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)

Typing for antigens HLA-A,B,C and DR was performed on 165 rheumatoid arthritis patients (14 black, 151 white) who had received gold therapy to determine the relationship between HLA antigens and gold dermatitis, stomatitis, thrombocytopenia, and proteinuria. Dermatitis and stomatitis occurred in both black and white patients. Thrombocytopenia and proteinuria occurred only among the white patients studied. The absence of thrombocytopenia and proteinuria among the black patients was not statistically significant. Antigen HLA-DR7 was uncommon among black and white subjects with dermatitis (0 of 6 blacks, 4 of 48 whites), but this decrease in frequency was not statistically significant. Antigen HLA-DR3 was an important risk factor for thrombocytopenia (relative risk = 11.8, P = .0043) and proteinuria (RR = 5.8, P = .032). These results are consistent with previous studies of HLA-DR3 and gold toxicity. The only black patient with stomatitis possessed the A1B8DR3 phenotype. Future studies should examine whether the same HLA antigen confers risk of different gold toxicities in different racial groups, and whether there are HLA antigens that provide a protective effect.
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PMID:Immunogenetic and racial determinants of gold toxicity in rheumatoid arthritis. 297 88

To elucidate the natural course of the nephropathy associated with penicillamine and thereby facilitate its clinical management 33 patients with rheumatoid arthritis who developed proteinuria during treatment with oral penicillamine were studied in detail throughout their renal illness. Renal biopsies were performed, and creatinine clearance and proteinuria were measured serially for 74 months (range 16-148 months). Fourteen patients developed proteinuria within six months after the start of treatment and 27 within 12 months. When treatment was stopped the proteinuria reached a median peak of 4.2 g/24 h (range 0.3-15.0 g/24 h) at one month (range 0-7 months) before resolving spontaneously by six months (12 patients), 12 months (21), or 18 months (29). In all patients but one, who developed carcinoma of the renal pelvis, proteinuria resolved by 21 months and its median duration was eight months. The median first and last measurements of creatinine clearance showed no appreciable change (80 ml/min and 78 ml/min), and no patient died from or needed treatment for renal failure. The HLA-B8 or HLA-DR3 alloantigen, or both, were identified in 10 patients. Renal biopsy specimens showed membranous glomerulonephritis in 29 patients, minimal change nephropathy in two, and electron dense deposits in the mesangial regions in two. In all the patients whose nephropathy was due solely to treatment with penicillamine the proteinuria resolved completely when the drug was withdrawn; renal function did not deteriorate, and corticosteroids were unnecessary.
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PMID:Natural course of penicillamine nephropathy: a long term study of 33 patients. 313 18

Ninety-five rheumatoid arthritis patients treated with aurothiomalate and/or D-penicillamine have been studied for possible associations between HLA-A, -B, -DR antigens and various toxic reactions to the above drugs. HLA-DR3 and -DRw6 had a higher frequency in patients with toxic reactions (all types) than in patients without toxic reactions (28.5 per cent vs 13.0 per cent and 26.5 per cent vs 4.3 per cent, chi 2 = 2.6 and 7.2, respectively). HLA-B8 was found at a higher frequency in patients with proteinuria and other types of renal involvement (20.0 per cent vs 7.4 per cent in controls), whereas skin manifestations were mainly associated with the presence of HLA-DRw6. The lowest frequency of side-effects was seen in patients with HLA-DR1 and DR2 (10.2 per cent vs 28.3 per cent and 28.5 per cent vs 54.3 per cent, chi 2 = 3.9 and 5.5, respectively). In addition, seropositive patients possessing HLA-DR1, showed toxic reactions less frequently.
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PMID:HLA-A,-B, and -DR antigens in relation to gold and D-penicillamine toxicity in Greek patients with RA. 313 53

In order to define genetic, immunological and metabolic risk factors and markers associated with diabetic neuropathy (DN) 47 insulin-dependent diabetic patients with neuropathy were compared to 30 age-matched insulin-dependent diabetes mellitus (IDDM) patients without neuropathy. Patients with diabetic neuropathy more often had proliferative retinopathy and Albustix positive proteinuria than patients without neuropathy. Judged by haemoglobin A1 (HbA1) concentrations measured during the preceding two years glycaemic control was worse in patients with than without diabetic neuropathy. The frequency of HLA-antigens DR3, DR4, DR3/DR4, B8, and B15 were increased and those of DR2 and B7 decreased in the diabetic patients. The frequency of any of these HLA-antigens did not differ in patients with or without diabetic neuropathy. There were no significant differences in the frequencies of insulin antibodies or proliferative responses to insulin antigens between patients with or without diabetic neuropathy. However, patients who were HLA-DR3/DR4 heterozygotes and had diabetic neuropathy responded to insulin antigens more often by proliferation than DR3/DR4 positive patients without diabetic neuropathy. Thus poor glycaemic control is associated with an increased risk for diabetic neuropathy. Patients with DR3/DR4 heterozygocity and failing to respond to insulin antigens by proliferation seem to be less prone to develop diabetic neuropathy.
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PMID:HLA-antigens and immunity to insulin in insulin-dependent diabetics with or without diabetic neuropathy. 323 12

