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Prog Cardiovasc Dis. 2014 Jan-Feb;56(4):415-25. doi: 10.1016/j.pcad.2013.10.005. Epub 2013 Oct 9.

Obesity paradox in end-stage kidney disease patients.

Author information

1
Harold Simmons Center for Kidney Disease Research and Epidemiology, University of California Irvine, School of Medicine, Orange, CA, USA; Division of Nephrology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Republic of Korea. Electronic address: jonghaparkmd@gmail.com.
2
Harold Simmons Center for Kidney Disease Research and Epidemiology, University of California Irvine, School of Medicine, Orange, CA, USA.
3
Centers for Disease Control and Prevention (CDC), Hyattsville, MD.
4
Harold Simmons Center for Kidney Disease Research and Epidemiology, University of California Irvine, School of Medicine, Orange, CA, USA; Department of Statistics, University of California Irvine, Irvine, CA.
5
Division of Nephrology, Memphis Veterans Affairs Medical Center, Memphis, TN, USA; Division of Nephrology, University of Tennessee Health Science Center, Memphis, TN, USA.
6
Harold Simmons Center for Kidney Disease Research and Epidemiology, University of California Irvine, School of Medicine, Orange, CA, USA; Department of Epidemiology, UCLA Fielding School of Public Health, Los Angeles, CA. Electronic address: kamkal@ucla.edu.

Abstract

In the general population, obesity is associated with increased cardiovascular risk and decreased survival. In patients with end-stage renal disease (ESRD), however, an "obesity paradox" or "reverse epidemiology" (to include lipid and hypertension paradoxes) has been consistently reported, i.e. a higher body mass index (BMI) is paradoxically associated with better survival. This survival advantage of large body size is relatively consistent for hemodialysis patients across racial and regional differences, although published results are mixed for peritoneal dialysis patients. Recent data indicate that both higher skeletal muscle mass and increased total body fat are protective, although there are mixed data on visceral (intra-abdominal) fat. The obesity paradox in ESRD is unlikely to be due to residual confounding alone and has biologic plausibility. Possible causes of the obesity paradox include protein-energy wasting and inflammation, time discrepancy among competitive risk factors (undernutrition versus overnutrition), hemodynamic stability, alteration of circulatory cytokines, sequestration of uremic toxin in adipose tissue, and endotoxin-lipoprotein interaction. The obesity paradox may have significant clinical implications in the management of ESRD patients especially if obese dialysis patients are forced to lose weight upon transplant wait-listing. Well-designed studies exploring the causes and consequences of the reverse epidemiology of cardiovascular risk factors, including the obesity paradox, among ESRD patients could provide more information on mechanisms. These could include controlled trials of nutritional and pharmacologic interventions to examine whether gain in lean body mass or even body fat can improve survival and quality of life in these patients.

KEYWORDS:

BMI; CKD; CVD; Dialysis; ESRD; HD; Obesity paradox; PD; PEW; Reverse epidemiology; Visceral fat; body mass index; cardiovascular diseases; chronic kidney disease; end-stage renal disease; hemodialysis; peritoneal dialysis; protein energy wasting

PMID:
24438733
PMCID:
PMC4733536
DOI:
10.1016/j.pcad.2013.10.005
[Indexed for MEDLINE]
Free PMC Article

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