Kumano K, Sakai T, Kuwao S, Ise M
Kidney Center, Kitasato University Hospital, Japan.
Int J Artif Organs. 1992 Dec;15(12):708-14.
Excess protein intake enhances the progression of renal failure. The oral carbonaceous adsorbent, AST-120, was found experimentally and clinically to retard the progression of renal failure. This study was designed to determine whether deterioration of renal function by dietary protein loading can be prevented or mitigated by this oral adsorbent. Rats with uremia induced by partial renal infarction were fed a normal or high-protein diet for 70 days with or without AST-120, in which the inorganic phosphate content was adjusted to the same level. The survival rate deteriorated with the high dietary protein, but was improved from 30% to 100% with AST-120. Dietary protein loading reduced renal function, based on creatinine clearance. AST-120 improved renal function and renal histopathology not only in the normal diet group but in the high-protein group as well. The progression of renal failure induced by protein loading is thus shown to be prevented by oral AST-120. The mechanism for its action remains to be clarified.
蛋白质摄入过量会加速肾衰竭的进展。实验和临床研究发现，口服碳质吸附剂AST-120可延缓肾衰竭的进展。本研究旨在确定这种口服吸附剂能否预防或减轻因饮食中蛋白质负荷导致的肾功能恶化。通过部分肾梗死诱导尿毒症的大鼠，在无机磷酸盐含量调整至相同水平的情况下，给予正常或高蛋白饮食70天，同时给予或不给予AST-120。高蛋白质饮食使大鼠存活率降低，但AST-120可将存活率从30%提高至100%。基于肌酐清除率，饮食中蛋白质负荷会降低肾功能。AST-120不仅改善了正常饮食组大鼠的肾功能和肾脏组织病理学，也改善了高蛋白饮食组大鼠的情况。因此，口服AST-120可预防蛋白质负荷诱导的肾衰竭进展。其作用机制仍有待阐明。
