title: Birth weight--a risk factor for progression in diabetic nephropathy?
abstract: OBJECTIVE
  Intrauterine growth retardation, as seen in individuals with low weight at birth, may give rise to a reduction in nephron number. Oligonephropathy has been linked to hypertension and renal disease in adult life. We tested the concept that low weight at birth acts as a risk factor for progression of diabetic nephropathy.
  
  
  METHODS
  We performed an observational follow-up study of 161 (97 men) type 1 diabetic patients with diabetic nephropathy [mean age (SD): 35 (11) years, mean duration of diabetes: 22 (8) years]. All patients had been followed for at least 3 years [median (range): 8 (3-20)] with at least three measurements [9 (3-31)] of glomerular filtration rate (GFR) (51Cr-EDTA). Information about birth size was obtained from midwife registrations.
  
  
  METHODS
  Steno Diabetes Center, a tertiary referral centre.
  
  
  METHODS
  Loss of kidney function according to birth weight and weight/length ratio at birth.
  
  
  RESULTS
  There was no correlation in univariate analysis between birth weight or weight/length ratio and rate of decline in GFR, neither in men nor in women. Furthermore, the 27 patients with birth weights below the 20th centile had a rate of decline in GFR [median (range)] similar to the 134 patients above: 2.6 (-4.7; 9.6) vs. 3.4 (-2.3; 19.3) mL min(-1) year(-1), respectively (NS). A multiple regression analysis revealed that albuminuria, arterial blood pressure, and haemoglobin A1C during follow-up showed a significant correlation with the decline in GFR [R2 (adjusted) = 0.34], whereas birth weight and birth weight/length ratio did not.
  
  
  CONCLUSIONS
  Our study does not suggest that weight at birth is associated with progression of established diabetic nephropathy in type 1 diabetic patients, whilst several other potential modifiable risk factors were identified.
authors.affiliation: Steno Diabetes Center, Gentofte, Denmark. pkjacobsen@adalnet.dk
authors.forename: P
authors.initials: P
authors.lastname: Jacobsen
authors.forename: P
authors.initials: P
authors.lastname: Rossing
authors.forename: L
authors.initials: L
authors.lastname: Tarnow
authors.forename: P
authors.initials: P
authors.lastname: Hovind
authors.forename: H-H
authors.initials: HH
authors.lastname: Parving
mesh_terms: D000328:Adult; D001827:Body Height; D003922:Diabetes Mellitus, Type 1 / Q000196:embryology / Q000209:etiology*; D003928:Diabetic Nephropathies / Q000196:embryology / Q000209:etiology*; D018450:Disease Progression; D005260:Female; D005317:Fetal Growth Retardation / Q000503:physiopathology; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D007230:Infant, Low Birth Weight / Q000502:physiology*; D007231:Infant, Newborn; D007677:Kidney Function Tests; D008297:Male; D012044:Regression Analysis; D012307:Risk Factors