[Study on the pathogenetic factors of the progression of renal insufficiency, with special reference to the effects of dietary protein intake].

The effects of dietary protein intake on the progression of renal insufficiency were studied in daunomycin (DMC) induced nephrotic rats (DMC rats) and also patients with chronic renal diseases. In the first study, the author examined which treatment among enalapril (E) and indomethacin (I) and dietary protein restriction was the most effective to prevent proteinuria and glomerulosclerosis, and then the effect of dietary protein restriction on renal content of malondialdehyde (MDA) and superoxide dismutase (SOD) in DMC rats. These rats were divided into four groups as follows: group PL and group PH were isocaloric diets containing either 5% or 24% protein, respectively and group PE and PI were given orally E (100 mg/l drinking water) or I (50 mg/l drinking water) with diets of 24% protein, respectively. In group PL, urinary protein excretion (U-Protein) rates and renal damage index were significantly lower than those in other three groups. In group PE, renal damage index was significantly improved although U-Protein showed no reduction in contrast with these in group PH. Renal MDA in group PL was lower than that in group PH was significantly lower than that in group PL. In this study dietary protein restriction was the most effective treatment for the prevention of progressive renal insufficiency. In the second study, patients with chronic renal diseases were divided into two groups according to their Ccr: group I; Ccr greater than or equal to 60 ml/min, group II; Ccr less than 60 ml/min. All patients orally received diets of high protein (1.4 g/kgBW) and subsequently of low protein (0.7 g/kgBW). Ccr, U-Protein, serum MDA and serum SOD were estimated at the end of each dietary period. In group I, Ccr was significantly lower on low protein diet than that on high protein diet, although these were no significant changes in Ccr in group II. The low protein diet caused a significant decrease in U-Protein in both groups. Serum MDA in group I was significantly lower on low protein diet than that on high protein diet, but not in group II. Serum SOD activity showed no changes. It is suggested that dietary protein restriction might reduce oxidant stress to the kidney, in addition to renal hemodynamic changes induced by prostaglandin and renin-angiotensin system, resulting in the prevent of progress of renal insufficiency.