Independence of onset of compensatory kidney growth from changes in renal function

Abstract

Renal function was measure before and shortly after uninephrectomy in mice to evaluate if work expended in the reabsorption of glomerular filtrate plays a role in the initiation of compensatory growth. To exclude the possibility of small but undetectable increments in glomerular filtration rate and absolute sodium reabsorption these functions were experimentally reduced immediately after uninephrectomy and sham nephrectomy. The onset of growth was indicated by an increased rate of [14C]choline incorporation into phospholipid in renal cortical slices. [14C]choline incorporation increased significantly only after uninephrectomy and remained unchanged after sham operation regardless of the magnitude or direction of the concurrent change in sodium reabsorption. The rate of incorporation increased by 40 +/- 8% (P less than 0.005) in uninephrectomized animals whose sodium reabsorption was reduced by 34 +/- 6% (P less than 0.001) and rose 45 +/- 11% (P less than 0.005) when sodium reabsorption remained unchanged. These results indicate that compensatory kidney growth is not triggered by an increase in renal work expended in the reabsorption of glomerular filtrate; in fact, it can occur when reabsorptive work is substantially decreased.

Endothelial-Directed Hepatic Regeneration After Partial Hepatectomy

“…1 Certain tissues, such as the liver, spleen, and kidney, have the ability to regenerate after injury. [2][3][4] The regenerative capacity of these tissues is tightly controlled with a finite endpoint, similar to physiologic phenomena known to be angiogenesis-mediated.…”

Increased kidney size, glomerular filtration rate and renal plasma flow in short-term insulin-dependent diabetics

“…The cause of the kidney enlargement in the two above mentioned conditions remains unknown. Increased work-load has been suggested in both conditions, but recent studies on kidney growth following reduction in renal mass do not support this hypothesis [7,10]. Such studies are lacking in diabetic animals.…”

Presence of renotrophic factor in plasma of unilaterally nephrectomized rats.

“…Though the role of a humoral factor in the mechanism of compensatory renal growth appears to be well established and though the compensatory hypertrophy has been repeatedly shown to occur independently from changes in renal function (Katz, 1970;Katz, Toback & Lindheimer, 1976 Obertop & Malt, 1977), the possibility that the early adaptation of the remaining kidney may play a contributory role in the onset of renal hypertrophy cannot definitely be ruled out (G. C. R. Morris, 1976).…”