Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although IgA nephropathy (IgA N) is reportedly the most common form of primary glomerulonephritis worldwide, there is a very low incidence of IgA N in Black Americans, and IgA N in Black patients with renal allografts has not been reported. In this report, we present the case of a Black patient with endstage renal disease presumed secondary to hypertensive nephrosclerosis who developed nephrotic range proteinuria due to IgA N in a cadaveric renal allograft 2 years following transplantation. Biopsy of the allograft in the immediate post-transplantation period had revealed no evidence of IgA N. Chronic active hepatitis related to hepatitis C preceded the development of proteinuria by approximately 1 year, raising the possibility that IgA N in the renal allograft was secondary to the liver disease. The clinical and histological features of primary IgA N and IgA N secondary to liver diseases are discussed.
 ...
PMID:Immunoglobulin A nephropathy in a renal allograft of a black transplant recipient. 141 57

In this work, 180 golden hamsters were infected with Schistosoma mansoni and 30 hamsters matched for age and sex served as controls. According to the number of injected cercariae, infected hamsters were divided into six main groups (20, 50, 100, 150, 200 and 250 cercariae). Each group was divided into five subgroups, according to the duration of infection after which animals were sacrificed (4, 6, 8, 12 and 24 weeks). Control and infected hamsters were subjected to laboratory evaluations (serum creatinine, blood urea nitrogen, cholesterol, albumin, total protein and urine protein concentration) and histopathologic examinations of kidney and liver tissues. A significant proteinuria, hypoalbuminemia and hypercholesterolemia was observed in schistosome infected (50 cercariae or more) but not in the controls and the group infected with 20 cercariae. There was significant correlation between these changes and duration of infection and the number of adult worm recovered from the mesenteric circulation at the end of the experiments. Histopathologic evaluation showed appearance of the circulating schistosome antigens, circulating anodic antigen (CAA) and circulating cathodic antigen (CCA), and of IgG glomerular deposits by the 6th week following infection; mesangial hypercellularity appeared early after infection (6-8 weeks), renal amyloid deposition appeared later (8-12 weeks). Egg antigens were not detected in the renal glomeruli. There was a significant correlation between the pathologic changes and duration of infection and the number of recovered adult worms from the mesenteric circulation. No histopathologic lesions were detected in controls and the group injected with 20 cercariae. A significant correlation was found between hepatic periportal fibrosis, amyloidosis and immune complex, deposition in the renal glomeruli. Hamsters did not tolerate infection with 150 cercariae or more for more than 12 weeks, and 20 cercariae caused no detectable glomerular disease. From this study, we concluded that S. mansoni infection causes nephropathy in the Syrian golden hamster. The disease became biochemically and histopathologically manifest by the 6th week following infection. Both immune complex deposition and renal amyloidosis stand as major pathogenic mechanisms. CAA and CCA are the major responsible antigens. Hepatic disease has an impact on the kidney lesion. 50 cercariae are the best dose to produce disease without early death of the animal. There is a significant correlation between the kidney disease and the duration and the load of S. mansoni infection.
 ...
PMID:Schistosoma mansoni nephropathy in Syrian golden hamsters: effect of dose and duration of infection. 194 25

Six patients with histologically proven HBsAg-negative chronic active hepatitis (CAH), who were initially treated successfully with prednisolone with or without azathioprine, developed unacceptable adverse effects due to prednisolone. In all six patients the liver disease relapsed on reduction of the prednisolone dose and they subsequently entered a trial of low dose D-penicillamine. Two of the patients required early withdrawal of D-penicillamine and a third patient, who had a good clinical and biochemical response initially, developed heavy proteinuria at 14 months. In the remainder, D-penicillamine was well tolerated and the liver disease satisfactorily controlled permitting reduction of the prednisolone dose to 2.5 mg daily. We conclude that in this subgroup of patients with HBsAg-negative CAH and major prednisolone-induced adverse effects, D-penicillamine is an effective alternative therapy although side effects are common.
 ...
PMID:D-penicillamine therapy in patients with HBsAg-negative chronic active hepatitis and major prednisolone-induced adverse effects. 229 22

