骨骼和肾脏

P. Miller, M. Pazianas
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引用次数: 0

摘要

慢性肾脏疾病(CKD)患者骨质疏松症的管理往往是非常具有挑战性的,它应该考虑两种疾病的病理生理。4-5期CKD患者发生脆性骨折和继发性死亡率增加的风险尤其高。鉴别骨质疏松症和CKD-MBD最好通过定量骨组织形态学来完成,但骨转换的生化标志物,特别是完整的甲状旁腺激素(PTH)和骨特异性碱性磷酸酶,也可能有所帮助。一种抗吸收性骨质疏松治疗可能不安全的肾性骨病是特发性肾动力骨病。不建议使用骨质疏松药物治疗的两种肾性骨病是骨软化症和原发性甲状旁腺功能亢进骨病,这两种骨病可以通过确定高骨特异性碱性磷酸酶的潜在原因或确定高完整甲状旁腺激素的原因来排除。如果4-5期CKD易碎性骨折患者认为骨质疏松是导致骨折的主要潜在代谢性骨病,FDA批准的治疗骨质疏松的药物在标签上或标签外都是有益的。
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Bones and the Kidney
Management of osteoporosis in patients with chronic kidney disease (CKD) is often very challenging and it should consider the pathophysiology of both disorders. Patients with stage 4–5 CKD are especially at very high risk for fragility fractures and secondary increase in mortality. Discriminating between osteoporosis and CKD-MBD is best accomplished with quantitative bone histomorphometry but biochemical markers of bone turnover, especially intact parathyroid hormone (PTH) and bone-specific alkaline phosphatase, also may be helpful. The one renal bone disease where antiresorptive osteoporosis therapies would be potentially unsafe is idiopathic renal adynamic bone disease. The two renal bone diseases where an osteoporosis pharmacological agent would not be advised are osteomalacia and primary hyperparathyroid bone disease which can be excluded by defining the underlying cause of a high bone-specific alkaline phosphatase or defining the cause of a very high intact PTH. If a stage 4–5 CKD patient with fragility fractures is felt to have osteoporosis as the major underlying metabolic bone disease causing fractures, FDA approved pharmacological agents for the treatment of osteoporosis can be beneficial on or off label.
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