The compensatory growth of the remaining kidney following unilateral nephrectomy has, over the years, been referred to alternatively as hypertrophy or hyperplasia, but the relative importance of these processes is a long-standing and still unresolved question. Since the in-vestigations of Arataki I and Moore2 it has been an accepted fact that mature nephrons can increase in size but not in number, and in this sense compensatory renal enlargement is purely hypertrophic. At the cellular level, however, there has been a variance of opinion. Initially it was thought that renal epithelium, like neurons, could not be stimulated to divide and that nephrons could increasein size only as a result of cellular hypertrophy. This concept dates back to I902, when Galeotti and Villa-Santal found no evidence that hyperplasia played any role in the enlargement of the adult kidney. Twenty-five years later Saphir, 4 in a study of compensatory growth of the rabbit kidney, stated definitely that he saw no mitotic figures in glomeruli or renal tubular epithelium, and again attributed the renal enlargement wholly to cellular hypertrophy. This remained the prevailing opinion, as reflected by standard pathology textbooksof that time, 5 until I949, when RollasonI demonstrated a briefburst of mitotic activity in young rats, chiefly in con-voluted tubular epithelium, within the first few days after unilateral nephrectomy. In addition to this clear-cut cellular hyperplasia, Rollason saw an increase in size of epithelial cells and concluded that both cellular hypertrophy and hyperplasia contributed to compensatory renal growth.