Severe hepatotoxicity from phenobarbital occurred in an infant boy who had a complicated illness with chronic bilateral subdural hematomas and sepsis. Skin rash began after 2 weeks of treatment, and signs of hepatocellular failure developed 3 weeks after phenobarbital had been started. Signs of severe liver disease included elevated aminotransferases, conjugated hyperbilirubinemia, significant coagulopathy, hepatosplenomegaly and ascites. Other features of this adverse drug reaction were unremitting fever, leukocytosis with eosinophilia and atypical lymphocytosis, and proteinuria. Sepsis, viral hepatitis, and metabolic liver disease were excluded. The child was on no other medication and had been previously well. In-vitro rechallenge of the patient's lymphocytes with cytochrome P-450 generated metabolites of phenobarbital showed extensive cytotoxicity compared to control. These data support the hypothesis that a defect in drug detoxification was responsible for the child's susceptibility to this drug hepatotoxicity.
 ...
PMID:Phenobarbital hepatotoxicity in an 8-month-old infant. 233 96

Four previously healthy children presented in a 6-week period with marked hypoproteinemia without liver disease, malnutrition, or significant proteinuria. They all had strikingly similar radiographic findings consisting of enlarged folds confined to the fundus and body of the stomach. Three of the children had prodromal symptoms suggesting a viral illness. Cytomegalovirus was cultured from the urine in all cases and from the gastric biopsy specimens in three patients. Two of these patients also showed intranuclear inclusions in their biopsy specimens compatible with cytomegalovirus. It is not certain if cytomegalovirus was the cause of the illness.
 ...
PMID:Pediatric hypertrophic gastropathy. 302 Sep 54

Familial LCAT deficiency is due to deficiency of plasma lecithin-cholesterol acyltransferase. The plasma is rich in free cholesterol and lecithin while cholesterol ester and lysolecithin levels are reduced. Analysis of the abnormal lipoproteins has helped our understanding of plasma lipid and lipoprotein metabolism in normals and in patients with liver disease. Proteinuria and anaemia are common and there is marked corneal lipid deposition. Eventually renal function deteriorates and dialysis and/or renal transplantation may be necessary. The human LCAT gene has been sequenced and been shown to be present on chromosomal segment 16q22-the region predicted on the basis of recombination studies as the site of the LCAT deficiency gene. The gene defect has been identified in some cases, but the mechanism remains unclear as the mutations were not in the region presumed to be the enzyme's active site. Only three cases of fish-eye disease have been described; all were elderly and had obvious corneal opacities. They had fasting hypertriglyceridaemia and increased VLDL. IDL and LDL were increased and were triglyceride rich. HDL, reduced by 90%, was mainly HDL3--with a high free and low ester cholesterol. LCAT activity in fish-eye plasma was normal but when measured in an exogenous substrate it was only 10-15% of normal. Fish-eye HDL is a substrate for purified LCAT, but fish-eye LCAT does not esterify free cholesterol of HDL (normal or fish-eye), although it esterifies free cholesterol of VLDL and LDL. It has been suggested that one type of LCAT activity acts on HDL (alpha-LCAT) and another on VLDL and LDL (beta-LCAT)--and that fish-eye disease is due to alpha-LCAT deficiency, and classical familial LCAT deficiency due to lack of both components.
 ...
PMID:Familial LCAT deficiency and fish-eye disease. 314 86

Except for infections (pyelonephritis, abscess of the kidney), which cause symptoms such as pyuria, pain and fever, most diseases of the renal parenchyma were unknown in Greek and Roman antiquity. Even in the Renaissance they were not yet properly identified. Edema was generally thought to be related to liver disease. Proteinuria was discovered at the end of the 18th century. In 1827 Bright provided the first, almost complete clinical description of the various forms of acute and chronic glomerulonephritis and showed that they were accompanied by macroscopic changes in the kidneys. Between 1850 and 1885, Frerichs, Klebs and Langhans described the primary glomerular lesions. The amount of new knowledge acquired during the 20th century has been tremendous, and covers the mechanism of urine formation, the role of sodium retention in edematous states, the physiology and physiopathology of the renin-angiotensin-aldosterone system, the glomerular origin of the nephrotic syndrome, new methods of investigation, progress in histology and immunology, the discovery of many tubular syndromes, the introduction of antibiotics and antihypertensive drugs, and the development of dialysis and transplantation.
 ...
PMID:[On the history of kidney disease]. 355 Oct 58

