We examined whether deficits in glomerular capillary surface area associated with a congenital nephron deficit could be corrected by glomerular hypertrophy. Using unbiased stereological techniques we examined the time course and mode of glomerular hypertrophy in mice lacking one allele for glial cell line-derived neurotrophic factor (GDNF). These GDNF heterozygous (Het) mice are born with ~30% less nephrons than wild-type (WT) littermates. An additional group of GDNF Het mice received the AT1-receptor antagonist candesartan (Cand; 10mg/kg/day) from 5 weeks of age to determine the role of AT1-receptors in the compensatory hypertrophy. At 10 weeks of age, the total volume of renal corpuscles, glomerular capillary surface area and length of glomerular capillaries in the kidneys of GDNF Het mice were all markedly (~45%) less than that of WT mice (P<0.001). However, by 30-weeks, and persisting at 60-weeks of age, GDNF Het and WT mice did not significantly differ in any of these parameters. Further, conscious 24 h mean arterial pressure (MAP) did not differ between GDNF Het and WT mice at any time point. MAP of GDNF Het-Cand mice was 20-30 mmHg less than that of GDNF Het-Veh mice at all three ages, but Cand treatment did not significantly alter glomerular capillary dimensions. In conclusion, we have demonstrated that the deficit in glomerular capillary surface area associated with a congenital nephron deficit can be corrected for in adulthood by an increase in the total length of glomerular capillaries. This process does not require AT1-receptor activation.