Although it has been repeatedly shown that the oral carbonaceous absorbent
AST-120 ameliorates the progression of
chronic renal failure, the mechanisms remain unknown.
METHODS: Male Sprague-Dawley rats (6 weeks old), weighing 180-210 g, were 4/5 nephrectomized, and were divided into two groups: one given
AST-120 (0.4 g/100 g
body weight BW; n= 9) and the other not given
AST-120 ( n = 9).
Body weight, blood pressure, and serum and urine chemistry, as well as the plasma components of the renin-angiotensin system, were measured for 22 weeks.
RESULTS:
Proteinuria was significantly greater in the controls than in the
AST-120 group (102 +/- 22 vs 51 +/- 7 mg/day at 22 weeks).
Urea clearance was lower in the former (3.7 +/- 0.4 vs 3.9 +/- 0.4 ml/min). There were no differences in plasma
renin activity (1.4 +/- 0.3 vs 1.9 +/- 0.4 mg/ml per h), or in
angiotensin I (756 +/- 119 vs 1042 +/- 168 pg/ml) and II (35.1 +/- 7.4 vs 46.6 +/- 7.6 pg/ml) or
angiotensin-converting enzyme activity (39.0 +/- 2.4 vs 37.9 +/- 2.2 IU/l) between the two groups.
Protein intake, estimated from urinary
urea appearance, was not different. Serum
phosphate concentration (6.6 +/- 0.3 vs 5.9 +/- 0.3 mg/dl) was higher in the control than in
AST-120, while the urinary
phosphate excretion rate (31.5 +/- 0.8 vs 28.1 +/- 1.8 mg/day) tended to be lower in the latter. Conclusions.
AST-120 retarded the progression of
renal failure in the 4/5 renal ablation model without affecting the plasma renin-angiotensin system or
protein intake, both of which were the most important risk factors for the progression of
renal failure. We hypothesize that the renal protective effects of the oral absorbent
AST-120 may be, at least in part, due to its lowering
phosphate absorption from the diet as a
phosphorus binder.