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

Little is known about the effect of posture on the circulatory abnormalities of advanced cirrhosis. We evaluated the systemic hemodynamics, measured by Doppler-echocardiography, atrial natriuretic factor, plasma renin activity and plasma norepinephrine, in 10 patients with cirrhosis and ascites and 10 healthy controls, after 2 h of standing and during lying down for a further 2 h. Standing hemodynamic patterns of controls and patients with cirrhosis did not differ significantly. The latter, however, showed higher plasma renin activity, norepinephrine and atrial natriuretic factor. The assumption of the supine position led to greater increases in cardiac index and atrial natriuretic factor, and reduction in systemic vascular resistance in patients with cirrhosis. Norepinephrine and plasma renin activity declined in both groups to a similar extent, while heart rate only slowed in controls. Thus, after 2 h in the supine position, patients with cirrhosis showed hyperdynamic circulation with increased cardiac index and heart rate and reduced systemic vascular resistance. Norepinephrine, plasma renin activity and atrial natriuretic factor were also elevated. The hyperdynamic circulation in advanced cirrhosis appears during or is enhanced by lying down. This finding suggests that this syndrome is, at least in part, attributable to excessive blood volume translocation towards the central area. However, the persistent activation of renin-angiotensin and sympathoadrenergic systems suggests that a concomitant reduced vascular sensitivity to vasoconstrictors concurs in its development.
 ...
PMID:Hyperdynamic circulation of advanced cirrhosis: a re-appraisal based on posture-induced changes in hemodynamics. 760 82

In order to elucidate a participation of intact parathyroid hormone (PTH(1-84)) in blood pressure (BP) and body fluid homeostasis, we studied fluctuations of PTH(1-84) during manipulations of BP in hyperparathyroid and healthy subjects, and during manipulations of blood volume in patients with glomerulonephritis or liver cirrhosis and in controls. Angiotensin II induced BP elevation was associated with increased values of PTH(1-84) both in healthy subjects (12-25 ng l-1, medians, p < 0.01), in patients with primary hyperparathyroidism (94-125 ng l-1, p < 0.01), in patients with low calcium due to end stage renal disease before requirement of dialysis (95-151 ng l-1, p < 0.02), and in patients with tertiary hyperparathyroidism (221-264 ng l-1, p < 0.05), but not in dialysis patients without hypercalcaemia (126-174 ng l-1, NS). The changes could not be attributed to reduction of serum calcium, but probably to the increase of plasma angiotensin II, which was positively correlated to the increase of serum PTH(1-84) in the healthy subjects (p = 0.619, n = 15, p < 0.05) and in the patients with primary hyperparathyroidism (p = 0.549, n = 18, p < 0.05). Noradrenaline induced BP elevation did not have a similar effect on PTH(1-84), and changes of PTH(1-84) were not related to changes of BP. Volume depletion after furosemide injection, also accompanied by increased levels of angiotensin II, resulted in elevation of PTH(1-84) in controls, cirrhotics, patients with glomerulonephritis without the nephrotic syndrome, but not in nephrotic patients. Volume depletion induced by bolus injection of atrial natriuretic peptide (ANP) was associated with decreased PTH(1-84) in healthy subjects (20-18 ng l-1, p < 0.02), but not in patients with nephrotic syndrome and liver cirrhosis. Volume expansion induced by albumin infusion caused increased plasma levels of ANP, but PTH(1-84) was unaltered. Thus, angiotensin II may be able to stimulate, and ANP to inhibit release of PTH(1-84), and PTH(1-84) may be involved in the regulation of BP and body fluid homeostasis. BP changes or changes in blood volume per se do not seem to influence PTH(1-84) levels.
 ...
PMID:Parathyroid hormone in blood pressure and volume homeostasis in healthy subjects, hyperparathyroidism, liver cirrhosis and glomerulonephritis. A possible interaction with angiotensin II and atrial natriuretic peptide. 786 30

This study investigated the relationship between changes in renal sympathetic activity as assessed by renal norepinephrine spill-over and the onset of renal sodium retention in the phenobarbital/carbon tetrachloride model of experimental cirrhosis in rats. In this model, sodium retention occurs when hepatic function, assessed by the aminopyrine breath test (ABT), falls below a critical threshold. Three groups of rats, studied on a constant salt diet, included a group with cirrhosis and sodium retention, a group with cirrhosis of similar duration and no sodium retention and a time-control phenobarbitaltreated group. ABT, renal plasma flow (RPF), glomerular filtration rate (GFR) and mean arterial pressure (MAP) were measured at the time of catecholamine sampling in anesthetized rats. Cirrhosis was associated with reductions in MAP, no change in RPF and GFR, and an ABT below the threshold in rats with sodium retention. In contrast, rats without sodium retention had liver function above the threshold. Renal norepinephrine spill-over increased continuously from controls to non-sodium retaining and sodium retaining animals. The difference between sodium retaining animals and controls was significant. Norepinephrine spill-over correlated to ABT and MAP but not urinary salt excretion. The data suggest that, under these experimental conditions, increased sympathetic activity may contribute to the onset of sodium retention. A plausible explanation for the continuous increase is that catecholamines are released as a compensatory mechanism in response to a primary yet undefined vasodilator.
 ...
PMID:Relationship between oxidative hepatic metabolism, urinary sodium excretion and sympathetic nerve activity in experimental cirrhosis in the rat. 788 79

