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)

To clarify the characteristics of renal pathology and its correlation with disease-modifying antirheumatic drugs (DMARDs) in patients with rheumatoid arthritis (RA), renal biopsy findings from 158 Japanese RA patients with urinary abnormalities and/or renal dysfunction were analyzed retrospectively in the period between 1979 and 1996. Urologic abnormality and urinary tract infection were ruled out in all patients. Light and immunofluorescence (IF) microscopy were performed in all patients. Mesangial proliferative glomerulonephritis (MesPGN) was diagnosed in 54 patients, membranous nephropathy (MN) in 49, and secondary amyloidosis (AM) in 30. Renal dysfunction was more frequent in patients with AM (22/30) than in patients without (40/128). Forty of 49 MN patients developed renal disorders during DMARDs therapy. The prevalence of DMARD-related MN increased during the period of observation. The fact that DMARDs are of very frequent use in recent Japanese RA patients may reflect the prevalence of MN in this study. Two thirds of patients with MesPGN developed renal disorders when no DMARDs were used. One half of 54 MesPGN patients demonstrated IgA glomerulonephritis (GN) by IF. The prevalence of primary renal diseases in Japan may reflect the frequency of IgA GN in Japanese RA patients. Furthermore, diffuse thinning of the glomerular basement membrane (GBM) was observed in 30 of 81 patients with electron microscopy. RA itself may underlie the pathogenesis of GBM thinning, and drugs used for RA treatment may also accelerate the development of this lesion. In conclusion, although MesPGN, MN, and AM may be relatively more common, IgA GN and GBM thinning also were other frequent entities in Japanese RA patients. No correlation was observed between DMARDs and renal disorders excepting MN.
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PMID:Analysis of renal pathology and drug history in 158 Japanese patients with rheumatoid arthritis. 977 18

A 30-year-old man had been treated for malignant rheumatoid arthritis from 1989 with a non-steroidal anti-inflammatory drug, then bucillamine for six months and prednisolone. Mild proteinuria appeared in May 1994, 4 years after bucillamine therapy was conducted. The patient was admitted to our hospital for a renal biopsy in July 1994. The specimen revealed secondary amyloidosis and membranous nephropathy (MGN). These findings suggest that MGN unrelated to bucillamine therapy might have occurred with secondary amyloidosis in rheumatoid arthritis.
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PMID:[A case of malignant rheumatoid arthritis complicated by secondary amyloidosis and membranous nephropathy]. 989 61

The causes of autoimmune responses leading to human kidney pathology remain unknown. However, environmental agents such as microorganisms and/or xenobiotics are good candidates for that role. Metals, either present in the environment or administered for therapeutic reasons, are prototypical xenobiotics that cause decreases or enhancements of immune responses. In particular, exposure to gold and mercury may result in autoimmune responses to various self-antigens as well as autoimmune disease of the kidney and other tissues. Gold compounds, currently used in the treatment of patients with progressive polyarticular rheumatoid arthritis, can cause a nephrotic syndrome. Similarly, an immune-mediated membranous nephropathy frequently occurred when drugs containing mercury were commonly used. Recent epidemiologic studies have shown that occupational exposure to mercury does not usually result in autoimmunity. However, mercury induces antinuclear antibodies, sclerodermalike disease, lichen planus, or membranous nephropathy in some individuals. Laboratory investigations have confirmed that the administration of gold or mercury to experimental animals leads to autoimmune disease quite similar to that observed in human subjects exposed to these metals. In addition, studies of inbred mice and rats have revealed that a few strains are susceptible to the autoimmune effects of gold and mercury, whereas the majority of inbred strains are resistant. These findings have emphasized the importance of genetic (immunogenetic and pharmacogenetic) factors in the induction of metal-associated autoimmunity. (italic)In vitro(/italic) and (italic)in vivo(/italic) research of autoimmune disease caused by mercury and gold has already yielded valuable information and answered a number of important questions. At the same time it has raised new issues about possible immunostimulatory or immunosuppressive mechanisms of xenobiotic activity. Thus it is evident that investigations of metal-induced renal autoimmunity have the potential to produce new knowledge with relevance to autoimmune disease caused by xenobiotics in general as well as to idiopathic autoimmunity.
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PMID:Metals and kidney autoimmunity. 1050 42

