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)

Immunohistologic and electron microscipic studies were performed on the kidneys of rabbits given daily intravenous injections of porcine thyroglobulin in amounts adjusted to the immune response of the individual rabbits. Glomerular lesions were restricted to the mesangium, were characterized by varying degrees of proliferation of mesangial cells and increase of mesangial matrix, and were accompanied by accumulations of rabbit immunoglobulins, C3, and porcine thyroglobulin. Electron-dense deposits were localized to the mesangium and the adjacent subendothelial space. Less than 10 per cent of the animals with mesangila lesions developed obvious impairment of glomerular function. Thyroglobulin-containing immune complexes were found to be rapidly removed from the mesangium, so that overloading of the mesangium and consequent accumulation of complexes in the adjacent capillary loops could not occur. Thus, the results provide further evidence that when immune complex deposition is restricted to the mesangium, relatively little interference with glomerular function results. This situation is paralleled in man by the lesions of subclinical lupus nephritis, chance proteinuria and hematuria, and the early lesions of Berger's disease.
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PMID:Immune complex disease. VII. Experimental mesangiopathic glomerulonephritis produced by chronic immunization with thyroglobulin. 14 59

Hypothyroidism, microscopic hematuria, and proteinuria developed in an 11-year-old girl. A renal biopsy specimen showed increased mesangial cells and matrix with focal glomerular basement membrane thickening. Three years later, a pronounced increase in proteinuria was detected. Elevated levels of antibody to thyroid microsomal antigen and thyroglobulin were found in the serum. A renal biopsy specimen showed a pronounced increase in mesangial cells and matrix with generalized glomerular basement membrane thickening. Electron microscopic studies demonstrated granular deposits in the capillary walls and mesangium. Immunofluorescent studies revealed granular deposits of IgG, IgM, and C3, primarily on the glomerular basement membrane. By indirect immunofluorescence, granular glomerular basement membrane and mesangial staining were detected with antibody specific for thyroglobulin and thyroid microsomal antigen. These observations suggest development of immune complex glomerulonephritis mediated by thyroid antigens.
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PMID:Immune complex glomerulonephritis mediated by thyroid antigens. 15 97

A 60 year old hyperthyroid black woman with long-standing Graves' disease treated with methimazole presented with anasarca and congestive heart failure. She was found to have the nephrotic syndrome with a urinary protein excretion of 32 g/day. Light and electron microscopy revealed a stage II membranous glomerulopathy. Direct and indirect immunofluorescence demonstrated immunoglobulin G (IgG), immunoglobulin M (IgM), third component of complement and thyroglobulin in a granular diffuse pattern consistent with an immune complex glomerulonephritis. Total thyroidectomy led to a decrease in proteinuria with little change in glomerular filtration rate during an 11 month follow-up period. We believe this to be the first report of immune complex glomerulonephritis associated with thyroid antigen in Graves' disease.
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PMID:Thyroid antigen associated immune complex glomerulonephritis in Graves' disease. 58 94

Association between auto-immune dysthyroidism and glomerulonephritis is quite rare. The authors report 3 cases with proteinuria varying from 2.72 to 6.06 g/day and hypothyroidism. Nephrotic syndrome was found in 2 cases and thyroid auto-antibodies (microsomal and thyroglobulin) and circulating immun complexes (C.I.C.) in 1 case, complement fractions C3 and C4 were normal in all cases. Renal biopsy showed membranous glomerulonephritis in 2 cases and minimal lesions in the third case. Proteinuria disappeared with glucocorticoids and thyroxine in 1 case, with thyroxine alone in an other case and persisted in the third case with normal thyroid function.
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PMID:[Primary hypothyroidism and glomerular involvement]. 181 33

We describe a patient with Graves' disease in whom marked proteinuria, microhematuria and hypoalbuminemia were associated. Renal biopsy demonstrated electrondense deposits in the capillary basement membrane, a finding consistent with immune complex glomerulonephritis. Indirect immunofluorescent examination with rabbit antihuman thyroglobulin indicated that these electron-dense deposits were thyroid antigen-mediated immune complexes.
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PMID:Thyroid antigen-mediated glomerulonephritis in Graves' disease. 252 88

Hyperthyroidism, microscopic hematuria, and proteinuria developed in an 11-year-old girl. Proteinuria decreased during treatment of hyperthyroidism with an antithyroid drug. On admission, serum anti-thyroglobulin antibody, antimicrosomal antibody, and immune complex were present. The thyrotropin binding inhibitory immunoglobulin (TBII) level was low. On the other hand, an antibody to the ganglioside component (fucosyl-GM1) was detected by an enzyme linked immunosolvent assay (ELISA). A thyroid biopsy specimen showed massive lymphocytic infiltration and interstitial fibrosis. A renal biopsy specimen showed marked proliferation of mesangial cells and increased mesangial matrix with focal segmental capillary wall abnormality. Electron microscopec studies demonstrated mild paramesangial dense deposits. By indirect immunofluorescence, granular glomerular basement membrane and mesangial staining were not detected with rabbit antibody to thyroglobulin, but were detected with rabbit antibody to fucosyl GM1. Fucosyl GM1 was also seen along the basilar aspect of the thyroid follicular epithelial cells. These observation suggests the development of glomerulonephritis mediated by thyroid antigen, particularly ganglioside component.
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PMID:Thyroid antigen-antibody nephritis: possible involvement of fucosyl-GM1 as the antigen. 331 41

