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[运动性蛋白尿的机制——力竭运动后蛋白质尿排泄与乳酸之间的关系]

[The mechanisms of exercise-induced proteinuria--relationship between urinary excretion of proteins and lactate after exhaustive exercise].

作者信息

Suzuki M, Ikawa S

机构信息

Department of Laboratory Medicine, Tokyo Jikei-kai University School of Medicine.

出版信息

Nihon Jinzo Gakkai Shi. 1991 Apr;33(4):357-64.

PMID:1875555
Abstract

Exercise-induced proteinuria is of the mixed glomerular-tubular type and has been thought to be due to increased glomerular permeability to macromolecular proteins in response to activation of the renin-angiotensin system and catecholamines and a reduction in renal hemodynamics. The excretion of the tubular type of proteins, however, can't be explained by the above mechanism. Two groups, consisting of subjects with the highest (H-alb, n = 20) and the lowest (L-alb, n = 20) excretion of albumin 30 min after exhaustive exercise were selected from a total of 69 normal male participants. No differences in VO2max, maxHR, changes in plasma angiotensin II, catecholamines, urine volume, or Ccr following exercise were observed between the two groups. The increase in blood lactate concentration immediately after exercise, increases in urinary excretion of lactate, pyruvate, alpha 1 M, beta 2 M, albumin and decrease in Cl- excretion 30 min after exercise in the H-alb group were significantly greater than in the L-alb group. The greater the urinary excretion of lactate and pyruvate, the greater the excretion of albumin, alpha 1M and beta 2M, and the less the urinary excretion of Cl-. The coefficient of correlation between the urinary excretion of lactate and beta 2M was 0.757, and between urinary excretion of albumin and beta 2M, 0.756 (p less than 0.001). These results suggest that exercise-induced organic acids and/or decrease in renal circulatory pH caused by organic acids may alter renal glomerular permeability and inhibit renal tubular reabsorption of low molecular weight proteins (alpha 1M, beta 2M). The permeability of the glomerular basement membrane (GBM) to macromolecular proteins may be altered by a reduction in the charge barrier of the GBM, which may be caused by the over-production of organic acids and a lower pH.

摘要

运动性蛋白尿属于肾小球 - 肾小管混合型,一直被认为是由于肾素 - 血管紧张素系统和儿茶酚胺激活后,肾小球对大分子蛋白质的通透性增加以及肾血流动力学降低所致。然而,肾小管型蛋白质的排泄不能用上述机制来解释。从69名正常男性参与者中选出两组,一组是力竭运动后30分钟白蛋白排泄量最高的受试者(H - alb组,n = 20),另一组是白蛋白排泄量最低的受试者(L - alb组,n = 20)。两组之间在最大摄氧量(VO2max)、最大心率(maxHR)、运动后血浆血管紧张素II、儿茶酚胺、尿量或内生肌酐清除率(Ccr)的变化方面均未观察到差异。H - alb组运动后即刻血乳酸浓度的升高、运动后30分钟尿乳酸、丙酮酸、α1微球蛋白(α1M)、β2微球蛋白(β2M)、白蛋白排泄量的增加以及Cl - 排泄量的减少均显著大于L - alb组。乳酸和丙酮酸的尿排泄量越大,白蛋白、α1M和β2M的排泄量就越大,而Cl - 的尿排泄量就越少。乳酸尿排泄量与β2M之间的相关系数为0.757,白蛋白尿排泄量与β2M之间的相关系数为0.756(p < 0.001)。这些结果表明,运动诱导的有机酸和/或有机酸导致的肾循环pH值降低可能会改变肾小球通透性,并抑制肾小管对低分子量蛋白质(α1M、β2M)的重吸收。肾小球基底膜(GBM)对大分子蛋白质的通透性可能会因GBM电荷屏障的降低而改变,而这可能是由有机酸的过度产生和较低的pH值引起的。

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