ABSTRACT
Nitric oxide [NO], an extensively studied endothelium - derived relaxing factor, seems to be a very potent regulator of intrarenal hemodynamics. Rats with chronic renal failure have a low nitric oxide [NO] production and a diminished NO excretion.The supplementation of L-arginine has an inhibitory effect on the progression of renal insufficiency. The Present study was designed to determine whether chronic renal failure patients have a low NO production. Plasma and urine nitrate [N03] and nitrite [N02] stable metabolites of NO, were measured in 50 patients with chronic renal failure. The 50 chronic renal failure patients were divided into five groups; group 1, mild renal failure [Creatinine clearance> 60 ml / min / 1.73 m[2]]; group 2, moderate renal failure [Creatinine Clearance> 30 < 60 ml / min. / 1.73 m[2]] and group 3, severe renal failure [Creatinine Clearance < 30 ml / min. / 1.73. m[2]], group 4, severe renal failure under hemodialysis, group 5, transplanted group. Each group was 10 patients. The study included also 10 healthy subjects matched for age, gender, body mass index and diet served as controls. Results showed that the daily urinary NO excretion was significantly lower in patients with moderate and severe renal failure as compared with those with mild renal failure and normal controls [P < 0.01]. At the same time the daily urinary NO excretion was not statistically significant in transplanted group when compared with those of controls [P > 0.05], but was statistically significant in severe CRF patients under haemodialysis when compared with controls [P < 0.01]. Plasma NO was significantly elevated in chronic renal failure patients as compared with normal controls [P < 0.05]. But increase in plasma NO in transplanted group was statistically not significant when compared with controls [P > 0.05]. The 24 - hour urinary NO excretion was correlated with creatinine clearance in chronic renal failure patients [P < 0.05 and P < 0.01] respectively, in different groups, but not correlated with 24 hour urinary protein [P> 0.05]. Plasma NO in renal failure patients was not correlated with creatinine clearance or 24 hour urinary protein [P > 0.05]. In conclusion, we found that chronic renal failure is a state of NO deficiency. Treatment stategies to increase NO production [L-arginine supplementation or other NO compounds] may prove to be useful in maintaining the renal function and slow the progression of renal disease