Logo image
Back
Maladaptation of Renal Hemodynamics Contributes to Kidney Dysfunction Resulting from Thoracic Spinal Cord Injury in Mice
Journal article   Open access   Peer reviewed

Maladaptation of Renal Hemodynamics Contributes to Kidney Dysfunction Resulting from Thoracic Spinal Cord Injury in Mice

Patrick Osei-Owusu, Eileen Collyer, Shelby A. Dahlen, Raisa E. Echols Adams and Veronica J. Tom
American journal of physiology. Renal physiology, v 323(2), pp F120-F140
06 Jun 2022
DOI: https://doi.org/10.1152/ajprenal.00072.2022
PMID: 35658716
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://doi.org/10.1152/ajprenal.00072.2022View
Published, Version of Record (VoR)Open Access (License Unspecified),  Open

Abstract

Renal dysfunction is a hallmark of spinal cord injury (SCI). Several SCI sequalae are implicated, however, the exact pathogenic mechanism of renal dysfunction is unclear. Herein, we found that T3 (T3Tx) or T10 (T10Tx) complete thoracic spinal cord transection induced hypotension, bradycardia, and hypothermia immediately after injury. T3Tx-induced hypotension but not bradycardia or hypothermia slowly recovered to levels in T10Tx SCI and uninjured mice ~16 h after injury as determined by continuous radiotelemetry monitoring. Both types of thoracic SCI led to a marked decrease in albuminuria and proteinuria in all phases of SCI, while the kidney injury marker, NGAL, rapidly increased in the acute phase, remaining elevated in the chronic phase of T3Tx SCI. Renal interstitial and vascular elastin fragmentation after SCI were worsened during chronic T3Tx SCI. In the chronic phase, renal vascular resistance response to a step increase in renal perfusion pressure or a bolus injection of Ang II or NE was almost completely abolished after T3Tx SCI. Bulk RNAseq analysis showed enrichment of genes involved in extracellular matrix (ECM) remodeling and chemokine signaling in the kidney from T3Tx SCI mice. Serum levels of interleukin 6 was elevated in the acute but not chronic phase of T3Tx and T10Tx SCI, while serum amyloid A1 level was elevated in both acute and chronic phases. We conclude that tissue fibrosis and hemodynamic impairment are involved in renal dysfunction resulting from thoracic SCI; these pathological alterations, exacerbated by high thoracic-level injury, is mediated at least partly by renal microvascular ECM remodeling.

Metrics

14 Record Views
11 citations in Web of Science
9 citations in Scopus

Details

UN Sustainable Development Goals (SDGs)

This publication has contributed to the advancement of the following goals:

#3 Good Health and Well-Being

InCites Highlights

Data related to this publication, from InCites Benchmarking & Analytics tool:

Collaboration types
Domestic collaboration
Web of Science research areas
Physiology
Urology & Nephrology
Logo image