A computational model for simulating solute transport and oxygen consumption along the nephrons.

Published

Journal Article

The goal of this study was to investigate water and solute transport, with a focus on sodium transport (TNa) and metabolism along individual nephron segments under differing physiological and pathophysiological conditions. To accomplish this goal, we developed a computational model of solute transport and oxygen consumption (QO2 ) along different nephron populations of a rat kidney. The model represents detailed epithelial and paracellular transport processes along both the superficial and juxtamedullary nephrons, with the loop of Henle of each model nephron extending to differing depths of the inner medulla. We used the model to assess how changes in TNa may alter QO2 in different nephron segments and how shifting the TNa sites alters overall kidney QO2 Under baseline conditions, the model predicted a whole kidney TNa/QO2 , which denotes the number of moles of Na+ reabsorbed per moles of O2 consumed, of ∼15, with TNa efficiency predicted to be significantly greater in cortical nephron segments than in medullary segments. The TNa/QO2 ratio was generally similar among the superficial and juxtamedullary nephron segments, except for the proximal tubule, where TNa/QO2 was ∼20% higher in superficial nephrons, due to the larger luminal flow along the juxtamedullary proximal tubules and the resulting higher, flow-induced transcellular transport. Moreover, the model predicted that an increase in single-nephron glomerular filtration rate does not significantly affect TNa/QO2 in the proximal tubules but generally increases TNa/QO2 along downstream segments. The latter result can be attributed to the generally higher luminal [Na+], which raises paracellular TNa Consequently, vulnerable medullary segments, such as the S3 segment and medullary thick ascending limb, may be relatively protected from flow-induced increases in QO2 under pathophysiological conditions.

Full Text

Duke Authors

Cited Authors

  • Layton, AT; Vallon, V; Edwards, A

Published Date

  • December 2016

Published In

Volume / Issue

  • 311 / 6

Start / End Page

  • F1378 - F1390

PubMed ID

  • 27707705

Pubmed Central ID

  • 27707705

Electronic International Standard Serial Number (EISSN)

  • 1522-1466

International Standard Serial Number (ISSN)

  • 1931-857X

Digital Object Identifier (DOI)

  • 10.1152/ajprenal.00293.2016

Language

  • eng