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The literature on the treatment of lupus nephritis is scattered, much of it in rheumatological rather than nephrological journals. Whatever our ignorance of the nature and genesis of lupus nephritis, under empirical treatment the prognosis, especially for severe forms, has improved dramatically during the past 20 years. For severe lupus nephritis, the evidence that the addition of cytotoxic agents to corticosteroids improves outcome is now secure, and discussion centres mainly on which drug to use and by what route. Intravenous methylprednisolone is at least as effective as high-dose tapering oral therapy for initial treatment, and carries fewer side-effects. The role of plasma exchange in lupus remains undefined: it may have a role in the treatment of cerebral manifestations or otherwise resistant patients, but controlled trials have failed to show benefit. Future developments will probably centre around the use of specific monoclonal antibodies which target specific groups and subgroups of cells, "humanised" by the splicing of human Fc piece to rodent (fab)2, perhaps bearing toxins. To use these agents to best advantage, however, we will have to understand better than we do today the nature of the cellular defects in the immune response which underlie the lupus syndrome.
The literature on the treatment of lupus nephritis is scattered, much of it in rheumatological rather than nephrological journals. Whatever our ignorance of the nature and genesis of lupus nephritis, under empirical treatment the prognosis, especially for severe forms, has improved dramatically during the past 20 years. For severe lupus nephritis, the evidence that the addition of cytotoxic agents to corticosteroids improves outcome is now secure, and discussion centres mainly on which drug to use and by what route. Intravenous methylprednisolone is at least as effective as high-dose tapering oral therapy for initial treatment, and carries fewer side-effects. The role of plasma exchange in lupus remains undefined: it may have a role in the treatment of cerebral manifestations or otherwise resistant patients, but controlled trials have failed to show benefit. Future developments will probably centre around the use of specific monoclonal antibodies which target specific groups and subgroups of cells, "humanised" by the splicing of human Fc piece to rodent (fab)2, perhaps bearing toxins. To use these agents to best advantage, however, we will have to understand better than we do today the nature of the cellular defects in the immune response which underlie the lupus syndrome.
This paper sets out the arguments for drug treatment of chronic glomerulonephritides (GN). Although the pathogenesis and mechanism of progression of chronic GN remained to be clarified, on the basis of controlled studies performed to date, there is a strong case to be made for an aggressive treatment approach to this disease spectrum. For instance, in patients with idiopathic membranous glomerulonephritis a six months treatment with chlorambucil (0.2 mg/KG/day) or prednisone (0.6 mg/KG/day) each given once a day over a period of three months has recently been shown to improve the outcome of the renal functional parameters after three years follow up. In another controlled trial a daily dose of 225 mg dipyridamole and 975 mg aspirin given over 12 months in patients with membrano-proliferative GN type I has been reported to normalize the increased platelet consumption rate and to stabilize the glomerular filtration rate. A third trial has demonstrated that the combined use of cyclophosphamide (100 mg/day) and prednisone (30 mg/day) over several months was superior to the use of prednisone alone (40 mg/day) in improving the long-term prognosis of diffuse-proliferative lupus nephritis (type IV, WHO). In some entities, however, as in IgA-nephritis there is still no evidence for a specific treatment improving the course of the chronic glomerular disease. Other therapeutic problems have to be solved: thus, in patients with minimal change nephropathy with a steroid dependent nephrotic syndrome the benefit of cyclophosphamide (given over three months) or of cyclosporin A is still being investigated. Furthermore, there is some evidence that progression of chronic GN, particularly that of glomerular sclerosing, can be prevented by a low protein diet. The role of eicosanoides and their inhibitors in this context has not yet been fully investigated. The different drug trials and new therapeutic concepts indicate a rapid development of chronic GN treatment. Therefore, a failure to treat actively is difficult to understand.
A 29-year-old white female with longstanding classical rheumatoid arthritis (RA) developed clinical and serological manifestations of systemic lupus erythematosus (SLE) with prominent signs of diffuse proliferative lupus nephritis. She fulfilled the ARA criteria for the classification of SLE as well as the ARA criteria for classical RA. The concomitant presence of these two affections in the same patient is rare and the discriminating features suggest that this coexistence may be coincidental. With respect to treatment, our patient had good relief of symptoms by a combined administration of methylprednisolone pulses and cyclophosphamide.
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