We have investigated the prevalence of proteinuria in patients with Graves' disease and chronic autoimmune thyroiditis attending a routine thyroid clinic. Using the urine protein creatinine index, proteinuria was found in 29.8% of patients with autoimmune thyroid disease and in 9.5% of patients attending the same clinic but without these conditions. When patients with Graves' disease were treated with 131I, proteinuria measured by 24 h collections developed in 9 of 14 patients without pre-existing proteinuria and appeared to diminish in 4 patients in whom proteinuria had been present before treatment. The prevalence and fluctuation of proteinuria was independent of thyroglobulin and microsomal antibody levels. We were unable to confirm previous reports of a high prevalence of circulating immune complexes in autoimmune thyroid disease; complexes were detected in only 7.9% of patients and did not correlate with proteinuria. The causes of mild proteinuria in autoimmune thyroid disease are not apparent, but previous case reports suggesting that membranous glomerulonephritis is associated with Graves' disease, albeit rarely, indicate that immunological mechanisms may be implicated.
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PMID:Proteinuria in autoimmune thyroid disease. 383 19

A 54-year-old woman who had proteinuria due to stage II membranous nephropathy is reported. She was treated with indomethacin for proteinuria and developed drug-induced hepatitis four months later. Liver dysfunction gradually recovered, but hormonal studies revealed abrupt fall of T3 and T4 and concomitant elevation of TSH levels within a month. Pathological findings of thyroid specimen and positive antithyroglobulin and antimicrosomal antibodies were compatible to chronic thyroiditis. In the second renal biopsy, glomerular deposits of thyroglobulin, thyroid microsomal antigens and IgG were demonstrated by immunofluorescence. Therefore, membranous nephropathy in this patient is presumed to be caused by immune complexes mediated by thyroid constituents. We believe that this is a precious case because continuous changes in T3, T4 and TSH were followed in a course of chronic thyroiditis, especially in the stage of progress to hypothyroidism, and the chronic thyroiditis was shown to be involved in the membranous nephropathy.
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PMID:A case of membranous nephropathy associated with thyroid antigens. 706 40

Repeated exposure of Brown Norway (BN) rats to relatively low doses of HgCl2 induces autoantibodies to renal antigens (e.g., laminin) and a membranous glomerulonephropathy characterized by proteinuria. In contrast, Lewis (LEW) rats are "resistant" to the autoimmune effects of mercury and, when exposed to this metal, are protected against experimental autoimmune encephalomyelitis (EAE) and Heymann's nephritis. To date, there is no information on "suppressive" effects of mercury in naturally occurring (so-called "spontaneous") rat models of autoimmune disease. Therefore, we have administered HgCl2 to diabetes-prone (DP) BB rats, animals that spontaneously develop both insulin-dependent diabetes mellitus (IDDM) and thyroiditis. We found that DP rats treated with mercury or water for a period of 40-125 days developed autoantibodies to thyroglobulin, with a higher incidence in HgCl2-injected animals (92% vs. 56% in H2O-injected controls). A novel finding of our study was the detection of autoantibodies to laminin in the same rats, again with an increased incidence after HgCl2 treatment (83% vs. 44%). IgG2a was the most frequently detected isotype of antibodies to laminin, followed by IgG1, IgG2b and IgG2c. The IgG isotype profile suggests that treatment with HgCl2 may activate both Th1 and Th2 lymphocytes in BB rats. In spite of these stimulatory effects on autoantibody responses, we found that there was no difference in the incidence of IDDM and thyroiditis between HgCl2-treated and control animals. We conclude that the suppressive effects of mercury previously observed in EAE and Heymann's nephritis of LEW rats do not occur in "spontaneous" autoimmune IDDM and thyroiditis of BB rats. Therefore, immune suppression caused by HgCl2 cannot be considered a common phenomenon, but may be a genetically determined characteristic of LEW rats, possibly related to a specific or unique cytokine profile of this particular rat strain. In contrast, while mercury does not seem to recruit, induce or rescue regulatory T cell function in DP rats, it does stimulate autoantibody responses in these animals.
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PMID:Effects of HgCl2 on the expression of autoimmune responses and disease in diabetes-prone (DP) BB rats. 955 Feb 85

Several cases of glomerular disease have been associated to thyroid diseases. The most frequent lesion described is membranous glomerulopathy, presented as a nephrotic syndrome. Here we report a 67-year-old man who developed a nephrotic syndrome accompanied by rapid derangement of renal function shortly after the onset of a primary hypothyroidism due to autoimmune thyroiditis. High titers of circulating anti-thyroglobulin and anti-microsomal thyroid antigen antibodies were detected. Serum levels of C3 and C4 fractions of complement were markedly decreased. Renal biopsy showed a membranoproliferative glomerulonephritis with severe mesangial proliferation, a type of glomerular involvement non-described previously in the literature, in relation with thyroid diseases. Four boluses of intravenous steroids were administered, followed by oral prednisone for three months. A dramatic recovery of renal function, together with normalization of urinary sediment, proteinuria decrease and normalization of serum complement were observed. Three years later, the patient suffered from a similar event, with a positive response to steroids again. One year later, the patient had a new recurrence and was treated with mycophenolate mofetil , improving his clinical situation.
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PMID:[Membranoproliferative glomerulonephritis associated with autoimmune thyroiditis]. 1521 68


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