method is of a special advantage because of an overall improvement in condition, making surgery possible. Complications resulting from reinjection were insignificant and transitory. As a whole, our results (sixteen patients in satisfactory condition), showed that Continuous Venous Reinjection of peritoneal fluid, even though a palliative method, represents a significant step forward in the treatment of Ascites in the severely ill.
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PMID:[Treatment of cirrhotic ascites by means of venous concentrated reinjected of the peritoneal fluid]. 99 28


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