Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

"Refractory" ascites was drained off by combinations of antialdosterone (spironolactone, canrenone) and pseudoantialdosterone (triamterene, amiloride) drugs inducing as high sodium excretion as 100 mEq per day in two patients with liver cirrhosis kept on a 9 mEq Na diet. Potentiation of the natriuretic effects of the two types of antikaliuretic drugs occurred by real synergism rather than addition. Although natriuretic acitivity showed a typical dose-related pattern, potassium excretion was unpredictable. Significant increase in potassium excretion (reversal of the suppression) occurred when 300 mg triamterene was combined with 200 mg canrenone in one of the two patients and when the dose of spironolactone or canrenone was increased from 200 mg to 600 mg within the combinations with 300 mg triamterene or 20 mg amiloride in the other. Parallel increase in sodium and potassium excretions might be caused by a proximal tubular effect or by inhibition of potassium reabsorption along with sodium in Henle's loop. The vasopressin (DDAVP) refractory distorsion of the relationship between osmolal clearance and free water reabsorpton (induced by pseudo-antialdosterone agents and potentiated by antialdosterone drugs) observed in all the 6 cases of the present patient material favoured the "loop hypothesis".
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PMID:Reversal of the suppressed potassium excretion during treatment with combinations of antikaliuretic drugs (spironolactone, canrenone, triamterene, amiloride) in patients with liver cirrhosis. 100 53

In order to study the role of renin in regulating blood pressure in normotensive states, saralasin (P113) was infused into normal subjects and patients with cirrhosis of the liver and ascites. In normal subjects on a normal sodium intake, P113 infusion had no effect on blood pressure. Only after the combined stress of a low sodium diet and the upright position did P113 lower the blood pressure. In two of the six cirrhotic patients, P113 caused a significant decrease in BP in the supine position. There was no consistent effect of the P113 infusion on plasma aldosterone or plasma renin activity in the normal or cirrhotic subjects.
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PMID:The role of renin in the control of blood pressure in normotensive man. 101 62

1-Sarcosine, 8-isoleucine angiotensin II (Sar1-Ile8-AII) was infused intravenously in 5 normal volunteers and 66 subjects with various hypertensive, fluid and electrolyte disorders. Changes of blood pressure (BP), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were studied. In normal subjects, Sar1-Ile-AII showed pressor (agonistic) activity, which was related to both dosage and sodium intake. Hyporeninaemic hypertensive subjects (pirmary aldosteronism) showed pressor responses to a smaller dose of this compound than the dose employed in normal subjects. Hyporeninaemic hypertensive subjects and normal volunteers after 3 days of high sodium intake showed significant elevations of BP and PAC and reduction of PRA. Changes of BP, PAC and PRA in normoreninaemic subjects including those with Bartter's syndrome, renal tubular acidosis or liver cirrhosis with ascites showed reduction of BP and PAC and elevation of PRA. The results indicate that the compound has both agonistic and antagonistic activities for blood pressure; which of these is obtained apparently depends upon endogenous angiotensin II levels, as well as the dosage employed. The results in subjects with high and low PRA suggest that the compound has antagonist and agonist actions at 3 sites of angiotensin II action, i.e. peripheral vascular bed, renin release mechanism from juxta-glomerular apparatus and the zona glomerulosa of the adrenals.
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PMID:Changes of blood pressure, plasma renin activity and plasma aldosterone concentration following the infusion of Sar1-Ile8-angiotensin II in hypertensive, fluid and electrolyte disorders. 101 63

3 patients with hepatic cirrhosis and ascites underwent increased diuresis on six occasions, closely related to episodes of gastrointestinal bleeding. In each instance the increased urine volume was preceded by a sharp increase in blood urea nitrogen, presumably due to absorption of nitrogenous compounds from the gastrointestinal tract, suggesting a mechanism of osmotic diuresis. In each case there was a signigicant increase in serum sodium and osmolality, related to the greater-water-than-sodium diuresis induced by urea, which was promptly reversed by the administration of water or isotonic solution. Clinically this syndrome may be defined as the association of hypernatremia and hyperosmolality due to osmotic diuresis from urea appearing in a cirrhotic patient with ascites and gastrointestinal bleeding.
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PMID:Hypernatremia following gastrointestinal bleeding in cirrhosis with ascites. 107 10

After a diffuse introductory discussion on S-adenosylmethionine methyltransferase activity, the results of an experimental trial carried out on 70 hospitalized patients with chronic hepatitis either persistent or aggressive, and with hepatic cirrhosis at various degrees, are reported. A first group of patients was treated with SAMe (S-adenosylmethionine) intravenously administered for 20 days at two daily doses of 15 mg. The second group was instead-receiving, still by i.v. route, 20 mg of fructose-1-6-diphosphage sodium salt, as a drug for comparison given twice a day at the doses of 2.5 over a 20 days' period. The protidemia picture and in particular the albuminic fraction, generally altered in all the cases under study, have been rapidly and significantly restored only in the group of patients treated with SAMe this indicating the efficacy of this molecule on the liver function.
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PMID:[Relations between protidopoiesis and biological transmethylations: action of S-adenosylmethionine on protein crasis in chronic hepatopathies]. 109 63

