title: Cardiac disease in young adult patients with end-stage renal disease since childhood: a Dutch cohort study.
abstract: BACKGROUND
  Cardiovascular disease is the most important cause of death in patients with pediatric end-stage renal disease (ESRD). Yet, few data exist on cardiac function in these patients. We assessed the extent of cardiac abnormality and analyzed its association with potential determinants in young adult patients with pediatric ESRD in a long-term follow-up study.
  
  
  METHODS
  All Dutch living adult patients with ESRD onset at age of 0 to 14 years between 1972 and 1992 were invited for echocardiography and blood pressure assessment. Special attention was paid to evidence of left ventricular hypertrophy (LVH), diastolic dysfunction, and aortic valve calcification. We collected data on determinants by review of all medical charts.
  
  
  RESULTS
  Of all the 187 living patients, 140 participated in the study. Of those, 110 patients had received a transplant and 30 patients were on dialysis. Mean age was 29.2 (20.7 to 41.8) years. Left ventricular mass index (LVMI) exceeded 150 g/m2 in 47% of all male patients and 120 g/m2 in 39% of all female patients, both consistent with LVH. Diastolic dysfunction, defined as an early over atrial transmitral blood flow velocity (E/A ratio) <1, was found in 18 (13%) patients; 27 (19%) had aortic valve calcification. Multiple regression analysis revealed the following: a high LVMI was associated with a current high blood pressure (beta=0.46, P < 0.001) and male gender (beta=0.21, P=0.009), a low E/A ratio with aging (beta=-0.28, P < 0.001) and a glomerular filtration rate (GFR) <25 mL/min/1.73 m2 (beta=-0.29, P < 0.001), and aortic valve calcification with prolonged peritoneal dialysis (beta=0.36, P < 0.001).
  
  
  CONCLUSIONS
  Young adult patients with pediatric ESRD are at risk for LVH caused by hypertension and for aortic valve calcification. Diastolic function decreases with age and is enhanced by a current low GFR. Prolonged peritoneal dialysis may enhance aortic valve calcification.
authors.affiliation: Department of Pediatrics, Emma Children's Hospital AMC, Amsterdam, The Netherlands.
authors.forename: Mariken P
authors.initials: MP
authors.lastname: Gruppen
authors.forename: Jaap W
authors.initials: JW
authors.lastname: Groothoff
authors.forename: Martin
authors.initials: M
authors.lastname: Prins
authors.forename: Poll
authors.initials: P
authors.lastname: van der Wouw
authors.forename: Martin
authors.initials: M
authors.lastname: Offringa
authors.forename: Willem Jan
authors.initials: WJ
authors.lastname: Bos
authors.forename: Jean Claude
authors.initials: JC
authors.lastname: Davin
authors.forename: Hugo S A
authors.initials: HS
authors.lastname: Heymans
mesh_terms: D000328:Adult; D017668:Age of Onset; D001024:Aortic Valve Stenosis / Q000453:epidemiology; D002114:Calcinosis / Q000453:epidemiology; D002648:Child; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D003971:Diastole; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000453:epidemiology*; D007668:Kidney / Q000502:physiology; D007676:Kidney Failure, Chronic / Q000453:epidemiology* / Q000503:physiopathology; D008297:Male; D009426:Netherlands / Q000453:epidemiology; D015995:Prevalence; D012189:Retrospective Studies; D012307:Risk Factors; D014463:Ultrasonography