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It was generally admitted that there was no specific rheumatoid lesion in the kidney and that most renal disease in patients with rheumatoid arthritis (RA) was usually linked to amyloid or secondary effects of drugs. Nevertheless, the necropsy study of Boerset al had shown that 19.7% of RA patients had a glomerulonephritis (GN) at death.1 Recent review of renal biopsy findings in RA patients showed that the most common histopathological finding was mesangial GN followed by amyloidosis and membranous GN.2 3 To evaluate the renal involvement in Chinese patients with RA, a short retrospective clinical study was performed from data of 1468 inpatients of a rheumatology section from 1984 to 1996. Patients having transient mild proteinuria, haematuria or both were not included in the current analysis. Only RA patients with persistent abnormality of haematuria (at least 4 RBC/high power field in two consecutive urine samples), increased proteinuria (daily urinary protein more than 1.0 g) or renal function insufficiency for at least three months (total 14 patients), or all three, had a renal biopsy. The specimens were then examined under light microscope. Immunohistological examination revealed linear IgG deposition along base membrane, IgA deposition in mesangium in patient 5, and non-specific finding in some of the patients taking Chinese herb drugs.
Two categories of patients were found (table 1). Group 1: nephrotic syndrome (NS) with daily protein more than 3.5 g after receiving gold salt or D-penicillamine (D-PC) treatment. Membranous GN in these three patients (patients 1–3) was thought to be related to the drugs themselves. The rest of the patients in this group developed NS or increased proteinuria after receiving disease modified anti-rheumatic drugs (DMARDs) other than gold or D-PC (patients 4–8). Renal biopsy had shown NS with membraneous GN in three patients, IgA nephropathy in one patient, and focal proliferative GN in one patient. Few reports have supported the association between methotrexate, antimalarial drugs, sulphasalazine, and renal disease. It was supposed that renal pathogenesis might be related to RA itself. Serum IgA was comparatively high with positive ANA in this patient group. It was deduced that RA patient with increased IgA is a marker of RA subset with tendency of renal involvement. The relation between IgA, IgA-RF and renal disease in patients with RA was not clear, but the affinity of IgA for mesangium, skin, and synovium might explain the particular clinical presentation of RA with high serum concentration of IgA.4-8 A similar association was also noted in a patient with Henoch-Schonlein purpura and ankylosing spondylitis with IgA nephropathy. Group 2: Chinese herbs instead of the traditional DMARD treatment (patients 9–14). Distinctive changes in renal biopsy (chronic tubulointerstitial nephritis with renal insufficiency, focal segmental global sclerosis, and diffuse global sclerosis with chronic renal failure) were found in contrast with mesangial proliferative or membraneous GN in most of the patients in the DMARD group. Patients in this group denied having received non-steroid anti-inflammatory drugs (NSAIDs) and any form of DMARDs. Unfortunately, the regimens of herbs were too heterogeneous to draw any meaningful conclusion.
In agreement with the data of Helin, NSAID induced nephropathy (chronic interstitial nephritis and ischaemic change) and systemic rheumatoid vasculitis (necrotising vasculitis) were rare in our RA patients.2 Renal amyloidosis was not found in our patients, in contrast with that reported in a white population in whom renal amyloidosis was a common finding in longstanding RA patients.2 Recent reports with special reference to pathological aspects of rapidly extensive interstitial fibrosis with atrophy and loss of tubules in young women with use of slimming regimen including Chinese herbs (Stephania tetrandra andMagnolia officinalis) have pointed out the potential hazard of renal damage by herbs.9 10 The glomeruli were relatively spared. Thickening of Bowman’s capsule was the rule. Although not found in our biopsy samples, many patients used herbs to treat synovitis. The events highlight the dangers of continuously uncontrolled use of herbs in Chinese patients with RA. Repeat biopsies were not performed in our patients. Irreversible renal damage was noted through the disease course in the group of patients taking Chinese herbs. Proteinuria and haematuria improved after the drugs were withdrawn in the other two groups. Finally, these results of a retrospective study cannot be generalised to reflect the prevalence of renal disease in Chinese patients with RA as a whole because of the material analysed. Renal disease occurring in RA patients may be under-represented in this review.
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