Changes in inflammatory biomarkers after renal revascularization in atherosclerotic renal artery stenosis

Wei Wang, Ahmed Saad, Sandra Herrmann, Alfonso Eirin, Michael A. McKusick, Sanjay Misra, Lilach O Lerman, Stephen C Textor

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Background. Atherosclerotic renal artery stenosis (ARAS) activates oxidative stress and chronic inflammatory injury. Contrast imaging and endovascular stenting pose potential hazards for acute kidney injury, particularly when superimposed upon reduced kidney perfusion. Methods. We measured sequential early and long-term changes in circulating inflammatory and injury biomarkers in 12 ARAS subjects subjected to computed tomography imaging and stent revascularization compared with essential hypertensive (EH) subjects of similar age under fixed sodium intake and medication regimens in a clinical research unit. Results. NGAL, TIMP-2, IGFBP7, MCP-1 and TNF-α all were elevated before intervention. Post-stenotic kidney volume, perfusion, blood flow and glomerular filtration rate (GFR) were lower in ARAS than in EH subjects. TIMP-2 and IGFBP7 fell briefly, then rose over 18 h after contrast imaging and stent deployment. Circulating NGAL decreased and remained lower for 27 h. These biomarkers in ARAS returned to baseline after 3 months, while kidney volume, perfusion, blood flow and GFR increased, but remained lower than EH. Conclusions. These divergent patterns of inflammatory signals are consistent with cell cycle arrest (TIMP-2, IGFBP7) and relative protection from acute kidney injury after imaging and stenting. Sustained basal elevation of circulating and renal venous inflammatory biomarkers support ongoing, possibly episodic, renal stress in ARAS that limits toxicity from stent revascularization.

Original languageEnglish (US)
Pages (from-to)1437-1443
Number of pages7
JournalNephrology Dialysis Transplantation
Volume31
Issue number9
DOIs
StatePublished - Sep 1 2016

Fingerprint

Renal Artery Obstruction
Tissue Inhibitor of Metalloproteinase-2
Biomarkers
Kidney
Stents
Perfusion
Blood Volume
Glomerular Filtration Rate
Acute Kidney Injury
Wounds and Injuries
Cell Cycle Checkpoints
Oxidative Stress
Sodium
Tomography
Research

Keywords

  • acute kidney injury
  • atherosclerotic renal artery stenosis (ARAS)
  • biomarkers
  • endovascular stenting
  • ischemic preconditioning (IPC)

ASJC Scopus subject areas

  • Nephrology
  • Transplantation

Cite this

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title = "Changes in inflammatory biomarkers after renal revascularization in atherosclerotic renal artery stenosis",
abstract = "Background. Atherosclerotic renal artery stenosis (ARAS) activates oxidative stress and chronic inflammatory injury. Contrast imaging and endovascular stenting pose potential hazards for acute kidney injury, particularly when superimposed upon reduced kidney perfusion. Methods. We measured sequential early and long-term changes in circulating inflammatory and injury biomarkers in 12 ARAS subjects subjected to computed tomography imaging and stent revascularization compared with essential hypertensive (EH) subjects of similar age under fixed sodium intake and medication regimens in a clinical research unit. Results. NGAL, TIMP-2, IGFBP7, MCP-1 and TNF-α all were elevated before intervention. Post-stenotic kidney volume, perfusion, blood flow and glomerular filtration rate (GFR) were lower in ARAS than in EH subjects. TIMP-2 and IGFBP7 fell briefly, then rose over 18 h after contrast imaging and stent deployment. Circulating NGAL decreased and remained lower for 27 h. These biomarkers in ARAS returned to baseline after 3 months, while kidney volume, perfusion, blood flow and GFR increased, but remained lower than EH. Conclusions. These divergent patterns of inflammatory signals are consistent with cell cycle arrest (TIMP-2, IGFBP7) and relative protection from acute kidney injury after imaging and stenting. Sustained basal elevation of circulating and renal venous inflammatory biomarkers support ongoing, possibly episodic, renal stress in ARAS that limits toxicity from stent revascularization.",
keywords = "acute kidney injury, atherosclerotic renal artery stenosis (ARAS), biomarkers, endovascular stenting, ischemic preconditioning (IPC)",
author = "Wei Wang and Ahmed Saad and Sandra Herrmann and Alfonso Eirin and McKusick, {Michael A.} and Sanjay Misra and Lerman, {Lilach O} and Textor, {Stephen C}",
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T1 - Changes in inflammatory biomarkers after renal revascularization in atherosclerotic renal artery stenosis

