CALCIUM-OXALATE INTERACTION IN MODULATION OF STONE FORMATION

点击翻译按钮获取中文摘要

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. This project addresses a topic that has raised considerable interest recently, dealing with the possibility that dietary calcium restriction is either ineffective or may exaggerate stone formation. The basis for this concern is the so-called calcium-oxalate interaction that occurs in the bowel and in urine. We were among the first to describe oxalate-calcium interaction in the bowel, i.e., changes in urinary oxalate excretion from binding of oxalate by calcium in the intestinal tract. During low calcium intake, there is inadequate luminal calcium to bind oxalate, increasing oxalate absorption and urinary oxalate. In AH, urinary oxalate may be mild-moderately increased, because increased intestinal absorption of calcium leaves insufficient amount of calcium to bind oxalate. A high calcium intake would be expected to eliminate or attenuate the rise in urinary oxalate. The limiting factor is dietary oxalate content, since it is dietary oxalate that is bound by luminal calcium. This component is directed at elucidating the "calcium-oxalate interaction", a process by which calcium affects the amount of total oxalate in urine by binding oxalate in the intestinal tract, as well as the amount of ionic oxalate in urine by complexing oxalate. By this process, calcium restriction could increase urinary oxalate, attenuating the decline in urinary saturation of calcium oxalate that might ensue from the fall in urinary calcium. Conversely, a high calcium intake could lower total and ionic oxalate in urine, opposing the rise in urinary saturation of calcium oxalate that might occur from increased urinary calcium. The overall hypothesis to be tested is that calcium-oxalate interaction is dependent on dietary oxalate restriction, the state of intestinal absorption of calcium or the degree of hypercalciuria, and on whether calcium is provided as food or supplement. The objective of this component is to complete remaining studies required to test the above hypothesis.