Bushinsky D A, Grynpas M D, Asplin J R
Nephrology Unit, University of Rochester School of Medicine, Rochester, New York 14642, USA.
Kidney Int. 2001 Apr;59(4):1415-23. doi: 10.1046/j.1523-1755.2001.0590041415.x.
We have successively inbred over 45 generations a strain of rats to maximize urine calcium excretion. The rats now consistently excrete 8 to 10 times as much calcium as controls and uniformly form poorly crystalline calcium phosphate kidney stones. In humans with calcium nephrolithiasis, consumption of a diet high in acid precursors is often cited as a risk factor for the development of calcium-based kidney stones; however, the effect of this diet on urinary supersaturation with respect to the common solid phases found in kidney stones has not been determined.
To determine the effect of the addition of an acid precursor on urine ion excretion, supersaturation, and stone formation, we fed these genetic hypercalciuric stone-forming (GHS) rats 13 g/day of a 1.2% calcium diet with 0.0, 0.5, 1.0, or 1.5% NH4Cl in the drinking water for 14 weeks (N = 8 for each). Urine was collected and analyzed every two weeks.
As expected, the addition of dietary NH4Cl led to a progressive fall in urine pH and urine citrate, while urine ammonium increased. Urine calcium and phosphorus increased, while urine oxalate fell. Increasing dietary NH4Cl led to a fall in supersaturation with respect to CaHPO4 (brushite) and CaOx and a rise in supersaturation with respect to uric acid. In spite of differences in supersaturation, most rats in each group formed stones that contained calcium phosphate and not calcium oxalate.
Thus, while the provision of additional dietary acids alters urinary ion excretion and lowers supersaturation with respect to CaHPO4 and CaOx, it does not change the character or rate of stone formation in the GHS rats.
我们已经连续对一个大鼠品系进行了45代以上的近亲繁殖，以最大限度地提高尿钙排泄量。现在这些大鼠的钙排泄量始终是对照大鼠的8至10倍，并且均一形成结晶性差的磷酸钙肾结石。在患有钙肾结石的人类中，摄入富含酸前体的饮食常被认为是钙基肾结石形成的危险因素；然而，这种饮食对肾结石中常见固相的尿过饱和度的影响尚未确定。
为了确定添加酸前体对尿离子排泄、过饱和度和结石形成的影响，我们给这些遗传性高钙尿结石形成（GHS）大鼠喂食13克/天的1.2%钙饮食，饮用水中添加0.0%、0.5%、1.0%或1.5%的氯化铵，持续14周（每组N = 8）。每两周收集并分析尿液。
正如预期的那样，添加膳食氯化铵导致尿液pH值和尿柠檬酸盐逐渐下降，而尿铵增加。尿钙和磷增加，而尿草酸盐下降。增加膳食氯化铵导致相对于磷酸氢钙（透钙磷石）和草酸钙的过饱和度下降，而相对于尿酸的过饱和度上升。尽管过饱和度存在差异，但每组中的大多数大鼠形成的结石含有磷酸钙而非草酸钙。
因此，虽然提供额外的膳食酸会改变尿离子排泄并降低相对于磷酸氢钙和草酸钙的过饱和度，但它不会改变GHS大鼠结石形成的特征或速率。
