LOW-BIRTH-WEIGHT - A RISK FACTOR FOR DEVELOPMENT OF DIABETIC NEPHROPATHY

It has been demonstrated that intrauterine growth retardation, defined as birth weight below the 10th percentile, gives rise to a reduction in nephron number. Oligonephropathy has been suggested to increase the risk for systemic and glomerular hypertension in adult life as well a s enhance risk for expression of renal disease after exposure to poten tially injurious renal stimuli. The aim of this study was to determine if low birth weight is a risk factor for development of diabetic neph ropathy. In a case-control study, we investigated 184 (110 men) insuli n-dependent diabetes mellitus (IDDM) patients with diabetic nephropath y (persistent albuminuria >300 mg/24 h) (age [mean +/- SD] 41.0 +/- 9. 3 years, duration of diabetes 26.9 +/- 8.2 years) and 182 (111 men) no rmoalbuminuric (<30 mg/24 h) IDDM patients (age 42.1 +/- 9.8 years, du ration of diabetes 25.8 +/- 8.6 years). Information about weight at bi rth was obtained from the midwife's original registrations. In women b elow the 10th percentile in birth weight (less than or equal to 2,700 g, n = 16), 75% had nephropathy compared with only 35% among patients whose birth weights were above the 90th percentile (14,000 g, n = 17) (P = 0.05). In men below the 10th percentile in birth weight less than or equal to 2,910 g, n = 22), the prevalence of patients with nephrop athy (50%) was similar to the prevalence among patients above the 90th percentile in birth weight (greater than or equal to 4,200 g, n = 24) (54%). Weights at birth (means +/- SD) were similar in patients with and without diabetic nephropathy: men, 3,548 +/- 554 and 3,555 +/- 493 g; women, 3,265 +/- 621 and 3,373 +/- 577 g, respectively. Adult heig ht was significantly correlated with weight at birth (r = 0.18, P = 0. 008 for men; r = 0.28, P < 0.001 for women). Men with diabetic nephrop athy were significantly shorter than men with normoalbuminuria (176.9 +/- 7.1 vs. 179.4 +/- 6.5 cm, P < 0.01). In conclusion, our study supp orts the hypothesis that genetic predisposition or factors operating i n utero or early childhood or both contribute to the development of di abetic nephropathy.