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口服糖胺聚糖纠正特发性草酸钙肾结石患者的红细胞异常并降低尿草酸水平

Correction of erythrocyte abnormalities in idiopathic calcium-oxalate nephrolithiasis and reduction of urinary oxalate by oral glycosaminoglycans.

作者信息

Baggio B, Gambaro G, Marchini F, Marzaro G, Williams H E, Borsatti A

机构信息

Division of Nephrology, University of Padova, Italy.

出版信息

Lancet. 1991 Aug 17;338(8764):403-5. doi: 10.1016/0140-6736(91)91030-x.

DOI:10.1016/0140-6736(91)91030-x
PMID:1678082
Abstract

Calcium-oxalate nephrolithiasis is associated with a defect in erythrocyte oxalate self-exchange and an abnormal rate of erythrocyte membrane protein phosphorylation. There is evidence that glycosaminoglycans (GAGs) have a regulatory effect on both of these processes. This study tested the hypothesis that modifications of erythrocyte oxalate self-exchange induced by oral GAGs are paralleled by similar changes in overall oxalate metabolism. 40 patients with idiopathic calcium-oxalate nephrolithiasis were treated for 15 days with 60 mg/day of a mixture of GAGs. By day 15 of treatment there were significant reductions from baseline in erythrocyte oxalate self-exchange (mean [SD] 1.67 [1.18] vs 2.59 [1.63] x 10(2) per min; p less than 0.005) and erythrocyte membrane protein phosphorylation (55.8 [7.3] vs 72.9 [6.8] x 10(-3) cpm/mg protein; p less than 0.005), but also in urinary oxalate excretion (0.24 [0.09] vs 0.31 [0.15] mmol/24 h; p less than 0.005). This finding suggests similar changes in both erythrocytes and other cells more important in oxalate handling. The changes had reversed by 15 days after withdrawal of treatment. Acute intravenous administration of GAGs (60 mg) induced a fall in carbon-14-labelled oxalate renal clearance (143 [13] vs 169 [28] ml/min; p less than 0.005), which strongly suggests the participation of the kidney. However, reduced oxalate absorption from the intestine, and even decreased synthesis of oxalate, cannot be ruled out.

摘要

草酸钙肾结石与红细胞草酸自我交换缺陷及红细胞膜蛋白磷酸化异常速率有关。有证据表明糖胺聚糖(GAGs)对这两个过程均有调节作用。本研究检验了以下假设:口服GAGs诱导的红细胞草酸自我交换改变与草酸盐整体代谢的类似变化平行。40例特发性草酸钙肾结石患者接受60mg/天的GAGs混合物治疗15天。治疗第15天时,红细胞草酸自我交换(平均[标准差]1.67[1.18]对2.59[1.63]×10²/分钟;p<0.005)和红细胞膜蛋白磷酸化(55.8[7.3]对72.9[6.8]×10⁻³cpm/mg蛋白;p<0.005)较基线均显著降低,尿草酸排泄也降低(0.24[0.09]对0.31[0.15]mmol/24小时;p<0.005)。这一发现提示红细胞和其他在草酸处理中更重要的细胞均发生了类似变化。停药15天后这些变化逆转。急性静脉注射GAGs(60mg)导致¹⁴C标记的草酸肾清除率下降(143[13]对169[28]ml/分钟;p<0.005),这强烈提示肾脏参与其中。然而,不能排除肠道草酸吸收减少甚至草酸合成减少的可能性。

相似文献

1
Correction of erythrocyte abnormalities in idiopathic calcium-oxalate nephrolithiasis and reduction of urinary oxalate by oral glycosaminoglycans.口服糖胺聚糖纠正特发性草酸钙肾结石患者的红细胞异常并降低尿草酸水平
Lancet. 1991 Aug 17;338(8764):403-5. doi: 10.1016/0140-6736(91)91030-x.
2
Effects of the oral administration of glycosaminoglycans on cellular abnormalities associated with idiopathic calcium oxalate nephrolithiasis.
Eur J Clin Pharmacol. 1991;40(3):237-40. doi: 10.1007/BF00315202.
3
Glycosaminoglycan content, oxalate self-exchange and protein phosphorylation in erythrocytes of patients with 'idiopathic' calcium oxalate nephrolithiasis.“特发性”草酸钙肾结石患者红细胞中的糖胺聚糖含量、草酸盐自我交换及蛋白质磷酸化
Clin Sci (Lond). 1990 Aug;79(2):113-6. doi: 10.1042/cs0790113.
4
Idiopathic calcium oxalate nephrolithiasis: a cellular disease.
Scanning Microsc. 1992 Mar;6(1):247-54.
5
An inheritable anomaly of red-cell oxalate transport in "primary" calcium nephrolithiasis correctable with diuretics.“原发性”钙肾结石中可通过利尿剂纠正的红细胞草酸转运的遗传性异常。
N Engl J Med. 1986 Mar 6;314(10):599-604. doi: 10.1056/NEJM198603063141002.
6
[Abnormalities in the erythrocyte membrane transport of oxalate in calcium oxalate lithogenesis].
Nephrologie. 1984;5(4):173-4.
7
Raised transmembrane oxalate flux in red blood cells in idiopathic calcium oxalate nephrolithiasis.特发性草酸钙肾结石患者红细胞中跨膜草酸通量升高。
Lancet. 1984 Jul 7;2(8393):12-3. doi: 10.1016/s0140-6736(84)91998-6.
8
Erythrocyte transmembrane flux and renal clearance of oxalate in idiopathic calcium nephrolithiasis.
Kidney Int. 1995 Nov;48(5):1549-52. doi: 10.1038/ki.1995.445.
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Oxalate metabolism in renal stone disease with special reference to calcium metabolism and intestinal absorption.肾结石病中的草酸盐代谢,特别涉及钙代谢和肠道吸收。
Scand J Urol Nephrol Suppl. 1989;119:1-53.
10
Calcium oxalate nephrolithiasis: defective oxalate transport.
Kidney Int. 1991 Jun;39(6):1283-98. doi: 10.1038/ki.1991.162.

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Occup Environ Med. 1996 Sep;53(9):595-600. doi: 10.1136/oem.53.9.595.
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Glycosaminoglycans and other sulphated polysaccharides in calculogenesis of urinary stones.糖胺聚糖及其他硫酸化多糖在尿路结石形成过程中的作用
World J Urol. 1994;12(1):43-8. doi: 10.1007/BF00182050.
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Effect of second messenger systems on oxalate uptake in renal epithelial cells.第二信使系统对肾上皮细胞草酸摄取的影响。
Urol Res. 1995;23(2):89-94. doi: 10.1007/BF00307938.