title: Rapid cortical bone loss in patients with chronic kidney disease.
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.
authors: Columbia University Medical Center, Department of Medicine, Division of Nephrology, New York, NY, USA. tln2001@columbia.edu
authors: Thomas L
authors: TL
authors: Nickolas
authors: Emily M
authors: EM
authors: Stein
authors: Elzbieta
authors: E
authors: Dworakowski
authors: Kyle K
authors: KK
authors: Nishiyama
authors: Mafo
authors: M
authors: Komandah-Kosseh
authors: Chiyuan A
authors: CA
authors: Zhang
authors: Donald J
authors: DJ
authors: McMahon
authors: Xiaowei S
authors: XS
authors: Liu
authors: Stephanie
authors: S
authors: Boutroy
authors: Serge
authors: S
authors: Cremers
authors: Elizabeth
authors: E
authors: Shane
mesh_terms: D015502:Absorptiometry, Photon; D000368:Aged; D015415:Biomarkers / Q000378:metabolism; D015519:Bone Density; D016723:Bone Remodeling; D001862:Bone Resorption / Q000150:complications* / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D001842:Bone and Bones / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D005260:Female; D005500:Follow-Up Studies; D006728:Hormones / Q000378:metabolism; D006801:Humans; D016014:Linear Models; D008137:Longitudinal Studies; D008297:Male; D009929:Organ Size; D006435:Renal Dialysis; D051436:Renal Insufficiency, Chronic / Q000150:complications* / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D006728:Hormones
keywords: CHRONIC KIDNEY DISEASE; CORTICAL BONE; DXA; HRpQCT; RENAL OSTEODYSTROPHY