title: Relationship between glomerular dysfunction and left-ventricular mass independent of haemodynamic factors in a community sample.
abstract: OBJECTIVE
  To evaluate whether the relationship between early glomerular dysfunction and left-ventricular mass (LVM) occurs in a community sample and whether this relationship depends on haemodynamic factors.
  
  
  METHODS
  In 621 randomly selected participants from a community sample (332 were normotensive), estimated glomerular filtration rate (eGFR), LVM and dimensions were determined using echocardiography, and aortic blood pressure (BP) assessed from applanation tonometry and SphygmoCor software. Aortic pulse wave velocity (PWV) and high-quality 24-h BP values were available from 554 and 437 participants, respectively.
  
  
  RESULTS
  With adjustments for confounders (including clinic SBP), eGFR was associated with LVM index (LVMI) and LVM in excess of that predicted from stroke work (inappropriate LVM, LVMinappr) in all participants (LVMI: partial r = -0.18, P < 0.0001; LVMinappr: partial r = -0.17, P < 0.0001) and normotensive (LVMI: partial r = -0.23, P < 0.0001; LVMinappr: partial r = -0.22, P < 0.0001) separate from hypertensive patients. Marked differences in LVMinappr were noted in the eGFR range below 132 compared to at least 132 ml/min per 1.73 m (P < 0.0005). When replacing clinic BP with either aortic SBP, 24-h BP, PWV, stroke work (for LVMI), left-ventricular end-diastolic diameter (LVEDD), or circumferential wall stress in the regression models, eGFR retained strong associations with LVMI (P = 0.01 to <0.0001) and LVMinappr (P < 0.005 to <0.0001) and these effects were replicated in normotensive separate from hypertensive patients.
  
  
  CONCLUSIONS
  Strong relationships between eGFR and LVM occur at a community level irrespective of the presence of hypertension and independent of 24-h and aortic BP, PWV, LVEDD, stroke work and wall stress. Non-haemodynamic factors explain a considerable proportion of the relationship between early glomerular dysfunction and left-ventricular hypertrophy.
authors.affiliation: Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, University of the Witwatersrand, Johannesburg, South Africa.
authors.forename: Fabian
authors.initials: F
authors.lastname: Maunganidze
authors.forename: Gavin R
authors.initials: GR
authors.lastname: Norton
authors.forename: Muzi J
authors.initials: MJ
authors.lastname: Maseko
authors.forename: Carlos D
authors.initials: CD
authors.lastname: Libhaber
authors.forename: Olebogeng H I
authors.initials: OH
authors.lastname: Majane
authors.forename: Pinhas
authors.initials: P
authors.lastname: Sareli
authors.forename: Angela J
authors.initials: AJ
authors.lastname: Woodiwiss
mesh_terms: D000328:Adult; D005260:Female; D005919:Glomerular Filtration Rate; D006352:Heart Ventricles / Q000503:physiopathology*; D006801:Humans; D007678:Kidney Glomerulus / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D055815:Young Adult