CALCIUM-OXALATE INTERATION IN MODULATING CALCIUM OXALATE STONE FORMATION

这一部分的目的是阐明“钙-草酸相互作用”，即膳食钙通过结合肠道中的草酸，减少草酸的吸收，以及通过络合减少尿离子草酸，从而影响尿草酸的过程。总的假设是，钙-草酸盐的相互作用取决于膳食草酸、肠道钙吸收状态以及钙作为食物或补充剂的输送。 在目标1中，我们的目标是证明对于正常受试者来说，钙-草酸相互作用发生在自由但不限制草酸摄入的过程中。我们的假设是，尿草酸的下降将与补钙相关的尿钙上升相反，从而最大限度地减少尿草酸钙饱和度的变化。在这项由安慰剂和碳酸钙组成的两阶段随机交叉试验中，10名接受代谢饮食的正常受试者将在每一阶段的最后两天收集两份24小时尿样。在目标2中，我们的目标是证明与正常的肠道钙吸收相比，在吸收性高钙尿(AH)状态下，钙-草酸相互作用被夸大。在一项两阶段随机交叉试验中，我们将测试16名接受代谢性饮食的AH患者在草酸限制期间补充碳酸钙与安慰剂的效果。我们预计尿草酸钙饱和度会有轻微但显著的增加，程度低于正常受试者。在目标3中，我们的目标是表明，由于食物中潜在的保护性营养物质的相互作用，作为食物的钙促进的钙-草酸盐相互作用比作为补充剂的钙更少。通过对10名正常受试者进行的两阶段随机交叉研究，我们预计，在高钙饮食期间，由于尿草酸的下降，尿草酸钙饱和度的增加会减弱。在目标4中，我们验证了当限制草酸时，草酸钙的饱和度依赖于尿钙浓度的假设。使用来自完成动态评估的患者登记的数据，随机和限制饮食收集的24小时尿草酸钙的尿草酸钙RSR将被计算出来，并与AH-I、AH-II和正常钙尿患者组中相应的尿钙和草酸浓度相关联。

The objective of this component is to elucidate the "calcium-oxalate interaction", a process by which dietary calcium affects urinary oxalate by binding oxalate in the intestine, reducing the amount of absorbed oxalate, and by reducing urinary ionic oxalate through complexation. The overall hypothesis is that calcium-oxalate interaction is dependent on dietary oxalate, the state of intestinal calcium absorption and on the delivery of calcium as food or supplement. In Aim 1, our objective is to demonstrate that for normal subjects calcium-oxalate interaction occurs during a liberal, but not restricted oxalate intake. Our hypothesis is that the decline in urinary oxalate will oppose the rise in urinary calcium associated with calcium supplementation, minimizing the change in urinary saturation of calcium oxalate. In this 2-phase randomized crossover trial comprised of placebo and calcium carbonate phases, 10 normal subjects maintained on a metabolic diet will collect two 24-hour urine specimens on the last 2 days of each phase. In Aim 2, our objective is to demonstrate that calcium-oxalate interaction is exaggerated in states of absorptive hypercalciuria (AH) compared with normal intestinal calcium absorption. In a 2-phase randomized crossover trial, we will test the effect of calcium carbonate supplementation versus placebo during oxalate restriction in 16 AH patients on a metabolic diet. We expect a modest but significant increase in urinary saturation of calcium oxalate, to a lesser degree than seen in normal subjects. In Aim 3, our objective is to show that calcium delivered as food promotes less calcium-oxalate interaction than calcium delivered as a supplement due to the interaction of potentially protective nutrients in food. From a 2-phase randomized crossover study conducted in 10 normal subjects maintained on a low or a high calcium diet with a liberal oxalate intake, we expect an attenuated rise in urinary saturation of calcium oxalate during a high calcium diet due to a decline in urinary oxalate. In Aim 4, we test the hypothesis that saturation of calcium oxalate is dependent on urinary calcium concentration when oxalate isrestricted. Using data from a registry of patients who completed an ambulatory evaluation, the urinary RSR of calcium oxalate derived from 24-hour urines collected on random and restricted diets will be calculated and correlated with corresponding urinary calcium and oxalate concentrations in AH-I, AH-II and normocalciuric patient groups.