Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003873 (rheumatoid arthritis)
 53,068 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum immunoglobulins IgG, IgA, and IgM, serum complement components C3 and C4, circulating immune complexes, antinuclear antibodies, and rheumatoid factor were measured in 56 patients with rheumatoid arthritis (RA) and nephropathy (23 with mesangial glomerulopathy; 13 with membranous glomerulonephritis; and 20 with amyloidosis) and 35 patients with RA without nephropathy (controls). Renal immunofluorescence findings in patients with mesangial glomerulopathy were compared with the serologic data. There were no differences in the occurrence of rheumatoid factor, antinuclear antibodies, and circulating immune complexes and the concentrations of serum complement C3 and C4 between various RA nephropathy groups and controls. Serum IgA and IgM concentrations were significantly higher in patients with mesangial glomerulopathy and amyloidosis than in controls. In patients with mesangial glomerulopathy glomerular IgM, IgA, and C3 were the most prominent findings in immunofluorescence examination. The serum IgA concentration was significantly higher in those patients with mesangial glomerulopathy with mesangial IgA deposits than in those without (4.97 (SD 1.03) g/l v 2.07 (1.21) g/l). The highest serum IgA concentrations (5.08 (1.39) g/l) were seen in the four patients with IgA glomerulonephritis. The prevalence of IgA glomerulonephritis in the renal biopsy material of the patients with RA was 5%, which possibly differs little from that seen in the general population. The results suggest that circulating immune complexes may not have any major role in the pathogenesis of various nephropathy types in patients with RA, contrary to their role in most extra-articular manifestations of RA.
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PMID:Immunological comparison of patients with rheumatoid arthritis with and without nephropathy. 233 1

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

Seven female patients with classical rheumatoid arthritis (RA), treated successfully with injectable gold salts (Fosfocrisolo ICI, 0.10 g/week, with a serum gold concentration of 200-400 mcg/dl), experienced severe gold side-effects after 3 to 20 months of therapy, requiring their withdrawal from gold despite the good results in both clinical and laboratory findings. Four patients showed mucocutaneous side-effects (2 dermatitis and 2 stomatitis) and three a moderate or severe proteinuria. Renal biopsy was performed in these patients, with a histological picture of membranous glomerulonephritis referable to gold therapy. Remission inducing drug (R.I.D.) therapy being mandatory in patients with a chronic progressive disease, and in view of the previous efficacy of gold salts, the patients were put on oral gold, Auranofin being administered 3 mg b.i.d. Both the mucocutaneous side-effects and the proteinuria ameliorated within 2 to 6 months, and the remission of the disease was maintained. The chemical and pharmacokinetic differences between the above two gold compounds are discussed.
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PMID:Injectable gold dermatitis and proteinuria: retreatment with auranofin. 293 99

The renal glomeruli are vulnerable to injury by a number of drugs and other toxic agents. These agents may lead to damage by one of two basic mechanisms: direct, dose-related toxic injury; indirect, immunologically mediated injury, largely dose-independent. Proteinuria is the simplest and most important functional indicator of glomerular injury. It occurs almost immediately in direct toxic injury, but there is a latent period of weeks to months with immunologically mediated processes. Of the two mechanisms, the second is by far the more common in clinical settings. The best studied experimental agent causing direct toxic injury is the aminonucleoside of puromycin. Clinically, perhaps the most important agent is Cyclosporine A. Although this agent is usually thought of primarily as a tubular toxin, it is capable of giving rise to a microangiopathic glomerular lesion similar to that in the hemolytic uremic syndrome. The classic model for immunologic glomerular lesion is Heymann nephritis, which produces a membranous glomerulopathy. Clinically, most drug mediated glomerulopathies also take the form of a membranous nephropathy, usually with a frank nephrotic syndrome. Among the more common offenders are penicillamine, gold salts used in rheumatoid arthritis, and captopril used in hypertension. The other common type of drug-related glomerulopathy occurs as part of a lupus-like syndrome induced by a variety of drugs, including hydralazine, procainamide, and penicillamine. All of these give rise to a variety of antibodies, most prominently antinuclear antibodies, and in the more severe cases there may be lupus-like glomerular lesions as well.
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PMID:Drug-associated glomerulopathies. 294 Jun 67