Nineteen patients with idiopathic membranous nephropathy were typed for HLA pattern and analyzed for the Fc receptor function of splenic macrophages by detecting in vivo the clearance of IgG-sensitized 51Cr-labelled autologous erythrocytes. Seven out of 19 patients were found to have a macrophage dysfunction. This defect was not related to any HLA-A, B, C, DR, DQ antigen tested nor to the levels of IgG-containing immune complexes, as detected by a Clq solid phase test, nor to the magnitude of proteinuria. Since HLA-B8 and HLA-DR3 antigens were significantly more frequent in patients than in the control group, the factors that may impair the macrophage system in individuals predisposed to this nephropathy are discussed.
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PMID:Failure to relate mononuclear phagocyte system function to HLA-A, B, C, DR, DQ antigens in membranous nephropathy. 347 35

One hundred and forty-one patients with rheumatoid arthritis treated with aurothiopropanol sulphonate or D-penicillamine, or both were examined for HLA antigens to investigate the genetic influence on the occurrence of different adverse reactions during therapy. All 13 patients possessing HLA-DR3 had toxic reactions. The relative risk for DR3 positives of developing skin eruptions or proteinuria was calculated to be 10.5 times and seven times respectively that of DR3 negatives. The incidence of DR7 antigen in 94 patients with toxic reactions was significantly decreased (11% compared with 28% in controls) suggesting a protective role for this antigen.
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PMID:HLA antigens and toxic reactions to sodium aurothiopropanol sulphonate and D-penicillamine in patients with rheumatoid arthritis. 387 81

HLA typing studies were performed on 60 consecutive patients with seropositive definite or classical rheumatoid arthritis (RA). Patients were treated with gold and were followed for a minimum of 18 months for identification of adverse reactions to gold therapy. HLA-DR3 was increased significantly in patients who developed gold induced rash, proteinuria or thrombocytopenia. On the other hand, the incidence of HLA-DR4 was lower in patients with these adverse reactions. Our results demonstrate that patients with RA carrying DR3 are at a higher risk of developing adverse reactions to gold. The most interesting finding was the low incidence of DR4 in patients who developed adverse reactions to gold, suggesting that DR4 positive patients may have some degree of protection against gold toxicity.
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PMID:HLA antigens and toxic reactions to sodium aurothiomalate in patients with rheumatoid arthritis. 623 91

One hundred sixty-two consecutive patients with rheumatoid arthritis (RA) were studied for possible association between HLA antigens, particularly DR antigens, and disease characteristics and adverse reactions to gold or D-penicillamine treatment. The frequency of HLA-DR4 was significantly increased: 62% in RA compared to 23% in controls. An association of HLA-DR4 with a positive family history for RA was also found. HLA-DR4 was not associated with subcutaneous nodules or keratoconjunctivitis, presence of rheumatoid factor, or ANA positivity. No increased prevalence of HLA-DR3 was found in patients who developed drug related toxicity (e.g., proteinuria for gold or D-penicillamine). Of the 27 patients in whom proteinuria developed, only 5 were DR3 positive. A significant association with D-penicillamine induced proteinuria and HLA-B8 gene was found. Our results obtained in a systematic survey do not confirm previous reports of a significant association between HLA-DR3 and drug toxicity, but confirm the association between HLA-DR4 and the development of RA and HLA-B8 and D-penicillamine induced proteinuria.
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PMID:A systematic survey of HLA-A,B,C and D antigens and drug toxicity in rheumatoid arthritis. 637 99

By means of a case-control study we investigated the association between HLA phenotypes and the development of proteinuria after aurothioglucose or D-penicillamine treatment in patients with rheumatoid arthritis (RA). HLA-DR3 was markedly increased in 44 treatment cases compared with 66 RA controls (46 versus 18%, p = 0.002). HLA-DR3 positive patients were at greater risk during treatment with D-penicillamine (RR 10.1, p = 0.001) than gold treated cases (RR 1.7, p = 0.365). The associations between HLA-DR3 and nephrotic syndrome (RR = 6.3, p = 0.004) and early onset proteinuria (RR = 5.4, p less than 0.001) were stronger compared with uncomplicated proteinuria (RR = 3.1, p = 0.017) and late-onset proteinuria (RR = 1.6, p = 0.459), respectively. It appears that genetic factors in RA influence the development, the degree and the time of onset of drug induced proteinuria.
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PMID:HLA-DR antigens and proteinuria induced by aurothioglucose and D-penicillamine in patients with rheumatoid arthritis. 642 May 62

We studied patients with rheumatoid arthritis who have been treated with aurothioglucose (Au) and subsequently with D-penicillamine (DP), and who developed drug-induced proteinuria, over a 10-year period. Twelve patients developed Au-induced and 19 DP-induced proteinuria. Of the 12 patients with Au-induced proteinuria, only 2 (17%) developed DP-induced proteinuria, indicating a slightly increased risk as compared with the overall incidence (9.3%) of this reaction in 168 DP-treated patients. In addition, only a minority (2 out of 19, 10.6%) of patients with DP-induced proteinuria had previous Au-induced proteinuria. These data may indicate that different mechanisms are operative in Au and DP-induced proteinuria, as is also suggested by the finding that HLA-DR3 was present more frequently in the latter (50%) than in the former (21%). A history of previous Au-induced proteinuria is insufficient reason to deny these patients the benefits of subsequent treatment with DP.
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PMID:The relationship between aurothioglucose- and D-penicillamine-induced proteinuria. 644 Dec 48


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