Altered Metabolism in the ex vivo Remnant Kidney

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Abstract
Oxygen consumption is increased in the rat remnant kidney (RK), but the basis of this enhanced metabolic activity has not been defined fully. To characterize the hypermetabolism further, isolated RK and normal kidneys (NK) were perfused using a range of perfusion pressures and substrates, and at varying times after 5/6 nephrectomy. Altered and increased RK metabolism was found as early as 1 week after 5/6 nephrectomy. The rate of net glucose consumption was higher in RK than NK (e.g., 0-30 min, 2.42 ± 0.28 vs. 1.21 ± 0.33 μmol·min-1 g-1), a difference not explained by changes in oxygen delivery or glycosuria. Ammonia production was significantly greater early in perfusion in RK than NK. Calculated nephron oxygen consumption (QO2) was greater in RK than NK for all substrates tested (e.g., pyruvate 5 ml: 552.3 ± 43.1 vs. 173.3 ± 25.6 pmol min-1, p 2 and net sodium reabsorption (TNa+) better than site II substrates. In RK, QO2 did not change with increasing perfusion pressure, and TNa+ rose only slightly for pressures ≥ 120 mm Hg. In summary, RK hypermetabolism is characterized by increased oxygen consumption, glycolysis and ammoniagenesis, is not substrate-specific and does not appear to be an artefact of the altered physiology of remnant perfusion.

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