The SNO-GSNOR mediated alternate source of NO supports renal function in eNOS−/−:VEGFKD (− dox) mice, but it fails to do so when podocyte VEGFKD is induced (+ dox), leading to massive proteinuria and renal failure, as well as severe diffuse glomerulosclerosis, suggesting incomplete compensation or an additional VEGFKD related pathway, including iNOS activation, which we have not evaluated. This evidence concerns the gene ADH5 and Renal insufficiency.