title: Role of adipose tissue in determining muscle mass in patients with chronic kidney disease.
abstract: OBJECTIVE
  Malnutrition is a powerful predictor of mortality in chronic kidney disease (CKD). However, its etiology is unclear. We hypothesized that the adipocyte-derived proteins leptin and adiponectin, inflammation (as measured by C-reactive protein, CRP), and insulin resistance (as measured by homeostasis model assessment, HOMA), implicated in the malnutrition-inflammation complex syndrome commonly seen in maintenance dialysis patients, would be associated with the loss of muscle mass in earlier stages of CKD. Arm muscle area was used as an indicator of muscle mass.
  
  
  METHODS
  The Modification of Diet in Renal Disease Study cohort of people with CKD stages 3 and 4 was used for analysis (N = 780).
  
  
  METHODS
  Regression models were carried out to examine the relationships of leptin, adiponectin, CRP, and HOMA with arm muscle area (the main study outcome).
  
  
  RESULTS
  Arm muscle area was 39 +/- 15 cm(2) (mean +/- SD), and adiponectin levels were 13 +/- 7 microg/mL. Median and interquartile range (IQR) concentrations were: 9.0 (13.6) ng/mL for leptin, 2.3 (4.9) mg/L for CRP, and 2.4 (2.0) for HOMA. Higher leptin (beta coefficient and 95% confidence interval, -6.9 [-8.7 to -5.1], P < .001) and higher CRP (beta coefficient and 95% confidence interval, -2.7 [-3.9 to -1.4], P < .001) were associated with lower arm muscle area. There was a trend toward lower arm muscle area with higher adiponectin (P = .07), but no association with HOMA (P = .80).
  
  
  CONCLUSIONS
  Leptin and CRP were associated with lower muscle mass in subjects with CKD at stages 3 and 4. Further studies are needed to understand the mechanisms underlying these associations, and to develop targeted interventions for this patient population.
authors.affiliation: Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston, Massachusetts 02111, USA. cvsceppa@comcast.net
authors.forename: Carmen
authors.initials: C
authors.lastname: Castaneda-Sceppa
authors.forename: Mark J
authors.initials: MJ
authors.lastname: Sarnak
authors.forename: Xuelei
authors.initials: X
authors.lastname: Wang
authors.forename: Tom
authors.initials: T
authors.lastname: Greene
authors.forename: Magdalena
authors.initials: M
authors.lastname: Madero
authors.forename: John W
authors.initials: JW
authors.lastname: Kusek
authors.forename: Gerald
authors.initials: G
authors.lastname: Beck
authors.forename: Joel D
authors.initials: JD
authors.lastname: Kopple
authors.forename: Andrew S
authors.initials: AS
authors.lastname: Levey
authors.forename: Vandana
authors.initials: V
authors.lastname: Menon
mesh_terms: D052242:Adiponectin / Q000097:blood; D000273:Adipose Tissue / Q000378:metabolism / Q000502:physiology*; D000293:Adolescent; D000328:Adult; D000368:Aged; D000886:Anthropometry; D001132:Arm; D015415:Biomarkers / Q000097:blood; D001823:Body Composition; D002097:C-Reactive Protein / Q000378:metabolism; D015331:Cohort Studies; D018450:Disease Progression; D005260:Female; D006801:Humans; D007333:Insulin Resistance; D007676:Kidney Failure, Chronic / Q000178:diet therapy / Q000378:metabolism* / Q000628:therapy; D020738:Leptin / Q000097:blood; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism / Q000502:physiology*; D009752:Nutritional Status; D011379:Prognosis; D012044:Regression Analysis; D006435:Renal Dialysis; D012720:Severity of Illness Index
chemical_list: D052242:Adiponectin; D015415:Biomarkers; D020738:Leptin; D002097:C-Reactive Protein