Department of Nephrology, Abdominal Center, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Kuopio Musculoskeletal Research Unit (KMRU), University of Eastern Finland, Kuopio, Finland.
PLoS One. 2022 Mar 29;17(3):e0261686. doi: 10.1371/journal.pone.0261686. eCollection 2022.
Disordered mineral metabolism reverses incompletely after kidney transplantation in numerous patients. Post-transplantation bone disease is a combination of pre-existing chronic kidney disease and mineral disorder and often evolving osteoporosis. These two frequently overlapping conditions increase the risk of post-transplantation fractures.
We studied the prevalence of low bone volume in bone biopsies obtained from kidney transplant recipients who were biopsied primarily due to the clinical suspicion of persistent hyperparathyroidism between 2000 and 2015 at the Hospital District of Helsinki and Uusimaa. Parameters of mineral metabolism, results of dual-energy x-ray absorptiometry scans, and the history of fractures were obtained concurrently. One hundred nine bone biopsies taken at a median of 31 (interquartile range, IQR, 18-70) months after transplantation were included in statistical analysis. Bone turnover was classified as high in 78 (72%) and normal/low in 31 (28%) patients. The prevalence of low bone volume (n = 47, 43%) was higher among patients with low/normal turnover compared to patients with high turnover [18 (58%) vs. 29 (37%), P = 0.05]. Thirty-seven fragility fractures in 23 (21%) transplant recipients corresponding to fracture incidence 15 per 1000 person-years occurred during a median follow-up 9.1 (IQR, 6.3-12.1) years. Trabecular bone volume did not correlate with incident fractures. Accordingly, low bone mineral density at the lumbar spine correlated with low trabecular bone volume, but not with incident fractures. The cumulative corticosteroid dose was an important determinant of low bone volume, but not of incident fractures.
Despite the high prevalence of trabecular bone loss among kidney transplant recipients, the number of fractures was limited. The lack of association between trabecular bone volume and fractures suggests that the bone cortical compartment and quality are important determinants of bone strength and post-transplantation fracture.
在许多患者中，肾移植后矿物质代谢紊乱不能完全恢复。移植后骨病是既有慢性肾脏病和矿物质紊乱，又经常进展为骨质疏松症的一种综合病症。这两种经常重叠的病症增加了移植后骨折的风险。
我们研究了 2000 年至 2015 年间在赫尔辛基和乌西玛地区医院区因临床疑似持续性甲状旁腺功能亢进而接受肾移植活检的患者的骨活检中低骨量的患病率。同时获取矿物质代谢参数、双能 X 射线吸收仪扫描结果和骨折史。将 109 例移植后中位数为 31（四分位距，IQR，18-70）个月的骨活检纳入统计分析。骨转换被分为高转换 78 例（72%）和低/正常转换 31 例（28%）。与高转换患者相比，低/正常转换患者低骨量（n = 47，43%）的患病率更高[18（58%）比 29（37%），P = 0.05]。23 例（21%）移植受者发生 37 例脆性骨折（37 例对应骨折发生率为 15/1000 人年），中位随访时间为 9.1（IQR，6.3-12.1）年。小梁骨体积与骨折事件无相关性。相应地，腰椎骨密度与低小梁骨体积相关，但与骨折事件无关。累积皮质激素剂量是低骨量的重要决定因素，但不是骨折事件的决定因素。
尽管肾移植受者的小梁骨丢失发生率较高，但骨折的数量有限。小梁骨体积与骨折之间缺乏关联表明，皮质骨和骨质量是骨强度和移植后骨折的重要决定因素。
