Alteration in the normal development of the kidney is likely to be a major contributing factor to programming of adult disease. Renal disease is reaching epidemic proportions in some sectors of the community and is often found in association with the two most characterised adult onset diseases, hypertension and noninsulin dependent diabetes mellitus. Epidemiological studies in humans have identified various maternal states such as anemia, diabetes and protein/micronutrient deficiency as causing renal abnormalities, often in association with decreased birth weight. Animal models of maternal protein/nutrient deficiency as well as maternal glucocorticoid exposure generally results in a reduction in glomerular (and thus nephron) number in the offspring along with increases in blood pressure. It is important to note that the stimulus has the greatest effect when applied at the beginning of metanephric development. The decrease in nephron endowment probably results from changes in expression of genes identified to be critical for normal branching morphogenesis in the kidney. However, other compensatory changes in the kidney may involve alteration of the renal renin-angiotensin system and changes in channels involved in sodium transport. Further research into genes/proteins altered in various "programmed" models, along with use of careful stereological methodology for determining glomerular number are essential to further our understanding of renal involvement in the programming of adult disease.