Sanai T, Okuda S, Onoyama K, Motomura K, Osato S, Hori K, Iseki K, Fujishima M
Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Miner Electrolyte Metab. 1991;17(3):160-5.
To investigate the effects of aluminium hydroxide (AH), a phosphate binder, on the progress of chronic renal diseases, high doses (9.6 g/kg/day, group ADR-H), moderate doses (2.4 g/kg/day, group ADR-M), and low doses (1.2 g/kg/day, group ADR-L) of the compound, were orally administered for 34 weeks to rats with Adriamycin (ADR)-induced focal glomerular sclerosis. Serum creatinine and blood urea nitrogen were significantly lower in either group ADR-H or ADR-M than in group ADR at week 34. Urinary protein excretion was significantly lower in group ADR-H than in group ADR in all observation periods and was also lower in group ADR-M than in group ADR at weeks 28 and 32. Both glomerular sclerosis and tubular change were significantly less severe in group ADR-H, while tubular change was less marked in group ADR-M than in group ADR. These results revealed that phosphate depletion was induced, and progressive renal failure was ameliorated in proportion to the dosing of AH. On the other hand, body weight was significantly smaller in group ADR-H than in group ADR in more than half of the observation period. In conclusion, a high dose of AH may adversely affect the nutritional state irrespective of having an extremely protective effect on progress of renal dysfunction. Appropriate doses of AH should be used to prevent the renal deterioration.