The factors involved in renin release have been extensively evaluated. The primary determinants are the transmural pressure at the afferent arteriole, sodium delivery to the macula densa, and the activity of the adrenergic nervous system. Other possible factors include circulating catecholamines, the serum and cerebrospinal fluid sodium concentration, serum potassium concentration, angiotensin II concentration, and antidiuretic hormone release. There is no convincing evidence that the renin-angiotensin system mediates renal autoregulation. Plasma renin activity is altered in a number of clinical settings. This parameter is elevated in most patients with cirrhosis and the nephrotic syndrome as well as in individuals with severe congestive heart failure. Despite inappropriately large weight gains, plasma renin suppresses normally with increased salt intake in edematous patients who have a normal glomerular filtration rate. The mechanisms of the alteration in the renin-angiotensin system in Bartter's syndrome is still not clear.
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PMID:Renin and the kidney. 110 Oct 89

Plasma renin activity and aldosterone metabolism were investigated in patients with cirrhosis and refractory ascites. All patients initially showed marked elevations of plasma and renin activity and plasma aldosterone. Although metabolic clearance of aldosterone was reduced, increased secretion rate was the major factor leading to elevated plasma levels. The elevated plasma renin activity and plasma aldosterone were only minimally affected by posture, dietary sodium restriction, and diuretic administration, suggesting a near-maximal degree of secondary aldosteronism. In most patients plasma renin activity and plasma aldosterone returned to normal when spontaneous natriuresis appeared. However, in 2 patients during spontaneous diuresis and in all 3 given aminoglutethimide, sodium excretion was poorly correlated with plasma renin activity and plasma aldosterone, suggesting that other tubular and/or vascular factors are important in the intense sodium reabsorption found with cirrhosis and ascites.
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PMID:Studies of renin and aldosterone in cirrhotic patients with ascites. 115 87

The hepatorenal syndrome following right hemiphepatectomy is reported in a previously healthy patient who sustained a shotgun wound in the abdomen. In spite of the development of severe oliguric renal insufficiency and the administration of massive amounts of volume expanders and furosemide, the urine sodium concentration remained very low, therby excluding the diagnosis of acute tubular necrosis. Although severe hyperbilirubinemia developed, the prothrombin time was only slightly abnormal and the liver doubled in size in the 2 weeks after surgery. The study of functional renal failure in patients with liver disease other than decompensated cirrhosis and with significant preservation of hepatic function may suggest that factors other than a circulating toxin participate in mediating the hepatorenal syndrome.
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PMID:Hepatorenal syndrome following hemihepatectomy. 126 Nov 3

Previous studies from this laboratory have demonstrated that the redistribution of blood volume and concomitant central hypervolemia induced by water immersion to the neck (NI) results in a significant natriuresis, kaliuresis, and diuresis. The NI model was utilized to assess the role of "effective volume" and hyperaldosteronism in the impairment of sodium and water handling in cirrhosis. Eleven cirrhotic patients were studied twice while in balance on a 10 mEq. Na, 100 mEq. K diet: control and NI. The conditions of seated posture and time of day were identical. UNaV was constant throughout C, ranging from 1 to 2 muEq per minute. During NI, UNaV increased progressively from 1 +/- 1 (S.E.M.) during the prestudy hour to 89 +/- 32 muEq per minute during hour 5 of NI (p less than 0.02), greatly exceeding the comparable value found in normal subjects on an identical diet. (See article).
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PMID:Determinants of deranged sodium and water homeostasis in decompensated cirrhosis. 127 Aug 90

1. Dogs with bile-duct ligation retain salt and water and form ascites. The present study was under-taken to examine the role of haemodynamic factors in the aetiology of this sodium retention. 2. Haemodynamic studies were performed in five dogs before and 5 weeks after bile-duct ligation. 3. After the operation there was an insignificant fall in mean arterial pressure, a significant rise in mean cardiac index and significant fall in mean total peripheral resistance. 4. It is concluded that heart failure is not a factor in renal sodium retention of the dog with bile-duct ligation, since the central venous pressure was not elevated. 5. The haemodynamic pattern and the tendency to salt retention in the dog with chronic bile-duct ligation closely resemble findings reported in patients with cirrhosis of the liver, and it is suggested that oedema formation in patients with cirrhosis of the liver and dogs with chronic bile-duct ligation shares a common aetiology.
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PMID:Haemodynamic studies in dogs with chronic bile-duct ligation. 127 59


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