Cited by 269Chronic Kidney Disease and DiabetesAcute Kidney Injury ResearchRenal and Vascular Pathologies

Determinants of kidney oxygen consumption and their relationship to tissue oxygen tension in diabetes and hypertension

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Hansell, Peter, Welch, William J, Blantz, Roland C, Palm, Fredrik·2013·Clinical and Experimental Pharmacology and Physiology

Abstract

Summary: The high renal oxygen (O 2) demand is associated primarily with tubular O 2 consumption (Qo2) necessary for solute reabsorption. Increasing O 2 delivery relative to demand via increased blood flow results in augmented tubular electrolyte load following elevated glomerular filtration, which, in turn, increases metabolic demand. Consequently, elevated kidney metabolism results in decreased tissue oxygen tension. The metabolic efficiency for solute transport (Qo2/T Na) varies not only between different nephron sites, but also under different conditions of fluid homeostasis and disease. Contributing mechanisms include the presence of different Na+ transporters, different levels of oxidative stress and segmental tubular dysfunction. Sustained hyperglycaemia results in increased kidney Qo2, partly due to mitochondrial dysfunction and reduced electrolyte transport efficiency. This results in intrarenal tissue hypoxia because the increased Qo2 is not matched by a similar increase in O 2 delivery. Hypertension leads to renal hypoxia, mediated by increased angiotensin receptor tonus and oxidative stress. Reduced uptake in the proximal tubule increases load to the thick ascending limb. There, the increased load is reabsorbed, but at greater O 2 cost. The combination of hypertension, angiotensin II and oxidative stress initiates events leading to renal damage and reduced function. Tissue hypoxia is now recognized as a unifying pathway to chronic kidney disease. We have gained good knowledge about major changes in O 2 metabolism occurring in diabetic and hypertensive kidneys. However, further efforts are needed to elucidate how these alterations can be prevented or reversed before translation into clinical practice.

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  • In the human kidney outer medulla, O2 partial pressure falls to approximately 5-25 mmHg.

    “falls to ∼5–25 mmHg in the outer medulla”

    From Material-dependent oxygen transport governs ischemia-reperfusion injury and drug response in a kidney microphysiological system (2026) · cites this paper as Hansell et al., 2013

    The Introduction states that oxygen partial pressure is lower in the medulla than in the cortex and describes a gradient along medullary structures. It does not give a 5–25 mmHg range for the human outer medulla; the human finding discussed in the hypertension section is a relative difference, not an absolute value. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • In the human kidney, cortical O2 partial pressure is approximately 50 mmHg under physiological conditions.

    “in the human kidney, the cortical O2 partial pressure is approximately 50 mmHg under physiological conditions”

    From Material-dependent oxygen transport governs ischemia-reperfusion injury and drug response in a kidney microphysiological system (2026) · cites this paper as Hansell et al., 2013

    The Introduction says cortical PO2 is higher than medullary PO2, but gives no normal cortical value. A search of our copy for 50 mmHg and for cortical oxygen tension in healthy humans found no passage establishing approximately 50 mmHg in the human kidney under physiological conditions. (LLM, conf=0.73)

    Experimental — accuracy not yet measured
  • During ischemia, tissue PO2 can fall below approximately 5 mmHg.

    “during ischemia, tissue PO2 can fall below ∼5 mmHg”

    From Material-dependent oxygen transport governs ischemia-reperfusion injury and drug response in a kidney microphysiological system (2026) · cites this paper as Hansell et al., 2013

    The Introduction discusses low renal tissue PO2 and says acute hypotension can paradoxically increase medullary PO2. The hypertension section reports PO2 as low as 12 mmHg in hypertensive rats. Searches for ischemia and 5 mmHg found no passage stating that tissue PO2 falls below approximately 5 mmHg during ischemia. (LLM, conf=0.73)

    Experimental — accuracy not yet measured

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Authors
Hansell, P., Welch, W. J., Blantz, R. C., & Palm, F.
Affiliations
  • Uppsala University (SE)
  • Georgetown University (US)
  • University of California San Diego (US)
  • Linköping University (SE)
Corresponding author
Hansell, Peter
Venue
Clinical and Experimental Pharmacology and Physiology
Publisher
Wiley
Published
2013-01-29
Volume
40
Issue
2
Pages
123-137
ISSN
  • 0305-1870 (ISSN-L)
  • 1440-1681
OpenAlex
W1967360868
Cited by
269
References
4
Citations by year
2026: 13 · 2025: 15 · 2024: 21 · 2023: 35 · 2022: 21 · 2021: 25 · 2020: 27 · 2019: 27 · 2018: 19 · 2017: 19 · 2016: 18 · 2015: 8 · 2014: 11 · 2013: 6 · 2012: 3
FWCI
1.31
Type
journal article
Language
en
Open access
Locations
  • Clinical and Experimental Pharmacology and Physiology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Heart, Lung, and Blood Institute (HL-068686, R01HL089583, HL089583, P01HL068686)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK028602, P30DK079337)
Topics
  • Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
  • Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Renal and Vascular Pathologies
Keywords
renal oxygen consumption, tissue oxygen tension, renal hypoxia, diabetic nephropathy, hypertension, chronic kidney disease, oxidative stress, mitochondrial dysfunction, hyperglycemia, angiotensin II, thick ascending limb, proximal tubule, renal blood flow, solute reabsorption
MeSH terms
Animals, Diabetes Mellitus, Humans, Hypertension, Kidney, Oxygen, Oxygen Consumption, Oxidative Stress

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

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