PMID- 30904069
OWN - NLM
STAT- MEDLINE
DCOM- 20200214
LR  - 20231103
IS  - 1523-1755 (Electronic)
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 95
IP  - 4
DP  - 2019 Apr
TI  - Tissue hypoxia, inflammation, and loss of glomerular filtration rate in human 
      atherosclerotic renovascular disease.
PG  - 948-957
LID - S0085-2538(19)30031-6 [pii]
LID - 10.1016/j.kint.2018.11.039 [doi]
AB  - The relationships between renal blood flow (RBF), tissue oxygenation, and 
      inflammatory injury in atherosclerotic renovascular disease (ARVD) are poorly 
      understood. We sought to correlate RBF and tissue hypoxia with glomerular 
      filtration rate (GFR) in 48 kidneys from patients with ARVD stratified by single 
      kidney iothalamate GFR (sGFR). Oxygenation was assessed by blood oxygenation 
      level dependent magnetic resonance imaging (BOLD MRI), which provides an index 
      for the levels of deoxyhemoglobin within a defined volume of tissue (R2*). sGFR 
      correlated with RBF and with the severity of vascular stenosis as estimated by 
      duplex velocities. Higher cortical R2* and fractional hypoxia and higher levels 
      of renal vein neutrophil-gelatinase-associated-lipocalin (NGAL) and 
      monocyte-chemoattractant protein-1 (MCP-1) were observed at lower GFR, with an 
      abrupt inflection below 20 ml/min. Renal vein MCP-1 levels correlated with 
      cortical R2* and with fractional hypoxia. Correlations between cortical R2* and 
      RBF in the highest sGFR stratum (mean sGFR 51 +/- 12 ml/min; R = -0.8) were 
      degraded in the lowest sGFR stratum (mean sGFR 8 +/- 3 ml/min; R = -0.1). Changes 
      in fractional hypoxia after furosemide were also absent in the lowest sGFR 
      stratum. These data demonstrate relative stability of renal oxygenation with 
      moderate reductions in RBF and GFR but identify a transition to overt hypoxia and 
      inflammatory cytokine release with severely reduced GFR. Tissue oxygenation and 
      RBF were less correlated in the setting of reduced sGFR, consistent with variable 
      oxygen consumption or a shift to alternative mechanisms of tissue injury. 
      Identifying transitions in tissue oxygenation may facilitate targeted therapy in 
      ARVD.
CI  - Copyright (c) 2019 International Society of Nephrology. Published by Elsevier Inc. 
      All rights reserved.
FAU - Abumoawad, Abdelrhman
AU  - Abumoawad A
AD  - Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA.
FAU - Saad, Ahmed
AU  - Saad A
AD  - Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA; 
      Department of Family Medicine, Creighton University, Omaha, Nebraska, USA.
FAU - Ferguson, Christopher M
AU  - Ferguson CM
AD  - Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA.
FAU - Eirin, Alfonso
AU  - Eirin A
AD  - Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA.
FAU - Woollard, John R
AU  - Woollard JR
AD  - Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA.
FAU - Herrmann, Sandra M
AU  - Herrmann SM
AD  - Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA.
FAU - Hickson, LaTonya J
AU  - Hickson LJ
AD  - Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA.
FAU - Bendel, Emily C
AU  - Bendel EC
AD  - Department of Radiology, Mayo Clinic, Rochester, Minnesota, USA.
FAU - Misra, Sanjay
AU  - Misra S
AD  - Department of Radiology, Mayo Clinic, Rochester, Minnesota, USA.
FAU - Glockner, James
AU  - Glockner J
AD  - Department of Radiology, Mayo Clinic, Rochester, Minnesota, USA.
FAU - Lerman, Lilach O
AU  - Lerman LO
AD  - Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA.
FAU - Textor, Stephen C
AU  - Textor SC
AD  - Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA. 
      Electronic address: stextor@mayo.edu.
LA  - eng
GR  - K23 DK109134/DK/NIDDK NIH HHS/United States
GR  - K08 DK118120/DK/NIDDK NIH HHS/United States
GR  - R01 DK100081/DK/NIDDK NIH HHS/United States
GR  - P01 HL085307/HL/NHLBI NIH HHS/United States
GR  - R01 DK073608/DK/NIDDK NIH HHS/United States
GR  - R01 HL098967/HL/NHLBI NIH HHS/United States
GR  - UL1 RR024150/RR/NCRR NIH HHS/United States
GR  - R01 DK102325/DK/NIDDK NIH HHS/United States
PT  - Clinical Trial, Phase I
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Atherosclerosis/*complications/physiopathology
MH  - Cell Hypoxia
MH  - Cross-Sectional Studies
MH  - Female
MH  - *Glomerular Filtration Rate
MH  - Humans
MH  - Inflammation/etiology/pathology/*physiopathology
MH  - Kidney/diagnostic imaging/*pathology/physiopathology
MH  - Magnetic Resonance Imaging
MH  - Male
MH  - Middle Aged
MH  - Oxygen/analysis/blood
MH  - Oxygen Consumption
MH  - Renal Artery Obstruction/etiology/pathology/*physiopathology
MH  - Renal Circulation
PMC - PMC6738340
MID - NIHMS1519409
OTO - NOTNLM
OT  - BOLD MR
OT  - GFR
OT  - NGAL
OT  - VEGF-A
OT  - cortical
OT  - hypertension
OT  - hypoxia
OT  - medullary
OT  - renal artery stenosis
OT  - renal blood flow
OT  - renovascular disease
OT  - revascularization
EDAT- 2019/03/25 06:00
MHDA- 2020/02/15 06:00
PMCR- 2020/04/01
CRDT- 2019/03/25 06:00
PHST- 2018/09/04 00:00 [received]
PHST- 2018/11/15 00:00 [revised]
PHST- 2018/11/29 00:00 [accepted]
PHST- 2019/03/25 06:00 [entrez]
PHST- 2019/03/25 06:00 [pubmed]
PHST- 2020/02/15 06:00 [medline]
PHST- 2020/04/01 00:00 [pmc-release]
AID - S0085-2538(19)30031-6 [pii]
AID - 10.1016/j.kint.2018.11.039 [doi]
PST - ppublish
SO  - Kidney Int. 2019 Apr;95(4):948-957. doi: 10.1016/j.kint.2018.11.039.