Renal tubular solute transport and oxygen consumption: insights from computational models

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Purpose of review

To maintain electrolyte homeostasis, the kidneys reabsorb more than 99% of the filtered Na+ under physiological conditions, resulting in less than 1% of the filtered Na+ excreted in urine. In contrast, due to distal tubular secretion, urinary K+ output may exceed filtered load. This review focuses on a relatively new methodology for investigating renal epithelial transport, computational modelling and highlights recent insights regarding renal Na+ and K+ transport and O2 consumption under pathophysiological conditions, with a focus on nephrectomy.

Recent findings

Recent modelling studies investigated the extent to which the adaptive response to nephrectomy, which includes elevation in single-nephron glomerular filtration rate and tubular transport capacity, may achieve balance but increases O2 consumption per nephron. Simulation results pointed to potential mechanisms in a hemi-nephrectomized rat that may attenuate the natriuresis response under K+ load, or that may augment the natriuretic, diuretic and kaliuretic effects of sodium glucose cotransporter 2 inhibition.


Computational models provide a systemic approach for investigating system perturbations, such as those induced by drug administration or genetic alterations. Thus, computational models can be a great asset in data interpretation concerning (but not limited to) renal tubular transport and metabolism.

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