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 DR3 and of extended haplotypes bearing DR3 was studied in three groups of subjects: 35 patients with rheumatoid arthritis (RA) with gold induced thrombocytopenia or proteinuria, 185 patients with RA without these side effects, and 300 normal healthy controls. The extended haplotypes bearing DR3 were analysed with cDNA probes for DR alpha, DR beta, DQ alpha, and DQ beta genes. The data showed that the prevalence of DR3 was significantly higher in patients who developed gold induced thrombocytopenia or proteinuria than in normal controls or patients with RA without these side effects. Distribution of three extended haplotypes bearing DR3 (B8, DR3; B18,DR3; non-B8,non-B18,DR3) in patients with RA with thrombocytopenia or proteinuria was significantly different from that in normal controls, but not from that in patients with RA without these toxic reactions. Southern blot analysis of DR, DQ genes with cDNA probes showed that the extended haplotype bearing B8,DR3, which carries DQA2.1 and DQB2.1 genes, was present in a significantly higher proportion of patients with RA with gold induced thrombocytopenia or proteinuria (22/24, 92%) than in patients with RA without these side effects (32/45, 71%) or normal subjects (40/61, 66%). The data suggest that the genomic region on chromosome 6 involved in susceptibility to gold induced thrombocytopenia or proteinuria should be extended to the DQA2, DQB2 gene loci.
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PMID:Polymorphism of major histocompatibility complex extended haplotypes bearing HLA-DR3 in patients with rheumatoid arthritis with gold induced thrombocytopenia or proteinuria. 239 62

Our investigation included 20 patients with rheumatoid arthritis and a negative routine (albustix) proteinuria test, and 20 healthy controls. The albustix test was compared with a method based on multifractional Cellogel RS electrophoresis of urinary proteins. The albustix test was found to be not reliable in patients with RA. Microproteinuria was in fact detected by the electrophoresis method in 12 out of 20 RA patients. Eleven patients showed glomerular type proteinuria (which was "selective" in 5 patients and "non-selective" in 6 patients), and 1 patient showed mixed type proteinuria. Electrophoresis failed to show microproteinuria in the controls. The high sensitivity, easy handling and low cost of multifractioned electrophoresis (which does not involve disturbing the patients) suggest its introduction as a routine test for all RA patients, thus achieving both accurate clinical assessment of proteinuria and a rational therapeutic approach.
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PMID:Microproteinuria as an index of initial renal lesion in patients with rheumatoid arthritis. 239 28

As the semiautomated electrophoretic analysis of proteinuria still needs technical experience, interest was focused on easy-to-perform methods of urinary protein measurement. SRID-tests for albumin, transferrin, IgG, alpha-1-microglobulin and a spectrophotometrical test for beta-NAG were carried out in 50 normal controls and compared to PCI/ECI-values of patients suffering from rheumatoid arthritis (n = 52) and various types of chronic glomerulonephritis (n = 41). Elevated levels of alpha-1-M and beta-NAG in chronic glomerulonephritis were interpreted as indicative for tubulointerstitial involvement in the chronic inflammatory process. PCI/ECI elevation in individual RA-samples may be caused by functional impairment of tubular protein handling due to chronic ingestion of non-steroid analgesics. The serum assays for transferrin (TF) and IgG based on SRID technique turned out to be too insensitive for the application on unconcentrated urine of normal control persons. In renal patients, however, TF-PCI values above 30 mg/g crea and IgG-PCI values above 50 mg/g crea have to be interpreted as pathologic indicating damage of the glomerular basement membrane. To elucidate TF- and IgG-values in urines with low protein content, highly sensitive nephelometric methods should be used. Concentration of urinary proteins using membrane filters may lead to protein losses, resulting in miscalculation of PC-indices.
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PMID:Application of urinary indicator proteins in the non-invasive assessment of glomerulo-tubular lesions in patients with chronic glomerulonephritis and rheumatoid arthritis. 247 10

