Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN, USA.
Department of Medicine, Division of Nephrology, Indiana University School of Medicine, Indianapolis, IN, USA.
J Bone Miner Res. 2022 Jul;37(7):1297-1306. doi: 10.1002/jbmr.4574. Epub 2022 Jun 3.
Chronic kidney disease (CKD) affects 15% of Americans and greatly increases fracture risk due to elevated parathyroid hormone, cortical porosity, and reduced bone material quality. Calcimimetic drugs are used to lower parathyroid hormone (PTH) in CKD patients, but their impact on bone matrix properties remains unknown. We hypothesized that tissue-level bone quality is altered in early CKD and that calcimimetic treatment will prevent these alterations. To test this hypothesis, we treated Cy/+ rats, a model of spontaneous and progressive CKD-mineral and bone disorder (CKD-MBD), with KP-2326, a preclinical analogue of etelcalcetide, early in the CKD disease course. To measure tissue-level bone matrix composition and material properties, we performed colocalized Raman spectroscopy and nanoindentation on new periosteal bone and perilacunar bone using hydrated femur sections. We found that CKD and KP treatment lowered mineral type B carbonate substitution whereas KP treatment increased mineral crystallinity in new periosteal bone. Reduced elastic modulus was lower in CKD but was not different in KP-treated rats versus CTRL. In perilacunar bone, KP treatment lowered type B carbonate substitution, increased crystallinity, and increased mineral-to-matrix ratio in a spatially dependent manner. KP treatment also increased reduced elastic modulus and hardness in a spatially dependent manner. Taken together, these data suggest that KP treatment improves material properties on the tissue level through a combination of lowering carbonate substitution, increasing mineral crystallinity, and increasing relative mineralization of the bone early in CKD. As a result, the mechanical properties were improved, and in some regions, were the same as control animals. Therefore, calcimimetics may help prevent CKD-induced bone deterioration by improving bone quality in new periosteal bone and in bone tissue near osteocyte lacunae. © 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).
慢性肾脏病(CKD)影响了 15%的美国人,并由于甲状旁腺激素升高、皮质多孔性和骨材料质量降低而大大增加了骨折风险。钙敏感受体激动剂被用于降低 CKD 患者的甲状旁腺激素(PTH),但它们对骨基质特性的影响尚不清楚。我们假设早期 CKD 会改变组织水平的骨质量,钙敏感受体激动剂治疗将预防这些改变。为了验证这一假设,我们用 KP-2326 治疗 Cy/+大鼠,一种自发性和进行性 CKD-矿物质和骨疾病(CKD-MBD)的模型,在 CKD 病程的早期用 KP-2326 治疗。为了测量组织水平的骨基质组成和材料特性,我们对新骨膜下骨和骨陷窝旁骨进行了共定位拉曼光谱和纳米压痕分析,使用了水合股骨切片。我们发现,CKD 和 KP 治疗降低了矿化类型 B 的碳酸盐取代物,而 KP 治疗增加了新骨膜下骨的矿化结晶度。CKD 时弹性模量降低,但 KP 治疗组与对照组相比无差异。在骨陷窝旁骨中,KP 治疗以空间依赖的方式降低了 B 型碳酸盐取代物,增加了结晶度,并增加了矿化相对于基质的比例。KP 治疗还以空间依赖的方式增加了弹性模量降低和硬度。总的来说,这些数据表明,KP 治疗通过降低碳酸盐取代物、增加矿化结晶度和增加早期 CKD 时骨的相对矿化,改善了组织水平的材料特性。因此,机械性能得到了改善,在某些区域与对照动物相同。因此,钙敏感受体激动剂可能通过改善新骨膜下骨和骨陷窝旁骨组织的骨质量来帮助预防 CKD 引起的骨恶化。