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)

Kidney and liver diseases induce alterations in drug binding to plasma proteins. These alterations are caused by qualitative and quantitative changes of plasma proteins and the presence of endogenous substances which act as competitive inhibitors of drug binding to plasma proteins. These changes are the most prominent in nephrotic syndrome and uremia among kidney diseases and in cirrhosis among liver diseases. The more important drugs in which the free fraction is changed in these entities are listed in the tables. The changes in drug distribution caused by plasma protein alterations may induce significant changes in entire drug pharmacokinetics. Discussed are theoretically expected and experimentally proven changes in plasma proteins in kidney and liver diseases and their influence to drug action and dosing regimen.
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PMID:[Changes in plasma proteins and drug distribution in kidney and liver diseases]. 817 1

The radiographic appearance of intestinal edema, including colonic edema, has been well described in the literature. Severe wall circumferential thickening can occur within the colon in a number of conditions. This includes edema secondary to colitis, allergy, ischemia, and infiltrative neoplastic processes. Edema may be secondary to low protein levels, as from protein losing enteropathy, nephrotic syndrome, and hepatic cirrhosis. The following case, in which there was severe ascending colonic wall thickening due to edema, is unusual in two respects: it had well-developed demonstrated "protective" right colonic varices and a normal protein level.
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PMID:CT demonstration of ascending colon varices. 818 Aug 60

We previously studied fibrinolysis and fibrinogenolysis by analyzing fragments of fibrin/fibrinogen degradation products (FDP) employing sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting. In this report, we characterized the fragments of FDP in three patients with increased serum FDP, that were caused by various diseases. In the patient suffering from tuberculous constrictive pericarditis (case 1), the most part of the FDP fragments were DD and D. In the patient suffering from infection in addition to liver cirrhosis (case 2), the most part of the FDP fragments were high molecular weight (HMW) and D. In case 1 and 2, serum FDP levels were increased in parallel with the elevations of CRP levels. Although DD and HMW fragments were remarkably increased in case 1 and 2 with our immunoblotting analysis, DD levels assayed with LPIA system were much lower than FDP levels. The reason this discrepancy was explained by the observation that affinities of the monoclonal antibody used in LPIA system with DD and HMW fragment were markedly lower than that to DD-E fragment. In the patient suffering from deep vein thrombosis probably caused by steroid therapy of nephrotic syndrome (case 3), the most part of detected FDP fragments were DD and HMW in the period when APTT was shorter than normal, whereas D was mainly observed in the period when APTT was normal. In case 3, FDP and DD levels were increased in parallel with the shortening of APTT. In these non-DIC patients, increased serum FDP levels were induced by the presence of ascites and/or pleural effusion plus infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Studies on the fragments of FDP in 3 non-DIC patients with increased FDP levels in the sera]. 836 Oct 25

A case of spontaneous bacterial peritonitis (SBP) developed in an old man whose ascitic fluid was related neither to portal hypertension nor nephrotic syndrome, but with severe hypoalbuminemia emerged after a massive bleeding from a gastric ulcer in a malnutrition state. Ascitic fluid, increasing day by day, yielded Enterobacter cloacae and Bacteroides fragilis. Though autopsy was not carried out because of refusal of his family, neither liver necropsy, nor abdominal CT scan nor repeated abdominal ultrasonography showed findings suggesting existence of liver cirrhosis. In the presence of his ascites, the extent of a chemiluminescence (CL) response of polymorphonuclear cells from volunteers was significantly lower than that of his serum. This report shows that SBP can develop in a patient with ascites unrelated to portal hypertension when ascitic fluid induces little CL response.
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PMID:[A case of spontaneous bacterial peritonitis with ascites caused by hypoproteinemia after a massive bleeding from a gastric ulcer]. 845 Feb 77

The possibility of open tubular capillary electrophoresis for clinical diagnostic use is examined. Capillary electrophoresis was performed in an untreated 50 microns (i.d.) x 100 cm (65 cm to detector) capillary with detection of absorbance at 200 nm. Conditions for the separation of serum proteins without adsorption to the capillary surface were established. Quantitative analyses of serum samples from 38 patients with liver cirrhosis, nephrotic syndrome, or polyclonal gammopathy by capillary electrophoresis were done and the results were compared with those by conventional agarose gel electrophoresis and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. All samples were analyzed in duplicate. We evaluated linearity of response, within-run CV, and the correlation between capillary electrophoresis and agarose gel electrophoresis.
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PMID:Quantitative analysis of serum proteins separated by capillary electrophoresis. 847 68

The specific renal effect of diuretics is due to the fact that their concentrations is almost 100-fold greater in the renal tubule than in the plasma. The function of the different segments of the nephron may be altered following changes in the effective arterial blood volume (EABV) and the extracellular fluid volume (ECFV). In diseases with reduced EABV, e.g., congestive heart failure, decompensated cirrhosis of the liver, and the nephrotic syndrome, proximal tubular hyperreabsorption of sodium occurs, leaving only a low Na+ load in the distal segments of the nephron, the site of diuretic action. Clinically, the response to diuretics is reduced or resistance to diuretics may even ensue, which can be predicted by a FENa < 0.2%. Resistance to diuretics can be overcome by short-term comedication with acetazolamide, which increases Na+ delivery to the site of action of the other diuretics used concomitantly. In states with increased ECFV, e.g. in chronic renal failure, there is distal tubular Na+ rejection, leading to a greater increase in FENa the more GFR is reduced. The remaining intact nephrons present a relatively increased response to diuretics. The efficacy of diuretic treatment in renal failure can be optimised by combining loop diuretics with thiazides. In conclusion, low-dose combination therapy, inducing "segmental blockade of the nephron", meets the functional changes along the nephron. It is therefore more effective and safer than high-dose monotherapy.
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PMID:Low-dose segmental blockade of the nephron rather than high-dose diuretic monotherapy. 848 49

