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2015 ; 5
(4
): 231-42
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Mineral and bone disorder after kidney transplantation
#MMPMID26722650
Taweesedt PT
; Disthabanchong S
World J Transplant
2015[Dec]; 5
(4
): 231-42
PMID26722650
show ga
After successful kidney transplantation, accumulated waste products and
electrolytes are excreted and regulatory hormones return to normal levels.
Despite the improvement in mineral metabolites and mineral regulating hormones
after kidney transplantation, abnormal bone and mineral metabolism continues to
present in most patients. During the first 3 mo, fibroblast growth factor-23
(FGF-23) and parathyroid hormone levels decrease rapidly in association with an
increase in 1,25-dihydroxyvitamin D production. Renal phosphate excretion resumes
and serum calcium, if elevated before, returns toward normal levels. FGF-23
excess during the first 3-12 mo results in exaggerated renal phosphate loss and
hypophosphatemia occurs in some patients. After 1 year, FGF-23 and serum
phosphate return to normal levels but persistent hyperparathyroidism remains in
some patients. The progression of vascular calcification also attenuates. High
dose corticosteroid and persistent hyperparathyroidism are the most important
factors influencing abnormal bone and mineral metabolism in long-term kidney
transplant (KT) recipients. Bone loss occurs at a highest rate during the first
6-12 mo after transplantation. Measurement of bone mineral density is recommended
in patients with estimated glomerular filtration rate > 30 mL/min. The use of
active vitamin D with or without bisphosphonate is effective in preventing early
post-transplant bone loss. Steroid withdrawal regimen is also beneficial in
preservation of bone mass in long-term. Calcimimetic is an alternative therapy to
parathyroidectomy in KT recipients with persistent hyperparathyroidism. If
parathyroidectomy is required, subtotal to near total parathyroidectomy is
recommended. Performing parathyroidectomy during the waiting period prior to
transplantation is also preferred in patients with severe hyperparathyroidism
associated with hypercalcemia.
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