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)

A study of early glomerular lesions was made in 8 patients infected with Schistosoma mansoni but having no clinical evidence of renal disease. Electron-microscopy of renal biopsies showed the presence of electron-dense deposits in basement membranes and of laminated bodies near the mesangial cells. Immunofluorescence showed that the deposits corresponded to IgG in 8 cases and to IgM in 2 cases. These lesions are comparable with those found in the kidneys of patients with cirrhosis of the liver.
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PMID:Kidney biopsy in the hepatosplenic form of infection with Schistosoma mansoni in man. 492 May 46

Although functional renal failure has been reported in patients with malignant disease of the liver, renal haemodynamics and function have not been investigated. Renal and intrarenal blood flow was measured using the (133)Xenon washout technique and creatinine clearances by the standard method in 14 patients with a variety of primary and secondary tumours of the liver in the absence of cirrhosis and without evidence of renal disease. In 11 patients renal and outer cortical blood flow was reduced and this was sometimes accompanied by a reduction in glomerular filtration rate. The pattern of renal circulatory changes was similar to that seen in renal dysfunction associated with hepatic cirrhosis. Possible causes of these disturbances and their significance in relation to the aetiology of functional renal failure in liver disease are discussed.
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PMID:Renal blood flow in malignant disease of the liver. 504 Aug 31

The effects of diseases of the liver, the thyroid, and the kidneys on the retinol-binding protein (RBP)-prealbumin (PA) system responsible for the transport of vitamin A in plasma were examined, using a radial gel diffusion immunoassay for PA and the previously described radioimmunoassay for RBP. Measurements were made on plasma samples from 118 normal subjects, 31 patients with cirrhosis, 5 with chronic active hepatitis, 27 with acute viral hepatitis, 14 patients with hyperthyroidism, 7 with hypothyroidism, and 26 patients with chronic renal disease of varying etiologies. In the patients with liver disease, the levels of vitamin A, RBP, and PA were all markedly decreased and were highly significantly correlated over a wide range of concentrations. Serial samples were available in 19 patients with acute hepatitis; as the disease improved the plasma concentrations of vitamin A, RBP, and PA all increased. In patients with acute hepatitis RBP concentrations correlated negatively with the levels of plasma bilirubin, glutamic-oxaloacetic transaminase, and alkaline phosphatase. In the hyperthyroid patients both RBP and PA concentrations were significantly lower than normal; in hypothyroidism, neither protein showed levels significantly different from normal. In both hyper- and hypothyroidism and in liver disease, the molar ratios of RBP:PA and of RBP:vitamin A were not significantly different from normal.Patients with chronic renal disease had marked abnormalities in the plasma concentrations of RBP and vitamin A and in the molar ratios examined. In renal disease the levels of both RBP and vitamin A were greatly elevated, while the PA levels remained normal. The molar ratios of RBP:PA and of RBP:vitamin A were both markedly elevated. In many patients RBP was present in molar excess as compared with PA. The presence of a relatively large proportion of free RBP, not complexed to PA, in some patients with chronic renal disease was confirmed by gel filtration. The free RBP, present in molar excess, was capable of forming a complex with additional purified PA added to the plasma. The kidneys appear to play an important role in the normal metabolism of RBP.
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PMID:The effects of diseases of the liver, thyroid, and kidneys on the transport of vitamin A in human plasma. 509 25

Fifty-nine case of ascites not due to cardiac or renal disease were subjected to clinical, endoscopic and laboratory investigations, including bacteriology and histopathology. Provisional diagnosis divided the cases into 38 patients with ascites as the main finding, and 21 patients with liver cirrhosis and ascites. After investigation, the final diagnosis was totally different from the provisional in 15 cases. Predominance of tuberculosis of the peritoneum per se or in addition to liver cirrhosis was striking, and its documentation was possible only through laparoscopy and biopsy. Oesophagoscopy, a simple procedure, revealing varices in undiagnosed ascites, points to liver cirrhosis. Laparoscopy confirms the diagnosis and reveals other additional factors for ascites as malignancy or tuberculosis.
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PMID:Endoscopic diagnosis of ascites in Assiut province, upper Egypt. 622 21

The behaviour of prekallikrein (PKK), factor XII, high molecular weight kininogen (HMWK) and kallikrein-inhibitor (KK-I) in 367 patients with various diseases is described. Malignancies lead to elevation of factor XII and KK-I, and reduction of PKK. The effect is more pronounced in patients with metastases. In renal diseases also one or more of the above mentioned parameters are abnormal. Defects requiring dialysis treatment significantly impair the contact factors. In this group low levels of PKK, Factor XII and HMWK and increased KK-I are common. In chronic renal disease patients, only F XII and KK-I are elevated, whereas PKK and HMWK are normal. Kidney transplantation leads to a rise in KK-I and reduction of PKK and HMWK. The values almost normalize few days after the operation. Factor XII, slightly increased immediately after transplantation, remains high in long term transplant recipients, whereas HMWK falls below normal. In liver disease patients, acute and chronic hepatitis, cirrhosis of the liver and coma, PKK is reduced. In cases with acute hepatitis PKK raises with recovery. Cirrhosis and coma lead to low HMWK and factor XII concentrations. KK-I is mostly affected during acute hepatitis, and is then highly increased. Our results clearly demonstrate that the biologic activity of one or more of contact factors is affected in many diseases.
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PMID:Prekallikrein, HMW-kininogen and factor XII in various disease states. 635 59

