title: Role of lean body mass in estimating glomerular filtration rate in Alzheimer disease.
abstract: BACKGROUND
  The association between estimated glomerular filtration rate (eGFR) and progression of Alzheimer disease (AD), as measured by cognitive decline and brain atrophy, has been infrequently studied. Since AD is characterized by sarcopenia and other changes in body composition, which are known to influence GFR, a determination of how lean mass (LM) affects estimation of GFR in AD patients is important.
  
  
  METHODS
  Participants were drawn from a prospective longitudinal study of brain ageing and AD in community-dwelling individuals. Control (n = 60) and AD (n = 61) participants were enrolled. Estimated GFR was calculated using the four-variable Modification of Diet in Renal Disease (MDRD), Cockroft-Gault, Macdonald appendicular LM and Taylor LM equations. Association of eGFR with 2-year change in cognitive function and brain volume was assessed.
  
  
  RESULTS
  Individuals with AD demonstrated a paradoxical finding in which lower baseline MDRD eGFR was associated with less cognitive decline (P = 0.04) and brain atrophy (P = 0.02), a phenomenon not observed in non-AD controls. This finding was abolished in the AD patients when either the Macdonald appendicular LM or Taylor LM equations were used. While significant group-by-eGFR interactions were present for cognitive decline (P = 0.006) and brain atrophy (P = 0.001) when the MDRD equation was used, no group-by-eGFR interactions were present when either the Macdonald LM (P = 0.58 and P = 0.10 for cognitive decline and brain atrophy, respectively) or Taylor LM (P = 0.97 and P = 0.55) equations were used.
  
  
  CONCLUSIONS
  Accounting for measures of LM in GFR estimation appears to significantly mitigate counterintuitive relationships between measures of AD progression and eGFR as calculated by more traditional measures of renal function. This suggests that consideration of LM in eGFR calculations may be important in patients with sarcopenia, such as the AD population.
authors.affiliation: Department of Medicine, Division of Nephrology and Hypertension and The Kidney Institute, University of Kansas Medical Center, Kansas City, KS 66160, USA. jwetmore@kumc.edu
authors.forename: James B
authors.initials: JB
authors.lastname: Wetmore
authors.forename: Robyn A
authors.initials: RA
authors.lastname: Honea
authors.forename: Eric D
authors.initials: ED
authors.lastname: Vidoni
authors.forename: Ammar
authors.initials: A
authors.lastname: Almehmi
authors.forename: Jeffrey M
authors.initials: JM
authors.lastname: Burns
mesh_terms: D000368:Aged; D000544:Alzheimer Disease / Q000150:complications / Q000503:physiopathology*; D001823:Body Composition; D015992:Body Mass Index; D003071:Cognition / Q000502:physiology; D003404:Creatinine / Q000378:metabolism; D003704:Dementia / Q000503:physiopathology*; D005260:Female; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate; D006801:Humans; D007674:Kidney Diseases / Q000209:etiology / Q000473:pathology*; D007677:Kidney Function Tests; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D011446:Prospective Studies; D012307:Risk Factors; D013851:Thinness
chemical_list: D003404:Creatinine