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Background: Chronic Kidney Disease associated with Mineral Bone Disease (CKD-MBD) is frequent in kidney transplant patients. Post-transplantation bone disease is complex, especially in patients with pre-existing metabolic bone disorders that are further affected by immunosuppressive medications and changes in renal allograft function. Main biochemical abnormalities of mineral metabolism in kidney transplantation (KTx) include hypophosphatemia, hyperparathyroidism (HPTH), insufficiency or deficiency of vitamin D, and hypercalcemia. Objective: This review aimed to summarize the pathophysiology and main biomarkers of CKD-MBD in KTx. Methods: A comprehensive and non-systematic search in PubMed was independently made with an emphasis on biomarkers in mineral bone disease in KTx. Results: CKD-MBD can be associated with numerous factors including secondary HPTH, metabolic dysregulations before KTx, and glucocorticoids therapy in post-transplant subjects. Fibroblast growth factor 23 (FGF23) reaches normal levels after KTx with good allograft function, while calcium, vitamin D and phosphorus, ultimately, result in hypercalcemia, persistent vitamin D insufficiency, and hypophosphatemia respectively. As for PTH levels, there is an initial tendency of a significant decrease, followed by a raise due to secondary or tertiary HPTH. In regard to sclerostin levels, there is no consensus in the literature. Conclusion: KTx patients should be continuously evaluated for mineral homeostasis and bone status, both cases with successful kidney transplantation and those with reduced functionality. Additional research on CKD-MBD pathophysiology, diagnosis, and management is essential to guarantee long-term graft function, better prognosis, good quality of life, and reduced mortality for KTx patients.
Background: Chronic Kidney Disease associated with Mineral Bone Disease (CKD-MBD) is frequent in kidney transplant patients. Post-transplantation bone disease is complex, especially in patients with pre-existing metabolic bone disorders that are further affected by immunosuppressive medications and changes in renal allograft function. Main biochemical abnormalities of mineral metabolism in kidney transplantation (KTx) include hypophosphatemia, hyperparathyroidism (HPTH), insufficiency or deficiency of vitamin D, and hypercalcemia. Objective: This review aimed to summarize the pathophysiology and main biomarkers of CKD-MBD in KTx. Methods: A comprehensive and non-systematic search in PubMed was independently made with an emphasis on biomarkers in mineral bone disease in KTx. Results: CKD-MBD can be associated with numerous factors including secondary HPTH, metabolic dysregulations before KTx, and glucocorticoids therapy in post-transplant subjects. Fibroblast growth factor 23 (FGF23) reaches normal levels after KTx with good allograft function, while calcium, vitamin D and phosphorus, ultimately, result in hypercalcemia, persistent vitamin D insufficiency, and hypophosphatemia respectively. As for PTH levels, there is an initial tendency of a significant decrease, followed by a raise due to secondary or tertiary HPTH. In regard to sclerostin levels, there is no consensus in the literature. Conclusion: KTx patients should be continuously evaluated for mineral homeostasis and bone status, both cases with successful kidney transplantation and those with reduced functionality. Additional research on CKD-MBD pathophysiology, diagnosis, and management is essential to guarantee long-term graft function, better prognosis, good quality of life, and reduced mortality for KTx patients.
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