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

A patient with Goodpasture's syndrome is described in whom pulmonary manifestations were dramatic, but in whom renal abnormalities were minor and only found on fluorescent and electron microscopy. His urine showed no proteinuria and no increase in cells in quantitative counts, and renal function was normal. It is suggested that there may be an indication for carrying out renal biopsies in patients with idiopathic pulmonary haemosiderosis and that this may lead to an early diagnosis of Goodpasture's syndrome.
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PMID:Goodpasture's syndrome: normal renal diagnostic findings. 109 Feb 23

Plasma lipoprotein distribution and apolipoprotein concentrations, as well as kidney function and histopathology of heart, aorta, liver and kidney were investigated in 1-year-old Nagase analbuminemic rats (NAR) and control Sprague-Dawley rats (SDR). The NAR, particularly the females, were found to be severely hyperlipidemic. Plasma total cholesterol in non-fasted animals was 6.1 +/- 0.3 mM in the female NAR vs. 2.5 +/- 0.2 mM in the female SDR (P less than 0.01). Most of the cholesterol was located in the LDL (1.019-1.063 g/ml) and HDL2 (1.063-1.125 g/ml) density range. Plasma triglycerides were 6.1 +/- 0.6 mM in the female NAR vs. 1.3 +/- 0.3 mM (P less than 0.01) in the female SDR. Plasma phospholipids were raised up to 5.4 +/- 0.3 mM vs. 2.4 +/- 0.1 mM (P less than 0.01). NAR have increased concentrations of plasma apolipoproteins A-I (about 3-4-fold) and B (about 2-fold), but the levels of apolipoproteins A-IV and E are not increased. There was less proteinuria in the male NAR than in the male SDR (P less than 0.01). Relevant histopathological findings in the NAR included hepatocytic lipofuscinosis and hemosiderosis in Kupffer cells. Tubular lesions were more common in kidneys from NAR than from SDR, and included protein casts, cortical lipofuscinosis, proximal tubular hyperplasia and proliferative interstitial nephritis. Glomerular changes were similar in both strains. Calcinosis of the aortic media and the corticomedullary region of the kidney was characteristically present in the female SDR but absent in the female NAR. Atherosclerotic lesions were not observed. In summary, 1-year-old NAR maintained on standard rat chow, are hyperlipoproteinemic. The increased levels of plasma LDL and HDL cholesterol are not associated with an increase in the incidence or severity of atherosclerotic or glomerular lesions.
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PMID:Hyperlipoproteinemia in one-year-old analbuminemic rats. 187 8

Hemolytic disease characterized by slight anemia, reticulocytosis, hemosiderosis, extramedullary hematopoiesis, and positive indirect antiglobulin (Coombs') tests and renal disease with proteinuria, hypoalbuminemia, and glomerular lesions were produced in Swiss mice by neonatal intraperitoneal inoculation of cell-free filtrates prepared from the spleens of old NZB/Bl mice. Lymphoid cell and plasma cell hyperplasia as well as hypergammaglobulinemia occurred in some of these inoculated mice. Type "C" murine oncogenic virus-like particles, indistinguishable from those previously described (1), were shown by electron microscopic study to be present in distinctive locations, notably in the basal foldings of convoluted tubules in the kidneys of a newborn NZB/Bl mouse, old NZB/Bl mice, a CBA x NZB F(1) hybrid mouse, and a Swiss mouse inoculated with NZB/Bl spleen cell-free filtrate. These observations point to two (perhaps related) circumstances which may be requisites for the pathogenic action of this newly discovered virus within and outside the strain NZB: infection of newborn, or infant, mice; persistent, possibly tolerant, infection of adult mice.
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PMID:Immunopathology of NZB/BL mice. VI. Virus separable from spleen and pathogenic for Swiss mice. 602 47

The chronic administration of captopril to Sprague-Dawley rats was performed under the barrier system by feeding ad libitum with mixed diet in various concentrations of captopril with 3 months recovery period. The number of animals was 180 female and 180 male including 5 groups of control, 30, 100, 300 and 900 mg/kg/day. The maximum nontoxic dose was estimated as about 30 mg/kg/day for male but a little more than this for female rats. Body weight increase was significantly reduced in male but for the first 3 months in female rats. No death was ascribed to the toxic effect of captopril. Polydipsia and polyuria in male, and the significant increase in values of BUN and inorganic phosphate in both sexes were observed. The reduction in erythrocyte count, values of hemoglobin and hematocrit, hemosiderosis in reticulum cells of the spleen and Kupffer cells in the liver and the increase of erythropoieses indicated hemolytic anemia. Heart weight reduced while kidney weight increased. Pathological examination revealed hypertrophia and hyperplasia of JG cells and thickening of walls of afferent arterioles with hyperplasia of vascular smooth muscle cells and increase of collagen fibers. Thickening of walls extended to walls of the interlobular arteries which remained after withdrawal of captopril for 3 months though JG granules attenuated. The age-related increases of incidences of proteinuria and myocardial fibrosis were attenuated dose-dependently which are probably due to hypotension induced by captopril.
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PMID:[Twelve month studies on the chronic toxicity of captopril in rats]. 627 84

