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)

D-penicillamine (DPA) leads to side effects in different ways: collagen and elastin crosslinking are inhibited, which results in thin and vulnerable skin, cutis laxa, elastosis perforans serpiginosa, wound healing defects and embryopathy. Toxic influences effect thrombo- and leukocytopenia (incidence 5-15%), gastrointestinal disturbances (10-30%), changes or loss of taste (5-30%), loss of hair (1-2%), and partly proteinuria (5-20%). Acute hypersensitive reactions include DPA-allergy (2-10%). Severe adverse effects are autoimmune phenomena such as pemphigus, DPA-induced lupus erythematosus, polymyositis/dermatomyositis, membranous glomerulopathy and hypersensitivity pneumonitis (like Good-pasture's syndrome) and myasthenia (all less than 1%). In addition there are a number of rare side effects, often single observations. Risk factors include a genetic disposition (especially HLA-B8 and -DR3), poor sulphoxidizers and, to a certain degree, higher age. During pregnancy and in clinically relevant disturbances of bone marrow, liver and renal function DPA is contraindicated. The total incidence of side effects amounts to 30-60%, the withdrawal rate is 20-30%; therefore clear indications and a regular survey of DPA therapy are necessary.
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PMID:[D-penicillamine--side effects, pathogenesis and decreasing the risks]. 306 3

When captopril was first introduced, it was used in high doses for severe hypertension, often in the presence of renal insufficiency, and side effects such as proteinuria, rash, neutropenia, and altered taste sensation were noted. Upon analysis, these effects were most commonly seen in patients with renal disease, autoimmune disease, or collagen vascular disease. These complications usually reversed rapidly upon discontinuation of treatment. In contrast, the growing use of the angiotensin converting enzyme inhibitors, captopril and enalapril, for treating mild to moderate hypertension and the trend toward the use of lower doses has shown these agents to be well tolerated with a low frequency of troublesome adverse effects. In fact, the original spectrum of adverse effects has virtually disappeared with the use of lower doses in patients with uncomplicated hypertension. In low doses, the converting enzyme inhibitors produce remarkably few incidences of symptomatic discomfort; the most common is skin rash, which often responds to dosage reduction. Cough and rare occurrences of angioedema have also been reported. Moreover, evidence is evolving that indicates that the converting enzyme inhibitors may sometimes decrease proteinuria and improve renal function; these effects may be especially important in diabetic hypertensive patients. Of note, these drugs can also attenuate the unwanted metabolic side effects of concurrent diuretic treatment.
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PMID:Safety issues during antihypertensive treatment with angiotensin converting enzyme inhibitors. 306 5

Diabetic nephropathy due to glomerulosclerosis develops in 40% of patients with type I diabetes (in type II the incidence is only around 5%). Two mechanisms are of pathogenetic importance: hemodynamic changes with glomerular hyperfiltration leading to glomerulosclerosis and proteinuria, and biochemical alterations of the glomerular basement membrane consisting of an increase and glycosylation of collagen IV as well as a decrease in negatively charged proteoglycans and sialic acid. Diabetic nephropathy runs through several stages, the first being characterized by hyperfunction and hypertrophy. The appearance of microalbuminuria after 10-15 years of diabetes seems to be a good indicator of the later development of clinically overt nephropathy with large urinary protein losses and decreasing renal function. Successful treatment of hypertension may slow the decrease of renal function. For those patients who have reached terminal renal failure, the treatment modalities of hemodialysis, continuous ambulatory peritoneal dialysis (CAPD) and renal transplantation offer a reasonable chance of prolonging life, although the results are generally less good than in non-diabetic renal patients of the same age group. However, the ultimate goal of therapy must remain the successful prevention of the devastating late sequelae of diabetes, including diabetic nephropathy.
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PMID:[Early recognition of and treatment possibilities in diabetic nephropathies]. 308 5

