UROLITHIASIS--ROLE OF NEPHRON DYSFUNCTION/INJURY

草酸是新陈代谢的最终产物，是80%的 肾结石及其尿药浓度的微小变化 影响草酸钙结晶。一个家庭的高频率 “特发性”肾结石的病史提示了一些人 研究人员认为尿石症可能是一种以代谢紊乱为特征的疾病 由细胞草酸运输的缺陷所致。中的遗传缺陷 红细胞钙和草酸转运最近在 肾结石患者，强化了这样一种观点 细胞运输异常可能在“特发性”中起主要作用 钙结石的形成。然而，草酸的细胞转运已经 在肾脏中没有特征，特别是在乳头细胞中 草酸钙结晶通常发生。 因此，这项提议的目的是； 1.研究草酸在肾皮质和肾乳头中的转运 细胞。 2.在实验模型中评估草酸盐处理的变化 以肾单位功能障碍或损伤为特征的肾结石。 这些研究将有助于阐明肾单位功能障碍或损伤的作用。 在草酸钙肾结石的发病机制中的作用 关于如何预防这种疾病的见解。

Oxalate, an end product of metabolism, is a major component of 80% of kidney stones, and small changes in its urinary concentration critically influence calcium oxalate crystallization. The high frequency of a family history in "idiopathic" renal stone disease has suggested to some investigators that urolithiasis may be a metabolic disorder characterized by a defect in cellular oxalate transport. Inherited defects in erythrocyte calcium and oxalate transport have been recently identified in patients with kidney stones, strengthening the contention that abnormalities in cellular transport may play a primary role in "idiopathic" calcium stone formation. However, the cellular transport of oxalate has not been characterized in the kidney, particularly in papillary cells where calcium oxalate crystallization usually occurs. The aims of this proposal, thus are; 1. To characterize oxalate transport in renal cortical and papillary cells. 2. To assess alterations in oxalate handling in experimental models of nephrolithiasis that feature nephron dysfunction or injury. These studies will help elucidate the role of nephron dysfunction or injury in the pathogenesis of calcium oxalate nephrololithiasis and may give us insights on how to prevent this disease.