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)

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

One hundred and thirty-two patients with rheumatoid arthritis treated with gold have been studied for possible associations between HLA DR antigens and different adverse reactions occurring during such therapy. Patients possessing HLA DR3 had a significantly greater frequency of side effects than patients lacking this antigen. It was particularly noticed that DR3 positive patients on gold treatment had an 11 times higher risk of getting proteinuria than those without DR3. The lowest frequency of side effects was seen in DR7 positives. No significant differences between the DR antigen groups with respect to skin eruptions, liver reactions, or leucopenia were evident.
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PMID:HLA DR antigens and gold toxicity. 640 93

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

This report describes 2 siblings with IgA nephropathy. Patient No. 1 was a 38-year-old woman with hematuria and proteinuria of 19 years duration. Her blood ABO type was A and Rh positive. She was found to have HLA-A2,Aw24; Bw54 , Bw48 ;Cwl,C-;DR1,DR4. Her renal specimen was diagnosed as the advanced stage of IgA nephropathy histologically. Patient No. 2 was a 41-year-old man who was a brother of patient No. 1. His blood ABO type was O and Rh positive. His serotype for the HLA was found to be HLA-Aw24,A-;Bw35, Bw54 ;Cw1,Cw3;DR4, DRw9 . His renal histology showed the advanced stage of IgA nephropathy. It is suggested that an abnormal immune response linked to gene coding for HLA-DR4 antigen might be involved in the development of IgA nephropathy.
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PMID:IgA nephropathy associated with HLA-DR4 antigen. 643 88

One hundred sixty-eight patients with rheumatoid arthritis treated with chloroquine (n = 87), gold salts (n = 133) and/or penicillamine (n = 77) were investigated for possible associations between HLA antigens and toxic reactions. Patients with 2 or more side effects to gold and/or penicillamine had a significantly increased frequency of antigens HLA-B8 and DR3 compared to patients with one or without adverse reactions. Proteinuria to gold or penicillamine was significantly associated with HLA-B8 (relative risk [RR] 4.2) and DR3 (RR 14.0) whereas nonnephrologic side effects to gold or penicillamine were associated with B7 and DR2 (RR 3.5 and 2.8). Patients with skin reactions to gold had a significantly greater frequency of HLA-B7. We found no correlation between chloroquine side effects and any HLA antigen. The results suggest a genetic predisposition to toxic reactions to gold or penicillamine based on an immunologic dysregulation.
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PMID:HLA antigens and toxicity to gold and penicillamine in rheumatoid arthritis. 643 66

This study of risk factors for diabetic nephropathy in juvenile Type 1 (insulin-dependent) diabetes mellitus compares two carefully characterised groups of patients, one with proteinuria (n = 23), the other a control group (n = 24) with no evidence of nephropathy despite more than 25 years of diabetic life. No significant difference was observed between the groups in any HLA-A, -B or -DR antigen of Bf allotype. DR3 was present in 87% of patients with proteinuria and 75% of the diabetic control group; DR4 was present in 48% of patients with proteinuria and 63% of diabetic controls; BfFl was present in 17% of patients with nephropathy and 9% of the diabetic control group. Compared with the control group, patients with proteinuria had significantly higher mean diabetic-clinic blood glucose concentrations before the diagnosis of microvascular disease, a significantly earlier age at diagnosis of diabetes, and had more often been treated with once-daily as opposed to twice-daily insulin regimens. Susceptibility to nephropathy in Type 1 diabetes appears to be determined by the quality of metabolic control and age of onset of diabetes; although the number of subjects studied was relatively small no evidence was found of any influence of HLA or Bf phenotype.
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PMID:HLA antigens and risk factors for nephropathy in type 1 (insulin-dependent) diabetes mellitus. 659 Apr 2

