Professor David Barker proposed that an individual could be 'programmed' in-utero to develop chronic diseases in adulthood such as hypertension and ischaemic heart disease. Professor Barry Brenner proposed that essential hypertension was the result of reduction in glomerular number which resulted in reduced total glomerular filtration surface area. It is possible to make a unification of the Barker hypothesis and Brenner hypothesis: Intrauterine growth retardation, caused by any kind of mechanism, generates babies with a low birth weight. These smaller babies have smaller kidneys with fewer glomeruli. Fewer glomeruli result in a decreased total glomerular filtration surface area, giving rise to individual glomerular hypertension due to a reduced renal functional reserve. The patients with the fewest glomeruli will then be more prone to develop irreversible renal failure when exposed to a renal insult in later life. With the invention of design-based stereological methods it is possible to estimate the number of glomeruli unbiasedly in animal kidneys as well as in human kidneys. Data from animal studies using various models for generating low nephron numbers together with measurement of blood pressure will be presented and a few human studies will also be presented.