UROLITHIASIS: ROLE OF NEPHRON DYSFUNCTION/INJURY

草酸盐是代谢的最终产物，是80%的 肾结石，并在其尿液浓度的微小变化至关重要 影响草酸钙结晶。 一个家庭的高频率 “特发性”肾结石病的历史表明， 研究人员认为尿石症可能是一种代谢紊乱， 细胞草酸盐运输缺陷引起的 遗传缺陷 红细胞钙和草酸盐转运最近已被确定， 肾结石患者，加强了论点， 细胞转运异常可能在"特发性" 钙结石形成。 然而，草酸盐的细胞转运 在肾脏中，特别是在乳头状细胞中， 通常发生草酸钙结晶。 因此，本提案的目的是： 1. 描述肾皮质和肾皮质中草酸盐转运的特征， 乳头状 细胞 2. 为了评估实验中草酸盐处理的改变， 模型 以肾单位功能障碍为特征的肾结石，或 损伤 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，并可能给我们 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.