Pylypchuk G, Ehrig U, Wilson D R
Can Med Assoc J. 1978 Apr 8;118(7):792-6.
To clarify further the beneficial effect of thiazide diuretics on recurrent calcium nephrolithiasis, the effect of short-term hydrochlorothiazide therapy on urine saturation with brushite (CaHPO(4).2H(2)O), in vitro collagen calcification by urine, and urinary inhibitors of calcification was studied.In 22 patients with idiopathic calcium oxalate/phosphate stones the urine calcium excretion decreased, the urine magnesium excretion increased and the urine magnesium/calcium ratio increased significantly (P < 0.001) during hydrochlorothiazide therapy. Supersaturation of the urine with brushite, which was present in 19 of the 22 patients, was reduced significantly (P < 0.001) in all during thiazide therapy, and to the undersaturated range in 16. The ability of urine to calcify collagen in vitro also decreased significantly (P < 0.001) during thiazide therapy, a change that correlated significantly (r = 0.4513, P < 0.05) with the decrease in brushite saturation. The concentration of urinary inhibitors of calcification, as determined with an in vitro collagen calcification system, was decreased significantly (P < 0.01) by thiazide therapy.It was concluded that, in addition to decreasing urine calcium excretion and increasing urine magnesium excretion, thiazide diuretics decrease the urinary brushite saturation and thus may prevent spontaneous nucleation or crystal growth, or both, of calcium phosphate. The ability of thiazides to decrease collagen calcification in vitro suggests that they may also prevent crystal growth on a nidus of organic matrix. Thiazides do not appear to act by increasing the excretion of urinary inhibitors of calcification.
为了进一步阐明噻嗪类利尿剂对复发性钙肾结石的有益作用，研究了短期氢氯噻嗪治疗对透钙磷石（CaHPO₄·2H₂O）尿液饱和度、尿液对体外胶原钙化的作用以及尿液钙化抑制剂的影响。在22例特发性草酸钙/磷酸盐结石患者中，氢氯噻嗪治疗期间尿钙排泄减少，尿镁排泄增加，尿镁/钙比值显著升高（P<0.001）。22例患者中有19例存在透钙磷石尿液过饱和情况，在噻嗪类治疗期间所有患者的过饱和度均显著降低（P<0.001），16例降至不饱和范围。噻嗪类治疗期间尿液体外钙化胶原的能力也显著降低（P<0.001），这一变化与透钙磷石饱和度降低显著相关（r=0.4513，P<0.05）。通过体外胶原钙化系统测定，噻嗪类治疗使尿液钙化抑制剂浓度显著降低（P<0.01）。得出的结论是，除了减少尿钙排泄和增加尿镁排泄外，噻嗪类利尿剂还降低尿液透钙磷石饱和度，从而可能预防磷酸钙的自发成核或晶体生长，或两者兼而有之。噻嗪类药物在体外降低胶原钙化的能力表明它们也可能防止晶体在有机基质核心上生长。噻嗪类药物似乎不是通过增加尿液钙化抑制剂的排泄起作用。
