Bone Mineral Disease After Kidney Transplantation.


Journal

Calcified tissue international
ISSN: 1432-0827
Titre abrégé: Calcif Tissue Int
Pays: United States
ID NLM: 7905481

Informations de publication

Date de publication:
04 2021
Historique:
received: 04 03 2021
accepted: 09 03 2021
pubmed: 26 3 2021
medline: 19 8 2021
entrez: 25 3 2021
Statut: ppublish

Résumé

Chronic kidney disease-mineral bone disorder (CKD-MBD) after kidney transplantation is a mix of pre-existing disorders and new alterations. The final consequences are reflected fundamentally as abnormal mineral metabolism (hypercalcemia, hypophosphatemia) and bone alterations [high or low bone turnover disease (as fibrous osteitis or adynamic bone disease), an eventual compromise of bone mineralization, decrease bone mineral density and bone fractures]. The major cause of post-transplantation hypercalcemia is the persistence of severe secondary hyperparathyroidism, and treatment options include calcimimetics or parathyroidectomy. On turn, hypophosphatemia is caused by both the persistence of high blood levels of PTH and/or high blood levels of FGF23, with its correction being very difficult to achieve. The most frequent bone morphology alteration is low bone turnover disease, while high-turnover osteopathy decreases in frequency after transplantation. Although the pathogenic mechanisms of these abnormalities have not been fully clarified, the available evidence suggests that there are a number of factors that play a very important role, such as immunosuppressive treatment, persistently high levels of PTH, vitamin D deficiency and hypophosphatemia. Fracture risk is four-fold higher in transplanted patients compared to general population. The most relevant risk factors for fracture in the kidney transplant population are diabetes mellitus, female sex, advanced age (especially > 65 years), dialysis vintage, high PTH levels and low phosphate levels, osteoporosis, pre-transplant stress fracture and high doses or prolonged steroids therapy. Treatment alternatives for CKD-MBD after transplantation include minimization of corticosteroids, use of calcium and vitamin D supplements, antiresorptives (bisphosphonates or Denosumab) and osteoformers (synthetic parathyroid hormone). As both mineral metabolism and bone disorders lead to increased morbidity and mortality, the presence of these changes after transplantation has to be prevented (if possible), minimized, diagnosed, and treated as soon as possible.

Identifiants

pubmed: 33765230
doi: 10.1007/s00223-021-00837-0
pii: 10.1007/s00223-021-00837-0
doi:

Substances chimiques

FGF23 protein, human 0
Minerals 0
Parathyroid Hormone 0
Fibroblast Growth Factor-23 7Q7P4S7RRE

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

551-560

Références

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Auteurs

Josep-Vicent Torregrosa (JV)

Nephrology & Renal Transplant Department - Hospital Clínic, Barcelona, Spain. vtorre@clinic.cat.
Universidad de Barcelona, Barcelona, Spain. vtorre@clinic.cat.

Ana Carina Ferreira (AC)

Nephrology Department, Centro Hospitalare, Universitário de Lisboa Central, Lisbon, Portugal.
Nova Medical School, Nova University, Lisbon, Portugal.

David Cucchiari (D)

Nephrology & Renal Transplant Department - Hospital Clínic, Barcelona, Spain.

Aníbal Ferreira (A)

Nephrology Department, Centro Hospitalare, Universitário de Lisboa Central, Lisbon, Portugal.
Nova Medical School, Nova University, Lisbon, Portugal.

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