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

Tubular handling of sodium and phosphate were studied in 4 patients with cirrhosis and ascites. The control group consisted of 5 patients with cirrhosis without sodium retention. The degree of phosphaturia was assumed to reflect proximal tubular reabsorption. Whereas fractional excretion of phosphate was comparable in both groups, fractional excretion of sodium was strikingly diminished in the patients with ascites. This observation suggests that sodium retention in these patients occurs beyond the proximal tubule. This interpretation is in accord with our previous observation, based on clearance data, that the proximal tubular reabsorption of sodium in cirrhosis may be normal even in the face of edema formation.
Nephron 1978
PMID:Tubular handling of sodium and phosphate in cirrhosis with salt retention. 62 15

A 62-year-old woman gave clinical manifestation of liver cirrhosis. Urinary protein was false positive, no uremia was found and renal changes were entirely overlooked. Deposition of abundant lipids (globoside and ceramide trihexoside) was found in the kidneys; essentially degenerative changes of the tubular epithelia were noted. These renal changes were compared with those in Fabry's disease.
Nephron 1975
PMID:Renal accumulation of glycosphingolipids. Report of a case and a review of literature. 80 60

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.
Nephron 1975
PMID:Renin and the kidney. 110 Oct 89

Carbon tetrachloride (CCl4) was intraperitoneally injected into Balb/c mice 4 times at biweekly intervals, and the morphological changes of the liver and kidney were examined during 12 weeks after the last injection. The renal injuries progressed in spite of cessation of CCl4 treatment; microcysts with tubular-cell degeneration were manifest on day 42 after the last injection of CCl4. At the end of the experiment, however, interstitial fibrosis with inflammatory cell infiltration was much more prominent. Glomerular changes with IgG deposits also developed following the tubulointerstitial changes. The CCl4 treatment induced liver damage as well, but it promptly subsided without formation of cirrhosis. The CCl4 nephrotoxicity was completely inhibited by whole body irradiation (200 rad) exposed at each injection of CCl4. In contrast, the hepatic damage was not changed by irradiation. These results seem to indicate etiologic independence of renal and hepatic events induced by CCl4 treatment. It is also suggested that chronic CCl4 nephrotoxicity is mediated, at least in part, by radiosensitive responses of the mice themselves.
Nephron 1992
PMID:Study on chronic renal injuries induced by carbon tetrachloride: selective inhibition of the nephrotoxicity by irradiation. 173 17

We examined endotoxins and limulus amebocyte lysate-reactive material (LAL-RM) in serum from 87 patients on hemodialysis, using the conventional chromogenic limulus test (CCLT) and a new specific endotoxin assay with factor G-free LAL (endotoxin-specific test: EST). All patients with regenerated cellulose dialyzers had increased CCLT values, whereas the EST values were not higher than in controls. This discrepancy can be explained by the LAL-RM which is cellulose-derived and cross-reacts with LAL via factor G. Using EST for measurements of endotoxin, 6 patients out of 87 had pathological endotoxemia and all of these patients were associated with either cirrhosis, infection, or malignancy. Some patients who had no complications showed fever before or during dialysis, but they did not have high endotoxin levels. EST is useful for the diagnosis of endotoxemia in patients on hemodialysis because of the presence of LAL-RM in serum. Endotoxemia is rare in patients on hemodialysis, if they are not associated with infection, cirrhosis, or other complications.
Nephron 1990
PMID:Endotoxemia in patients on hemodialysis. 223 48

A 41-year-old hemodialyzed woman developed ascites and was found to have secondary iron overload. The dose of administered iron was approximately 11-12 g, and her serum ferritin level was 15,000 ng/ml (15,000 micrograms/l). There were no signs of congestive heart failure, fluid overload, or liver cirrhosis. A program of weekly phlebotomy combined with recombinant human erythropoietin (rhEPO) therapy was tried to eliminate the iron congestion. After 9 months of this therapy, about 5 g of iron had been removed. The ascites completely disappeared, and her serum ferritin level fell to 5,800 ng/ml (5,800 micrograms/l). This suggests that such combined therapy would be useful when iron overload must be corrected rapidly. Before therapy, the sterile ascitic fluid showed exudative characteristics with 3.7 g/dl (37 g/l) of total protein. The serum-ascites albumin difference was 0.6 g/dl (6 g/l), and the fluid contained 1,400 inflammatory cells/mm3 (1.4 X 10(9)/l). Notably, the serum-ascites albumin difference increased in parallel with iron elimination. These findings suggested that iron deposition may have played a role in changing the permeability of the peritoneum, or in impairing lymphatic drainage, both of which are presumed to be pathogenetic factors of nephrogenic ascites.
Nephron 1990
PMID:Treatment of a patient with end-stage renal disease, severe iron overload and ascites by weekly phlebotomy combined with recombinant human erythropoietin. 236 36

