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Title: 尿路結石症基礎と臨床 : 促進物質としての蓚酸の役割
Other Titles: Oxalate as a promoter in calcium oxalate nephrolithiasis
Authors: 山川, 謙輔  KAKEN_name
加藤, 貴裕  KAKEN_name
有馬, 公伸  KAKEN_name
柳川, 真  KAKEN_name
川村, 寿一  KAKEN_name
Author's alias: Yamakawa, Kensuke
Katou, Takahiro
Arima, Kiminobu
Yanagawa, Makoto
Kawamura, Juichi
Keywords: Oxalate transport
Red blood cell
Issue Date: Oct-1991
Publisher: 泌尿器科紀要刊行会
Journal title: 泌尿器科紀要
Volume: 37
Issue: 10
Start page: 1111
End page: 1114
Abstract: 再発性蓚酸Ca結石患者10名,対照健常者15名でoxalate influx rateを測定した.赤血球膜においては,患者で亢進した.ラット小腸刷子縁膜ではNa-蓚酸共輸送系の存在が示唆された.塩化Naと蓚酸の同時摂取は蓚酸の腎負荷を増加させる
Oxalate transports on membranes of red blood cell, intestinal epithelium and proximal tubule cell were reviewed, and the new findings about oxalate transport across these membranes are reported. Red blood cell oxalate influx rate in a group of recurrent calcium oxalate stone formers was significantly higher than that of a control group. In the red blood cells of mammals, the band 3 protein transports oxalate. Although abnormal influx rate of red blood cells might be recognized as an expression of somatic cell abnormality of oxalate transport in some recurrent stone formers, the band 3 protein is not related to oxalate transport in both kidney and intestine. The study using brush border membrane vesicles suggested the presence of Na-oxalate co-transport. In humans, sodium intake increased the oxalate/creatinine ratio of urine. This indicated that excessive sodium intake might be a risk factor of stone formation. Further study of oxalate transport of both kidney and intestine will be required to elucidate an etiology of calcium oxalate nephrolithiasis.
PubMed ID: 1755400
Appears in Collections:Vol.37 No.10

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