Acta clinica Belgica · 2025
Bisphosphonates in a kidney transplant recipient with persistent hyperparathyroidism: think twice.
СтатьяКлинический случайНазвание и аннотация: Перевод в очереди
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Engelen Thijs, Evenepoel Pieter
Аннотация
INTRODUCTION: Bone disease after kidney transplantation is complex, converging features of senile, postmenopausal, glucocorticoid-induced, and chronic kidney disease (CKD)-associated osteoporosis.
CASE PRESENTATION: We present a case of a 60-year-old female kidney transplant recipient with osteoporosis, who failed to show an improvement in areal bone mineral density (aBMD) after 5 years of annual intravenous therapy with 5 mg zoledronate. After thorough examination, persistent hyperparathyroidism and subsequent hypophosphatemia were pointed to as the most likely explanation.
DISCUSSION: Persistent hyperparathyroidism is a common finding in kidney transplant patients. Therapy with antiresorptive agents may mask the bone phenotype of persistent hyperparathyroidism, delaying the initiation of parathyroid hormone (PTH) suppressive therapy. Meanwhile, PTH driven hypophosphatemia may be a cause of antiresorptive treatment failure.
CONCLUSION: Present case emphasizes the importance of controlling CKD-mineral and bone disorders prior to initiating bone targeting drugs, as also has been recommended by recent consensus manuscripts. In an era in which bone turnover markers gain importance in guiding PTH suppressive and osteoporosis therapy, antiresorptive agents may complicate the diagnosis of hyperparathyroidism by masking the bone phenotype.
CASE PRESENTATION: We present a case of a 60-year-old female kidney transplant recipient with osteoporosis, who failed to show an improvement in areal bone mineral density (aBMD) after 5 years of annual intravenous therapy with 5 mg zoledronate. After thorough examination, persistent hyperparathyroidism and subsequent hypophosphatemia were pointed to as the most likely explanation.
DISCUSSION: Persistent hyperparathyroidism is a common finding in kidney transplant patients. Therapy with antiresorptive agents may mask the bone phenotype of persistent hyperparathyroidism, delaying the initiation of parathyroid hormone (PTH) suppressive therapy. Meanwhile, PTH driven hypophosphatemia may be a cause of antiresorptive treatment failure.
CONCLUSION: Present case emphasizes the importance of controlling CKD-mineral and bone disorders prior to initiating bone targeting drugs, as also has been recommended by recent consensus manuscripts. In an era in which bone turnover markers gain importance in guiding PTH suppressive and osteoporosis therapy, antiresorptive agents may complicate the diagnosis of hyperparathyroidism by masking the bone phenotype.