Recent studies show nitric oxide (NO) deficiency is both a cause and consequence of chronic kidney disease (CKD). Reduced renal neuronal NO synthase (nNOS) abundance and activity parallels development of CKD with different models in the Sprague Dawley (SD) whereas Wistar Furth (WF) are protected against CKD and show preserved renal NO production. In this study, we compared renal NO in response to DOCA/salt-induced injury between the WF and SD. Studies were conducted on sham WF (n=6) and SD (n=6) and uninephrectized (UNX)+75mg DOCA+1% NaCl (WF n=9; SD n=10) followed for five weeks. Kidneys were harvested for Western blot, NOS activity and histology. Other measurements included creatinine clearance and 24h total NO production and urinary protein excretion. Absolute values of kidney weight were lower in WF than SD but showed similar % increases with UNX+DOCA/NaCl. Proteinuria and decreased creatinine clearance were present in the SD but not the WF following UNX+DOCA/NaCl. Glomerular injury was mild in the WF as compared to SD which showed many globally damaged glomeruli. Although renal nNOS abundance was decreased in both strains (higher baseline in WF), soluble NOS activity was maintained in the WF but significantly reduced in the SD. Renal endothelial (e)NOS abundance and membrane NOS activity was unaffected by treatment. In summary, WF showed resistance to UNX+DOCA/NaCl induced CKD with maintained renal NO production despite mild reduction in nNOS abundance. Further studies are needed to evaluate how WF maintains renal NO production despite similar changes in abundance as the vulnerable SD strain.