Hypoxia as a biomarker of kidney disease

Roger G. Evans, Julian A. Smith, Bruce S. Gardiner, David W. Smith, Amanda G. Thrift, Clive N. May, Yugeesh R. Lankadeeva, Andrew D. Cochrane

Research output: Chapter in Book/Report/Conference proceedingChapter (Book)Otherpeer-review

Abstract

All established (e.g., serum creatinine, albuminuria) and emerging (e.g., neutrophil gelatinase-associated lipocalin, cystatin C) biomarkers of kidney disease suffer from the disadvantage that they are markers of damage to the kidney or loss of renal function. Tissue hypoxia is believed to be an initiating factor, in both chronic kidney disease (CKD) and acute kidney injury (AKI), so may provide a physiological biomarker for early diagnosis of both conditions. Currently blood oxygen dependent magnetic resonance imaging (BOLD MRI) appears to have little diagnostic value in human CKD. On the other hand, the measurement of urinary oxygen tension (PO2) has potential as a biomarker of risk of AKI in a hospital setting because: (i) Hypoxia in the renal medulla plays a central role in AKI of multiple causes; (ii) The vasa recta are closely associated with collecting ducts in the medulla so that pelvic urinary PO2 would be expected to equilibrate with medullary tissue PO2; (iii) The PO2 of urine in both the renal pelvis and the bladder varies in response to stimuli that would be expected to alter medullary tissue PO2;and (iv) New fibre-optic methods make it feasible to measure bladder urine PO2 in patients with a bladder catheter. But translation of this approach to hospital practice requires: (i) A quantitative understanding of the impact of oxygen transport across the epithelium of the ureter and bladder on urinary PO2 measured from the bladder,(ii) confirmation that changes in urinary PO2 parallel those in medullary PO2 in physiology and pathology, and (iii) Studies of the prognostic utility of urinary PO2 in hospital settings associated with risk of AKI, such as in patients undergoing cardiac surgery with cardiopulmonary bypass, those at risk of sepsis, and those undergoing imaging procedures requiring administration of radiocontrast agents.
Original languageEnglish
Title of host publicationBiomarkers in Kidney Disease
EditorsVinood B. Patel, Victor R. Preedy
Place of PublicationUnited Kingdom
PublisherSpringer
Pages83-105
Number of pages23
ISBN (Electronic)9789400776999
ISBN (Print)9789400776982, 9789400777002
DOIs
Publication statusPublished - 2016

Publication series

NameBiomarkers in Disease
PublisherMethods, Discoveries and Applications
ISSN (Print)2542-3657

Keywords

  • acute kidney injury
  • BOLD MRI
  • cardiopulmonary bypass
  • chronic kidney disease
  • intensive care
  • sepsis
  • urinary oxygen tension

Cite this

Evans, R. G., Smith, J. A., Gardiner, B. S., Smith, D. W., Thrift, A. G., May, C. N., ... Cochrane, A. D. (2016). Hypoxia as a biomarker of kidney disease. In V. B. Patel, & V. R. Preedy (Eds.), Biomarkers in Kidney Disease (pp. 83-105). (Biomarkers in Disease). United Kingdom: Springer. https://doi.org/10.1007/978-94-007-7743-9_7-1
Evans, Roger G. ; Smith, Julian A. ; Gardiner, Bruce S. ; Smith, David W. ; Thrift, Amanda G. ; May, Clive N. ; Lankadeeva, Yugeesh R. ; Cochrane, Andrew D. / Hypoxia as a biomarker of kidney disease. Biomarkers in Kidney Disease. editor / Vinood B. Patel ; Victor R. Preedy. United Kingdom : Springer, 2016. pp. 83-105 (Biomarkers in Disease).
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abstract = "All established (e.g., serum creatinine, albuminuria) and emerging (e.g., neutrophil gelatinase-associated lipocalin, cystatin C) biomarkers of kidney disease suffer from the disadvantage that they are markers of damage to the kidney or loss of renal function. Tissue hypoxia is believed to be an initiating factor, in both chronic kidney disease (CKD) and acute kidney injury (AKI), so may provide a physiological biomarker for early diagnosis of both conditions. Currently blood oxygen dependent magnetic resonance imaging (BOLD MRI) appears to have little diagnostic value in human CKD. On the other hand, the measurement of urinary oxygen tension (PO2) has potential as a biomarker of risk of AKI in a hospital setting because: (i) Hypoxia in the renal medulla plays a central role in AKI of multiple causes; (ii) The vasa recta are closely associated with collecting ducts in the medulla so that pelvic urinary PO2 would be expected to equilibrate with medullary tissue PO2; (iii) The PO2 of urine in both the renal pelvis and the bladder varies in response to stimuli that would be expected to alter medullary tissue PO2;and (iv) New fibre-optic methods make it feasible to measure bladder urine PO2 in patients with a bladder catheter. But translation of this approach to hospital practice requires: (i) A quantitative understanding of the impact of oxygen transport across the epithelium of the ureter and bladder on urinary PO2 measured from the bladder,(ii) confirmation that changes in urinary PO2 parallel those in medullary PO2 in physiology and pathology, and (iii) Studies of the prognostic utility of urinary PO2 in hospital settings associated with risk of AKI, such as in patients undergoing cardiac surgery with cardiopulmonary bypass, those at risk of sepsis, and those undergoing imaging procedures requiring administration of radiocontrast agents.",
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Evans, RG, Smith, JA, Gardiner, BS, Smith, DW, Thrift, AG, May, CN, Lankadeeva, YR & Cochrane, AD 2016, Hypoxia as a biomarker of kidney disease. in VB Patel & VR Preedy (eds), Biomarkers in Kidney Disease. Biomarkers in Disease, Springer, United Kingdom, pp. 83-105. https://doi.org/10.1007/978-94-007-7743-9_7-1

