الفهرس 
DIABETIC NEPHROPATHYOnly 14 pages are availabe for public view
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Abstract
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 nondiabetic
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.