As a consequence of nephron loss, reflux nephropathy (RN) causes considerable glomerular hypertrophy. To examine the relative contributions of capillary dilatation and growth in producing hypertrophy, glomeruli contained in unscarred areas of renal biopsies from 19 children with RN were compared with those in 16 children with minimal change nephrotic syndrome and 16 with recurrent hematuria, who were used as controls representing normal childhood growth. Using computerized digitometry we measured the mean glomerular tuft area (GTA) in all complete, undistorted, nonsclerotic glomeruli in periodic acid-Schiff (PAS) stains. Measurements were repeated in four glomeruli of uniform size in periodic acid-silver methenamine stains, the results (GTA4) correlating significantly with GTA. In the same four glomeruli we measured the mean individual capillary luminal area (CLA) and counted the mean number of lumens per glomerulus (N). Mean mesangial area (MA) was calculated as GTA4 - (CLA x N). Cells per distal mesangial region were counted in PAS stains. GTA, GTA4, N, MA and mesangial cell counts were significantly greater in RN than controls, but CLA and fractional MA (MA/GTA%) did not differ. N correlated highly significantly with GTA4 in both RN and controls, but CLA did not do so. These findings are consistent with capillary growth by subdivision being the main mechanism of glomerular hypertrophy when nephron loss occurs during childhood, and the identity of the regressions of N versus GTA4 in RN and controls suggests that compensatory hypertrophy resembles the normal glomerular growth pattern in this age group.