A MATERNAL BUT NOT PATERNAL ASSOCIATION OF AMBULATORY BLOOD PRESSURE WITH ALBUMIN EXCRETION IN YOUNG OFFSPRING WITH TYPE 1 DIABETES

  1. M. Loredana Marcovecchio, MD1,
  2. Paivi H. Tossavainen, MD1,
  3. Carlo L. Acerini, MD1,
  4. Timothy G. Barrett, PhD2,
  5. Julie Edge, MD3,
  6. Andrew Neil, FRCP4,
  7. Julian Shield, MD5,
  8. Barry Widmer, BSC1,
  9. R. Neil Dalton, PhD6 and
  10. David B. Dunger, MD (dbd25{at}cam.ac.uk)1,7
  1. 1Department of Paediatrics, University of Cambridge, Cambridge, UK
  2. 2School of Clinical and Experimental Medicine, University of Birmingham, Birmingham, UK
  3. 3Department of Paediatric Endocrinology and Diabetes, Oxford Children's Hospital, Headington, Oxford, UK
  4. 4Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, UK
  5. 5Institute of Child Life & Health, UBHT Education Centre, Bristol, UK
  6. 6WellChild Laboratory, Evelina Children's Hospital, London, UK
  7. 7Institute of Metabolic Science, University of Cambridge, Cambridge, UK

    Abstract

    Objective. Familial predisposition to hypertension has been associated with the development of diabetic nephropathy in adults, but there are limited data in adolescents. Our aim was to assess whether parental ambulatory blood pressure (ABP) was associated with BP and albumin excretion in young offspring with type 1 diabetes.

    Research Design and Methods. 24-hour ABP monitoring was performed in 509 young offspring (mean age(±SD) 15.8±2.3yr) with type 1 diabetes, 311 fathers and 444 mothers. Systolic (SBP) and diastolic (DBP) BP during 24h, day (d) and night-time (n) were calculated. 3 early morning urinary albumin-creatinine ratios (ACR), HbA1c and anthropometric parameters were available for the offspring.

    Results. All paternal ABP parameters, except for nSBP, were independently related to the offspring's ABP (24h-SBP: β=0.18, 24h-DBP: β=0.22, dSBP β=0.25, dDBP β=0.23; nDBP β=0.18, all p<0.01). Maternal 24h-DBP (β=0.19 p=0.004), day-DBP (β=0.09 p=0.04) and nSBP (β=0.24 p=0.001) were related to the corresponding ABP parameter in the offspring.

    Significant associations were found between the offspring logACR and maternal ABP. The association with 24h-DBP (β=0.16 p=0.02), dDBP (β=0.16 p=0.02) and nDBP (β=0.15 p=0.03) persisted even after adjusting for the offspring's ABP. Mothers of offspring with microalbuminuria (MA) had higher ABP than mothers of offspring without MA (all p<0.05).

    Conclusions. In this cohort, parental ABP significantly influenced the offspring BP, therefore confirming familial influences on this trait. In addition, maternal ABP, particularly DBP, was closely related to ACR in the offspring, suggesting a dominant effect of maternal genes or an effect of the intrauterine environment on MA risk.

    Footnotes

      • Received June 25, 2009.
      • Accepted November 8, 2009.