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Published on: May 17, 2015
Sclerostin and Dickkopf-1 in post-menopausal renal allograft recipients
1Renal Unit, Department of Medicine, University-Hospital of Verona, Verona, Italy.
Background:
Age, pre-existing renal osteodistrophy, impaired renal function, and chronic use of immunosuppressive drugs are the main factors involved in the onset and development of bone metabolism disturbances and skeletal alterations occurring after renal transplantation. However, at the state of the art, no reports have analyzed the additional post-menopausal physiological mechanisms associated with the onset and development of bone complications in renal transplant recipients.
Methods:
We measured by means of molecular strategies (enzyme-linked immunoassay, chemiluminescence) the serum levels of Sclerostin and Dickkopf-1 (DKK1), two major antagonists of the Wnt/β-catenin pathway, and several bone resorption/formation biomarkers (N-terminal procollagen type 1, bone-specific alkaline phosphatase, and serum C-terminal telopeptides of type I collagen) in 19 post-menopausal kidney transplant patients and 12 post-menopausal chronic kidney disease patients (CKD group) matched for age and renal function.
Results:
Our results showed that the levels of both Wnt antagonists were similar in the two study groups (P=.15 and .96, respectively). Additionally, no correlation was found between Sclerostin and DKK1 serum levels in all patients included in the study (R2=0.03, P=.2). After statistical analysis, we found no differences in the bone resorption/formation biomarkers between renal transplant and CKD patients. Multivariate analysis showed that Sclerostin levels were significantly positively correlated with serum phosphorus levels (P=.008) and inversely correlated with renal function (P=.026). Surprisingly, no significant correlation was found between all the analyzed demographic and clinical parameters and DKK1.
Conclusions:
Our study demonstrated for the first time that renal transplantation per se and immunosuppressive treatments do not represent additional factors contributing to bone metabolic/biochemical alterations in post-menopausal women. However, our results emphasized that a better preservation of the graft function could significantly slow down the progression of bone metabolic deregulations and prevent clinical bone complications.
Insights
Renal transplantation does not worsen bone metabolism in post-menopausal women. Preserving kidney graft function is key to preventing bone complications and metabolic deregulations.
Area of Science:
- Nephrology
- Endocrinology
- Bone Metabolism
Background:
- Bone metabolism disturbances are common after kidney transplantation.
- Factors include age, renal osteodystrophy, impaired renal function, and immunosuppression.
- Post-menopausal physiological mechanisms in transplant recipients remain understudied.
Purpose of the Study:
- To investigate bone metabolic alterations in post-menopausal kidney transplant recipients.
- To compare bone biomarkers and Wnt antagonists (Sclerostin, DKK1) between transplant and CKD patients.
- To identify factors influencing bone complications post-transplantation.
Main Methods:
- Serum levels of Sclerostin and Dickkopf-1 (DKK1) were measured using immunoassay techniques.
- Bone resorption and formation biomarkers were quantified.
- 19 post-menopausal kidney transplant patients and 12 post-menopausal CKD patients were analyzed.
Main Results:
- Sclerostin and DKK1 levels were similar between kidney transplant and CKD groups.
- No significant differences in bone resorption/formation biomarkers were observed.
- Sclerostin correlated positively with phosphorus and inversely with renal function.
Conclusions:
- Renal transplantation and immunosuppression do not independently cause bone metabolic alterations in post-menopausal women.
- Preserving graft function is crucial for slowing bone metabolic deregulation.
- This study highlights the importance of graft function in managing bone health post-transplant.
