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

The development of severe proteinuria or nephrotic syndrome as an adverse reaction to gold therapy in rheumatoid arthritis is well known. Morphologic examination reveals membranous glomerulonephritis in almost all cases. Since the beginning of 1978 there has been a striking increase in the number of such cases seen at this institute. 5 patients aged from 17 to 65 years who had been treated with sodium aurothiomalate for rheumatoid arthritis developed severe proteinuria. In all cases only minimal glomerular changes were observable by light microscopy. Electron microscopy demonstrated multiple electrondense, subepithelial deposits which were confirmed by fluorescence microscopy. In all cases characteristic lysosomes ("aurosomes") were demonstrated in the cytoplasm, mainly of the epithelial glomerular cells. This unusual accumulation of almost identical cases coincides with the introduction of a new gold preparation, Na-aurothiomalate (Tauredon), containing 46% metallic gold.
 ...
PMID:[Conspicuous accumulation of membranous glomerulonephritis following gold therapy in chronic polyarthritis--a side effect of a new preparation?]. 10 66

This paper describes four cases (where rheumatoid arthritis is the basic ailment of the patients involved) of immune complex nephritis and stage I membranous glomerulonephritis, respectively. Treatment was by means of penicillamine. Also discussed are light-microscopical, immunohistological, and electron-optical results.
 ...
PMID:[Glomerulopathy in rheumatic patients due to penicillamine]. 13 94

Renal complications associated with gold salt treatment in rheumatoid arthritis occur in fewer than 5% of treated patients. Recent investigations have shown that the renal lesion manifested clinically as membranous glomerulonephritis is caused by immune complexes. This paper presents a hypothesis for the mechanism by which gold causes this lesion: autoimmunization due to released tubular antigen(s). This hypothetical mechanism is strikingly similar to that responsible for autologous autoimmune nephrosis in the rat (Heymann's nephritis).
 ...
PMID:Hypothesis for the pathogenesis of sodium aurothiomalate (Myocrisin) induced immune complex nephritis. 15 94

The solid phase Clq radioimmunoassay was used to detect immune complexes in sera from patients with systemic lupus erythematosus (14/25), rheumatoid arthritis (4/5), vasculitis (5/15), infective endocarditis (2/2), acute rheumatic fever (2/3), pre-eclamptic toxaemia (0/14), lung cancer (3/7), glomerulonephritis (26/98) and renal transplant patients (0/5). The best correlation with disease activity was seen in systemic lupus erythematosus and infective endocarditis where serial immune complex determinations were clearly of value in monitoring therapy. The findings in primary glomerulonephritis indicate only a limited usefulness of the assay in that serum immune complexes were detected in a minority (22/73) of patients with glomerular immune deposits. In particular the data do not support a role for Clq fixing immune complexes in the pathogenesis of membranous glomerulonephritis or in pre-eclamptic toxaemia.
 ...
PMID:Serum immune complexes and disease. 15 40

During gold therapy a patient with rheumatoid arthritis developed nephrotic syndrome, and a patient with juvenile chronic arthritis proteinuria. Electron microscopic examination of bioptic specimens of the kidneys revealed in both instances membranous glomerulonephritis with typical epimembranous deposits and intracellular gold inclusions. Immunofluorescent examination performed only in the second patient revealed that the deposits in the wall of the glomerular capillaries contain IgG which suggests an immunocomplex mechanism of the development of the renal disease, induced very probably by chrysotherapy.
 ...
PMID:Gold nephropathy in rheumatoid arthritis and in juvenile chronic arthritis. 53 99

Soluble immune complexes were detected using inhibition of antibody-dependent cell-mediated cytotoxicity (ADCC) in sera of patients with various diseases. Results were positive in 32/41 patients with rheumatoid arthritis (78%), in 27/38 systemic lupus erythematosus patients (71%), in 7/10 cutaneous lupus erythematosus patients (70%), in 6/8 mixed connective tissue disease patients (75%), in 11/26 membranous glomerulonephritis patients (42%), in 6/20 membranoproliferative glomerulonephritis patients (30%) and in 3/12 multiple sclerosis patients (25%). ADCC inhibition was compared with PEG precipitation technique and was found to be more sensitive for detecting soluble immune complexes. Various pitfalls are discussed.
 ...
PMID:Detection of soluble immune complexes by the technique of ADCC inhibition in human diseases. 53 26