Classically, the histological lesion observed in a drug-or heavy metal-induced nephrotic syndrome is membranous glomerulonephritis. We report two cases of "toxic" nephrotic syndrome with unusual histological features. One was secondary to mercury intoxication and the other, to D-penicillamine in a patient with rheumatoid arthritis. In both cases, renal biopsy revealed minimal glomerular changes. The proteinuria rapidly disappeared after exposure to the toxic agent was discontinued. Genetic factors and a disregulation of the immune system with lymphokine production may be responsible for these renal changes. This study demonstrates that renal biopsy is necessary in this clinical setting.
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PMID:[Lipoid nephrosis of toxic origin. 2 cases]. 294 17

To clarify the natural course of gold nephropathy and thereby facilitate its clinical management 21 patients with rheumatoid arthritis who developed proteinuria during treatment with intramuscular sodium aurothiomalate were studied in detail throughout their renal illnesses. Renal biopsies were performed, and creatinine clearance and proteinuria were measured serially for 60 months (range 16-130 months). Ten patients developed proteinuria after six months' treatment, 15 after 12 months, and 18 after 24 months. When treatment was stopped the proteinuria reached a median peak of 2.1 g/day (range 0.7-30.7 g/day) at two months (range 1-13 months) before resolving spontaneously, in eight patients by six months, in 13 by 12 months, and in 18 by 24 months. All patients were free of proteinuria by 39 months, the median duration being 11 months. The median first and last measurements of creatinine clearance showed no significant change (77 ml/minute and 59 ml/minute, respectively), and no patient died from or needed treatment for renal failure. HLA-B8 or DR3 alloantigens, or both, were identified in seven patients. Renal biopsy specimens showed membranous glomerulonephritis in 15 patients, a minimal change nephropathy in two, mesangial electron dense deposits in two, and no appreciable glomerular changes in two. In these 21 patients the proteinuria of gold nephropathy resolved completely when treatment was withdrawn. Renal function did not deteriorate, corticosteroids were unnecessary, and several different renal lesions were seen.
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PMID:The natural course of gold nephropathy: long term study of 21 patients. 311 21

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

A 16 year old girl with rheumatoid arthritis who had not received gold or penicillamine developed a nephrotic syndrome. Her renal biopsy specimen showed membranous glomerulonephritis by light, electron, and immunofluorescence microscopy.
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PMID:Membranous glomerulonephritis in rheumatoid arthritis unassociated with gold or penicillamine treatment. 363 71

Rheumatoid arthritis may be associated with several glomerular lesions including amyloidosis, mesangial proliferation and membranous glomerulonephritis. Systemic vasculitis is a well-recognized extra-articular complication of rheumatoid arthritis, but necrotizing glomerulonephritis, the glomerular expression of vasculitis, has been described infrequently. This report comprises four patients with rheumatoid arthritis who underwent renal biopsy for declining renal function, proteinuria and active urine sediments. Pathology revealed that three patients had segmental necrotizing glomerulonephritis without significant glomerular immunoglobulin deposition. The fourth had segmental necrosis associated with diffuse membranous glomerulonephritis. We conclude that necrotizing glomerulonephritis is part of the spectrum of glomerular lesions seen in patients with rheumatoid arthritis. Because of therapeutic considerations involving the use of cyclophosphamide, necrotizing glomerulonephritis should be a diagnostic consideration in the rheumatoid arthritis patient with signs of glomerulonephritis and rapidly deteriorating renal function.
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PMID:Necrotizing glomerulonephritis in rheumatoid arthritis. 380 89

In a series of 96 patients with membranous glomerulonephritis (MGN) there were 14 who had concomitant rheumatoid arthritis. Ten of these had been treated with gold or D-penicillamine; in four patients neither of these drugs could have been responsible for the MGN. One of them received intrasynovial osmium tetroxide two months before the clinical onset of MGN. Three of the patients had positive rheumatoid factor. HLA-type was examined in three patients and all showed B27 antigen but not DR3. No patient developed signs of systemic lupus erythematosus during the follow-up (mean 5.9 years). In two patients MGN persisted as judged from urinary abnormalities, one patient recovered after a relapse period and one developed secondary amyloidosis.
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PMID:Membranous glomerulonephritis in rheumatoid arthritis not related to gold or D-penicillamine therapy: a report of four cases and review of the literature. 382 81


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