To examine the subclinical renal damage in collagen disease, we analyzed the excretion pattern of microproteinuria. We studied 58 collagen disease patients including 25 RA (rheumatoid arthritis) patients, 15 SLE (systemic lupus erythematosus), 5 PSS (progressive systemic sclerosis), 4 MCTD (mixed connective tissue disease), and 9 others. Urinary protein was not detected by urine dipsticks in all patients. Urinary proteins, which were concentrated to 5 mg/ml, were subjected to linear gradient (4-30%) SDS-PAGE and then transferred to nitrocellulose membrane by electrophoretic blotting method. The membrane was stained with Auro Dye and the blotted proteins were identified by enzyme immunoassay using specific antibodies. The percentages of albumin of whole urinary proteins were 27.2 +/- 13.7% in RA and 25.8 +/- 12.6% in PSS, which were significantly lower than that of controls (42.1 +/- 15.3%). However no significant difference in the percentage of urinary albumin was noted between SLE and controls. The percentages of low molecular weight (MW) proteins (proteins having smaller MW than albumin) were higher in RA and PSS. Especially the bands with MW of 25,200 were prominent and these percentages were 11.3 +/- 6.1% in RA and 14.6 +/- 9.1% in PSS, which were significantly higher than controls (5.1 +/- 3.5%). These bands with MW of 25,200 were demonstrated to be free light chains of immunoglobulins by western blotting method. From the above observations, protein excretion patterns in RA or PSS patients were so-called tubular proteinuria, and especially free light chain excretion was increased. We proposed that tubular dysfunction and abnormal production of free light chain might exist frequently in collagen diseases, especially RA and PSS.
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PMID:[A study of microproteinuria in patients with collagen disease]. 259 19

Two cases of rheumatoid arthritis with renal lesions are presented. In one of the patients a mesangial IgM nephropathy and in the other patient a mesangiocapillary glomerulonephritis were proved clinically and by biopsy. In the first patient proteinuria was found only while in the second patient the proteinuria was combined with nephrotic syndrome and arterial hypertension. The various renal lesions in rheumatoid arthritis and their causes are discussed.
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PMID:[Kidney involvement in rheumatoid arthritis]. 263 86

A pooled estimate of the magnitude of the benefit and side effects of injectable gold salts in rheumatoid arthritis was computed using meta-analysis based upon available evidence in the literature. Active joint count, grip strength, functional capacity, hemoglobin concentration and erythrocyte sedimentation rate (ESR) were pooled. The change in percentage in favor of gold (adjusted for placebo) was as follows: active joint count 30.1%, (p less than 0.00001), grip strength 13.7% (p less than 0.013), functional capacity 13% (p less than 0.0005), hemoglobin concentration 5.3% (p less than 0.02), and ESR 19.6% (p less than 0.02). Pooling of side effects gave the following results: side effect withdrawals were 11% (p less than 0.01), dermatitis occurred in 15% and proteinuria in 0.7% more patients than in the placebo group.
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PMID:Meta-analysis of injectable gold in rheumatoid arthritis. 266 67

To elucidate the natural course of gold and penicillamine nephropathy and to facilitate appropriate clinical management 54 patients with rheumatoid arthritis who developed proteinuria during treatment with intramuscular gold thiomalate (21) or oral D penicillamine (33) were studied in detail throughout the whole of their renal illnesses. Renal biopsy was performed and creatinine clearance and proteinuria were measured serially for a median period of 60 months (range 16-130 months) in the gold treated and 74 months (range 13-158 months) in the penicillamine treated patients. During gold (penicillamine) treatment 48% (43%), 71% (82%) and 86% (91%) of patients had presented with proteinuria by 6, 12 and 24 months of treatment. After stopping gold (penicillamine) treatment proteinuria reached a median maximum of 2.1 g/day (4.2 g/day) at 2 months (1 month) before resolving spontaneously so that by 6, 12 and 18 months 38% (36%), 62% (64%) and 76% (88%) of patients were free of proteinuria. The median initial and most recent creatinine clearances of the gold (penicillamine) treated patients were 77 ml/min (80 ml/min) and 59 ml/min (78 ml/min) respectively and no patients died from or needed treatment for chronic renal failure. HLA B8 and/or DR3 alloantigens were identified in 64% of the gold treated and 56% of the penicillamine treated patients. In the gold (penicillamine) treated patients renal biopsy revealed membranous glomerulonephritis (GN) in 72% (88%), an immune complex mesangial glomerulonephritis in 10% (6%), minimal change nephropathy in 10% (6%) and no significant glomerular abnormalities in 8% (0%). The study has demonstrated the close similarity between gold and penicillamine nephropathy. It has also demonstrated that some 75% of cases develop during the first year of treatment, the proteinuria resolves completely when treatment is withdrawn, progressive deterioration of renal function is most uncommon, corticosteroid therapy is unnecessary and several different types of glomerulonephritis are associated with gold and penicillamine treatment.
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PMID:The natural course of gold and penicillamine nephropathy: a longterm study of 54 patients. 278 97

