Treatment of Lupus Nephritis

Abstract

The etiology of systemic lupus erythematosus is unknown. An unidentified causative agent [possibly viral] appears to initiate a series of intermediary disturbances of immune function, in particular of defective T [thymus-derived] cell function with consequent T-B [bone marrow-derived] cell imbalance, finally resulting in the production of a plethora of antibodies to various cytoplasmic and nuclear constituents, coupled with the formation of soluble immune complexes. There is evidence that lupus nephritis arises from the deposition of such circulating immune complexes. Despite what appears to be common etiologic and pathogenetic mechanism, the histologic expression of renal injury is diverse, ranging from trivial focal abnormalities to the most serious forms of diffuse inflammatory change. Despite relative lack of knowledge, limited success has been achieved in the therapy of lupus nephritis. To date, renal histology constitutes the most useful basis for determining the type of steroid regiment for effective therapy. Steroid and immunosuppressive [azathioprine, cyclophosphamide] therapy are discussed.