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Intrauterine growth restriction (IUGR) is associated with an increased prevalence of renal malfunction. Two principal pathogenetic pathways appear to be involved: on the one hand non-renal mechanisms such as hypertension and type 2 diabetes, both associated with previous IUGR, predispose to secondary renal damage; on the other hand, renal mechanisms are involved such as the reduced number of nephrons in low-birth-weight children, which is a risk factor for future renal failure. In addition, glomerular diseases show a severer course in IUGR children. The course of the nephrotic syndrome is less favourable, and IgA nephropathy is associated with a higher prevalence of glomerular sclerosis. Data from animal experiments suggest an increased susceptibility of glomeruli to inflammatory stimuli and reduced regenerative capacities. However, not only prenatal environment, but also postnatal hyperalimentation is responsible for the manifestation of renal disease after IUGR.