The altered permeability of the glomerular capillaries for plasmaproteins in nephrotic syndrome (NS) appears as a consequence of immunological or autoimmunological processes. Increasing knowledge concerning the action of cytokines on the permeability of the vascular barrier, and the possibility to suppress their production with ciclosporine A (CsA), especially of the cytokine interleukin-2, made its therapeutic use for the treatment of NS reasonable. On the basis of clinical data the following conclusions are made with respect to the relevancy of CsA for the treatment of NS: 1. CsA affects the NS of histological different glomerular diseases. 2. CsA acts better in steroid-sensitive or steroid-dependent NS than in steroid-resistant NS. 3. The response to CsA is higher in NS due to minimal change nephropathy (MCN) than in NS due to focal glomerular sclerosis (FSGS). 4. CsA seems to influence some of steroid-resistant NS due to FSGS, membranous glomerulonephritis (MGN) and IgA nephropathy (IgAN). 5. As with steroids, a relapse of NS due to CsA withdrawal and in consequence as dependancy may appear with a higher risk for side effects during long-term treatment.