Hyperplasia after unilateral nephrectomy and role of excretory load in its production

Abstract

Using P 32 uptake in DNA nucleotides as an index of mitoses, hyperplasia in the kidney has been studied in rats both after unilateral nephrectomy and after transplantation of one ureter into the peritoneal cavity. In the latter group, in which the excretory load on each kidney was increased without removing any kidney tissue, no increase in P 32 uptake was present 48 hr after operation, whereas in unilaterally nephrectomized animals the P 32 uptake was doubled at this time, compared to control animals. These results are interpreted as indicating that the increased work load on the remaining kidney after unilateral nephrectomy is not responsible for stimulating cell division. It is suggested that hyperplasia under these conditions is probably a result of the decrease in the number of kidney cells per se.