Decreased Circulating Sclerostin Levels in Renal Transplant Recipients With Persistent Hyperparathyroidism

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Sclerostin is an osteocyte-secreted soluble antagonist of the Wnt/β-catenin signaling pathway requisite for osteoblast development and activity. The regulation of sclerostin expression in bone is complex. Parathyroid hormone (PTH) is recognized to be an important suppressor. Circulating sclerostin levels are 2- to 4-fold higher in patients with end-stage renal disease as compared with individuals with normal renal function.


We performed a longitudinal observational cohort study and case-control study in 50 de novo renal transplant recipients, 50 chronic kidney disease (CKD) patients (n = 50) matched for age, sex, and estimated glomerular filtration rate, and 23 renal transplant recipients referred for parathyroidectomy to define the impact of renal transplantation on circulating sclerostin levels and to clarify the role of persistent (tertiary) hyperparathyroidism.


Sclerostin serum levels decreased by 61.2% (median) during the first 3 months after transplantation (1.24 vs 0.44 ng/mL, P < 0.0001) to increase thereafter toward levels observed in CKD counterparts (0.63 ng/ml). High PTH levels independently associated with low sclerostin levels, both at time of transplantation and at 1 year. Sclerostin levels significantly increased after parathyroidectomy (0.49 vs. 0.32 ng/ml, P < 0.0001). The time course of bone biomarkers after parathyroidectomy suggests that bone resorption normalizes earlier than bone formation.


Circulating sclerostin levels appear to show a biphasic pattern after renal transplantation with a rapid and profound decrease, followed by gradual increase towards levels observed in CKD counterparts. Our data support the notion that PTH is an important regulator of circulating sclerostin levels.

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