Differences in GFR and tissue oxygenation, and interactions between stenotic and contralateral kidneys in unilateral atherosclerotic renovascular disease

Sandra Herrmann, Ahmed Saad, Alfonso Eirin, John Woollard, Hui Tang, Michael A. McKusick, Sanjay Misra, James Glockner, Lilach O Lerman, Stephen C Textor

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14 Citations (Scopus)

Abstract

Background and objectives Atherosclerotic renal artery stenosis (ARAS) can reduce renal blood flow, tissue oxygenation, and GFR. In this study, we sought to examine associations between renal hemodynamics and tissue oxygenation with single-kidney function, pressor hormones, and inflammatory biomarkers in patients with unilateral ARAS undergoing medical therapy alone or stent revascularization. Design, setting, participants, & measurements Nonrandomized inpatient studies were performed in patients with unilateral ARAS (.60% occlusion) before and 3 months after revascularization (n=10) or medical therapy (n=20) or patients with essential hypertension (n=32) under identical conditions. The primary study outcome was change in single-kidney GFR. Individual kidney hemodynamics and volume were measured using multidetector computed tomography. Tissue oxygenation (using R2* as a measure of deoxyhemoglobin) was determined by blood oxygen level-dependent magnetic resonance imaging at 3 T. Renal vein neutrophil gelatinase-associated lipocalin (NGAL), monocyte chemoattractant protein-1 (MCP-1), and plasma renin activity were measured. Results Total GFR did not change over 3 months in either group, but the stenotic kidney (STK) GFR rose over time in the stent compared with the medical group (12.2[21.8 to 10.5] versus 25.3[27.3 to 20.3] ml/min; P=0.03). Contralateral kidney (CLK) GFR declined in the stent group (43.6619.7 to 36.6619.5 ml/min; P=0.03). Fractional tissue hypoxia fell in the STK (fraction R2*.30/s: 22.1%620% versus 14.9%618.3%; P,0.01) after stenting. Renal vein biomarkers correlated with the degree of hypoxia in the STK: NGAL(r=0.3; P=0.01) and MCP-1(r=0.3; P=0.02; more so after stenting). Renal vein NGAL was inversely related to renal blood flow in the STK (r=20.65; P,0.001). Biomarkers were highly correlated between STK and CLK, NGAL (r=0.94; P,0.001), and MCP-1 (r=0.96; P,0.001). Conclusions These results showed changes over time in single-kidney GFR that were not evident in parameters of total GFR. Furthermore, they delineate the relationship of measurable tissue hypoxia within the STK and markers of inflammation in human ARAS. Renal vein NGAL and MCP-1 indicated persistent interactions between the ischemic kidney and both CLK and systemic levels of inflammatory cytokines.

Original languageEnglish (US)
Pages (from-to)458-469
Number of pages12
JournalClinical Journal of the American Society of Nephrology
Volume11
Issue number3
DOIs
StatePublished - Mar 7 2016

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Kidney
Renal Artery Obstruction
Renal Veins
Chemokine CCL2
Stents
Biomarkers
Renal Circulation
Hemodynamics
Multidetector Computed Tomography
Renin
Inpatients
Magnetic Resonance Imaging
Outcome Assessment (Health Care)
Lipocalin-2
Hormones
Cytokines
Oxygen
Inflammation
Therapeutics

ASJC Scopus subject areas

  • Nephrology
  • Transplantation
  • Epidemiology
  • Critical Care and Intensive Care Medicine