Of 90 patients with membranous nephropathy proved by biopsy, 8 (8.9%) had pre-existing rheumatoid arthirtis. Four of these eight patients received systemic treatment with gold. Two others received only token amounts of gold. In two patients who received gold, the renal lesions did not occur until months after discontinuance of gold therapy. We found that clinically significant renal lesions (lesions associated with proteinuria) in patients with rheumatoid arthritis were more likely to be membranous nephropathy than occult amyloidosis or adult lipoid nephrosis. The membranous lesion in patients with rheumatoid arthritis may be difficult to identify by light microscopy, and, although special strains can be helpful, the pathology is frequently sufficiently subtle to require immunofluorescence and electron microscopy for definitive diagnosis. We postulate that chrysotherapy may not be the cause of membranous nephropathy in patients with classic rheumatoid arthritis in whom gold has been used. Whether it merely exacerbates a lesion already present in these patients, or whether it plays little or no role in the development of membranous nephropathy is an unsettled question. Our data lead to think that RA can induce MN and that gold is not the primary inciting agent.
 ...
PMID:Membranous nephropathy in patients with rheumatoid arthritis: relationship to gold therapy. 66 57

Two cases with different and not previously described fatal renal complications during treatment with penicillamine are reported. A man with seronegative rheumatoid arthritis with features of systemic lupus erythematosus was treated with penicillamine for six months and developed a mild membranous glomerulonephritis and a severe renal vasculitis leading to uremia and death. A woman with primary biliary cirrhosis was treated with penicillamine for nine months and developed a nephrotic syndrome, the renal biopsy showing minimal change glomerulonephritis. The nephrotic syndrome responded to prednisone but the patient died, probably from septicemia. Penicillamine may thus cause glomerular damage without deposition of immune complexes. A restricted use of the drug is recommended.
 ...
PMID:Fatal renal vasculitis and minimal change glomerulonephritis complicating treatment with penicillamine. Report on two cases. 76 Apr 1

Four patients with rheumatoid arthritis developed heavy proteinuria after five to 12 months of treatment with D-penicillamine. Light microscopy of renal biopsy samples showed minimal glomerular capillary wall thickening and mesangial matrix increase, or no departure from normal. Electron microscopy, however, revealed subepithelial electron-dense deposits, fusion of epithelial cell foot processes, and evidence of mesangial cell hyperactivity. Immunofluorescence microscopy demonstrated granular capillary wall deposits of IgG and C3. The findings were similar to those in early membranous glomerulonephritis, differences being observed however in the results of staining for the early-acting complement components C1q and C4. It is tentatively concluded that complement was activated by the classical pathway.
 ...
PMID:Immunopathology of penicillamine-induced glomerular disease. 95 Jun 31

Indentations of the glomerular basement membrane were observed by light microscopy in ultrathin Epon-embedded serial sections from the renal biopsies of patients who had membranous glomerulonephritis, minimal change glomerulonephrits, acute or resolving exudative glomerulonephritis and focal glomerulonephrits, interstitial nephritis, amyloidosis, rheumatoid arthritis, or ankylosing spondylitis. In patients with membranous glomerulonephritis, acute or resolving exudative glomerulonephritis, amyloidosis, or rheumatoid arthritis, the occurrence of indentations in the glomerular basement membrane differed significantly from that in controls. The presence of indentations did not correlate with proteinuria, hematuria, leukocyturia, arterial hypertension, or with the nephrotic syndrome or its treatment with steroids. Examination of alternate serial sections by light and be electron microscopy showed that the indentations that were light microscopically visible corresponded to craters on the epithelial surface of the glomerular basement membrane seen in the electron microscope. These craters contained protruding portions of the epithelial cells, extracellular electron-lucent material or electron-dense amorphous or striated membranous material. They were often surrounded by spikelike protrusions of the lamina densa. These indentations might represent solitary remnants of former subepithelial deposits.
 ...
PMID:Indentations of the glomerular basement membrane in renal diseases. A light and electron microscopic study on ultrathin serial sections. 97 63


1 2 3 4 5 6 7 8 9 10 Next >>