The transgenic SAD mouse which expresses a modified sickle hemoglobin, Hb SAD, displays in vivo hemoglobin polymerization and erythrocyte sickling. In the presence study functional and morphological renal analyses were performed in SAD mice in order to compare the renal pathology of SAD mice with the human disease. The SAD mice display renal hemosiderosis, microvascular occlusions, vascular thrombosis, cortical infarcts and papillary necrosis. In the medulla, hemoglobin polymers could be observed with infrequent erythrocyte sickling, which may explain the absence of significant renal concentration defect, whereas in humans, the difference in the vascularization network leads to more extensive sickling. Most animals develop glomerular hypertrophy and mesangial sclerosis which increases in frequency and severity with age. The glomerular damage is associated with functional defects, including increased blood urea nitrogen levels and non-selective proteinuria. The glomerular lesions of SAD mice strikingly mimic sickle cell glomerulosclerosis, the most severe renal complication of sickle cell disease in humans. In summary, the SAD mouse is a valuable model of the thrombotic and glomerulosclerotic complications of human sickle cell glomerulopathy and can serve for pathophysiologic studies, and, eventually, for prevention and therapy investigation.
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PMID:The transgenic SAD mouse: a model of human sickle cell glomerulopathy. 785 92

Anti-basement membrane antibody (anti-BM Ab) mediated disease is reported to be a rare disorder frequently leading to severe deterioration of renal function. It was our purpose to work out parameters necessary to predict the outcome reliably and to examine, who will benefit most from therapy. Data from 35 patients were evaluated retrospectively. Diagnosis was based on the detection of linear IgG staining (n = 28) along the glomerular basement membrane (GBM) in renal biopsies and/or on the demonstration of anti-BM Ab both by ELISA and immunoblotting (n = 35). Patients were followed up for at least 6 months. Several variables were analysed as to whether they are appropriate prognostic factors. Twenty patients (57%) presented with Goodpasture's syndrome, 13 (37%) had anti-GBM glomerulonephritis alone, whereas two patients suffered solely from pulmonary haemosiderosis. Frequent initial symptoms were haemoptysis (n = 18), haematuria (n = 26), proteinuria (n = 26) and elevated serum creatinine (n = 27). Among all, 10 patients improved, having stable renal function. Twenty-one patients developed end-stage renal failure and four died. Parameters indicating a poor prognosis were a serum(s)-creatinine greater than 600 mumol/l and crescent formation in more than 50% of the glomeruli on renal biopsy. By combining these two parameters the outcome could be reliably predicted. The initial antibody titre and cigarette smoking were without predictive value. In conclusion, the earlier therapy starts, the better will be the result. Patients presenting early with a serum creatinine < 200 mumol/l and without severe glomerular alterations gained the most benefit from therapy, indicating that outcome may be improved by early diagnosis.
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PMID:Course and prognosis of anti-basement membrane antibody (anti-BM-Ab)-mediated disease: report of 35 cases. 808 49

A 46-year-old man was admitted to our clinic because of acute heart failure. Six years before admission he was pointed out cardiomegary and hematuria. One year later, he was diagnosed as having jugular foramen syndrome. On admission, he had a fever and dyspnea. Pansystolic blowing murmur was audible at the apex. The chest ratio on his chest X-ray was 52.5%. An electrocardiogram showed left ventricular hypertrophy. An echocardiogram showed marked dilatation and severe dysfunction of left ventricle. Radionuclide scanning with technetium 99 m pyrophosphate identified inflammatory change in the apex. Myocardial biopsy showed fibrotic degeneration and IgG deposits in myocardium. Blood examination showed anemia, lymphopenia. positive anti-nuclear antibody (1000 times, shaggy pattern), positive anti ds-DNA antibody and hypocomplementemia. Furthermore, proteinuria was pointed out. Renal biopsy showed focal segmental glomerulonephritis with active necrotizing lesion (type III nephritis). Lupus myocarditis and nephritis was diagnosed. After prednisolone (80 mg/day) was administered. left ventricular function and hypocomplementemia improved. The ACE inhibitor was also used for proteinuria. In spite of a little amount of blood transfusion, he showed hepatic hemosiderosis. We suspect that the cause of hemosiderosis was related chronic inflammation of active lupus. It was treated with Erythropoietin.
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PMID:[A case of lupus myocarditis and nephritis with transient foramen jugular syndrome]. 939 74

