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)

The renal biopsies of 30 patients with rheumatoid arthritis and clinical evidence of renal disease were reviewed; only patients in whom the intravenous pyelogram was normal were subjected to biopsy, thus excluding those with papillary necrosis and chronic pyelonephritis. Tissue was studied by light, electron and immunofluorescence microscopy. There were 13 cases of mesangial change, 9 of membranous glomerulonephritis, 4 of tubulointerstitial change, 2 cases of focal segmental glomerulosclerosis, 1 case of amyloid and 1 of diffuse proliferative glomerulonephritis with crescents. All 9 patients with membranous glomerulonephritis but only 6 of 13 with mesangial change had received gold or penicillamine. We found no evidence of "glomerulitis" or of a rheumatoid vasculitis.
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PMID:Renal biopsy appearances in rheumatoid disease. 662 62

The nephrotic syndrome developed in a patient receiving therapy with gold for rheumatoid arthritis. The results of a histopathological examination of the renal biopsy specimen were unremarkable. Immunofluorescent studies showed deposits of immunoglobulins and C3 in a granular pattern in the glomerular basement membranes. Ultrastructurally, the discrete osmiophilic immune complexes were epimembranous. By x-ray microanalysis, gold that was complexed with sulfur was present in proximal tubular cytoplasmic vacuoles and nuclei. Gold and sulfur could not be demonstrated in glomerular epimembranous deposits. The results of these studies suggest that immune complex deposition does not involve gold and sulfur acting as haptens. Gold-salt therapy may result in damage to proximal tubules that leak renal tubular antigens, which in turn complex with autoantibody and produce an autoimmune membranous nephropathy. The evidence for this mechanism is not convincing. Although the data indicate an immune-complex cause for gold-salt nephropathy, the incident antigen (or antigens) and mechanism of action remain unidentified.
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PMID:Gold nephropathy. Ultrastructural, fluorescent, and energy-dispersive x-ray microanalysis study. 678 11

A case of definite ankylosing spondylitis (AS), classical rheumatoid arthritis (RA) and membranous nephropathy is presented. Concurrent presence of the HLA-B27 and HLA-DR4 antigens was demonstrated. The association of AS and RA as well as RA and membranous nephropathy are discussed and the literature reviewed.
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PMID:Coexistence of HLA-B27 ankylosing spondylitis and DR4 seropositive nodular rheumatoid arthritis in patient with membranous nephropathy. 697 78

Eleven patients with amyloidosis were treated for terminal renal failure by transplantation, receiving 12 cadaver allografts. In one patient the amyloidosis was primary and in the remaining 10 it was secondary to a chronic inflammatory disease. All of the patients were subjected to one or two fine-needle aspiration biopsies of the kidney graft during a followup of 11 to 68 months. The biopsies of three patients, one with primary amyloidosis and two with ankylosing spondylitis, revealed amyloid recurrence in the graft. These recurrences were diagnosed at 11, 28, or 37 months, respectively. The risk of amyloid recurrence is thus by no means negligible. The present study revealed no factors determining the development of recurrence. In two additional cases, membranous glomerulonephritis was observed in transplant biopsy. Both of these patients had rheumatoid arthritis as the underlying disease and were treated with gold salts before transplantation. It is suggested that an impaired immune response, related to amyloidosis and/or immunosuppressive therapy, may have favored the formation and deposition of circulating immune complexes.
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PMID:Recurrence of renal amyloid and de novo membranous glomerulonephritis after transplantation. 702 98

We have described a man with classic rheumatoid arthritis who had membranous nephropathy associated with nephrotic syndrome not related to gold or penicillamine therapy. Complete remission of the nephrosis occurred after discontinuation of hydroxychloroquine therapy. Further study is needed to determine the incidence of subclinical membranous nephropathy in patients with rheumatoid arthritis, and the effect of drugs in triggering clinical manifestations of this condition.
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PMID:Membranous nephropathy in rheumatoid arthritis. 707 45

The development of membranous glomerulonephritis in a 51 year old patient suffering from rheumatoid arthritis suggested drug toxicity, and particularly of a recently developed anti-inflammatory agent, diclofenac. The toxicity is discussed in relationship to the biochemical and pharmacological properties of the molecule, the therapeutic setting and the positivity of serological tests for rheumatoid arthritis in this particular case.
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PMID:[Membranous glomerulonephritis during rheumatoid arthritis. Probable toxicity of diclofenac (author's transl)]. 729 Feb 98