Immunohistologic studies in IgA nephropathy which have suggested activation of the alternative complement pathway prompted us to study serum complement components and control proteins in 28 patients with IgA nephropathy. Thirteen patients, 12 of whom were men, had or developed chronic renal failure (CRF) during 34 +/- 5 months of follow-up. These patients were more hypertensive and had heavier proteinuria than those with stable renal function. Their serum IgA concentrations were not different from patients with normal renal function. The prevalence of HLA antigens was similar to that for the reference population and BW35 was not associated with CRF. Serum C3, B, H and I concentrations in patients with stable normal renal function were higher than they were in patients with CRF. Four patients studied--two with normal renal function and two with CRF--had partial familial deficiencies of single complement proteins. Our data suggest that high serum levels of C3, B, H and I may be associated with stable normal glomerular filtration rate and that complement deficiencies are not infrequent in IgA nephropathy. How these findings relate to the pathogenesis and progression of IgA nephropathy requires further study. We also conclude that higher serum IgA concentrations and the presence of BW35 are not necessarily associated with progressive renal insufficiency in IgA nephropathy.
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PMID:Serum complement proteins in IgA nephropathy. 660 18

A collaborative study including seven kidney transplant centers in Paris recorded 19 new cases of "de novo" membranous glomerulonephritis (MGN) in a series of 1000 kidney graft biopsies over 1550 renal transplantations. This study represents the largest series "de novo" MGN in the literature. The mean time for the onset of the proteinuria was 26 months post-transplantation (extremes 2-58 months). None of the following factors seemed to be linked with the presence of MGN: age, sex, donor-recipient HLA phenotype, 1st graft vs 2nd graft, cadaver vs related graft, HLA matching, recipient treatment, number of transfused blood units, lymphocytotoxins, number of rejection episodes, number and length of acute tubular necrosis, viral or bacterial infections. These 19 new cases of MGN were compared to the other previously published 42 cases. They generally do not appear to be deleterious for the graft function.
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PMID:[Cooperative study of de novo extramembranous glomerulonephritis in renal allografts in humans: report of 19 new cases in 1550 renal transplant patients of the transplantation group of the Ile de France]. 675 63

To investigate the possible relation between certain HLA antigens and toxicity during treatment with sodium aurothiomalate of D-penicillamine, we studied 91 patients with rheumatoid arthritis. Seventy-one had toxic reactions to either drug or both drugs; the remaining 20 took one of the drugs for at least six months, without toxicity. Nineteen of 24 patients in whom proteinuria developed were positive for HLA-B8 and HLA-DRW3 antigens; 14 of 15 episodes of aurothiomalate-induced proteinura and nine of 13 episodes of penicillamine-induced proteinura occurred in patients with these antigens. All 13 episodes of proteinuria in which urinary protein exceeded 2 g in 24 hours occurred in patients with DRw3. The relative risk of proteinuria during treatment with aurothiomalate is increased 32 times in patients who are HLA-DRw3 positive. No significant associations were found between any HLA antigen and development of skin rashes or hematologic complications. Toxicity during aurothiomalate or penicillamine treatment for rheumatoid arthritis may be under genetic control.
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PMID:HLA-DR antigens and toxic reaction to sodium aurothiomalate and D-penicillamine in patients with rheumatoid arthritis. 677 Feb 69

Idiopathic mesangial glomerulonephritis with IgA deposits was observed in two relatives, father and son, in a family of 5 members. In the father the disease started at age 43 with relapsing macroscopic hematuria, proteinuria, renal failure and hypertension, with a progressive course in the ensuing four years. The affected son, the oldest of three brothers, developed relapsing macroscopic hematuria at age 16; two years later renal function was normal and there was no hypertension, but microhematuria persisted without proteinuria. The mother and the other two brothers had no clinical or biological signs of renal disease. Serum immunoglobulins (IgG, IgA, and IgM) and complement (C3, C4, C3 proactivator) were normal in the patients and their relatives. Histocompatibility typing demonstrated the presence of HLA-Bw35 in the father and the two unaffected sons, being negative in the mother and the affected son. The analysis of HLA-Bw35 in 23 patients with IgA mesangial glomerulonephritis gave positive results in 30% of them, while the control group had a positivity of 15% (p non significant with the X2 test). The present observations suggest that IgA mesangial glomerulonephritis is a potentially familial and hereditary renal disease. HLA-Bw35 antigen appears not to be a genetic marker of the disease in our geographical area.
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PMID:[Familial and hereditary mesangial glomerulonephritis with IgA deposits (author's transl)]. 701 69


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