In patients with cirrhosis and ascites decreased renal blood flow might be related to the severity of liver disease but the relationship between the severity of cirrhosis and renal perfusion has not yet been established. Thus we measured renal, systemic and splanchnic hemodynamics in 63 patients with ascites and in 28 without ascites. When compared to patients without ascites, patients with ascites had lower renal blood flow (1,170 +/- 100 vs. 935 +/- 55 ml/min/1.73 m2; mean +/- SEM, p < 0.05) and renal perfusion pressure (78 +/- 2 vs. 72 +/- 1 mm Hg, p < 0.05 and higher inferior vena cava pressure (6.5 +/- 0.7 vs. 10.7 +/- 0.7 mm Hg, p < 0.05). Patients with ascites had significantly higher serum bilirubin concentrations, hepatic venous pressure gradient and lower serum albumin concentrations, indocyanine green (ICG) extraction than patients without ascites. Renal vascular resistance, glomerular filtration rate, mean arterial pressure, cardiac index and systemic vascular resistance were not significantly different between the two groups. By multiple regression analysis no significant correlation was found between liver tests (i.e., prothrombin time, serum bilirubin and albumin concentrations, ICG extraction), hepatic venous pressure gradient, cardiac index and systemic vascular resistance on the one hand and renal blood flow on the other. No significant correlation was found between glomerular filtration rate and liver tests. In conclusion, in patients with cirrhosis and ascites, renal hypoperfusion is not related to the severity of liver disease.
Nephron 1993
PMID:Renal hemodynamics in patients with cirrhosis: relationship with ascites and liver failure. 828 84

Spontaneous bacterial peritonitis (SBP) is defined as infection of preexisting ascites without evidence for any intraabdominal source for secondary infection. SBP is now recognized with rising frequency and has mainly been reported in patients with alcohol-induced cirrhosis of the liver. We report SBP in a female dialysis patient whose ascites was not due to liver disease, but was possibly due to lupus erythematosus or represented 'nephrogenic ascites'. The patient had severe abdominal pain and a positive rebound phenomenon, fever and an elevated peripheral white cell count of 21,000 cells/microliters. Ascitic fluid analysis revealed an exudate with a protein concentration of 5.2 g/dl, 13,000 white cells/microliters with 94% neutrophils and positive cultures for Streptococcus morbillorum. Because of the dramatic clinical features the patient underwent laparotomy which did not reveal a source for secondary infection and in retrospect was unnecessary. The patient responded well to antibiotic therapy. This case report draws attention to SBP as a cause of acute abdomen in patients on chronic hemodialysis.
Nephron 1993
PMID:Spontaneous bacterial peritonitis in a hemodialysis patient with systemic lupus erythematosus. 779 66

Compared to healthy humans in most patients with cirrhosis and renal sodium and water retention, effects of atrial natriuretic peptide (ANP) on sodium and water excretion are reduced. It has been postulated that this impaired response to ANP is caused by renal vasoconstriction, induced by high levels of angiotensin II. To further investigate this issue, we studied renal hemodynamics (glomerular filtration rate, GFR, single nephron GFR, SNGFR, renal blood flow, RBF) and urinary sodium excretion (UNaV) in rats with CCl4-induced cirrhosis of the liver, before and during ANP infusion. The same parameters were determined in cirrhotic rats after a 4-day pretreatment with the angiotensin-converting enzyme (ACE) inhibitor captopril before and during ANP. Results were compared to those obtained in 2 control groups of healthy rats, one of them pretreated with captopril. Rats with cirrhosis had a significantly reduced GFR, SNGFR, RBF, UNaV and an elevated plasma renin activity compared to healthy controls. ANP caused a significant rise in UNaV (+198%) but no significant change of GFR, SNGFR and RBF in cirrhotic rats. Captopril-pretreated rats with cirrhosis had a significantly higher RBF (+26%) and 24-hour urinary sodium excretion (+52%) but no significant differences in GFR and SNGFR compared to cirrhotic rats without captopril pretreatment. Administration of ANP to cirrhotic rats pretreated with captopril resulted in a significant rise in GFR (+56%), SNGFR (+42%), RBF (+29%) and UNaV (+159%) compared to cirrhotic rats with ANP alone. In healthy rats, there was no additional effect of a combined therapy with captopril and ANP.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephron 1993
PMID:Renal effects of atrial natriuretic peptide in cirrhotic rats with and without captopril pretreatment. 832 62