Antibodies directed against tubular brush border antigens (RTE) are used to induce heterologous immune-complex nephritis. Among these antigens a glycoprotein with a molecular weight of 330 kilodaltons (gp330) has been shown to be of pathogenetic significance. We investigated whether antibodies other than those directed against gp330 are present in anti-RTE and whether they play a pathogenetic role. By using enzyme-linked immunosorbent assay techniques and Western blotting, we investigated polyclonal antibodies directed not only against crude RTE but also against RTEgp, a purified glycoprotein fraction of RTE, with respect to activity against glomerular basement membrane (GBM) components laminin, fibronectin, and type IV collagen. Both antibody preparations showed reactivity predominantly to the 220 kilodaltons subunit of laminin. Lower but nevertheless distinct reactivity to fibronectin and type IV collagen was also found. The antibody fraction directed against components of the GBM, which was isolated from anti-RTE IgG by affinity chromatography, showed linear binding to the GBM in indirect immunofluorescence studies. Injection of these antibodies into the renal artery also led to linear binding to the GBM with linear deposition of complement factors 3 and 9 and induced a weak and transient proteinuria. Immunoelectron microscopy revealed binding of the antibodies to glomerular epithelial and endothelial cell surfaces adjacent to the GBM. Injection of anti-RTE antibody absorbed to GBM components resulted in binding of antibodies and complement factors 3 and 9 in a fine granular pattern along the GBM, whereas injection of unabsorbed anti-RTE led to a course granular pattern. We conclude that the presence of antibodies (cross-)reacting with laminin, fibronectin, and type IV collagen in anti-RTE antibody has pathogenetic effects and could explain differences in pathogenicity between monospecific anti-gp330 antibody and polyclonal anti-RTE antibody.
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PMID:Antibodies to purified renal tubular epithelial antigens contain activity against laminin, fibronectin, and type IV collagen. 327 61

Relapsing polychondritis (RP) is a multisystem autoimmune disease characterized by the presence of antibodies to type II collagen. This collagen is found predominantly in cartilaginous tissues, vitreous humor, aorta and notochord. Involvement of the kidney is rare, only 7 cases having been recorded, and there is no type II collagen in glomeruli. Six of the previous cases had crescentic glomerulonephritis. We report here two cases of biopsy proven RP in which IgA nephropathy was seen, the first examples recorded. Both patients had hematuria and slight proteinuria, with mild impairment of renal function. The histological and immunofluorescence pattern on both biopsies was in keeping with IgA nephropathy. Both patients received steroids with diminution/disappearance of hematuria and proteinuria. In view of the potentially progressive nature of glomerular disease with RP, the renal status should be investigated in all patients with RP.
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PMID:IgA nephropathy in relapsing polychondritis. 328 8

A two-year-old child with the clinical stigmata of nail-patella syndrome, congenital urinary tract anomalies and proteinuria underwent renal biopsy. Electron microscopy revealed characteristic electron lucent areas and collagen fibril-like deposits in the glomerular basement membrane. Of special interest, electron dense deposits were seen in subendothelial areas of the capillary loops and immunofluorescent staining was striking, particularly for IgM, in a peripheral capillary loop pattern.
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PMID:Renal histopathology of the nail-patella syndrome in a two-year-old boy. 336 66

In order to investigate the effect of cadmium-metallothionein (Cd-MT) on renal reabsorption of collagen metabolites, urinary excretion of hydroxylysine (Hyl), glucosyl-galactosyl-Hyl (Glc-Gal-Hyl), galactosyl-Hyl (Gal-Hyl), and hydroxyproline (Hyp), which are unique collagen metabolites, was determined in rats. Administration of Cd-MT resulted in acute renal failure in the form of proteinuria, aminoaciduria and glycosuria. Protein content in urine was greatly increased 1 day after injection of Cd-MT and decreased from 5 days, while the maximum levels of excretion of amino acids and glucose were observed at 6 days post-injection. The urinary excretion of total Hyp and Hyl, including Glc-Gal-Hyl, Gal-Hyl and free Hyl, were significantly increased at 3, 6 and 8 days after injection of Cd-MT with the maximum level at 6 days. Moreover, the molar ratio of Glc-Gal-Hyl/Gal-Hyl of urine in the Cd-MT-treated group was almost the same as that in the controls. These results suggest that a portion of Hyp, Hyl and its glycosides is normally reabsorbed from the renal tubule in the controls, and Cd-MT exposure caused an increase in urinary excretions of Hyp and Hyl, including its glycosides, through a renal tubular defect in reabsorption of Hyl in the same manner as with common amino acids.
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PMID:Increased urinary excretion of collagen metabolites in cadmium-metallothionein nephropathy. 343 83

