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

Published

Journal Article (Review)

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. SUMMARY: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.

Full Text

Duke Authors

Cited Authors

  • Layton, AT; Vallon, V

Published Date

  • September 2018

Published In

Volume / Issue

  • 27 / 5

Start / End Page

  • 384 - 389

PubMed ID

  • 30016311

Pubmed Central ID

  • 30016311

Electronic International Standard Serial Number (EISSN)

  • 1473-6543

International Standard Serial Number (ISSN)

  • 1062-4821

Digital Object Identifier (DOI)

  • 10.1097/mnh.0000000000000435

Language

  • eng