Renal transplantation was performed in 2 patients with end-stage renal disease due to AA-type amyloidosis. One patient with amyloidosis of rheumatoid arthritis (RA) origin died twelve months after renal transplantation in cardiogenic shock. AA-amyloid deposits were demonstrated in the graft even though there were excellent function and no proteinuria. The second patient with amyloid nephropathy due to familial Mediterranean fever (FMF) showed no impairment of graft function 24 months after transplantation. These 2 cases are compared to an additional 31 cases of renal transplantation for amyloid nephropathy described in the literature. Proteinuria was reported in 32.3% and amyloid was detected in the functioning graft in 41.4%. The function was excellent even when small amyloid deposits were present in the graft. Renal transplantation is indicated in cases of amyloid nephropathy of the AA-type, provided life threatening amyloid involvement of other organs is not present.
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PMID:Renal transplantation in amyloid nephropathy. 280 85

One hundred eight-six patients with active rheumatoid arthritis were evaluated in a double-blind, randomized study that compared treatment with sulfasalazine (SSZ) (2 mg/day), gold sodium thiomalate (GST) (50 mg/week), and placebo (PBO). The 37-week course of therapy was completed by 109 patients. While marked improvement was seen in all 3 treatment groups, the only statistically significant differences between SSZ or GST and PBO were in a decreased erythrocyte sedimentation rate and increased grip strength in the right hand. GST is known to be superior to PBO, and the response of the GST-treated group was similar to that seen in other trials. The response of the PBO group, however, was much greater than in other placebo groups we have studied. SSZ was similar in efficacy to injectable gold, but was better tolerated. Because of adverse drug reactions (most commonly, rash, stomatitis, and proteinuria), 41% of patients were withdrawn from the GST treatment. Untoward drug effects (most frequently, rash and gastrointestinal distress) caused 16% of patients to be withdrawn from SSZ therapy.
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PMID:A controlled trial comparing sulfasalazine, gold sodium thiomalate, and placebo in rheumatoid arthritis. 289 44

Hematuria and proteinuria in rheumatoid arthritis (RA) are commonly associated with drug therapy but occur independently of drugs, amyloid or urologic disorders. The latter occurrences suggest a primary renal lesion associated with RA. Review of reported renal biopsies identifies mesangial glomerulopathy as a common finding in RA patients without associated drug therapy and that it is frequently associated with hematuria in nonrheumatoid patients. Moreover, immunoglobulins have been shown to concentrate in the mesangium in experimental animals, suggesting that a functional response by the kidney mesangium to remove IgM rheumatoid factor (RF)-IgG complexes could lead to this mesangial lesion. We describe 3 patients with RA who had a mesangiopathy characterized by increased quantities of mesangial matrix and deposition of IgM without other lesions. Together, these observations suggest that: (1) mesangial glomerulopathy is common in RA; (2) removal of circulating RF-IgG complexes is a function of the mesangium and might produce this renal lesion; (3) mesangial glomerulopathy may be responsible for much of the hematuria observed in RA patients and, in many cases, may not be drug related and thus may not require discontinuing beneficial therapy.
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PMID:Mesangial glomerulopathy and IgM rheumatoid factor in rheumatoid arthritis. 291 40


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