There are differences in the adaptations of tubular function in the early phase compared with the chronic phase following reduced renal mass. In several experimental models of reduced renal mass, fractional reabsorption of sodium is reduced acutely following nephrectomy but is rapidly restored to levels observed before nephrectomy.[37, 38] There are scant data available on compensatory adaptations in the acute phase in the human.

In one study, total sodium excretion was found to be similar to that observed before nephrectomy, by day 5 after uninephrectomy in kidney donors.[39] This adaptation was associated with a significant increase in lithium clearance (a semi-quantitative indicator of sodium learn more reabsorption in the proximal tubules).[39] Similarly in the rat, it was demonstrated that at 2–5 hours after uninephrectomy, absolute reabsorption of sodium was similar to that of the sham controls but fractional proximal reabsorption of sodium had decreased significantly.[38]

By day 30 after nephrectomy in the rat, fractional proximal reabsorption had been restored to levels observed in sham animals.[38] Total reabsorption of sodium is maintained immediately after nephrectomy, while fractional proximal reabsorption is reduced. Thus, the distal tubules, where reabsorption of sodium has been shown to increase almost 90%,[10] are suggested to make a critical contribution to maintenance of sodium homeostasis during this period.[37] Restoration of proximal reabsorption of sodium after the aforementioned Trichostatin A research buy initial decrease is associated with a significant increase in activity of apical antiporters and the basolateral pump.[40] Glomerular hyperfiltration occurs in response to a reduction in renal mass and is associated with significant glomerular hypertrophy. In the adult human, within a few weeks after donation of a kidney, GFR reaches 70% of its value before nephrectomy[41, 42] and remains stable for up to

15–20 years.[8, 43] Similar observations were made in the rat where GFR stabilized at 80% of the pre-nephrectomy value by day 32 after nephrectomy.[38, 44] The hyperfiltration following a reduction in renal mass is associated with increased effective renal plasma flow,[41] likely due to decreased afferent PLEKHB2 arteriolar resistance. Furthermore, following uninephrectomy in the rat, an increase in NO production has also been observed[45] which may promote the increase in renal blood flow and SNGFR following nephrectomy. Alterations in the TGF function likely contribute to the decrease in pre-glomerular resistance. Muller-Suur et al. showed that at 20 minutes after uninephrectomy in the adult rat, TGF sensitivity was reduced (rightward shift), but TGF reactivity was increased (downward shift) and the authors concluded that the decrease in TGF sensitivity may facilitate the rise in SNGFR following nephrectomy.[46] In contrast, Blantz et al.