Wesseling-Perry Katherine
Pediatric Nephrology, David Geffen School of Medicine at UCLA, A2-383 MDCC, 650 Charles Young Dr, Los Angeles, CA, 93001-1835, USA,
Curr Osteoporos Rep. 2015 Apr;13(2):98-105. doi: 10.1007/s11914-015-0253-4.
Although traditional diagnosis and treatment of renal osteodystrophy focused on changes in bone turnover, current data demonstrate that abnormalities in skeletal mineralization are also prevalent in pediatric chronic kidney disease (CKD) and likely contribute to skeletal morbidities that continue to plague this population. It is now clear that alterations in osteocyte biology, manifested by changes in osteocytic protein expression, occur in early CKD before abnormalities in traditional measures of mineral metabolism are apparent and may contribute to defective skeletal mineralization. Current treatment paradigms advocate the use of 1,25(OH)2vitamin D for the control of secondary hyperparathyroidism; however, these agents fail to correct defective skeletal mineralization and may exacerbate already altered osteocyte biology. Further studies are critically needed to identify the initial trigger for abnormalities of skeletal mineralization as well as the potential effects that current therapeutic options may have on osteocyte biology and bone mineralization.
尽管传统的肾性骨营养不良诊断和治疗主要关注骨转换的变化，但目前的数据表明，骨骼矿化异常在儿童慢性肾脏病（CKD）中也很普遍，并且可能导致继续困扰该人群的骨骼疾病。现在很清楚，在传统矿物质代谢指标出现异常之前，早期CKD就会发生以骨细胞蛋白表达变化为特征的骨细胞生物学改变，这可能导致骨骼矿化缺陷。目前的治疗方案主张使用1,25(OH)2维生素D来控制继发性甲状旁腺功能亢进；然而，这些药物无法纠正骨骼矿化缺陷，并且可能会加剧已经改变的骨细胞生物学状态。迫切需要进一步的研究来确定骨骼矿化异常的初始触发因素，以及目前的治疗选择可能对骨细胞生物学和骨矿化产生的潜在影响。
