Retard de croissance intra-utérin et déficit en néphrons

Abstract

The number of nephrons at birth is normally quite fixed in any species. Severe renal hypoplasia is readily detected because of functional insufficiency, but moderate inborn nephron deficits may exist, yeat remain undetected. A systematic anatomical study revealed a large quantitative variation of the number of nephrons at birth m man (600000-1400000). Inborn nephron deficits were found to correlate very strongly with birth weight in the rat. The same correlation exists in man : intrauterine growth retardation may be a major cause of inborn nephron deficit, pointing to the possible involvement of common growth factors responsible for fetal development and determination Of the number of kidney functional units. Inborn nephron deficit may also proceed from drug toxicity, as described for gentamicin. The deficit is usually compensated for by hypertrophy of the remnant nephrons and hyperfiltration. This may lead to accelerated glomerulosclerosis, as shown in the rat, and be responsible for subsequent proteinuria, renal insufficiency and arterial hypertension. Epidenuologic and experimental studies are now necessary to verify this hypothesis and analyze the underlying mechanisms leading from intrauterine growth retardation to hypertension in the adulthood.