Rapid cortical bone loss in patients with chronic kidney disease. (18th July 2013)

• Record Type: Journal Article
• Authors: Nickolas, Thomas L; Stein, Emily M; Dworakowski, Elzbieta; Nishiyama, Kyle K; Komandah‐Kosseh, Mafo; Zhang, Chiyuan A; McMahon, Donald J; Liu, Xiaowei S; Boutroy, Stephanie; Cremers, Serge; Shane, Elizabeth
• Is Part Of: Journal of bone and mineral research. Volume 28:Number 8(2013:Aug.)
• Page Start: 1811
• Page End: 1820
• Publication Date: 2013-07-18
• Subjects: CHRONIC KIDNEY DISEASE -- CORTICAL BONE -- RENAL OSTEODYSTROPHY -- HRpQCT -- DXA; Bones -- Metabolism -- Periodicals; Mineral metabolism -- Periodicals; 612.392
• DOI: 10.1002/jbmr.1916
• Languages: English
• ISSNs: 0884-0431

Abstract

ABSTRACT: Chronic kidney disease (CKD) patients may have high rates of bone loss and fractures, but microarchitectural and biochemical mechanisms of bone loss in CKD patients have not been fully described. In this longitudinal study of 53 patients with CKD Stages 2 to 5D, we used dual‐energy X‐ray absorptiometry (DXA), high‐resolution peripheral quantitative computed tomography (HRpQCT), and biochemical markers of bone metabolism to elucidate effects of CKD on the skeleton. Median follow‐up was 1.5 years (range 0.9 to 4.3 years); bone changes were annualized and compared with baseline. By DXA, there were significant declines in areal bone mineral density (BMD) of the total hip and ultradistal radius: −1.3% (95% confidence interval [CI] −2.1 to −0.6) and −2.4% (95% CI −4.0 to −0.9), respectively. By HRpQCT at the distal radius, there were significant declines in cortical area, density, and thickness and increases in porosity: −2.9% (95% CI −3.7 to −2.2), −1.3% (95% CI −1.6 to −0.6), −2.8% (95% CI −3.6 to −1.9), and +4.2% (95% CI 2.0 to 6.4), respectively. Radius trabecular area increased significantly: +0.4% (95% CI 0.2 to 0.6), without significant changes in trabecular density or microarchitecture. Elevated time‐averaged levels of parathyroid hormone (PTH) and bone turnover markers predicted cortical deterioration. Higher levels of serum 25‐hydroxyvitamin D predicted decreases in trabecular network heterogeneity. These data suggest that significant cortical loss occurs with CKD, which is mediated by hyperparathyroidism and elevated turnover. Future investigations are required to determine whether these cortical losses can be attenuated by treatments that reduce PTH levels and remodeling rates.