Abstract
The definition of Chronic Kidney Disease - Mineral Bone Disorder (CKD-MBD) has suffered significant changes over the last decade as our knowledge on the matter grows. The complexity of this subject is even bigger if you consider renal transplant recipients (RTRs) - they already have a legacy of CKD-MBD previous to transplant, their bones will be under the direct and indirect effects of immunosuppression and they will develop CKD-MBD secondary to their graft (dis) function.
Highlights
The Kidney Disease Improving Global Outcome (KDIGO) has greatly contributed to the Chronic Kidney Disease - Mineral Bone Disorder (CKD-MBD)’s definition in CKD population
The definition of Chronic Kidney Disease - Mineral Bone Disorder (CKD-MBD) has suffered significant changes over the last decade as our knowledge on the matter grows. The complexity of this subject is even bigger if you consider renal transplant recipients (RTRs) - they already have a legacy of CKD-MBD previous to transplant, their bones will be under the direct and indirect effects of immunosuppression and they will develop CKD-MBD secondary to their graft function
Special consideration should be given to the orthopedic management in RTRs regarding fracture risk and avascular necrosis of the major joints, the femoral head, due to the effects of immunosuppression
Summary
When a functioning kidney is implanted in a patient with CKD stage 5, high levels of FGF23 and PTH will suddenly act on a responsive organ, resulting in an important and immediate decrease of phosphate levels, immediate rise of calcium levels, progressive rise in 1,25-dihydroxy vitamin D and, by feedback, a theoretically normalization of FGF 23 and PTH [21,22]. Hypophosphatemia is registered in more that 90% of RTRs in the first month This is the result of the inhibition of phosphate reabsorption in proximal tubule by FGF 23, PTH and probably other phosphatonines [23,24]. At least one third of patients still have high levels of PTH [26] This is mainly explained by hyperplasia of parathyroid gland previous to transplantation with less calcium sensing receptors in the gland, resulting a decreased response to hypercalcemia. A single center study with 140 patients showed that persistent hyperparathyroidism on the third month after transplant was an independent risk factor for fracture with a 7.5 fold increase risk [30]. Osteodensitometry at day 14 and day 264 post-renal transplantation and concluded that higher levels of FGF-23 at the time of the transplant were associated with higher risk for bone mineral density loss during the first-year post-transplant [31]
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