Cite this

@article{1f5d6d1d6dcc4406b74332875984c386,
title = "Differences in GFR and tissue oxygenation, and interactions between stenotic and contralateral kidneys in unilateral atherosclerotic renovascular disease",
abstract = "Background and objectives Atherosclerotic renal artery stenosis (ARAS) can reduce renal blood flow, tissue oxygenation, and GFR. In this study, we sought to examine associations between renal hemodynamics and tissue oxygenation with single-kidney function, pressor hormones, and inflammatory biomarkers in patients with unilateral ARAS undergoing medical therapy alone or stent revascularization. Design, setting, participants, & measurements Nonrandomized inpatient studies were performed in patients with unilateral ARAS (.60{\%} occlusion) before and 3 months after revascularization (n=10) or medical therapy (n=20) or patients with essential hypertension (n=32) under identical conditions. The primary study outcome was change in single-kidney GFR. Individual kidney hemodynamics and volume were measured using multidetector computed tomography. Tissue oxygenation (using R2* as a measure of deoxyhemoglobin) was determined by blood oxygen level-dependent magnetic resonance imaging at 3 T. Renal vein neutrophil gelatinase-associated lipocalin (NGAL), monocyte chemoattractant protein-1 (MCP-1), and plasma renin activity were measured. Results Total GFR did not change over 3 months in either group, but the stenotic kidney (STK) GFR rose over time in the stent compared with the medical group (12.2[21.8 to 10.5] versus 25.3[27.3 to 20.3] ml/min; P=0.03). Contralateral kidney (CLK) GFR declined in the stent group (43.6619.7 to 36.6619.5 ml/min; P=0.03). Fractional tissue hypoxia fell in the STK (fraction R2*.30/s: 22.1{\%}620{\%} versus 14.9{\%}618.3{\%}; P,0.01) after stenting. Renal vein biomarkers correlated with the degree of hypoxia in the STK: NGAL(r=0.3; P=0.01) and MCP-1(r=0.3; P=0.02; more so after stenting). Renal vein NGAL was inversely related to renal blood flow in the STK (r=20.65; P,0.001). Biomarkers were highly correlated between STK and CLK, NGAL (r=0.94; P,0.001), and MCP-1 (r=0.96; P,0.001). Conclusions These results showed changes over time in single-kidney GFR that were not evident in parameters of total GFR. Furthermore, they delineate the relationship of measurable tissue hypoxia within the STK and markers of inflammation in human ARAS. Renal vein NGAL and MCP-1 indicated persistent interactions between the ischemic kidney and both CLK and systemic levels of inflammatory cytokines.",
author = "Sandra Herrmann and Ahmed Saad and Alfonso Eirin and John Woollard and Hui Tang and McKusick, {Michael A.} and Sanjay Misra and James Glockner and Lerman, {Lilach O} and Textor, {Stephen C}",
year = "2016",
month = "3",
day = "7",
doi = "10.2215/CJN.03620415",
language = "English (US)",
volume = "11",
pages = "458--469",
journal = "Clinical Journal of the American Society of Nephrology",
issn = "1555-9041",
publisher = "American Society of Nephrology",
number = "3",

}

TY - JOUR

T1 - Differences in GFR and tissue oxygenation, and interactions between stenotic and contralateral kidneys in unilateral atherosclerotic renovascular disease

AU - Herrmann, Sandra

AU - Saad, Ahmed

AU - Eirin, Alfonso

AU - Woollard, John

AU - Tang, Hui

AU - McKusick, Michael A.

