Aluminium and bone disease in chronic renal failure
Aluminium and bone disease in chronic renal failure
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DOI：
10.1093/ndt/17.suppl_2.21
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发表时间：
2002-01-01
影响因子：
6.1
通讯作者：
Malluche, HH
中科院分区：
文献类型：
--
作者：
Malluche, HH
铝被肠道吸收并迅速转运到骨骼中，在那里它破坏矿化和骨细胞的生长和活性。它的毒性导致或加剧疼痛形式的肾性骨营养不良，最显著的是粘连性骨病和骨软化症，但也有其他形式的疾病。因为铝会在骨骼中被长时间隔离。其毒性作用是累积的。结果。即使间歇或低剂量使用铝基磷酸盐结合剂也会增加骨中该毒素的总负荷;因此，即使是用于“抢救适应症”，铝的使用也是不可取的。血液中的铝水平不是透析患者铝吸收或器官负荷的可靠标志：只有矿化前沿的铝才能反映骨中观察到的组织病理变化。因此，骨活检仍然是铝相关骨病的唯一确诊方法。最重要的是，毒素的整体器官浓度之间缺乏相关性。如铝，病理变化不排除毒性。因此。毒素的特定定位比整个器官浓度更重要。在25年的研究中对铝所观察到的情况可能会在其他金属中重现，这些金属在骨骼中被吸收，运输和积累。我们所了解的铝的毒性应告知我们的其他金属为基础的治疗肾病患者的研究数据的解释。这就要求对任何新引入的治疗缺乏排泄肾功能的骨病的药物进行仔细的评估。
Aluminium is absorbed by the intestines and is rapidly transported into bone, where it disrupts mineralization and bone cell growth and activity. Its toxicities result in or exacerbate painful forms of renal osteodystrophy, most notably adynamic bone disease and osteomalacia, but also other forms of the disease. Because aluminium is sequestered in bone for long periods. its toxic effects are cumulative. As a result. even intermittent or lowdose use of aluminium-based phosphate binders adds to the total load of this toxin in the bone; thus, aluminium use is inadvisable, even for a 'rescue indication'. Aluminium blood levels are not a reliable marker of aluminium absorption or organ load in dialysis patients: only stainable aluminium at the mineralization front reflects the histo pathological changes observed in bone. Therefore, bone biopsies remain the only approach for definitive diagnosis of aluminium-related bone disease. Most importantly, lack of correlation between overall organ concentrations of a toxin., such as aluminium, and pathological changes does not rule out toxicity. Thus. the specific localization of the toxin is more important than overall organ concentration. What has been observed with aluminium during 25 years of research might be reproduced with other metals that are absorbed, transported and accumulated in bone. What we have learned about the toxicity of aluminium should inform our interpretation of data from studies of other metal-based therapeutics for renal patients. This calls for careful evaluation of any newly introduced therapeutic agents for bone disease in patients lacking excretory kidney function.