A variety of renal histopathologic lesions, such as amyloidosis, mesangial proliferative glomerulonephritis, and membranous glomerulonephritis (MGN), are associated with rheumatoid arthritis (RA). Bucillamine (BCL), a disease-modifying antirheumatic drug, has a chemical structure and side-effect profile similar to that of d-penicillamine, which can induce MGN in RA. There are a few reports of MGN occurring in association with BCL treatment. However, lacking detailed analyses of immunoglobulin deposition in glomerular lesions, these studies did not elucidate the pathogenesis of BCL-induced MGN. We evaluated seven biopsy specimens from six patients with RA who had undergone BCL treatment with a mean BCL dose of 72.5 g before the appearance of proteinuria. Light microscopic evaluation showed mild to moderate mesangial proliferation. Two biopsy specimens showed spikes along glomerular capillary walls. Granular deposition of immunoglobulin G (IgG) along glomerular capillary walls was seen in all cases, and five specimens showed deposition of IgG2 and/or IgG3 components, in addition to IgG4. Furthermore, subepithelial dense deposits were distributed segmentally in four biopsy specimens on electron microscopy. IgG4, reported to be the predominant IgG subclass deposited, is distributed diffusely in idiopathic MGN. Thus, there were obvious differences between BCL-induced and idiopathic MGN in regard to both IgG subclasses deposited and deposition pattern within the glomerulus. Because IgG3 has the strongest affinity for C1q, these findings suggest that BCL-induced MGN activates the classical pathway more efficiently than idiopathic MGN and that the pathogenesis is different between these two diseases.
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PMID:Bucillamine induces membranous glomerulonephritis. 1192 Mar 35

We report a rare case of nephrotic syndrome in an elderly woman with positive antineutrophil cytoplasmic antibody(ANCA). The patient was 81 years of age and had a history of interstitial pneumonia. She was diagnosed rheumatoid arthritis(RA) at admission. Rapidly progressing renal damage was found with mild microscopic hematuria and positive ANCA. The renal biopsy findings indicated membranous nephropathy. Neither gold nor anti-rheumatic drugs had been previously administered. She may have had an RA-specific membranous nephropathy. Crescentic formation was not clear. With hematuria, the leukocyte infiltration in the capillary lumen and the change in epithelial cells of Bowman's capsules would be histological findings suggesting ANCA-associated nephritis. This is a rare report on membranous nephropathy in an RA patient with ANCA-associated nephritis.
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PMID:[An elderly case of ANCA-positive membranous nephropathy]. 1192 46

Virus C infection has been associated with a broad spectrum of extrahepatic diseases such as essential mixed cryoglobulinemia, membranous glomerulonephritis, vasculitis, rheumatoid arthritis and lupus erythematosus. The etiologic role of virus C has also been observed in some neoplasms such as non-Hodgkin's lymphoma and the monoclonal gammapathies. Many studies also support the link between this virus and porphyria cutanea tarda (PCT). Isolated cases suggest a relationship with dermatomyositis. Herein, we report the coexistence of PCT, non-Hodgkin's lymphoma and dermatomyositis in the same patient affected with virus C infection which has never previously been described.
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PMID:Porphyria cutanea tarda, dermatomyositis and non-Hodgkin lymphoma in virus C infection. 1280 96

