title: Diabetic nephropathy in pregnancy: suboptimal hypertensive control associated with preterm delivery.
abstract: BACKGROUND
  Nephropathy complicates 5% to 10% of pregnancies in women with diabetes and is associated with adverse outcomes. Given the importance of blood pressure (BP) control in reducing cardiovascular and renal complications outside of pregnancy, we hypothesized that poorly controlled hypertension in early pregnancy among women with diabetic nephropathy would be associated with adverse outcomes.
  
  
  METHODS
  To examine the impact of hypertensive control in early pregnancy on perinatal outcomes, we performed a retrospective cohort study of pregnancies complicated by diabetic nephropathy with "Above Target" mean arterial pressure (> or = 100 mm Hg; N = 21) and "Below Target" mean arterial pressure (< 100 mm Hg; N = 22), which approximates the American Diabetes Association and the Seventh Report of the Joint National Committee recommended target of 130/80 mm Hg, measured at < 20 weeks' gestation.
  
  
  RESULTS
  There were no differences in maternal age (mean +/- SEM: 27.2 +/- 1.2 v 29.5 +/- 1.0 years), duration of diabetes (median, range: 17.5, 13 to 24 v 16, 1 to 25 years), or glucose control (glycosylated hemoglobin [HbA1c] 8.0% +/- 0.3% v 8.1% +/- 0.4%) between the Above and Below Target groups. The Above Target group had more proteinuria (4.69 +/- 1.08 v 1.65 +/- 0.43 g/24 h; P = .007) and higher serum creatinine levels (1.23 +/- 0.17 v 0.85 +/- 0.06 mg/dL; P = .02). The Above Target group was more likely to deliver at < 32 weeks' gestation (38.1% v 4.6%; P = .007). The increased risk of preterm delivery remained significant after adjusting for duration of diabetes and glucose control.
  
  
  CONCLUSIONS
  Suboptimal control of hypertension in early pregnancy in women with diabetic nephropathy is associated with a significant risk of preterm delivery. Improved preconceptional control of hypertension may reduce adverse perinatal outcomes in women with diabetic nephropathy.
authors.affiliation: Department of Obstetrics and Gynecology, University of Washington, Seattle, Washington 98195-6460, USA. darcarr@u.washington.edu
authors.forename: Darcy B
authors.initials: DB
authors.lastname: Carr
authors.forename: Gretchen L
authors.initials: GL
authors.lastname: Koontz
authors.forename: Carolyn
authors.initials: C
authors.lastname: Gardella
authors.forename: Emily V
authors.initials: EV
authors.lastname: Holing
authors.forename: Debra A
authors.initials: DA
authors.lastname: Brateng
authors.forename: Zane A
authors.initials: ZA
authors.lastname: Brown
authors.forename: Thomas R
authors.initials: TR
authors.lastname: Easterling
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology*; D002302:Cardiac Output / Q000502:physiology; D003928:Diabetic Nephropathies / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D015994:Incidence; D007231:Infant, Newborn; D007752:Obstetric Labor, Premature / Q000453:epidemiology / Q000209:etiology*; D011247:Pregnancy; D011248:Pregnancy Complications; D011379:Prognosis; D012189:Retrospective Studies
chemical_list: D001786:Blood Glucose