A proliferative glomerulonephritis was induced in rats pre-immunized with rabbit IgG by injecting intravenously a sub-nephrotoxic dose of rabbit anti-glomerular basement membrane (GBM) IgG (A rats). Most rats (80%) developed a severe proteinuria (greater than 100 mg/24 hr) within two to five days after the injection of anti-GBM IgG. At the same time, microscopic examination of the kidneys revealed a glomerular infiltration by mononuclear phagocytes and a prominent decrease in the intensity of the colloidal iron reaction in glomeruli. A non-proliferative glomerular disease was induced in another group of rats (B rats) by intraperitoneal administration of aminonucleoside of puromycin. A marked proteinuria (greater than 100 mg/24 hr) occurred after six days in 90% of animals. Histochemical studies then revealed a decrease in staining intensity of glomeruli for polyanion. No glomerular hypercellularity was noted. In normal rats and in non-proteinuric A or B rats, the 24 hour urinary excretion of neutral proteinases ranged from 1.4 to 7.8 units (mean value +/- SEM, 4.69 +/- 0.60, N = 11), that of laminin ranged from 100 to 3,900 ng (mean value +/- SEM, 1,154 +/- 325, N = 10), and that of type IV collagen ranged from 160 to 420 ng (mean value +/- SEM, 306 +/- 26.5 ng, N = 8). In proteinuric rats from groups A (N = 11) and B (N = 9), the 24 hour urinary excretion of neutral proteinases significantly increased (mean values +/- SEM, 38.55 +/- 8.66 U for A rats and 42.17 +/- 7.92 U for B rats) and ran parallely with that of proteins, laminin and type IV collagen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary excretion of neutral proteinases in nephrotic rats with a glomerular disease. 355 Feb 15

The teratogenic effects of the dioxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) have previously been studied in several species, and hydronephrosis has been reported to be a frequent abnormality in near-term fetuses. C57BL/6N female mice, given 12 micrograms/kg TCDD, P.O., on day 10 of gestation were killed on days 14, 15, and 16; fetal kidneys were collected and prepared for either immunofluorescent localization of several extracellular matrix components (ECM) or transmission electron microscopy (TEM). The TCDD-treated and control kidneys showed the same pattern of staining for fibronectin, but TCDD-treated kidneys displayed a diminished overall intensity. The intensity of laminin and type IV collagen immunofluorescence also appeared to be decreased, and deviations in the pattern of antibody binding were detected for differentiating TCDD-treated nephrons. Binding of the laminin antibody to the basal lamina was decreased in the parietal layer of Bowman's capsules in more advanced stages of differentiation. TEM analysis focused on the basal lamina of the tubules and Bowman's capsule. In TCDD-exposed kidneys, ECM components adjacent to differentiating nephrons were less abundant, and the basal lamina of the developing Bowman's capsules had a diminished lamina densa. The earliest nephrons to develop display these defects and comprise the first functional filtration units of the metanephric kidney. These ultrastructural changes noted in TCDD-exposed nephrons may promote proteinuria, a condition normally observed in the developing kidney when the filtration barrier is immature.
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PMID:TCDD alters the extracellular matrix and basal lamina of the fetal mouse kidney. 362 14

The aim of the present study was to find out whether the basement-membrane proteins laminin and type IV collagen are involved in the development of aminonucleoside-induced nephrosis. These proteins were measured by specific radioimmunoassays in serum, urine and kidney-cortex samples, and they were localized in the glomeruli by indirect immunofluorescence. Nephrosis was induced in rats with a single intraperitoneal injection of puromycin aminonucleoside. Serum laminin concentrations, detected by a radioimmunoassay for the P2 domain of the protein, increased to reach a maximum at days 5-7, and they remained elevated until at least day 14. The increase preceded the development of proteinuria, suggesting a role for laminin in glomerular function. Concomitant with proteinuria, increasing amounts of laminin antigenicity were also found in the urine. The size of the laminin antigen in serum was estimated by gel filtration, and the serum forms were found to contain both the P1 and the P2 regions of the intact laminin molecule. On the other hand, there were no changes in the serum or urinary concentrations of type-IV-collagen-derived antigens, as detected by a radioimmunoassay for the 7S collagen domain of this protein. The total content of laminin in kidney cortex, measured after digestion of the tissue with trypsin and collagenase, was, at day 9, still comparable with normal values, and the distribution of both basement-membrane proteins in the glomeruli, studied by indirect immunofluorescence, was similar to that in the controls. The tissue damage induced by aminonucleoside, however, seems to stimulate collagen biosynthesis, as the activities of prolyl 4-hydroxylase, lysyl hydroxylase and galactosylhydroxylysyl glucosyltransferase in kidney tissue increased significantly, with maxima at days 8-10.
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PMID:Effects of experimental nephrosis on basement-membrane components and enzymes of collagen biosynthesis in rat kidney. 388 96


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