[Cyclosporin in the treatment of idiopathic nephrotic syndrome].

Two years after the marketing of cyclosporine A (CsA) in the field of organ transplantation the molecule was tried in idiopathic nephrotic syndrome (INS).The first trials were conducted by Meyrier et al in adults [18] and by Tejani et al in children [35] and followed by a few letters on this new treatment mode of INS [10, 14]. The first results were presented at the 18th Annual Meeting of the American Society of Nephrology and published, respectively in the British Medical Journal [19] and in Kidney International [36]. The rationale for treating INS with CsA was rather fragile. It had been established that CsA impairs the production of IL-2 and of γ interferon. At this time, the prevailing hypothesis (the "Shalhoub hypothesis") [34] was that INS was caused by a lymphokine that diminished the negative, anionic charges of the filtration barrier, especially those present on the glomerular basement membrane (GBM), this polyanion repulsing the negatively charged albumin molecules and hampering their egress into the urinary chamber [14; 39; 13; 33]. Soon after the first trials, which raised considerable interest, several investigators tried the effect of CsA in various glomerulopathies. Some, like systemic lupus erythematosus were undoubtedly immunologic in nature. Favre et al, [8] studied the effect of CsA in lupus nephritis and obtained very favorable results. Regrettably no further trials of CsA have been conducted in this indication. Other trials were undertaken in glomerulopathies of immunologic origin, such as membranous glomerulopathy [6], IgA nephropathy [15], proliferative GN, Schönlein-Henoch purpura [3], Wegener's granulomatosis [2, 7, 9], crescentic glomerulopathies [32] and recurrent or de novo post-transplantation GN. However some trials were done in glomerulopathies with obviously no immunological basis, such as Alport's syndrome [4] and diabetic glomerulopathy [20, 21]. As early as in 1989 a review of the literature [21] retrieved 538 patients treated with CsA for such disparate diseases. On the whole, it was observed that, irrespective of the immunologic or non-immunologic nature of the disease, CsA obtained a significant reduction of proteinuria [23, 27].