DIET, VITAMIN-D AND VERTEBRAL MINERAL DENSITY IN HYPERCALCIURIC CALCIUM STONE FORMERS
DIET, VITAMIN-D AND VERTEBRAL MINERAL DENSITY IN HYPERCALCIURIC CALCIUM STONE FORMERS
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DOI：
10.1038/ki.1991.151
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发表时间：
1991-06-01
影响因子：
19.6
通讯作者：
SEBERT, JL
中科院分区：
文献类型：
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作者：
BATAILLE, P;ACHARD, JM;SEBERT, JL
为了阐明饮食钙非依赖性高钙尿症的病理生理学，选择了42名钙结石形成者（Ca SF），因为他们在自由饮食中的钙尿症大于0.1 mmol/kg/天。 通过排除乳制品，使其接受钙限制饮食（Ca RD）4天。 分别于第4天、第5天晨空腹2 h、口服钙负荷1 g后4 h取尿，测定肌酐、Ca、PO4、尿素和总羟脯氨酸尿（THP）。 在第5天空腹血浆浓度的Ca，PO4，完整的PTH，Gla蛋白，calcidiol和骨化三醇进行了测量。 根据钙RD高钙尿消失与否，将患者分为饮食性高钙尿症（DH，18例）和饮食性非钙依赖性高钙尿症（IH，24例）。 将IH患者分为正常空腹尿钙所致吸收性高钙尿症（AH）8例和空腹高钙尿症（AH）16例。 根据PTH水平将空腹高钙尿症患者分为肾性高钙尿症（RH，1例）和未确定的高钙尿症（UH，15例）。 此外，通过定量计算机断层扫描测量了他们的椎体矿物质密度（VMD），在DH中正常（年龄和性别的正常平均值的91 +/-6%），但在IH中降低至69 +/-4%。 AH和UH的VMD无差异。 尿中尿素、磷酸盐和THP的排泄量IH高于DH，AH和UH相当。 所有组和亚组的钠排泄量Ca RD以及血浆参数均相同。 血浆骨化三醇增加IH和DH相对正常，尽管正常的血浆骨化二醇。 口服钙负荷后尿钙增加，钙吸收的指数，IH高于对照组，IH和DH以及IH的三个亚组之间相当。 根据这些数据和IH的相关研究，得出以下结论：（1）。伴有IH的钙结石患者VMD降低，但伴有DH的患者VMD未降低，这使得这两组高钙尿症患者的差异具有临床意义。 （2.） IH中AH、RH和UH的进一步区分不是很合理，因为RH是例外，而VMD和其他生化参数（用于亚分类的参数除外）在AH和UH之间没有差异。 （3.） 由于IH患者的空腹羟脯氨酸尿和空腹钙尿高于对照组，而血浆PTH浓度低于正常（RH患者除外），空腹钙尿与空腹羟脯氨酸尿相关，因此提示原发性骨吸收过度，而不是原发性肾钙渗漏或原发性肠吸收过度，是IH的主要原因。 （四） IH是与较高的尿素排泄的自由和钙R饮食比对照组，这表明更高的蛋白质摄入量没有乳制品来源。 由于空腹钙尿和羟脯氨酸尿与尿素排泄相关，因此较高的摄入量可能有利于骨吸收。（5.） 在IH时，钙负荷后，钙三醇与VMD和尿钙呈正相关，与空腹尿钙呈负相关，提示钙三醇通过增加钙的吸收来减轻骨吸收。 （6.） 在IH中，血浆骨化三醇与骨化二醇正相关，与血浆磷酸盐负相关，血浆磷酸盐保持在正常范围内。 因此，IH时血浆骨化三醇增加可能是由于25（OH）维生素D1-α羟化酶对PPO 4的超敏反应，使其合成依赖于25（OH）D。 （7.）排除乳制品可能对钙结石形成者的骨骼有害。 应建议限制非乳制品来源的蛋白质摄入。
To elucidate the pathophysiology of dietary calcium independent hypercalciuria, 42 calcium stone formers (Ca SF) were selected because they had on free diet a calciuria greater than 0.1 mmol/kg/day. For four days they were put on a diet restricted in calcium (Ca RD) by exclusion of the diary products. They collected 24 hour urines on free diet and on day 4 of Ca RD as well as the two-hour fasting urines on the morning of the day 5 and the four-hour urines passed after an oral calcium load of 1 g, for measurement of creatinine, Ca, PO4, urea and total hydroxyprolinuria (THP). On day 5 fasting plasma concentrations of Ca, PO4, intact PTH, Gla protein, calcidiol and calcitriol were measured. The patients were firstly classified into dietary hypercalciuria (DH, 18 patients) and dietary calcium-independent hypercalciuria (IH, 24 patients) on the basis of the disappearance or not of hypercalciuria on Ca RD. Then the patients with IH were subclassified into absorptive hypercalciuria (AH) because of normal fasting calciuria (8 patients) and into fasting hypercalciuria (16 patients). Fasting hypercalciuric patients were subsequently divided according to the PTH levels into renal hypercalciuria (RH, 1 patient) with elevated fasting PTH becoming normal after the Ca load and undetermined hypercalciuria (UH, 15 patients) with normal PTH levels. Furthermore, their vertebral mineral density (VMD) was measured by quantitative computerized tomography which was normal in DH (91 +/- 6% of the normal mean for age and sex) but was decreased in IH to 69 +/- 4%. No difference in VMD was observed between AH and UH. Urinary excretions of urea, phosphate and THP was higher in IH than in DH and comparable in AH and UH. Sodium excretion Ca RD was the same in all groups and subgroups as well as the plasma parameters. Plasma calcitriol was increased in IH and DH comparatively to normal in spite of normal plasma calcidiol. Calciuria increase after oral calcium load, an index of Ca absorption, was higher in IH than in controls and comparable in IH and DH as well as in the three subgroups of IH. From these data and correlation studies in IH it is concluded: (1.) VMD is decreased in Ca stone formers with IH but not in those with DH, making the distinction of these two groups of hypercalciuria patients clinically relevant. (2.) The further distinction within IH of AH, RH and UH is not very justified, since RH is exceptional and VMD and other biochemical parameters (with the exception of those taken for subclassification) are not different between AH and UH. (3.) Since in IH, fasting hydroxyprolinuria and fasting calciuria were greater than in control, whereas plasma PTH concentrations were low to normal (with the exception of the case with RH), and fasting calciuria was correlated to fasting hydroxyprolinuria, it is suggested that a primary bone hyperresorption, and not a primary renal leak of calcium or a primary intestinal hyperabsorption, is the main cause of IH. (4.) IH is associated with higher urea excretion on free and Ca R diets than in controls, suggesting a higher protein intake of no dairy origin. This higher intake may favor bone resorption since fasting calciuria and hydroxyprolinuria are correlated to urea excretion.(5.) In IH, the positive correlations of calcitriol with VMD and calciuria increase after Ca oral load, and the negative one between calcitriol and fasting calciuria, suggest that calcitriol attenuates bone resorption by increasing calcium absorption. (6.) In IH, plasma calcitriol is correlated positively to calcidiol and negatively to plasma phosphate which remains in the normal range. Therefore, increased plasma calcitriol in IH may be explained by a hypersensitivity of 25 (OH) vitamin D1-alpha hydroxylase to PPO4, making its synthesis dependent upon 25 (OH) D. (7.) Exclusion of dairy products might be deleterious for the skeleton in Ca stone formers. Restriction of protein intake of non-dairy origin should rather be advised.