title: Changes in inflammatory biomarkers after renal revascularization in atherosclerotic renal artery stenosis.
abstract: 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.
  
  
  
  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.
  
  
  
  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.
  
  
  
  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.
authors.affiliation: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA Department of Nephrology, Dalian Municipal Central Hospital Affiliated of Dalian Medical University, Dalian, Liaoning, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.affiliation: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.
authors.forename: Ahmed
authors.initials: A
authors.lastname: Saad
authors.affiliation: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.
authors.forename: Sandra M
authors.initials: SM
authors.lastname: Herrmann
authors.affiliation: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.
authors.forename: Alfonso
authors.initials: A
authors.lastname: Eirin Massat
authors.affiliation: Department of Radiology, Mayo Clinic, Rochester, MN, USA.
authors.forename: Michael A
authors.initials: MA
authors.lastname: McKusick
authors.affiliation: Department of Radiology, Mayo Clinic, Rochester, MN, USA.
authors.forename: Sanjay
authors.initials: S
authors.lastname: Misra
authors.affiliation: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.
authors.forename: Lilach O
authors.initials: LO
authors.lastname: Lerman
authors.affiliation: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.
authors.forename: Stephen C
authors.initials: SC
authors.lastname: Textor
mesh_terms: D000368:Aged; D050197:Atherosclerosis / Q000150:complications*; D015415:Biomarkers / Q000097:blood*; D018932:Chemokine CCL2 / Q000097:blood; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000175:diagnosis* / Q000209:etiology; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D011446:Prospective Studies; D012078:Renal Artery Obstruction / Q000175:diagnosis / Q000209:etiology / Q000628:therapy*; D015607:Stents; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015415:Biomarkers; C111835:CCL2 protein, human; D018932:Chemokine CCL2; C560823:TIMP2 protein, human; D014409:Tumor Necrosis Factor-alpha; D019716:Tissue Inhibitor of Metalloproteinase-2
keywords: acute kidney injury; atherosclerotic renal artery stenosis (ARAS); biomarkers; endovascular stenting; ischemic preconditioning (IPC)