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 as enhance risk for expression of renal disease after exposure to potentially injurious renal stimuli. The aim of this study was to determine if low birth weight is a risk factor for development of diabetic nephropathy. In a case-control study, we investigated 184 (110 men) insulin-dependent diabetes mellitus (IDDM) patients with diabetic nephropathy (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) normoalbuminuric (<30 mg/24 h) IDDM patients (age 42.1 +/- 9.8 years, duration of diabetes 25.8 +/- 8.6 years). Information about weight at birth was obtained from the midwife's original registrations. In women below 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 nephropathy (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 height 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 nephropathy were significantly shorter than men with normoalbuminuria (176.9 +/- 7.1 vs. 179.4 +/- 6.5 cm, P < 0.01). In conclusion, our study supports the hypothesis that genetic predisposition or factors operating in utero or early childhood or both contribute to the development of diabetic nephropathy.