Rossing P, Tarnow L, Nielsen F S, Hansen B V, Brenner B M, Parving H H
Ugeskr Laeger. 1996 Dec 30;159(1):41-4.
It has been demonstrated that intrauterine growth retardation gives rise to a reduction in nephron number. Oligonephropathy has been suggested to enhance the risk for expression of renal disease following exposure to potentially injurious renal stimuli. In a case-control study we investigated if low birth weight is a risk factor for development of diabetic nephropathy in 184 IDDM patients with diabetic nephropathy (persistent albuminuria > 300 mg/24 hours) and 182 normoalbuminuric (< 30 mg/24 hours) patients. In women with birthweight < 10 th centile (< or = 2,700 g, n = 16) 75% had nephropathy compared to only 35% among patients > 90 th centile (> or = 4,000 g, n = 17) (p = 0.05). In men with birth-weight < 10th centile (< or = 2,910 g, n = 22) the prevalence of nephropathy: 50%, was similar to the prevalence among patients > 90th centile (> or = 4,200 g, n = 24) 54%. Mean weight at birth were similar in patients with and without diabetic nephropathy. Men with diabetic nephropathy were significantly shorter than men with normoalbuminuria (176.9 (7.1) vs 179.4 (6.5), 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.