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)

Twenty-six of 300 patients (9%) with rheumatoid arthritis (RA) developed penicillamine-induced proteinuria. The mean daily dose and duration of therapy at onset of proteinuria were 591 mg and 9 months, respectively, while the mean duration of proteinuria was 5.5 months. However, six patients developed proteinuria at 250 mg/d and six after 9 months of therapy. Twelve patients were successfully either restarted (five) or maintained (seven) on penicillamine with resolution of proteinuria. No permanent renal impairment occurred. Positive risk factors included the presence of HLA-B8 and DR3 and prior gold-induced proteinuria. Patients with prior gold-induced proteinuria should be observed more carefully, but tissue typing is not recommended as proteinuria is reversible. Furthermore, penicillamine can be restarted or maintained in these patients if the RA has responded favorably to the drug.
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PMID:Penicillamine-induced proteinuria: risk factors. 348 19

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

We are reporting findings in 13 patients who presented with glomerulonephritis without evidence of systemic disease, but who were found to have positive antinuclear antibody results and immunoglobulin and/or complement deposits at the dermal-epidermal junction of normal skin not exposed to light. There was no evidence of other organ involvement, and serologic tests for systemic lupus erythematosus (SLE) gave negative results. The renal disease is characterized by severe proteinuria, focal or diffuse proliferative glomerular lesions on biopsy, with variable patterns of immunoglobulin deposits. No clinical manifestations or serologic results typical of SLE have developed during prolonged observation. HLA phenotyping carried out in eight of the 13 patients revealed DR2 or DR3 alloantigens or both in seven of the eight patients, an incidence similar to that in patients with overt SLE. Because of the specificity of the skin biopsy immunofluorescence, the similarity of HLA-DR antigens, and a favorable response of the renal disease to therapy, we believe that these patients have a variant of SLE.
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PMID:Triad of glomerulonephritis, antinuclear antibodies, and positive skin immunofluorescence. Variant of systemic lupus erythematosus. 633 92

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

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

An increase in the frequency of DR3 in rheumatoid arthritis (RA) patients exhibiting toxic reactions to chrysotherapy has been reported in several studies of white patients. This study was designed to compare DR antigen frequencies in local white RA patients undergoing chrysotherapy with their response to treatment. The results from our sample of RA patients (n = 148) confirm the fact that there is increased frequency of DR3 in patients who develop toxic reactions to gold therapy, as reported in other studies of white patients. The DR3 increase was attributable to those gold-treated patients who developed proteinuria, and was not observed in patients who developed skin toxicity. Interestingly, the associations were not as strong as those found in other reports. Only 21.1% of the patients with DR3 manifested toxic reactions overall, with only one-third of the patients with proteinuria being DR3 positive. There was also an association of toxicity, albeit not significant, with a decreased frequency of DR2, which is consistent with the suggestion that this phenotype may protect against adverse reactions to gold treatment. These results suggest that while DR3 is significantly associated with adverse response to gold treatment, the relationship is not as strong as that previously reported. Explanation of these differences remains to be elucidated.
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PMID:DR antigens and gold toxicity in white rheumatoid arthritis patients. 658 52

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

The aetiology and pathogenesis of focal glomerulosclerosis is poorly understood and many conflicting reports suggest HLA locus associations in both familial and non-familial glomerulosclerosis. We report a family in which 4 of 5 sisters developed proteinuria, 2 with hypertension and 1 progressing to end-stage renal failure (index case). Three underwent renal biopsy which displayed characteristic features of focal glomerulosclerosis and all shared the HLA alleles HLA-A1, B8, DR3, DR7. The index case received two cadaveric renal transplants from HLA-A1, B8, DR3 donors and developed chronic rejection with no histological evidence of recurrent glomerulonephritis in either kidney. The frequency of this haplotype in the Australian dialysis and transplant population with focal glomerulosclerosis was compared to that seen in the general Australian Caucasian population and was not significantly different suggesting that the presence of the HLA alleles HLA-A1, B8, DR3, DR7 may increase the predisposition to familial glomerulosclerosis but additional factors are required for disease development and progression.
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PMID:Familial focal glomerulosclerosis: a genetic linkage to the HLA locus? 750 47


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