AU - Misra, Sanjay

AU - Glockner, James

AU - Lerman, Lilach O

AU - Textor, Stephen C

PY - 2016/3/7

Y1 - 2016/3/7

N2 - Background and objectives Atherosclerotic renal artery stenosis (ARAS) can reduce renal blood flow, tissue oxygenation, and GFR. In this study, we sought to examine associations between renal hemodynamics and tissue oxygenation with single-kidney function, pressor hormones, and inflammatory biomarkers in patients with unilateral ARAS undergoing medical therapy alone or stent revascularization. Design, setting, participants, & measurements Nonrandomized inpatient studies were performed in patients with unilateral ARAS (.60% occlusion) before and 3 months after revascularization (n=10) or medical therapy (n=20) or patients with essential hypertension (n=32) under identical conditions. The primary study outcome was change in single-kidney GFR. Individual kidney hemodynamics and volume were measured using multidetector computed tomography. Tissue oxygenation (using R2* as a measure of deoxyhemoglobin) was determined by blood oxygen level-dependent magnetic resonance imaging at 3 T. Renal vein neutrophil gelatinase-associated lipocalin (NGAL), monocyte chemoattractant protein-1 (MCP-1), and plasma renin activity were measured. Results Total GFR did not change over 3 months in either group, but the stenotic kidney (STK) GFR rose over time in the stent compared with the medical group (12.2[21.8 to 10.5] versus 25.3[27.3 to 20.3] ml/min; P=0.03). Contralateral kidney (CLK) GFR declined in the stent group (43.6619.7 to 36.6619.5 ml/min; P=0.03). Fractional tissue hypoxia fell in the STK (fraction R2*.30/s: 22.1%620% versus 14.9%618.3%; P,0.01) after stenting. Renal vein biomarkers correlated with the degree of hypoxia in the STK: NGAL(r=0.3; P=0.01) and MCP-1(r=0.3; P=0.02; more so after stenting). Renal vein NGAL was inversely related to renal blood flow in the STK (r=20.65; P,0.001). Biomarkers were highly correlated between STK and CLK, NGAL (r=0.94; P,0.001), and MCP-1 (r=0.96; P,0.001). Conclusions These results showed changes over time in single-kidney GFR that were not evident in parameters of total GFR. Furthermore, they delineate the relationship of measurable tissue hypoxia within the STK and markers of inflammation in human ARAS. Renal vein NGAL and MCP-1 indicated persistent interactions between the ischemic kidney and both CLK and systemic levels of inflammatory cytokines.

AB - Background and objectives Atherosclerotic renal artery stenosis (ARAS) can reduce renal blood flow, tissue oxygenation, and GFR. In this study, we sought to examine associations between renal hemodynamics and tissue oxygenation with single-kidney function, pressor hormones, and inflammatory biomarkers in patients with unilateral ARAS undergoing medical therapy alone or stent revascularization. Design, setting, participants, & measurements Nonrandomized inpatient studies were performed in patients with unilateral ARAS (.60% occlusion) before and 3 months after revascularization (n=10) or medical therapy (n=20) or patients with essential hypertension (n=32) under identical conditions. The primary study outcome was change in single-kidney GFR. Individual kidney hemodynamics and volume were measured using multidetector computed tomography. Tissue oxygenation (using R2* as a measure of deoxyhemoglobin) was determined by blood oxygen level-dependent magnetic resonance imaging at 3 T. Renal vein neutrophil gelatinase-associated lipocalin (NGAL), monocyte chemoattractant protein-1 (MCP-1), and plasma renin activity were measured. Results Total GFR did not change over 3 months in either group, but the stenotic kidney (STK) GFR rose over time in the stent compared with the medical group (12.2[21.8 to 10.5] versus 25.3[27.3 to 20.3] ml/min; P=0.03). Contralateral kidney (CLK) GFR declined in the stent group (43.6619.7 to 36.6619.5 ml/min; P=0.03). Fractional tissue hypoxia fell in the STK (fraction R2*.30/s: 22.1%620% versus 14.9%618.3%; P,0.01) after stenting. Renal vein biomarkers correlated with the degree of hypoxia in the STK: NGAL(r=0.3; P=0.01) and MCP-1(r=0.3; P=0.02; more so after stenting). Renal vein NGAL was inversely related to renal blood flow in the STK (r=20.65; P,0.001). Biomarkers were highly correlated between STK and CLK, NGAL (r=0.94; P,0.001), and MCP-1 (r=0.96; P,0.001). Conclusions These results showed changes over time in single-kidney GFR that were not evident in parameters of total GFR. Furthermore, they delineate the relationship of measurable tissue hypoxia within the STK and markers of inflammation in human ARAS. Renal vein NGAL and MCP-1 indicated persistent interactions between the ischemic kidney and both CLK and systemic levels of inflammatory cytokines.

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JO - Clinical Journal of the American Society of Nephrology

JF - Clinical Journal of the American Society of Nephrology

SN - 1555-9041

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