We investigated the cause of membranous glomerulonephritis (MGN) in 24 patients with rheumatoid arthritis (RA). The class or stage of RA was diagnosed using the criteria of the American Rheumatism Association, and MGN was diagnosed using renal biopsy. Renal biopsy and laboratory findings, including serologic analysis, were evaluated. Eighteen patients had previously received one of the following antirheumatic agents: bucillamine (n = 13), D-penicillamine (n = 3), or gold (n = 2). The renal lesions of all 24 patients resembled lesions seen with idiopathic MGN on examination by light microscopy, electron microscopy, and immunofluorescence. We concluded that patients with RA are predisposed to develop MGN, whether or not they receive antirheumatic agents.
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PMID:Membranous glomerulonephritis in patients with rheumatoid arthritis. 769 79

Patients with rheumatoid arthritis who develop membranous glomerulonephritis associated with gold or penicillamine therapy have been shown to get better when the drugs are discontinued, whereas up to 50% of patients with idiopathic membranous glomerulonephritis develop renal failure. A feature of the lesion in rheumatoid disease is the presence of mesangial immune complex deposits in addition to the basement membrane deposits of classical idiopathic membranous glomerulonephritis. To determine whether the presence of mesangial immune complexes indicates a different renal outcome in membranous glomerulonephritis we studied 3 groups: group A 10 patients with rheumatoid arthritis and drug induced membranous glomerulonephritis with mesangial immune complex deposits, group B 14 patients with idiopathic membranous glomerulonephritis with additional mesangial immune complex deposits and group C 25 patients having classic idiopathic membranous glomerulonephritis with deposits solely in the glomerular basement membrane. After median follow up of 72 months, nephrotic range proteinuria resolved in all cases in group A after drug withdrawal, 93% of group B, but only 60% of group C (groups A + B vs C, X2 = 7.8, p < 0.01). Serum creatinine remains less than 500 mumol/l in all patients in group A, 93% of group B, but only 64% of group C (groups A + B vs C, X2 = 7.6, p < 0.01). Mesangial immune complex deposits were predominantly of the IgM isotype in both the rheumatoid and idiopathic membranous group. The presence of mesangial immune complex deposits suggests either a different pathogenesis or host responsiveness to that found in classic idiopathic membranous glomerulonephritis, and predicts a more favourable renal outcome.
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PMID:Do mesangial immune complex deposits affect the renal prognosis in membranous glomerulonephritis? 805 Feb 6

We discussed clinicopathological evaluation and treatment of bucillamine induced renal destruction. Thirteen cases of rheumatoid arthritis were investigated in whom proteinuria had developed while being treated with bucillamine. The dose of bucillamine ranged from 100 to 300 mg/day, and many of them were treated with a dose of 200-300 mg/day. The total dose was in the range of 9-57 g. Proteinuria had developed within 3 months after perceiving the efficacy of bucillamine in many of the cases. The details of renal histology revealed that membranous nephropathy was noted in all of the 13 cases and that mesangial proliferative gromerulonephritis was noted in eight cases (61.5%), thin basement membrane was noted in four cases (30.8%) and in one case (7.7%) amyloidosis were identified in parallel. After suspending further administration of bucillamine, the proteinuria was gradually reduced without any specific treatment or without increase in the dose of corticosteroid, and was eliminated in all cases within 10 months. There were some cases in whom proteinuria was eliminated within a short period of time by the administration of corticosteroid in a moderate dose (prednisolone 30 mg/day). It is necessary to initiate the administration of bucillamine from a small dose such as 100 mg/day and pay attention to onset of any side effect. It was also seemed necessary to confirm the renal histology by renal biopsy as far as feasible because a large variety of pathological findings are developed in the kidney of these cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinicopathological evaluation and treatment of bucillamine induced membranous nephropathy]. 834 63

We report a 58-year-old woman with classical rheumatoid arthritis (RA) who developed a membranous glomerulonephritis (MGN). She had never been treated with gold or D-penicillamine; other connective tissue diseases as well as hepatitis B were excluded. We suggest that the responsible cause of MGN is RA.
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PMID:Membranous glomerulonephritis in rheumatoid arthritis unrelated to gold, D-penicillamine or other connective tissue disease. 885 74


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