Bone loss and fracture are serious sequelae of kidney transplantation, associated with morbidity, mortality and high economic costs. The pathogenesis of post-transplantation bone loss is multifactorial and complex. Pre-existing bone mineral disease is responsible for a significant part, but it is aggravated by risk factors emerging after renal transplantation with immunosuppressive agents being one of the key contributors. The decrease in bone mass is particularly prominent during the first 6-12 months after transplantation, continuing at a lower rate thereafter. Bone mineral density measurements do not predict bone histology and bone biopsy findings reveal heterogeneous lesions, which vary according to time after transplantation. Currently, vitamin D and bisphosphonates are the most extensively tested therapeutic agents against this accelerated bone loss in renal transplant recipients. Both of these agents have proven effective, but there is no evidence that they decrease fracture risk. More studies are needed to examine the complex pathophysiologic mechanisms implicated in this population, as well as the effects of different therapeutic interventions on bone disorders after kidney transplantation.