Management of mineral and bone disorders in renal transplant recipients
Post‐transplantation bone loss is greatest in the first 6–12 months, and the majority of post‐transplantation fractures are peripheral. The incidence has been variably reported but exceeds 40% in some studies.3 In a study comparing recent renal transplant recipients to dialysis patients on the transplant waiting list, the relative risk of fractures is 34% higher in the first 6 month post‐transplantation.4 The use of prednisolone is the main cause of bone loss, as highlighted by a longitudinal bone biopsy study performed early post‐transplantation.5 The main findings were a decrease in osteoblast number, early posteoblast apoptosis, a reduced bone formation rate and prolonged mineralisation lag time. Significantly, these findings were present in patients with both high and low bone turnover, suggesting that these findings are independent of pre‐existing CKD‐MBD. Long‐term, a degree of recoupling between bone formation and resorption occurs, and depending on renal allograft function and abnormalities of mineral metabolism, BMD may stabilize or even improve post‐transplantation.6
Variable strategies and treatments are used to detect bone loss and preserve BMD after transplantation; however, none have been shown to clearly alter fracture risk. We now discuss the 2009 Kidney Disease Improving Global Outcomes (KDIGO) guidelines for the management of bone disease in RTRs and review recent evidence with a focus on implications for changes to clinical practice.