Proximal and distal sodium reabsorption values were calculated from lithium clearance in 63 patients with renal diseases, 13 cirrhotic patients with ascites and 12 control subjects. In the patients with renal diseases, fractional excretion of lithium (FELi) and fractional proximal reabsorption of sodium (FPRNa) were not changed in patients whose glomerular filtration rate (GFR), was over 30 mL/min, but FELi was increased and FPRNa was decreased when the GFR was lower than 30 mL/min. Moreover, fractional distal reabsorption of sodium (FDRNa) was decreased in patients whose GFR was under 40 mL/min. These results indicate that proximal tubular function is well adapted to the degree of renal function even if the etiologies of renal diseases are different. Five patients with nephrotic syndrome (minimal change type) were subjected to lithium clearance method before and after steroid treatment. FPRNa in nephrotic patients was reduced after the treatment, though there was no significant difference in FDRNa. In cirrhotic patients, FELi, FPRNa and FDRNa did not differ from the values in the control subjects, which were not influenced by the decrease in GFR. Thus, the reduction of FPRNa with GFR which was observed in renal disease, was absent in liver cirrhosis. In conclusion, these data indicate that renal adjustment of sodium excretion in chronic renal disease at first takes place in the distal parts of the nephron and later in the proximal tubule, and in addition, that in appropriate reabsorption of sodium from the proximal tubule probably plays a role in ascites formation in cirrhotic patients.
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PMID:[Clinical assessment of renal proximal tubular function using lithium clearance method]. 870 17

Characteristics of renal sympathetic nerve activity in conscious rats with established congestive heart failure, cirrhosis, or nephrotic syndrome were analyzed using three methods: mean integrated voltage over time, power spectrum analysis, and sympathetic peak detection analysis. Compared with control rats, all three disease models had increased mean integrated voltage. On power spectrum analysis, all three disease models had increased relative power at the heart rate frequency, indicating that it was related to renal sympathetic nerve discharge coupled to the cardiac cycle. Congestive heart failure and nephrotic syndrome rats showed increased relative power in the low-frequency range, whereas cirrhotic and nephrotic syndrome rats showed decreased relative power in the high-frequency range. On sympathetic peak detection analysis, the frequency of sympathetic peaks was greater in the three disease models compared with the control rats. In cirrhotic rats, the distribution of sympathetic peak heights was shifted toward an increased number of peaks of lesser height. It is concluded that basal renal sympathetic nerve activity is chronically increased in these disease models. This is manifest as increased power coupled to the cardiac cycle, which may reflect the disease-specific defects in arterial and cardiac baroreflex control. In cirrhosis, there is possible selective activation of a subgroup of renal sympathetic nerve fibers.
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PMID:Characteristics of renal sympathetic nerve activity in sodium-retaining disorders. 876 Feb 33

Resistance to the natriuretic action of atrial natriuretic peptide (ANP) is a hallmark of states of pathological sodium retention including congestive heart failure, cirrhosis of the liver, and nephrotic syndrome. A variety of mechanisms including reduced delivery of filtrate to ANP-sensitive sites in the inner medullary collecting duct and diminished receptor density in this tubular segment have been offered to account for this resistance. Recent studies in experimental nephrotic syndrome and in liver disease produced by ligation of the common bile duct in rats suggest that increased activity of cyclic guanosine 3',5'-monophosphate (cGMP) phosphodiesterase may be an important mediator of renal resistance to ANP. Such increased enzyme activity rapidly catabolizes the second messenger cGMP, normally formed when ANP interacts with its biologically active natriuretic peptide. A receptors, thereby leading to blunted ANP responsiveness. This increased phosphodiesterase activity offers a novel approach to the management of clinical conditions associated with sodium retention and edema formation.
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PMID:Phosphodiesterases (PDEs) hydrolyze the 3' phosphoester bond of the purine 3',5'-cyclic monophosphates, cAMP and cGMP. 876 Feb 35

Resistance to the natriuretic action of atrial natriuretic peptide (ANP) is a hallmark of states of pathological sodium retention including congestive heart failure, cirrhosis of the liver, and nephrotic syndrome. A variety of mechanisms including reduced delivery of filtrate to ANP-sensitive sites in the inner medullary collecting duct and diminished receptor density in this tubular segment have been offered to account for this resistance. Recent studies in experimental nephrotic syndrome and in liver disease produced by ligation of the common bile duct in rats suggest that increased activity of cyclic guanosine 3',5'-monophosphate (cGMP) phosphodiesterase may be an important mediator of renal resistance to ANP. Such increased enzyme activity rapidly catabolizes the second messenger cGMP, normally formed when ANP interacts with its biologically active natriuretic peptide A receptors, thereby leading to blunted ANP responsiveness. This increased phosphodiesterase activity offers a novel approach to the management of clinical conditions associated with sodium retention and edema formation.
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PMID:Phosphodiesterase activity as a mediator of renal resistance to ANP in pathological salt retention. 876 Feb 36


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