Gittes G K, Gittes R F
J Urol. 1984 Jun;131(6):1206-7. doi: 10.1016/s0022-5347(17)50873-3.
The "work" hypothesis of renal compensatory hypertrophy has always been opposed to the established observation that the peritoneal reabsorption of 1 rat kidney's excretion after ureteroperitoneostomy does not result in a compensatory increase in total renal mass. But urine peritonitis in the U-P rats could result in a lower intake of food and/or less efficient digestion, thus making it difficult for rats to undergo compensatory renal growth. To eliminate nutrition as a factor, all rats were fasted after undergoing either uninephrectomy, uretero- peritoneostomy , or a sham operation. Uninephrectomized rats maintained their residual renal mass better than their sham controls under fasting conditions (109 +/- 11.3 versus 95 +/- 5.7 mg. per 100 gm. body weight, p less than .001). But the final renal mass and body weight of uretero- peritoneostomized rats and sham-operated rats was the same. Thus the added excretory burden of uretero- peritoneostomized rats does not have the renal-sparing effect observed after uninephrectomy in fasted rats and urine peritonitis is not a sufficient explanation for this lack of response to uretero- peritoneostomy . It can be maintained that, since uretero- peritoneostomy has no renotrophic effect, there is a qualitative difference between uninephrectomy and uretero- peritoneostomy as stimuli for renal compensatory hypertrophy.
