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Insulin resistance and lower plasma adiponectin increase malignancy risk in nondiabetic continuous ambulatory peritoneal dialysis patients

Jung Tak Parka1, Tae-Hyun Yooa1, Tae Ik Changa, Dong Hyung Leea, Joo Hyun Leea, Jung Eun Leea, Hoon Young Choia, Shin-Wook Kanga, Dae-Suk Hana, Dong-Ryeol RyubCorresponding Author Informationemail address

Received 2 October 2009; accepted 8 February 2010. published online 19 March 2010.
Corrected Proof

Abstract 

End-stage renal disease patients have a higher risk for developing cancer. Although several causes for this increased risk have been proposed, the risk factors for cancer development in this population have not been elucidated. The aim of this study was to determine whether metabolic derangements, including insulin resistance and altered adipokines, increase the risk of developing malignancies in peritoneal dialysis (PD) patients, who are vulnerable to metabolic disorders because of excessive glucose absorbed from the dialysate. Study subjects comprised 106 nondiabetic PD patients who had been on PD for a minimum of 3 months with no overt malignancy. Baseline anthropometry, fasting glucose, insulin, and adiponectin were measured. The development of malignancy was evaluated during the follow-up period. During the mean follow-up of 47.0 ± 23.7 months, malignancy occurred in 15 patients (14.2%). The most common site of cancer was the kidney (26.7%), followed by thyroid (13.3%) and stomach (13.3%). Baseline insulin levels and homeostasis model assessment of insulin resistance were significantly higher, whereas plasma adiponectin levels were significantly lower, in patients who developed malignancy. Cox proportional hazards analysis revealed that insulin levels, homeostasis model assessment of insulin resistance, and lower adiponectin were independent predictors of malignancy. These findings demonstrate that insulin resistance and lower adiponectin levels could be risk factors for malignancy in nondiabetic PD patients.

a Department of Internal Medicine, College of Medicine, Brain Korea 21 for Medical Science, Yonsei University, Seoul, South Korea

b Department of Internal Medicine, School of Medicine, Ewha Womans University, Seoul 158-710, South Korea

Corresponding Author InformationCorresponding author. Tel.: +82 2 2650 2507; fax: +82 2 2650 2505.

1 These authors contributed equally to this work.

PII: S0026-0495(10)00060-0

doi:10.1016/j.metabol.2010.02.006

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