Changes of renal nitric oxide (NO) production have been associated with glomerular hyperfiltration, vascular permeability, albuminuria, glomerulosclerosis and tubulointerstitial fibrosis. In our study we tried to detect the role of expression of both iNOS and eNOS in Egyptian diabetic and non diabetic nephropathy. Renal biopsies and clinical data of thirty diabetic patients, ten non- diabetic patients with renal impairments and ten control subjects were selected. Glomerular and cortical endothelial NOS (eNOS) and inducible NOS (iNOS) were assessed by immunohistochemical staining and related to clinical data such as duration of diabetes, insulin therapy and arterial hypertension, albuminuria, proteinuria, glomerular filtration rate, presence of vascular complication or diabetic retinopathy. We found that both glomerular eNOS and iNOS expression increased in diabetic nephropathy and related to hypertension and peripheral arterial occlusive disease. With increased serum creatinine the expression of both iNOS and eNOS increased in these patients. Also iNOS increased in non-diabetic patients with renal impairment and control subject mainly at tubular cells and interstitial cells explaining their role in tubular injury. Also we detected a relation between expression of iNOS and eNOS and smoking in diabetic patients. We didn't find any relation between expression of both iNOS and eNOS and degree of proteinuria or the duration of insulin therapy. We can conclude that the presence of iNOS may lead to tubular damage as resulting in renal failure. The up-regulation of NO in DN may explain endothelial dysfunction which is associated with almost all diabetic complications.