Kasiske and colleagues studied mineral and bone metabolism after unilateral donor nephrectomy. Similar as to what is observed early in the course of chronic kidney disease, fibroblast growth factor 23 and parathyroid hormone concentrations were shown to be increased following kidney donation. High fibroblast growth factor 23 and parathyroid hormone concentrations most probably are a compensatory mechanism to maintain normophosphatemia. Bone biomarker profiles in the study suggest increased bone turnover as trade-off. Limitations inherent to the assessed biomarkers, however, warrant a prudent interpretation.