Cytotoxic therapy of lupus nephritis: recent developments

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Abstract
Until recently, the primary goal of most therapeutical trials in lupus nephritis (LN) has been to avoid treatment failure, namely death, end‐stage renal disease (ESRD) or doubling of serum creatinine (DSC). Fortunately, these poor outcomes have become relatively less frequent, particularly due to the early detection of kidney involvement by regular follow‐up in specialized institutions. As an alternative goal to the prevention of treatment failure, prompt achievement and long‐term maintenance of remission with less drug‐induced morbidity should become the primary treatment objectives. Such an ideal goal is, however, difficult to achieve for several distinct reasons. Firstly, LN is a heterogeneous disease, the prognosis of which is influenced by many variables such as race, gender, socio‐economic status, presenting features, initial renal pathology, the occurrence of renal flares, the presence of extra‐renal disease, the presence of antiphospholipid antibodies and as of yet unknown factors. Secondly, we still partially ignore the pathophysiological pathways operating in LN, thereby precluding a more specific—and hopefully less toxic—immunointervention. Besides the well known pathogenic role of anti‐DNA antibodies, interleukin‐10, CD40/CD40‐L and B7/CD28 interactions, other mechanisms implicated in the initiation and relapses of LN will hopefully be unravelled in the next decade. Thirdly, few controlled trials have been performed in this field, mostly due to the rarity of the disease and the need for long‐term follow‐up. Accordingly, the literature contains more reviews, comments and editorials (including this one!) than prospective controlled trials.

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