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[代谢性酸中毒对慢性肾衰竭患者氨基酸及酮酸代谢的影响]

[The effect of metabolic acidosis on amino acid and keto acid metabolism in chronic renal failure].

作者信息

Mochizuki T

机构信息

Department of Medicine, Kidney Center, Tokyo Woman's Medical College.

出版信息

Nihon Jinzo Gakkai Shi. 1991 Feb;33(2):213-24.

PMID:2051649
Abstract

The effect of metabolic acidosis (MA) on amino acid and keto acid metabolism was studied in fourteen patients with chronic renal failure (CRF) under the low protein diet (0.6-0.8 g/kgBW). The comparative study of five patients with renal tubular acidosis was carried out. Each patient was investigated before [MA(+)period] and after correction with sodium bicarbonate administration lasting 10 days [MA(-)period]. The correction of MA improved nitrogen balance and elevated plasma branched-chain amino acids (BCAA), keto acids (BCKA), glutamine and alanine concentrations. No effect was however, observed in change of plasma insulin and glucagon. Oral administration of the keto-analogues of BCKA [0.1 g/kgBW of alpha-ketoisovalerates (KIV) and alpha-keto-isocaproic acid (KIC)] is made for the purpose of investigating the change in the metabolic conversion rate to amino acids. As a result, MA (+) suppressed an increase in plasma KIV and KIC concentrations. Moreover, an increase in plasma valine and leucine concentrations were suppressed by MA (+). These results suggested that MA stimulates BCKA oxidation and suppresses the protein sparing effect of leucine and KIC, and accelerates the catabolism in CRF under the low protein diet. The correction of MA is ineffective in severe renal failure (serum creatinine above 10.0 mg/dl), because the other uremic factors appear to be affecting protein and amino acid metabolism. Therefore, it might be concluded that MA should be corrected at an earlier stage of CRF.

摘要

在14例接受低蛋白饮食(0.6 - 0.8g/kg体重)的慢性肾衰竭(CRF)患者中,研究了代谢性酸中毒(MA)对氨基酸和酮酸代谢的影响。对5例肾小管酸中毒患者进行了对比研究。每位患者在[MA(+)期]之前以及在持续10天给予碳酸氢钠纠正后[MA(-)期]进行了检查。MA的纠正改善了氮平衡,并提高了血浆支链氨基酸(BCAA)、酮酸(BCKA)、谷氨酰胺和丙氨酸的浓度。然而,未观察到血浆胰岛素和胰高血糖素的变化。为了研究代谢转化为氨基酸的速率变化,口服给予BCKA的酮类似物[0.1g/kg体重的α-酮异戊酸(KIV)和α-酮异己酸(KIC)]。结果,MA(+)抑制了血浆KIV和KIC浓度的升高。此外,MA(+)抑制了血浆缬氨酸和亮氨酸浓度的升高。这些结果表明,MA刺激BCKA氧化,抑制亮氨酸和KIC的蛋白质节省作用,并在低蛋白饮食下加速CRF中的分解代谢。在严重肾衰竭(血清肌酐高于10.0mg/dl)中,MA的纠正无效,因为其他尿毒症因素似乎在影响蛋白质和氨基酸代谢。因此,可以得出结论,应在CRF的早期阶段纠正MA。

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