Chronic kidney disease-mineral bone disorder (CKD-MBD) after kidney transplantation is a mix of pre-existing disorders and new alterations. The final consequences are reflected fundamentally as abnormal mineral metabolism (hypercalcemia, hypophosphatemia) and bone alterations [high or low bone turnover disease (as fibrous osteitis or adynamic bone disease), an eventual compromise of bone mineralization, decrease bone mineral density and bone fractures]. The major cause of post-transplantation hypercalcemia is the persistence of severe secondary hyperparathyroidism, and treatment options include calcimimetics or parathyroidectomy. On turn, hypophosphatemia is caused by both the persistence of high blood levels of PTH and/or high blood levels of FGF23, with its correction being very difficult to achieve. The most frequent bone morphology alteration is low bone turnover disease, while high-turnover osteopathy decreases in frequency after transplantation. Although the pathogenic mechanisms of these abnormalities have not been fully clarified, the available evidence suggests that there are a number of factors that play a very important role, such as immunosuppressive treatment, persistently high levels of PTH, vitamin D deficiency and hypophosphatemia. Fracture risk is four-fold higher in transplanted patients compared to general population. The most relevant risk factors for fracture in the kidney transplant population are diabetes mellitus, female sex, advanced age (especially > 65 years), dialysis vintage, high PTH levels and low phosphate levels, osteoporosis, pre-transplant stress fracture and high doses or prolonged steroids therapy. Treatment alternatives for CKD-MBD after transplantation include minimization of corticosteroids, use of calcium and vitamin D supplements, antiresorptives (bisphosphonates or Denosumab) and osteoformers (synthetic parathyroid hormone). As both mineral metabolism and bone disorders lead to increased morbidity and mortality, the presence of these changes after transplantation has to be prevented (if possible), minimized, diagnosed, and treated as soon as possible.

肾移植后慢性肾病-矿物质骨病 (CKD-MBD) 是既存疾病和新变化的混合体。最终后果从根本上反映为异常矿物质代谢（高钙血症、低磷血症）和骨骼改变[高或低骨转换疾病（如纤维性骨炎或无动力性骨病），最终损害骨矿化，降低骨矿物质密度和骨折] . 移植后高钙血症的主要原因是严重继发性甲状旁腺功能亢进的持续存在，治疗选择包括拟钙剂或甲状旁腺切除术。反过来，低磷血症是由高血 PTH 水平和/或高血 FGF23 水平持续引起的，其纠正很难实现。最常见的骨形态改变是低骨转换疾病，而高转换骨病在移植后频率降低。虽然这些异常的发病机制尚未完全阐明，但现有证据表明，有许多因素起着非常重要的作用，例如免疫抑制治疗、持续高水平的 PTH、维生素 D 缺乏和低磷血症。与一般人群相比，移植患者的骨折风险高出四倍。肾移植人群骨折的最相关危险因素是糖尿病、女性、高龄（尤其是 > 65 岁）、透析年份、高 PTH 水平和低磷酸盐水平、骨质疏松症、移植前应力性骨折和高剂量或长期类固醇治疗。移植后 CKD-MBD 的治疗替代方案包括尽量减少皮质类固醇、使用钙和维生素 D 补充剂、抗吸收剂（双膦酸盐或狄诺塞麦）和成骨剂（合成甲状旁腺激素）。由于矿物质代谢和骨骼疾病都会导致发病率和死亡率增加，因此必须尽快预防（如果可能）、尽量减少、诊断和治疗移植后这些变化的存在。