Hypoxia as a biomarker of kidney disease. / Evans, Roger G.; Smith, Julian A.; Gardiner, Bruce S.; Smith, David W.; Thrift, Amanda G.; May, Clive N.; Lankadeeva, Yugeesh R.; Cochrane, Andrew D.

Biomarkers in Kidney Disease. ed. / Vinood B. Patel; Victor R. Preedy. United Kingdom : Springer, 2016. p. 83-105 (Biomarkers in Disease).

Research output: Chapter in Book/Report/Conference proceedingChapter (Book)Otherpeer-review

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T1 - Hypoxia as a biomarker of kidney disease

AU - Evans, Roger G.

AU - Smith, Julian A.

AU - Gardiner, Bruce S.

AU - Smith, David W.

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AU - May, Clive N.

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N2 - All established (e.g., serum creatinine, albuminuria) and emerging (e.g., neutrophil gelatinase-associated lipocalin, cystatin C) biomarkers of kidney disease suffer from the disadvantage that they are markers of damage to the kidney or loss of renal function. Tissue hypoxia is believed to be an initiating factor, in both chronic kidney disease (CKD) and acute kidney injury (AKI), so may provide a physiological biomarker for early diagnosis of both conditions. Currently blood oxygen dependent magnetic resonance imaging (BOLD MRI) appears to have little diagnostic value in human CKD. On the other hand, the measurement of urinary oxygen tension (PO2) has potential as a biomarker of risk of AKI in a hospital setting because: (i) Hypoxia in the renal medulla plays a central role in AKI of multiple causes; (ii) The vasa recta are closely associated with collecting ducts in the medulla so that pelvic urinary PO2 would be expected to equilibrate with medullary tissue PO2; (iii) The PO2 of urine in both the renal pelvis and the bladder varies in response to stimuli that would be expected to alter medullary tissue PO2;and (iv) New fibre-optic methods make it feasible to measure bladder urine PO2 in patients with a bladder catheter. But translation of this approach to hospital practice requires: (i) A quantitative understanding of the impact of oxygen transport across the epithelium of the ureter and bladder on urinary PO2 measured from the bladder,(ii) confirmation that changes in urinary PO2 parallel those in medullary PO2 in physiology and pathology, and (iii) Studies of the prognostic utility of urinary PO2 in hospital settings associated with risk of AKI, such as in patients undergoing cardiac surgery with cardiopulmonary bypass, those at risk of sepsis, and those undergoing imaging procedures requiring administration of radiocontrast agents.

AB - All established (e.g., serum creatinine, albuminuria) and emerging (e.g., neutrophil gelatinase-associated lipocalin, cystatin C) biomarkers of kidney disease suffer from the disadvantage that they are markers of damage to the kidney or loss of renal function. Tissue hypoxia is believed to be an initiating factor, in both chronic kidney disease (CKD) and acute kidney injury (AKI), so may provide a physiological biomarker for early diagnosis of both conditions. Currently blood oxygen dependent magnetic resonance imaging (BOLD MRI) appears to have little diagnostic value in human CKD. On the other hand, the measurement of urinary oxygen tension (PO2) has potential as a biomarker of risk of AKI in a hospital setting because: (i) Hypoxia in the renal medulla plays a central role in AKI of multiple causes; (ii) The vasa recta are closely associated with collecting ducts in the medulla so that pelvic urinary PO2 would be expected to equilibrate with medullary tissue PO2; (iii) The PO2 of urine in both the renal pelvis and the bladder varies in response to stimuli that would be expected to alter medullary tissue PO2;and (iv) New fibre-optic methods make it feasible to measure bladder urine PO2 in patients with a bladder catheter. But translation of this approach to hospital practice requires: (i) A quantitative understanding of the impact of oxygen transport across the epithelium of the ureter and bladder on urinary PO2 measured from the bladder,(ii) confirmation that changes in urinary PO2 parallel those in medullary PO2 in physiology and pathology, and (iii) Studies of the prognostic utility of urinary PO2 in hospital settings associated with risk of AKI, such as in patients undergoing cardiac surgery with cardiopulmonary bypass, those at risk of sepsis, and those undergoing imaging procedures requiring administration of radiocontrast agents.

KW - acute kidney injury

KW - BOLD MRI

KW - cardiopulmonary bypass

KW - chronic kidney disease

KW - intensive care

KW - sepsis

KW - urinary oxygen tension

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Evans RG, Smith JA, Gardiner BS, Smith DW, Thrift AG, May CN et al. Hypoxia as a biomarker of kidney disease. In Patel VB, Preedy VR, editors, Biomarkers in Kidney Disease. United Kingdom: Springer. 2016. p. 83-105. (Biomarkers in Disease). https://doi.org/10.1007/978-94-007-7743-9_7-1