OPTIMAL CORRECTION OF ACIDOSIS CHANGES PROGRESSION OF DIALYSIS OSTEODYSTROPHY
OPTIMAL CORRECTION OF ACIDOSIS CHANGES PROGRESSION OF DIALYSIS OSTEODYSTROPHY
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DOI：
10.1038/ki.1989.309
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发表时间：
1989-12-01
影响因子：
19.6
通讯作者：
MORIEUX, C
中科院分区：
文献类型：
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作者：
LEFEBVRE, A;DEVERNEJOUL, MC;MORIEUX, C
为了研究酸中毒在血液透析性骨营养不良中的最终作用，我们前瞻性研究了21例患者，这些患者在透析液中使用不同量的碳酸氢盐透析18个月。根据研究前骨活检的骨形成率（BFR）水平，将患者分为两个亚组。在这两个亚组中，患者被随机分配到两个治疗组：10名患者（A组）用常规量的碳酸氢盐（33 . ±. 2 mmol/L）;其余患者（B组，N = 11）在透析液中加入7 - 15 mmol/L碳酸氢钠，以获得24 mEq的透析前碳酸氢盐血浆水平。B组透析前血浆碳酸氢盐水平较高（15.6 ± 0.01），表明酸中毒得到有效纠正。1组A vs. 24.0 . ±. 0.6 mEq/升B组，P < 0.005），其在研究开始后三个月达到。与研究前骨活检相比，在研究结束时进行的骨活检中，A组的类骨质和成骨细胞表面增加，但B组未增加。用与PTH分子44.68区交叉反应的抗血清测量的甲状旁腺素血浆水平（iPTH）在A组的研究期间增加，但在B组中没有增加。这一结果表明，继发性甲状旁腺功能亢进（HPT）的进展，只有在A组患者。在18个月的研究期间，两组的骨钙素血浆值均增加。因此，分别评价了基于BFR水平形成的两个患者亚组。研究前骨活检显示BFR正常-高的患者亚组在研究开始时具有高骨吸收和升高的iPTH和骨钙素血浆水平。在该亚组中，研究期间A组骨钙素血浆水平比B组升高更多。BFR正常-低的患者亚组骨钙素水平较低，10名患者中有7名在研究开始时患有再生障碍性骨病。在该亚组中，A组的骨钙素血浆值在研究期间没有变化，但B组增加。在研究期间，任何组的血浆或骨铝均未发生显著变化。因此，酸中毒的最佳纠正可以减少高骨转换患者的HPT进展，并刺激低骨形成患者的骨转换。
To investigate an eventual role of acidosis on hemodialysis osteodystrophy we prospectively studied 21 patients who were dialyzed with different amounts of bicarbonate in the dialysate for 18 months. According to the level of bone formation rate (BFR) on a prestudy bone biopsy, patients were split in two subgroups. Inside these two subgroups patients were randomly allocated to two therapeutics groups: 10 patients (group A) were dialyzed with the conventional amount of bicarbonate (33 .+-. 2 mmol/liter) in the dialysate; the rest of the patients (group B, N = 11) had 7 to 15 mmol/liter sodium bicarbonate added to the dialysate to obtain 24 mEq predialysis bicarbonate plasma levels. An effective correction of acidosis was shown in group B by a higher predialysis plasma bicarbonate level (15.6 .+-. 1 group A vs. 24.0 .+-. 0.6 mEq/liter group B, P < 0.005), which was reached three months after start of the study. Compared to the prestudy bone biopsy, osteoid and osteoblastic surfaces increased in group A but not in group B on the bone biopsies performed at the end of the study. Parathormone plasma level (iPTH), measured with an antiserum which cross reacts with the 44.68 region of PTH molecule, increased during the study in group A but not in group B. This findings suggested progression of secondary hyperparathyroidism (HPT) only in group A patients. Osteocalcin plasma values increased in both groups during the 18 months of the study. Consequently the two subgroups of patients formed on the basis of BFR level were evaluated separately. The subgroup of patients with normal-high BFR on the prestudy bone biopsy had a high bone resorption and elevated iPTH and osteocalcin plasma levels at start of the study. In this subgroup of patients with osteocalcin plasma level increased more in group A than in group B during the study. The subgroup of patients with normal-low BFR had lower osteocalcin levels, and seven of ten patients had aplastic bone disease at start of the study. In this subgroup, osteocalcin plasma values were unchanged during the study in group A but increased in group B. There was no significant modification of plasma or bone aluminium in any group during the time of the study. Therefore, an optimal correction of acidosis could decrease progression of HPT in patients with high bone turnover, and stimulate bone turnover in patients with low bone formation.