The impact of renal transplantation on trabecular and cortical bone mineral density (BMD) and cortical structure is unknown. We obtained quantitative computed tomography scans of the tibia in pediatric renal transplant recipients at transplantation and 3, 6, and 12 months; 58 recipients completed at least two visits. We used more than 700 reference participants to generate Z-scores for trabecular BMD, cortical BMD, section modulus (a summary measure of cortical dimensions and strength), and muscle and fat area. At baseline, compared with reference participants, renal transplant recipients had significantly lower mean section modulus and muscle area; trabecular BMD was significantly greater than reference participants only in transplant recipients younger than 13 years. After transplantation, trabecular BMD decreased significantly in association with greater glucocorticoid exposure. Cortical BMD increased significantly in association with greater glucocorticoid exposure and greater decreases in parathyroid hormone levels. Muscle and fat area both increased significantly, but section modulus did not improve. At 12 months, transplantation associated with significantly lower section modulus and greater fat area compared with reference participants. Muscle area and cortical BMD did not differ significantly between transplant recipients and reference participants. Trabecular BMD was no longer significantly elevated in younger recipients and was low in older recipients. Pediatric renal transplant associated with persistent deficits in section modulus, despite recovery of muscle, and low trabecular BMD in older recipients. Future studies should determine the implications of these data on fracture risk and identify strategies to improve bone density and structure. During childhood and adolescence, skeletal development is characterized by increases in trabecular and cortical bone mineral density (BMD) and cortical dimensions. 1 Children with CKD have numerous risk factors for impaired bone acquisition, including growth failure, delayed puberty, malnutrition, acidosis, vitamin D deficiency, muscle deficits, and secondary hyperparathyroidism. Successful renal transplantation corrects many of the underlying abnormalities contributing to bone deficits in childhood CKD. However, immunosuppressive therapies and persistent hyperparathyroidism may impair recovery of bone structure and strength. The risk of fracture among adult renal transplant recipients increases in the months after transplantation and then gradually declines. 2 The