TY - JOUR
T1 - Birth weight - A risk factor for progression in diabetic nephropathy?
AU - Jacobsen, Peter
AU - Rossing, P.
AU - Tarnow, L.
AU - Hovind, P.
AU - Parving, H. H.
PY - 2003/3/1
Y1 - 2003/3/1
N2 - Objectives. 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. Design and subjects. 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. Settings. Steno Diabetes Center, a tertiary referral centre. Main outcome measures. 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.
AB - Objectives. 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. Design and subjects. 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. Settings. Steno Diabetes Center, a tertiary referral centre. Main outcome measures. 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.
KW - Birth weight
KW - Diabetic nephropathy
KW - Glomerular filtration rate
KW - Type 1 diabetes mellitus
KW - Weight/length ratio
UR - http://www.scopus.com/inward/record.url?scp=0037335809&partnerID=8YFLogxK
U2 - 10.1046/j.1365-2796.2003.01109.x
DO - 10.1046/j.1365-2796.2003.01109.x
M3 - Article
C2 - 12603502
AN - SCOPUS:0037335809
SN - 0954-6820
VL - 253
SP - 343
EP - 350
JO - Journal of Internal Medicine
JF - Journal of Internal Medicine
IS - 3
ER -