During the past two decades, the essentiality of zinc for man has been established. Deficiency of zinc in man due to nutritional factors and several diseased states has been recognized. High phytate content of cereal proteins decreases availability of zinc; thus the prevalence of zinc deficiency is likely to be high in a population subsisting mainly on cereal proteins. Alcoholism is known to cause hyperzincuria and thus may play a role in producing zinc deficiency in man. Malabsorption, cirrhosis of the liver, chronic renal disease and other chronically debilitating diseases may similarly induce zinc deficiency in human subjects. A severe deficiency of zinc has recently been recognized to occur in patients with sickle cell anemia and a beneficial effect of zinc therapy in such patients has been reported. Growth retardation, male hypogonadism, skin changes, poor appetite, mental lethargy and delayed wound healing are some of the manifestations of chronically zinc-deficient human subjects. Taste abnormalities, correctable with zinc supplementation, have been observed in uremic subjects. Recently, abnormal dark adaptation related to zinc deficiency in patients with cirrhosis of the liver and sickle cell disease has been reported. In severely zinc-deficient patients, dermatological manifestations, diarrhea, alopecia, mental disturbances and intercurrent infections predominate and if untreated the condition becomes fatal. Zinc deficiency is known to affect testicular functions adversely in man and animals. This effect of zinc is at the end organ level and it appears that zinc is essential for spermatogenesis and testosterone steroidogenesis. Zinc is involved in many biochemical functions. Several zinc metalloenzymes have been recognized in the past decade. Zinc is required for each step of cell cycle in microorganisms and is essential for DNA synthesis. Thymidine kinase, RNA polymerase, DNA-polymerase from various sources and RNA-dependent DNA polymerase from viruses have been shown to be zinc-dependent enzymes. Zinc also regulates the activity of RNase; thus the catabolism of RNA appears to be zinc-dependent. The effect of zinc on protein synthesis may be attributable to its vital role in nucleic acid metabolism. The activities of many zinc-dependent enzymes have been shown to be affected adversely in zinc-deficient tissues. Three enzymes, alkaline phosphatase, carboxypeptidase and thymidine kinase, appear to be most sensitive to zinc restriction in that their activities are affected adversely within three to six days of institution of a zinc-deficient diet to experimental animals.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Zinc deficiency in human subjects. 636 78

In a survey the present possibilities are outlined to get knowledge about diseases of inner organs with the help of enzyme determinations in the urine. Here it is remarkable that changes of the enzyme excretion appear not only in renal disease with acute renal failure, pyelonephritis, glomerulonephritis, renal infarction and nephroptosis but are also to be observed in primarily extrarenal diseases such as diabetes mellitus, hyperthyroidism, thesaurismoses, myocardial infarction, hypertension, acute pancreatitis, epidemic hepatitis, liver cirrhosis, obstructive jaundice and rheumatoid arthritis. The causes of the changes of enzyme excretions are various. Since enzymes of different origin and localisation behave themselves variably, the simultaneous determination of a brush border marker (e.g. alanine aminopeptidase), a lysosomal enzyme (e.g. beta-glucuronidase or N-acetyl glucosaminidase) and a low molecular enzyme (e.g. lysozyme) is of use for the recognition of renal alterations. By the control of activities of urinary enzymes it is possible to get without risk informations about pathobiochemical processes in the kidney which are not to be gained by means of other methods.
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PMID:[Urinary enzyme excretion in diseases of the internal organs]. 636 87

The disposition of tocainide was studied in 15 patients with renal dysfunction. In 9 with total renal failure, the plasma half-life ranged from 16.6 to 42.7 h and total plasma clearance from 35 to 94 ml/min. The longest half-lives were found in 1 patient with cirrhosis, 3 taking the enzyme inhibitor allopurinol, and 1 on cimetidine. The mean half-life in the remaining patients was 22.3 +/- 4.8 h (+/- SD). During a 4 h haemodialysis, the half-life in the 9 patients decreased to 8.5 +/- 4.6 h, which was calculated to correspond to removal of 25 +/- 14% of the drug from the body. In 6 patients with impaired renal function (creatinine clearance 10-55 ml/min) the tocainide half-life ranged from 13.2 to 22.0 h and total plasma clearance from 72 to 122 ml/min. One patient was taking allopurinol and 1 dihydralazine, and the mean half-life in the others was 19.2 +/- 4.0 h. The apparent volume of distribution was similar to that found previously in healthy subjects. The results suggest that tocainide elimination is predictably reduced in patients with renal disease.
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PMID:Pharmacokinetics of tocainide in patients with renal dysfunction and during haemodialysis. 640 48

The administration of nonsteroidal antiinflammatory drugs (NSAID) may induce marked side effects, especially on renal function. Some of these side effects are the consequence of inhibition of prostaglandin (PG) synthesis. Patients who need an increase in PG synthesis to maintain renal function (congestive heart failure, cirrhosis of the liver, preexisting renal disease) appear to be particularly at risk. Regular checks on renal function are mandatory when prescribing NSAID to such patients.
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PMID:[Secondary effects of non-steroid anti-inflammatory agents on kidney function]. 661 81

On the basis of their own experience and data from the literature, the authors warn against the simultaneous administration of diuretic agents and non-steroidal antiinflammatory drugs. Apart from the drastic reduction in the natriuretic effects of some diuretics, this association may lead to acute non-oliguric renal failure in patients with one of the following predisposing factors: volemic depletion, effective circulating volume (cardiac insufficiency, liver cirrhosis), preexisting nephropathy (lupus erythematosus, chronic renal failure), or borderline renal function (geriatric patients, diabetics).
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PMID:[Non-steroid anti-inflammatory agents, diuretics and kidney function: a warning]. 662 43


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