title: Left ventricular mass progression despite stable blood pressure and kidney function in stage 3 chronic kidney disease.
abstract: OBJECTIVE
  Progressive chronic kidney disease (CKD) is associated with worsening cardiovascular (CV) risk not explained by traditional risk factors. Left ventricular (LV) hypertrophy (LVH) is an important CV risk factor, but its progression has not been documented in early CKD. We explored whether progression of LVH in early CKD would occur despite stable kidney function.
  
  
  METHODS
  We conducted a post hoc analysis of a 12-month study of lanthanum carbonate in stage 3 CKD, which included longitudinal assessments of CV biomarkers. Primary outcome for the analysis was the change in LV mass (LVM) indexed to height in meters(2.7) (LVM/Ht(2.7)). Secondary outcomes were changes in blood pressure (BP), pulse-wave velocity, LV systolic/diastolic function, fibroblast growth factor 23 (FGF23), klotho, and estimated glomerular filtration rate (eGFR).
  
  
  RESULTS
  Thirty-one of 38 original subjects had sufficient data for analysis. LVM/Ht(2.7) increased (47 ± 13 vs. 53 ± 13 g/m(2.7), p = 0.006) over 12 months despite stable BP, stable eGFR and normal LV systolic function. Vascular stiffness and LV diastolic dysfunction persisted throughout the study. Klotho levels decreased (748 ± 289 to 536 ± 410 pg/ml, p = 0.03) but were unrelated to changes in LVM/Ht(2.7). The change in FGF23/klotho ratio was strongly correlated with changes in LVM/Ht(2.7) (r2 = 0.582, p = 0.03).
  
  
  CONCLUSIONS
  Subjects with stage 3 CKD exhibited increasing LVM, persistent LV diastolic dysfunction and vascular stiffness despite stable kidney function, BP and LV systolic function. Abnormal FGF23 signaling due to reduced klotho expression may be associated with increasing LVM.
authors.affiliation: Division of Pediatric Nephrology, Southern Illinois University, Springfield, Ill., USA.
authors.forename: Michael E
authors.initials: ME
authors.lastname: Seifert
authors.forename: Lisa
authors.initials: L
authors.lastname: de las Fuentes
authors.forename: Charles
authors.initials: C
authors.lastname: Ginsberg
authors.forename: Marcos
authors.initials: M
authors.lastname: Rothstein
authors.forename: Dennis J
authors.initials: DJ
authors.lastname: Dietzen
authors.forename: Steven C
authors.initials: SC
authors.lastname: Cheng
authors.forename: Will
authors.initials: W
authors.lastname: Ross
authors.forename: David
authors.initials: D
authors.lastname: Windus
authors.forename: Victor G
authors.initials: VG
authors.lastname: Dávila-Román
authors.forename: Keith A
authors.initials: KA
authors.lastname: Hruska
mesh_terms: D000368:Aged; D001794:Blood Pressure; D001827:Body Height; D018450:Disease Progression; D005260:Female; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000097:blood; D005919:Glomerular Filtration Rate; D005966:Glucuronidase / Q000097:blood; D006352:Heart Ventricles / Q000473:pathology*; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000473:pathology* / Q000503:physiopathology; D000090265:Klotho Proteins; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D009929:Organ Size; D063177:Pulse Wave Analysis; D051436:Renal Insufficiency, Chronic / Q000097:blood / Q000503:physiopathology*; D059289:Vascular Stiffness; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*
chemical_list: C000717427:FGF23 protein, human; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23; D005966:Glucuronidase; D000090265:Klotho Proteins