AU - Wang, Wei

AU - Saad, Ahmed

AU - Herrmann, Sandra

AU - Eirin, Alfonso

AU - McKusick, Michael A.

AU - Misra, Sanjay

AU - Lerman, Lilach O

AU - Textor, Stephen C

PY - 2016/9/1

Y1 - 2016/9/1

N2 - Background. Atherosclerotic renal artery stenosis (ARAS) activates oxidative stress and chronic inflammatory injury. Contrast imaging and endovascular stenting pose potential hazards for acute kidney injury, particularly when superimposed upon reduced kidney perfusion. Methods. We measured sequential early and long-term changes in circulating inflammatory and injury biomarkers in 12 ARAS subjects subjected to computed tomography imaging and stent revascularization compared with essential hypertensive (EH) subjects of similar age under fixed sodium intake and medication regimens in a clinical research unit. Results. NGAL, TIMP-2, IGFBP7, MCP-1 and TNF-α all were elevated before intervention. Post-stenotic kidney volume, perfusion, blood flow and glomerular filtration rate (GFR) were lower in ARAS than in EH subjects. TIMP-2 and IGFBP7 fell briefly, then rose over 18 h after contrast imaging and stent deployment. Circulating NGAL decreased and remained lower for 27 h. These biomarkers in ARAS returned to baseline after 3 months, while kidney volume, perfusion, blood flow and GFR increased, but remained lower than EH. Conclusions. These divergent patterns of inflammatory signals are consistent with cell cycle arrest (TIMP-2, IGFBP7) and relative protection from acute kidney injury after imaging and stenting. Sustained basal elevation of circulating and renal venous inflammatory biomarkers support ongoing, possibly episodic, renal stress in ARAS that limits toxicity from stent revascularization.

AB - Background. Atherosclerotic renal artery stenosis (ARAS) activates oxidative stress and chronic inflammatory injury. Contrast imaging and endovascular stenting pose potential hazards for acute kidney injury, particularly when superimposed upon reduced kidney perfusion. Methods. We measured sequential early and long-term changes in circulating inflammatory and injury biomarkers in 12 ARAS subjects subjected to computed tomography imaging and stent revascularization compared with essential hypertensive (EH) subjects of similar age under fixed sodium intake and medication regimens in a clinical research unit. Results. NGAL, TIMP-2, IGFBP7, MCP-1 and TNF-α all were elevated before intervention. Post-stenotic kidney volume, perfusion, blood flow and glomerular filtration rate (GFR) were lower in ARAS than in EH subjects. TIMP-2 and IGFBP7 fell briefly, then rose over 18 h after contrast imaging and stent deployment. Circulating NGAL decreased and remained lower for 27 h. These biomarkers in ARAS returned to baseline after 3 months, while kidney volume, perfusion, blood flow and GFR increased, but remained lower than EH. Conclusions. These divergent patterns of inflammatory signals are consistent with cell cycle arrest (TIMP-2, IGFBP7) and relative protection from acute kidney injury after imaging and stenting. Sustained basal elevation of circulating and renal venous inflammatory biomarkers support ongoing, possibly episodic, renal stress in ARAS that limits toxicity from stent revascularization.

KW - acute kidney injury

KW - atherosclerotic renal artery stenosis (ARAS)

KW - biomarkers

KW - endovascular stenting

KW - ischemic preconditioning (IPC)

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