The loss of CD31 was evident 3 days after adriamycin administration then persisted until day 28 (Fig. 4A to E & K) while the expression of synaptopodin was significantly reduced 7 days after ADR administration (Fig. 4F to J & L), suggesting that glomerular endothelial cells with eNOS deficiency are more susceptible to injury than podocytes and that endothelial dysfunction plays a critical role in the development and progression of ADR-induced nephropathy. This evidence concerns the gene SYNPO and endothelial dysfunction.