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Treatment of nephrotic syndrome with cyclosporin A. What remains in 1994?

Ten years after treatment of idiopathic nephrotic syndrome was undertaken with cyclosporin A, its mode of action is still unclear. The drug appears not to be merely an immunosuppressive agent, but also seems endowed with nonspecific antiproteinuric properties, explaining partial remissions observed in various aetiologies of nephrotic syndrome, including some with no immunologic background [1]. Its indications continue to generate contradictory publications. Some affirm that it is a major advance in the treatment of nephrotic syndrome, while in other publications, prophets of doom fulminate caveats against those who undertake to destroy the kidneys of their renal patients with the nephrotoxic distillate of Tolypocladium inflatum (Gams). This stream of articles and oral presentations leaves the nephrologist more perplexed than enlightened. What aetiologies of nephrotic syndrome are the right indications? Is success predictable in a given patient? Should cyclosporin A be used alone or be boosted by steroids? What dosage should be used? Should it be titrated by monitoring blood levels? Or just according to serum creatinine fluctuations? Will steroid dependency invariably be traded off for cyclosporin dependency? If so, how many cyclosporin-dependent patients will have to pay the price of remission with relentless renal interstitial fibrosis?