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Volume 59, Issue 3, Pages 385-389 (March 2010)


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Obesity is associated with increased parathyroid hormone levels independent of glomerular filtration rate in chronic kidney disease

Georges SaababcCorresponding Author Informationemail address, Adam Whaley-Connellbc, Samy I. McFarlaned, Suying Lie, Shu-Cheng Chene, James R. Sowersbc, Peter A. McCulloughf, George L. Bakrisg, Kidney Early Evaluation Program Investigators

Received 22 July 2009; accepted 7 August 2009. published online 05 October 2009.

Abstract 

The objective of the study was to examine the relationship of obesity and parathyroid hormone (PTH) levels among persons with chronic kidney disease (CKD). This was a cross-sectional analysis of 4551 participants in the National Kidney Foundation–Kidney Early Evaluation Program found to have CKD (estimated glomerular filtration rate <60 mL/[min 1.73 m2]) examining the relationship of body mass index (BMI) and PTH levels. In unadjusted analysis, PTH levels increased with increasing BMI quartiles. After adjustment for age, race, sex, diabetes, calcium, phosphorus, estimated glomerular filtration rate, and presence of microalbuminuria, PTH levels were 7.3% (P = .008), 11.9% (P < .0001), and 18.1% (P < .0001) higher in the second, third, and fourth BMI quartiles, respectively, as compared with the first quartile. In a companion analysis, higher BMI was associated with increased odds of having an elevated PTH measurement (>70 pg/mL). Compared with the first quartile, odds ratios for elevated PTH were 1.26 (95% confidence interval, 1.06-1.50; P = .01), 1.38 (1.15-1.65, P = .0005), and 1.66 (1.37-2.00, P < .0001) for the second, third, and fourth quartiles, respectively. We found no effect modification by race, diabetes, or presence of microalbuminuria. Therefore, in a large community-dwelling population with CKD, the presence of obesity and of increasing BMI is associated with higher PTH levels independent of measured confounders and may be an additional target in the management of secondary hyperparathyroidism in CKD.

a Washington University School of Medicine, St Louis, MO 63110, USA

b University of Missouri-Columbia School of Medicine, Columbia, MO 65211, USA

c Harry S. Truman VA Hospital, Columbia, MO 65201, USA

d SUNY-Downstate Brooklyn, Brooklyn, NY 11203, USA

e KEEP Data Coordinating Center, Minneapolis Medical Research Foundation, Minneapolis, MN 55404, USA

f William Beaumont Hospital, Royal Oak, MI 48073, USA

g University of Chicago School of Medicine, Chicago, IL 60637, USA

Corresponding Author InformationCorresponding author. Renal Division, Department of Internal Medicine, Washington University School of Medicine, St Louis, MO 63110, USA. Tel.: +1 314 362 4547; fax: +1 314 362 2713.

PII: S0026-0495(09)00331-X

doi:10.1016/j.metabol.2009.08.007


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