The urinary excretion of aldosterone, kallikrein and prostaglandin E2 (PGE2) was studied in sodium-retaining (RC) and nonretaining (NRC), nonascitic cirrhotic rats, under basal conditions and after an oral sodium load (5 mmol). The glomerular synthesis of PGE2 was measured in RC rats under the same conditions. Both groups of cirrhotic animals showed a decreased urinary excretion of PGE2. Isolated glomeruli of RC rats produced less PGE2 than those of the control animals, both under basal conditions and after the sodium load. The NRC group was the only one able to increase the urinary excretion of kallikrein in response to the sodium load. These findings could contribute to explain the early physiopathological events of hepatic cirrhosis.
Nephron 1988
PMID:Urinary excretion and glomerular synthesis of prostaglandin E2 and prostaglandin F2 alpha in cirrhotic, non-ascitic rats: the effects of sodium overload. 316 14

In 5 patients with cirrhosis and ascites the glomerular filtration rate (GFR), free water clearance (CH2O) and urinary excretion of prostaglandin E2(PGE2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured before and after a 3-day treatment with sulindac (400 mg/day). The administration of sulindac induced a marked fall of urinary excretion of PGE2 (from 24.2 +/- 5.5 to 3.8 +/- 1.1 ng/h; p less than 0.05), 6-keto-PGF1 alpha (from 19.9 +/- 2.9 to 5.6 +/- 1.1 ng/h; p less than 0.02) GFR (from 111 +/- 15 to 67 +/- 10 ml/min; p less than 0.01) and CH2O (from 7 +/- 1.5 to 3.7 +/- 1.3 ml/min; p less than 0.02) in all patients studied. The plasma concentration of the active metabolite sulindac sulfide in cirrhotics was 400% of that found in 6 healthy volunteers (9.6 +/- 1.7 vs. 2.4 +/- 0.6 ng/ml). Our results indicate that sulindac, at a dose of 400 mg/day, inhibits the renal synthesis of prostaglandins and impairs renal function in cirrhotics with ascites. These effects are probably related to the marked alteration of sulindac kinetics that occurs in these patients.
Nephron 1986
PMID:Sulindac reduces the urinary excretion of prostaglandins and impairs renal function in cirrhosis with ascites. 351 19

An anuric ESRD patient on chronic hemodialysis with liver cirrhosis and refractory ascites was treated with ultrafiltration followed by head-out water immersion (HWI) and a new period of ultrafiltration. Despite anuria and the absence of peripheral edema, 4 h of HWI significantly raised the central venous pressure, diminished the abdominal girth by 5%, and successfully transfered at least 2.4 liters of ascitic fluid to the intravascular space made available to ultrafiltration. Dialysis or ultrafiltration alone were not effective in removing this amount of fluid or in reducing ascites.
Nephron 1986
PMID:Water immersion in an anuric cirrhotic patient. 371 43

We have suggested that cirrhotic patients with high uric acid clearances had an increased effective vascular volume. This hypothesis was tested by studying the relationship between the excretion of uric acid, sodium, potassium, and aldosterone in cirrhosis. In 29 consecutive cirrhotic patients, of whom 17 had ascites, and in a control group, the logarithm of urinary sodium and aldosterone excretion highly correlated in control (r = -0.79, p less than 0.001) and cirrhotic patients without (r = -0.72, p less than 0.01) and with (r = -0.80, p less than 0.001) ascites. The regression line significantly shifted to the left in the cirrhotic patients (p less than 0.001). The urinary ratio K/K + Na also correlated with urinary aldosterone in controls (r = +0.66, p less than 0.001) and in cirrhotic patients (r = +0.77, p less than 0.001); this regression line shifted to the right in cirrhosis patients (p less than 0.02). The fractional uric acid excretion significantly correlated with urinary aldosterone only in cirrhotic patients (r = -0.76, p less than 0.001). These data confirmed the existence of hypoaldosteronism in many cirrhotic patients and are consistent with tubular hypersensitivity to aldosterone and emphasize the major role of the effective vascular volume in the control of urid acid clearance in cirrhosis.
Nephron 1986
PMID:Relationship between aldosterone and sodium, potassium, and uric acid clearance in cirrhosis with and without ascites. 378 85


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