TY - JOUR
T1 - Changes in inflammatory biomarkers after renal revascularization in atherosclerotic renal artery stenosis
AU - Wang, Wei
AU - Saad, Ahmed
AU - Herrmann, Sandra M.
AU - Massat, Alfonso Eirin
AU - McKusick, Michael A.
AU - Misra, Sanjay
AU - Lerman, Lilach O.
AU - Textor, Stephen C.
N1 - Publisher Copyright:
© 2016 The Author. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.
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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U2 - 10.1093/ndt/gfv448
DO - 10.1093/ndt/gfv448
M3 - Article
C2 - 26908767
AN - SCOPUS:84994850823
SN - 0931-0509
VL - 31
SP - 1437
EP - 1443
JO - Nephrology Dialysis Transplantation
JF - Nephrology Dialysis Transplantation
IS - 9
ER -