Oral carbonaceous absorbent modifies renal function of renal ablation model without affecting plasma renin-angiotensin system or protein intake
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Background. 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.
Key wordsRenal failure Progression Renin-angiotensin system Protein intake Phosphate
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