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Two-year cortical and trabecular bone loss in CKD-5D: biochemical and clinical predictors

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Abstract

Summary

This prospective two-year study of patients on chronic dialysis measured changes in bone mineral density (BMD). Patients with higher baseline BMD and shorter dialysis vintage lost more bone. Treatment with anti-hypertensives acting on the central nervous system was protective against bone loss. Baseline serum levels of sclerostin and bone-specific alkaline phosphatase predicted bone loss.

Introduction

This prospective 2-year study of chronic kidney disease on dialysis (CKD-5D) patients assessed trabecular and cortical bone loss at the hip and spine and examined potential demographic, clinical, and serum biochemical predictors of bone loss.

Methods

Eighty-nine CKD-5D patients had baseline, year 1, and year 2 bone mineral density (BMD) measurements using dual X-ray absorptiometry (DXA) and quantitative computed tomography (QCT); concurrent blood samples were drawn and clinical variables recorded. No study treatments occurred.

Results

The 2-year total hip BMD change was − 5.9% by QCT and − 3.1% by DXA (p < 0.001). Spinal BMD was unchanged. QCT total hip cortical mass and volume decreased (− 7.3 and − 10.0%); trabecular volume increased by 5.9% (ps < 0.001). BMD changes did not vary with age, BMI, race, diabetes, smoking, or exercise. Patients with higher baseline BMD and shorter dialysis vintage lost more bone (p < 0.05). Vitamin D analogs and phosphate binders were not protective against bone loss; cinacalcet was protective by univariate but not by multivariable analysis. CNS-affecting antihypertensives were protective against loss of BMD, cortical mass, cortical volume (ps < 0.05) and trabecular mass (p = 0.007). These effects remained after adjustment. BSAP correlated with changes in BMD, cortical mass, and volume (p < 0.01) as did sclerostin (inversely).

Conclusions

There was severe cortical bone loss at the hip best recognized by QCT. Patients with shorter dialysis vintage and less pre-existing bone loss lost more bone, while treatment with CNS-acting antihypertensives was protective. BSAP and sclerostin were useful markers of bone loss.

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Acknowledgements

We thank the following colleagues for their support and making their patients available for our study: Dr. Nassair and colleagues of Nephrology Associates of Kentuckiana; Dr. Eleanor Lederer and colleagues of University of Louisville Division of Nephrology; Dr. Khalil Rahman and colleagues of Nephrology Associates of Lexington; Dr. Khalid Bhatti and Dr. Mahendra Patel of Nephrology Associates of Central Kentucky; Dr. Jyotin Chandarana, Dr. Rezkalla Butros, Dr. Ashutosh Lohe, Dr. Syed Hasni, and Dr. Harold Helton of Cumberland Nephrology; and Dr. Mostafa Amr of Central Kentucky Nephrology.

The authors would like to thank Kimberly McLaughlin and Nedda Hughes for their invaluable and knowledgeable work in patient enrollment and data collection. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

Funding

This study was funded in part by the National Institutes of Health, Grant RO1 080770, and the Kentucky Nephrology Research Trust. The project was supported by the National Center for Research Resources and the National Center for Advancing Translational Sciences, National Institutes of Health, through Grant UL1TR001998.

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Correspondence to H. H. Malluche.

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Malluche, H.H., Monier-Faugere, MC., Blomquist, G. et al. Two-year cortical and trabecular bone loss in CKD-5D: biochemical and clinical predictors. Osteoporos Int 29, 125–134 (2018). https://doi.org/10.1007/s00198-017-4228-4

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  • DOI: https://doi.org/10.1007/s00198-017-4228-4

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