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)

The distribution of HLA-D region antigens was studied in three groups (I, IIa, and IIb) of patients with rheumatoid arthritis (RA): group I comprised 43 patients with mild, non-progressive RA, controlled by non-steroidal anti-inflammatory drugs without progression or erosions; group II comprised 94 patients with severe disease, who had earlier been treated with non-steroidal anti-inflammatory drugs and all had incomplete response requiring treatment with gold (sodium aurothiomalate). Of these, 46 patients (group IIa) responded to gold and the disease was well controlled, and the remaining 48 patients (group IIb) did not respond to gold and developed gold induced toxic reactions, including thrombocytopenia or proteinuria, or both. HLA-D region antigens were defined by serological and molecular (Southern blot analysis and oligonucleotide typing) techniques. The results show that DR4 was significantly increased in all three groups of patients. The prevalence of DR1, or DR1 in DR4 negative patients, and DR3 and DR4 associated DQw7 specificities, however, showed differences in these three groups of patients. The prevalence of DR1 and of DR1 in DR4 negative patients was increased only in patients with mild (group I) RA, but not in patients with severe (groups IIa and IIb) disease. On the other hand, the prevalence of DR4 associated DQw7 was significantly increased in patients with severe disease, but not in patients with mild RA. In addition, DR3 was significantly increased only in patients with severe disease who developed gold induced toxic reactions (group IIb). These data suggest that the HLA-D region genes which cause susceptibility to mild RA may be different from those causing susceptibility to severe RA. The results suggest that both DR and DQ (A, B) genes may be important in conferring susceptibility to RA: DR in mild disease and DQ in severe RA.
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PMID:HLA-D region genes and rheumatoid arthritis (RA): importance of DR and DQ genes in conferring susceptibility to RA. 141 14

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

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

In order to examine the clinical characteristics and genetic background of secondary amyloidosis associated with rheumatoid arthritis, we analyzed clinical features and HLA typing of 85 patients in a multicenter study. Eighty-five patients with secondary amyloidosis associated RA were studied. The diagnosis of secondary amyloidosis were made on histological findings by biopsy or autopsy. The most common biopsy site was gastrointestinal tract (79.5%). Clinical symptom and the frequency at the time of diagnosis were; diarrhea (35 cases), abdominal pain (22 cases) and vomiting and nausea (16 cases). Abnormalities and the frequency in a laboratory test included proteinuria (49 cases), increased serum creatinine (32 cases), anemia (30 cases) and hematuria (15 cases). Twenty-eight patients were dead and 57 patients were alive at the time of the study. The average duration between diagnosis of amyloidosis and death was 19.4 +/- 18.5 (SD) months among the dead patients. The average duration after diagnosis of amyloidosis was 24.2 +/- 19.5 (SD) months in surviving patients. The causes of death were renal failure complicated with heart failure (6 patients), heart failure alone (3 patients) and renal failure alone (2 patients). Fifty-nine patients in the control group who were negative to amyloid deposition on biopsies at more than one site in the gastrointestinal tract, were clinically compared with patients in the amyloidosis group. No difference were noted in the age of RA occurrence and the stage between the two groups. As to the class, however, the number of patients with severe functional disorder (class 3 or severe) was larger in the amyloidosis group. There were no significant difference between the two groups in Lansbury's activity index. On hematology, biochemistry and urinalysis, the incidences of increased white blood cell count, anemia, increased platelet count, increased serum creatinine, hypoproteinemia, hypoalbuminemia, increased IgA, and increased urine and blood BMG were statistically significantly higher in the amyloidosis group than in the control group. HLA-A, -B, -C, and DR-locus antigens were compared in the 53 patients in the amyloidosis group and in the 59 subjects in the control group. There were no significant differences in frequency of HLA-A, and -B antigens between two groups. Frequency of CW7 antigen was significantly decreased in the amyloidosis group (13.2%) than in the control group (39.0%). Frequency of DR1 antigen was decreased in the amyloidosis group (3.8%) than in the control group (22.0%), although the difference was not significant. These findings suggest the possible involvement of genetic factors in the occurrence of amyloidosis. It is suggested that the occurrence of amyloidosis is suppressed by some genes which are linked with CW7 antigen.
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PMID:[Clinical characteristics and genetic background of secondary amyloidosis associated with rheumatoid arthritis in Japanese]. 871 35