In order to assess the role, if any, of atrial natriuretic peptide (ANP) and hemodynamic changes in diuretic response to concentrated ascitic fluid reinfusion (CAFR) in cirrhotic patients, we studied 10 patients with liver cirrhosis before and after aspiration, concentration and intravenous reinfusion of their ascitic fluid. Basal ANP levels were higher than in normal subjects, but not related to the degree of water and sodium excretion. CAFR induced a variable degree of ANP changes and diuretic response, and these two parameters were strictly correlated to each other. No major changes of cardiac output and systemic vascular resistances were observed after CAFR. In conclusion, the apparent resistance to ANP diuretic action observed in basal condition in cirrhotic patients seems to revert after expanding blood volume by CAFR.
Nephron 1993
PMID:Atrial natriuretic peptide and hemodynamic changes after concentrated ascitic fluid reinfusion in cirrhotic patients. 841 94

Clinical course and serial liver histology of a patient who developed fatal chronic active hepatitis C after renal transplantation are presented. This patient developed persistently deranged liver biochemistry 3 months after transplantation, despite normal liver enzyme values during the preceding 3 years on hemodialysis. In addition to increased parenchymal enzyme concentrations, the levels of ductal enzymes were also markedly elevated, with peak levels of alanine aminotransferase and gamma-glutamyl transpeptidase 7 and 100 times, respectively, the normal upper limit. The patient was persistently seronegative for hepatitis C virus (HCV) antibodies, but positive for HCV RNA. Treatment with alpha-interferon for 6 months, initiated after the development of early cirrhosis, resulted in no improvement, and the patient died from liver failure 36 months after renal transplantation. Serial liver histology, examined four times from 11 months to 36 months after transplantation, showed progressive deterioration from chronic active hepatitis to cirrhosis. This patient illustrates the uncommon complication of rapidly progressive and ultimately fatal liver disease due to HCV infection after renal transplantation. Early recognition with anti-HCV and HCV RNA assays as well as histologic assessment are crucial for the identification of patients with a poor prognosis who might benefit from therapeutic intervention before irreversible liver damage.
Nephron 1995
PMID:Clinicopathological features of hepatitis C virus antibody negative fatal chronic hepatitis C after renal transplantation. 856 57

A survey of hepatitis B surface antigen (HBSAG) and antibodies against hepatitis C virus (anti-HCV) in 173 patients undergoing hemodialysis in Taiwan revealed that 15 (9%) patients were positive for both HBSAG and anti-HCV, 106 (61%) were positive for anti-HCV alone, and 14 (8%) were positive for HBSAG alone. Most HBSAg positivity was acquired before the onset of hemodialysis. Anti-HCV positivity, however, was mainly acquired via the hemodialysis procedure. Patients with dual markers were younger (43.7 +/- 3.3 years old, p = 0.0274), had the longest period on hemodialysis (6.6 +/- 1.3 years, p < 0.001), and more severe liver dysfunction. When compared with those who were negative for both markers, patients with both HBSAG and anti-HCV had an increased incidence of chronicity (5/15 vs. 2/38; p < 0.05), ultrasonographic cirrhosis (5/15 vs. 1/38; p < 0.05), and clinical decompensation (2/15 vs. 0/38; p < 0.05). Their risk for developing ultrasonographic cirrhosis and clinical decompensation was also greater than that of patients with anti-HCV alone (5/15 vs. 8/106 and 2/15 vs. 2/106; p < 0.05 for both). The presence of HBSAG alone, however, did not increase the incidence of liver dysfunction. The presence of anti-HCV alone was only associated with a greater elevation of serum alanine aminotransferase (44.2 +/- 5.5 vs. 19.1 +/- 2.5 U/l; p < 0.05) and an increased incidence of chronicity (30/106 vs. 2/38; p < 0.05). Our results indicate that a high prevalence of HCV superinfection impose a significant risk on a large population of HBSAG-positive hemodialysis patients in Taiwan. As the coexistence of anti-HCV and HBSAG is associated with more severe liver dysfunction, it is urgent to devise effective methods to prevent HCV circulation in a hemodialysis environment-especially in a hepatitis B virus endemic area such as Taiwan.
Nephron 1996
PMID:Superinfection with hepatitis C virus in hemodialysis patients with hepatitis B surface antigenemia: its prevalence and clinical significance in Taiwan. 877 37

We analyzed 10 patients (male:female 9:1, mean age 64.2 years) who developed hepatocellular carcinoma during the observation period of 2 years among 2,164 chronic hemodialysis patients in 23 dialysis centers. Among them, 409 patients were positive for serum anti-HCV antibodies (19%). They were all positive for serum anti-HCV antibodies but negative for HBs antigen. None of the anti-HCV antibody-negative patients developed hepatocellular carcinoma during this period. Although liver function tests of the patients were almost normal, pathological examination of the liver revealed chronic active hepatitis or cirrhosis. Periodic ultrasonographic examination is necessary for early detection of hepatocellular carcinoma in chronic hemodialysis patients with positive anti-HCV antibodies even if liver function tests are within normal ranges.
Nephron 1996
PMID:Characteristics of anti-HCV antibody-positive patients with hepatocellular carcinoma on chronic hemodialysis: recommendation of periodic ultrasonography for early detection. 889 60


<< Previous 1 2 3 4 5 Next >>