The negative association between gout and rheumatoid arthritis is widely accepted, and gout is also speculated to be rare in systemic lupus erythematosus (SLE), as only a few sporadic cases have been reported. From 1985 to 2001 we encountered 15 lupus patients at Chang-Gung Memorial Hospital, including two with lupus-scleroderma and one with lupus-scleroderma-polymyositis overlap syndrome coexisting with gout. This study retrospectively analyses the clinical and laboratory characteristics of these patients. A lower female predominance is found, and most patients developed gout after the onset of SLE, although gout preceded SLE in two cases. Measurement of serum uric acid and 24-h urine uric acid found all of the patients to be hyperuricaemic and underexcretors of uric acid. Furthermore, most of the patients (14/15) were receiving diuretics. Also, many had hypertension and serious cardiovascular diseases. Renal impairment during gouty attacks seemed to be a predisposing factor for developing end-stage renal disease. Gouty arthritis usually occurred during relative SLE inactivity, podagra was frequent, and tophi were found in a few patients. Compared with the unselected population of SLE patients, the cases studied here had a higher incidence of chronic arthritis, malar rash, haematologic disorder, photosensitivity, serositis and neurologic disorder. Renal disease in the patients sampled was frequently membranous nephropathy.
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PMID:Gout in systemic lupus erythematosus and overlap syndrome - a hospital-based study. 1457 59

In patients with systemic lupus erythematosus(SLE), interstitial cystitis(lupus cystitis) is an uncommon, but important manifestation. We report two Japanese patients with lupus cystitis. Case 1 was a 49-year-old woman diagnosed as having rheumatoid arthritis and membranous nephropathy. She was treated with prednisolone(5 mg daily). Case 2 was a 41-year-old woman also diagnosed as having rheumatoid arthritis previously and treated with a non-steroidal anti-inflammatory drug. Both cases presented abdominal pain, vomiting, dysuria and frequency of micturition. We diagnosed these cases as SLE on the basis of arthritis, renal disorder(proteinuria and hematuria), and positive antinuclear and anti-dsDNA antibodies. In addition, bilateral hydronephrosis was found in both cases. Thus, they were also diagnosed as probable lupus cystitis. The patients were treated with one cycle of methylprednisolone pulse therapy. Thereafter they were treated with 60 mg/day of prednisolone and their symptoms resolved promptly. Furthermore, no abnormal finding was found by abdominal ultrasonography and/or the intravenous pyelogram after therapy. Renal biopsies were performed and both cases showed lupus glomerulopathy (case 1: WHO class Vb, case II: WHO class IVb). Abdominal pain and/or dysuria, which is common in SLE patients, requires further examinations to evaluate the lupus cystitis.
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PMID:[Two cases of lupus cystitis complicated by lupus nephritis treated successfully with steroid therapy]. 1473 94

Infliximab is a chimeric tumor necrosis factor-alpha (TNF-alpha) monoclonal antibody, which has been used extensively in patients with rheumatoid arthritis and inflammatory bowel disease. It also appears to be effective in other conditions such as psoriasis and ankylosing spondylitis. The major side effect of infliximab is infection. Renal complications are uncommon and not well recognized. This report describes a probable case of infliximab-induced membranous nephropathy.
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PMID:Infliximab and nephrotic syndrome. 1620 73

We experienced a case of rheumatoid arthritis with nephrotic syndrome. A renal biopsy specimen from this patient showed various renal histological changes. The patient was a 50-year-old man who was diagnosed as having rheumatoid arthritis in 1987. We performed a renal biopsy because he had persistent proteinuria from March in 2002. The renal biopsy specimen showed amyloid AA and P protein deposition in the glomeruli. Moreover mild mesangial proliferation was recognized. IgA-deposition in the mesangial area, and granular-deposition of IgG along the glomerular capillary wall were also observed. In electron microscopy, electron dense deposits were recognized in the mesangial area and subepithelium of the glomerular basement membrane. From these findings, we diagnosed amyloid nephropathy, IgA nephritis and membranous nephropathy. Renal biopsy of patients with RA is useful not only for precise diagnosis, but also for selection of the appropriate treatment.
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PMID:[Case of rheumatoid arthritis with various histological lesions of the kidney]. 1654 59


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