[Recent approaches to the pathogenesis of minimal change nephrotic syndrome].

Clinical and experimental observations suggest that lipoid nephrosis (Minimal change nephrotic syndrome) results from T cell dysfunction due to still unknown mechanisms. By substractive screening library, we identified 84 transcripts, of which 42 correspond to known genes, 12 match with proteins of yet unknown function and 30 are unknown clones. Among the 42 known transcripts, at least 18 are closely involved in the T-Cell Receptor mediated signaling cascades. This includes genes encoding components of the T-Cell Receptor and proteins associated with the cytoskeleton scaffold, as well as transcription factors. During the relapse phase, we have detected very low levels of IL12R beta 2 mRNA suggesting that the T-cell activation evolves toward a Th2 phenotype. Thus, the combination of substractive cloning and differential screening constitutes an efficient approach to identify genes likely involved in the pathophysiology of MCNS.