Bone Disease in Chronic Kidney Disease and Kidney Transplant
Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD) comprises alterations in calcium, phosphorus, parathyroid hormone (PTH), Vitamin D, and fibroblast growth factor-23 (FGF-23) metabolism, abnormalities in bone turnover, mineralization, volume, linear growth or strength, and vascular calcific...
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| Format: | Article |
| Language: | English |
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MDPI AG
2022-12-01
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| Series: | Nutrients |
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| Online Access: | https://www.mdpi.com/2072-6643/15/1/167 |
| _version_ | 1797440129439105024 |
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| author | Ezequiel Bellorin-Font Eudocia Rojas Kevin J. Martin |
| author_facet | Ezequiel Bellorin-Font Eudocia Rojas Kevin J. Martin |
| author_sort | Ezequiel Bellorin-Font |
| collection | DOAJ |
| description | Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD) comprises alterations in calcium, phosphorus, parathyroid hormone (PTH), Vitamin D, and fibroblast growth factor-23 (FGF-23) metabolism, abnormalities in bone turnover, mineralization, volume, linear growth or strength, and vascular calcification leading to an increase in bone fractures and vascular disease, which ultimately result in high morbidity and mortality. The bone component of CKD-MBD, referred to as renal osteodystrophy, starts early during the course of CKD as a result of the effects of progressive reduction in kidney function which modify the tight interaction between mineral, hormonal, and other biochemical mediators of cell function that ultimately lead to bone disease. In addition, other factors, such as osteoporosis not apparently dependent on the typical pathophysiologic abnormalities resulting from altered kidney function, may accompany the different varieties of renal osteodystrophy leading to an increment in the risk of bone fracture. After kidney transplantation, these bone alterations and others directly associated or not with changes in kidney function may persist, progress or transform into a different entity due to new pathogenetic mechanisms. With time, these alterations may improve or worsen depending to a large extent on the restoration of kidney function and correction of the metabolic abnormalities developed during the course of CKD. In this paper, we review the bone lesions that occur during both CKD progression and after kidney transplant and analyze the factors involved in their pathogenesis as a means to raise awareness of their complexity and interrelationship. |
| first_indexed | 2024-03-09T12:03:40Z |
| format | Article |
| id | doaj.art-63a39e8135394113ba5bf6345d62e40a |
| institution | Directory Open Access Journal |
| issn | 2072-6643 |
| language | English |
| last_indexed | 2024-03-09T12:03:40Z |
| publishDate | 2022-12-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Nutrients |
| spelling | doaj.art-63a39e8135394113ba5bf6345d62e40a2023-11-30T23:01:07ZengMDPI AGNutrients2072-66432022-12-0115116710.3390/nu15010167Bone Disease in Chronic Kidney Disease and Kidney TransplantEzequiel Bellorin-Font0Eudocia Rojas1Kevin J. Martin2Division of Nephrology and Hypertension, Saint Louis University, Saint Louis, MO 63103, USADivision of Nephrology and Kidney Transplantation, University Hospital of Caracas, Caracas 1053, VenezuelaDivision of Nephrology and Hypertension, Saint Louis University, Saint Louis, MO 63103, USAChronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD) comprises alterations in calcium, phosphorus, parathyroid hormone (PTH), Vitamin D, and fibroblast growth factor-23 (FGF-23) metabolism, abnormalities in bone turnover, mineralization, volume, linear growth or strength, and vascular calcification leading to an increase in bone fractures and vascular disease, which ultimately result in high morbidity and mortality. The bone component of CKD-MBD, referred to as renal osteodystrophy, starts early during the course of CKD as a result of the effects of progressive reduction in kidney function which modify the tight interaction between mineral, hormonal, and other biochemical mediators of cell function that ultimately lead to bone disease. In addition, other factors, such as osteoporosis not apparently dependent on the typical pathophysiologic abnormalities resulting from altered kidney function, may accompany the different varieties of renal osteodystrophy leading to an increment in the risk of bone fracture. After kidney transplantation, these bone alterations and others directly associated or not with changes in kidney function may persist, progress or transform into a different entity due to new pathogenetic mechanisms. With time, these alterations may improve or worsen depending to a large extent on the restoration of kidney function and correction of the metabolic abnormalities developed during the course of CKD. In this paper, we review the bone lesions that occur during both CKD progression and after kidney transplant and analyze the factors involved in their pathogenesis as a means to raise awareness of their complexity and interrelationship.https://www.mdpi.com/2072-6643/15/1/167CKD: chronic kidney diseasekidney transplantbone diseaserenal osteodystrophyCKD-MBDhyperparathyroidism |
| spellingShingle | Ezequiel Bellorin-Font Eudocia Rojas Kevin J. Martin Bone Disease in Chronic Kidney Disease and Kidney Transplant Nutrients CKD: chronic kidney disease kidney transplant bone disease renal osteodystrophy CKD-MBD hyperparathyroidism |
| title | Bone Disease in Chronic Kidney Disease and Kidney Transplant |
| title_full | Bone Disease in Chronic Kidney Disease and Kidney Transplant |
| title_fullStr | Bone Disease in Chronic Kidney Disease and Kidney Transplant |
| title_full_unstemmed | Bone Disease in Chronic Kidney Disease and Kidney Transplant |
| title_short | Bone Disease in Chronic Kidney Disease and Kidney Transplant |
| title_sort | bone disease in chronic kidney disease and kidney transplant |
| topic | CKD: chronic kidney disease kidney transplant bone disease renal osteodystrophy CKD-MBD hyperparathyroidism |
| url | https://www.mdpi.com/2072-6643/15/1/167 |
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