Abstract
Mineral and bone diseases (MBD) are common in patients with chronic kidney disease who undergo kidney transplantation. The incidence, types and severity of MBD vary according to the duration of chronic kidney disease, presence of comorbid conditions and intake of certain medications. Moreover, multiple types of pathology may be responsible for MBD. After successful reversal of uremia by kidney transplantation, many bone and mineral disorders improve, while immunosuppression, other medications, and new and existing comorbidities may result in new or worsening MBD. Chronic kidney disease is also common after kidney transplantation and may impact bone and mineral disease. In this article, we reviewed the prevalence, pathophysiology, and impact of MBD on post-transplant outcomes. We also discussed the diagnostic approach; immunosuppression management and potential treatment of MBD in kidney transplant recipients.
Highlights
Organ transplantation is considered the most effective treatment for end-stage renal disease (ESRD)
Using a large dialysis organization (LDO) database, we found that more than 14,000 kidney transplant recipients have CKD-mineral and bone diseases (MBD) data before transplantation
Vitamin D analogs and vitamin D receptor activators Josephson et al showed in a controlled, blinded study that kidney transplant recipients who were given calcium and calcitriol had less bone loss in the lumbar spine and increased Bone Mineral Density (BMD) in the distal radius compared with transplant patients given calcium alone or placebo [54]
Summary
Organ transplantation is considered the most effective treatment for end-stage renal disease (ESRD). It is characterized by marked increase in bone turnover, irregularly shaped trabecules displaying numerous abnormal remodeling sites, and an unusually high number of bone cells with irregular arrangement and shape It is characterized by reduced bone volume, and mineralization is paralleled by a decrease in bone formation. It is characterized by presence of few osteoid seams and few osteoblasts. There are conflicting data among the findings described in the various studies, but the main pathology in bone remodeling after renal transplantation consists of decreased bone formation and mineralization associated with persistent bone resorption. The pathological defective bone formation may be a consequence of decreased osteoblastogenesis, osteoblast function, or increased osteoblast death rate
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