In beta-thalassemia, profound anemia and severe hemosiderosis cause functional and physiological abnormalities in various organ systems. In recent years, there have been few published studies demonstrating proteinuria, aminoaciduria, low urine osmolality, and excess secretion of the tubular damage markers, such as urinary N-acetyl-D-glucosaminidase (U(NAG)) and beta2 microglobulin, in patients with thalassemia. The object of this study was to analyze renal tubular and glomerular function in pediatric patients with beta-thalassemia and to correlate the renal findings to iron overload. Thirty-seven patients with beta-thalassemia major and 11 with thalassemia intermedia were studied. Twelve children without iron metabolism disorders or renal diseases served as a control group. No difference in blood urea nitrogen (BUN), serum creatinine, creatinine clearance, electrolytes, fractional excretion of sodium and potassium, and tubular phosphorus reabsorption was found. Serum uric acid was equal in the two groups, but its urine excretion was significantly higher in the thalassemic group. U(NAG) and U(NAG) to creatinine ratio (U(NAG/CR)) were elevated in all patients with thalassemia compared with the control group (p < 0.001) and were directly correlated to the amount of transfused iron but not to actual ferritin level. We found that renal tubular function is impaired in children with beta- thalassemia major and intermedia. It is not known whether these functional abnormalities would have any long-term effects on the patients. Further studies are needed, and means of preventing these disturbances should be sought.
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PMID:Renal function in children with beta-thalassemia major and thalassemia intermedia. 1858 Nov 45

The prevalence of chronic infection with the hepatitis C virus (HCV) in patients with chronic kidney disease is higher than in the general population. The estimated prevalence is 13% in haemodialysis, with wide variations geographically and between units in the same country. A liver biopsy is a useful tool for deciding whether to start antiviral therapy and to exclude concomitant causes of liver dysfunction. Examples of this include non-alcoholic fatty liver disease, whose incidence is on the rise, and haemosiderosis, which may affect the progression of the disease and determine the response to antiviral therapy. In addition, the transjugular approach can be used to measure the hepatic venous pressure gradient and confirm the existence of portal hypertension. Chronic hepatitis due to HCV has been shown to reduce survival in haemodialysis, renal transplantation and graft survival. It is the fourth leading cause of death and the leading cause of post-renal transplantation liver dysfunction. HCV behaves as an independent risk factor for the occurrence of proteinuria; it increases the risk of developing diabetes mellitus, de novo glomerulonephritis and chronic allograft nephropathy; it leads to a deterioration in liver disease and causes a greater number of infections. An increased frequency of fibrosing cholestatic hepatitis has also been described which, together with the rapid evolution to cirrhosis, can significantly increase morbidity and mortality and lead to the need for liver transplantation. In addition, immunosuppression in renal transplantation predisposes a reactivation of HCV. However, as the pharmacokinetics of interferon and ribavirin is impaired in kidney failure and their use has adverse effects on function and graft survival, a combination therapy must be limited to non-transplanted individuals with an estimated glomerular filtration rate greater than 50ml/min, and with the interferon being used as monotherapy in dialysis. The fact that a quarter of HCV-positive patients evaluated for a renal transplant have bridging fibrosis or cirrhosis in the liver biopsy may renew renal pre-transplant treatment planning.
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PMID:Management of HCV infection in chronic kidney disease. 2195 30

Sickle cell disease is the most common inherited blood disorder in the United States. The primary driver of pathology is microvascular occlusion which affects multiple organ systems including the kidney. The renal pathology usually manifests as hematuria, proteinuria, or microalbuminuria, and up to 10% of individuals with homozygous sickle cell disease (HbSS) develop renal failure over their lifetime. At ultrasound, the most common finding is increased size with mild variation in echogenicity of the renal parenchyma. We report the ultrasound appearance of a case of acute sickle cell nephropathy with markedly abnormal, enlarged, and echogenic kidneys due to intravascular hemolysis and hemosiderosis, confirmed by biopsy. Knowledge of this potential presentation of sickle cell nephropathy may help aid in earlier diagnosis of renal complications and avoidance of unnecessary renal biopsies.
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PMID:An unusual ultrasound appearance of renal hemosiderosis in acute sickle cell nephropathy. 3176 62


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