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[骨质疏松症患者的肾酸化机制障碍]

[Renal acidification mechanism disorders in patients with osteoporosis].

作者信息

Sánchez A, Libman J

机构信息

Centro de Endocrinología, Rosario, Argentina.

出版信息

Medicina (B Aires). 1995;55(3):197-202.

PMID:8544715
Abstract

Eight patients (6 women and 2 men) with osteoporosis caused or aggravated by renal acidification defects are presented. Three of the female patients were premenopausal; the others were 9, 20 and 22 years postmenopausal, and two of them were on hormonal replacement therapy. Two patients had nephrolithiasis: one male with recurrent calcium phosphate stones and a left sided staghorn calculus, and one female with nephrocalcinosis due to medullary sponge kidney and hypercalciuria (patients No. 1 and 2, respectively, Table 1). In the remaining subjects, clinical suspicion was based on: a) Hip fracture in a 44-yr-old premenopausal female without any risk factor (No. 3, Table 2). b) Several vertebral compression fractures in a 45-yr-old male without hypogonadism or other predisposing factors (No. 7, Table 2). c) Lack of response to antiosteoporotic therapy in 3 women (patients No. 4, 6 and 8, Table 2). Serum bicarbonate levels and urine acidification capacity were studied in all patients. Three had low serum bicarbonate (two of whom showed high fractional excretion of bicarbonate), four had a distal defect, and one had a mixed form. Serum creatinine and potassium, and venous blood pH were normal in all cases, suggesting incomplete renal tubular acidosis. Bone mineral density in Z-score (means +/- s.e.m.) was - 1.75 +/- 0.08 in the lumbar spine (n = 8), and - 1.57 +/- 0.09 in the femoral neck (n = 4) [Tables 1 and 2; Figs 1 and 2]. Following one year treatment with oral sodium bicarbonate and potassium citrate, total skeletal calcium increased by 3-10% in five of the patients. Whereas the high prevalence of renal acidification defects among renal stone formers with or without hypercalciuria is well acknowledged, renal tubular acidosis is not included in the list of entities causing secondary osteoporosis. As shown in 6 patients of this series, incomplete RTA should be considered as another disease capable of causing osteoporosis or worsening involutional bone loss.

摘要

本文报告了8例因肾酸化缺陷导致或加重骨质疏松的患者(6名女性和2名男性)。其中3名女性患者处于绝经前;其他患者分别为绝经后9年、20年和22年,其中2名正在接受激素替代治疗。2例患者患有肾结石:1例男性有复发性磷酸钙结石和左侧鹿角形结石,1例女性因髓质海绵肾和高钙尿症出现肾钙质沉着(分别为表1中的患者1和2)。其余患者的临床怀疑依据为:a)一名44岁绝经前女性无任何危险因素却发生髋部骨折(表2中的患者3)。b)一名45岁男性无性腺功能减退或其他易感因素却出现多处椎体压缩性骨折(表2中的患者7)。c)3名女性对抗骨质疏松治疗无反应(表2中的患者4、6和8)。对所有患者进行了血清碳酸氢盐水平和尿液酸化能力研究。3例患者血清碳酸氢盐水平低(其中2例碳酸氢盐排泄分数高),4例有远端缺陷,1例为混合型。所有病例的血清肌酐、钾及静脉血pH值均正常,提示为不完全性肾小管酸中毒。腰椎的骨密度Z值(均值±标准误)为-1.75±0.08(n = 8),股骨颈为-1.57±0.09(n = 4)[表1和表2;图1和图2]。口服碳酸氢钠和枸橼酸钾治疗1年后,5例患者的全身骨骼钙含量增加了3% - 10%。虽然无论有无高钙尿症,肾结石患者中肾酸化缺陷的高患病率已得到充分认识,但肾小管酸中毒并未被列入导致继发性骨质疏松的疾病清单。正如本系列中的6例患者所示,不完全性肾小管酸中毒应被视为另一种可导致骨质疏松或加重绝经后骨质流失的疾病。

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