ADH5 and acute kidney injury: 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.