Heparin cofactor II (HC II) levels were measured by electro-immunoassay in healthy volunteers, and patients with liver disease, DIC, proteinuria or a history of venous thrombosis. Analysis of the data in 107 healthy volunteers revealed that plasma HC II increases with age (at least between 20 and 50 years). HC II was found to be decreased in most patients with liver disease (mean value: 43%) and only in some patients with DIC. Elevated levels were found in patients with proteinuria (mean value 145%). In 277 patients with a history of unexplained venous thrombosis three patients were identified with a HC II below the lower limit of the normal range (60%). Family studies demonstrated hereditary HC II deficiency in two cases. Among the 9 heterozygotes for HC II deficiency only one patient had a well documented history of unexplained thrombosis. Therefore the question was raised whether heterozygotes for HC II deficiency can also be found among healthy volunteers. When defining a group of individuals suspected of HC II deficiency as those who have a 90% probability that their plasma HC II is below the 95% tolerance limits of the normal distribution in the relevant age group, 2 suspected HC II deficiencies were identified among the healthy volunteers. In one case the hereditary nature of the defect could be established. It is concluded that hereditary HC II deficiency is as prevalent among healthy volunteers as in patients with thrombotic disease. Further it is unlikely that heterozygosity for HC II deficiency in itself is a risk factor for the development of venous thrombosis.
 ...
PMID:Hereditary heparin cofactor II deficiency and the risk of development of thrombosis. 360 11

This study reviews liver disease in toxemia of pregnancy based on 102 cases submitted to the Armed Forces Institute of Pathology. The common clinical features were right upper quadrant and epigastric pain, nausea, vomiting, and elevation of the serum transaminases. Jaundice occasionally developed. These occurred in severe preeclampsia or eclampsia and their cause was usually recognized. However, hepatic symptoms and signs did result in inappropriate diagnoses and misdirected therapy. Such confusion occurred when these were the initial problems confronting the clinician in women presenting with advanced toxemia due to poor prenatal care. They were also likely to be misleading when other more classic parameters, such as blood pressure and proteinuria, were only midly abnormal. Central nervous system complications were the common cause of death but liver disease could be partially or wholly responsible. Extensive periportal lesions, hepatic hematomas, spontaneous rupture, and infarction all contributed to hepatic injury and to morbidity. Fibrin deposition, hemorrhage, or both in the periportal areas was characteristic of the histopathology. Scanning electron microscopy validated this spectrum of change. A toxemic vasculopathy related to severe vasospasm in the hepatic arterial circulation may be responsible.
 ...
PMID:Liver disease in toxemia of pregnancy. 378 23

Using enzyme-linked immunosorbent assay technique (Boehring Institute Laboratory), eighty-one adult patients were studied for hepatitis Bs antigenaemia. Nine of the patients had asymptomatic persistent proteinuria, thirty-nine, nephrotic syndrome, and thirty-three had profuse proteinuria, azotoaemia and hypertension. The histopathology obtained in forty showed twenty-two with MCGN, four with focal glomerulosclerosis, three with proliferative glomerulonephritis, one with minimal change glomerulonephritis and ten with end-stage kidney disease. None of the patients had apparent clinical evidence of liver disease nor a past history of jaundice. One hundred and eighty apparently normal adults served as controls; 33.3% of the patients had positive hepatitis Bs antigenaemia, in contrast to 6% (P less than 0.001) in the normal controls. Hepatitis Bs antigenaemia was more prevalent in the groups with nephrotic syndrome and persistent asymptomatic proteinuria than in the group with advanced renal failure. Hepatitis Bs antigenaemia was detected in all histopathologic forms but was most prevalent in the MCGN (P less than 0.001) which is also the more commonly encountered lesion. The implications of these findings are discussed.
 ...
PMID:Role of hepatitis Bs antigen in chronic glomerulonephritides in Nigerians. 608 37


1 2 3 4 5 6 7 Next >>