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Journal Article Epublish 3 citations

PubMed: 32341794 DOI: 10.1136/bmjsem-2019-000662

Hypoxia is not the primary mechanism contributing to exercise-induced proteinuria.

BMJ Open Sport Exerc Med 6(1):e000662

Authors: Kelsley E Joyce, John Delamere, Susie Bradwell, Stephen David Myers, Kimberly Ashdown, Carla Rue, Samuel Je Lucas, Owen D Thomas, Amy Fountain, Mark Edsell, Fiona Myers, Will Malein, Chris Imray, Alex Clarke, Chrisopher T Lewis, Charles Newman, Brian Johnson, Patrick Cadigan, Alexander Wright, Arthur Bradwell

Affiliations

  • School of Sport, Exercise, and Rehabilitation Sciences, University of Birmingham, Birmingham, UK.
  • Birmingham Medical Research Expeditionary Society, University of Birmingham, Birmingham, UK.
  • Institute of Clinical Sciences, University of Birmingham, Birmingham, UK.
  • Medical School, East Surrey Hospital, Redhill, Surrey, UK.
  • Occupational Performance Research Group, University of Chichester Department of Sport and Exercise Sciences, Chichester, West Sussex, UK.
  • Research & Development, Binding Site Group Ltd, Edgbaston, Birmingham, UK.
  • St. George's University Hospital, University of London, London, UK.
  • School of Biological Sciences, University of Portsmouth, Portsmouth, UK.
  • Department of Anaesthesia, Ninewells Hospital, Dundee, UK.
  • Vascular Surgery, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK.
  • Department of Bioengineering, Imperial College London, London, UK.
  • Academic Foundation Programme, NHS Highland, Inverness, United Kingdom.
  • University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.
  • BASEM, Doncaster, UK.
  • Medical School, University of Birmingham, Birmingham, UK.

Abstract

INTRODUCTION

Proteinuria increases at altitude and with exercise, potentially as a result of hypoxia. Using urinary alpha-1 acid glycoprotein (α1-AGP) levels as a sensitive marker of proteinuria, we examined the impact of relative hypoxia due to high altitude and blood pressure-lowering medication on post-exercise proteinuria.

METHODS

Twenty individuals were pair-matched for sex, age and ACE genotype. They completed maximal exercise tests once at sea level and twice at altitude (5035 m). Losartan (100 mg/day; angiotensin-receptor blocker) and placebo were randomly assigned within each pair 21 days before ascent. The first altitude exercise test was completed within 24-48 hours of arrival (each pair within ~1 hour). Acetazolamide (125 mg two times per day) was administrated immediately after this test for 48 hours until the second altitude exercise test.

RESULTS

With placebo, post-exercise α1-AGP levels were similar at sea level and altitude. Odds ratio (OR) for increased resting α1-AGP at altitude versus sea level was greater without losartan (2.16 times greater). At altitude, OR for reduced post-exercise α1-AGP (58% lower) was higher with losartan than placebo (2.25 times greater, p=0.059) despite similar pulse oximetry (SpO) (p=0.95) between groups. Acetazolamide reduced post-exercise proteinuria by approximately threefold (9.3±9.7 vs 3.6±6.0 μg/min; p=0.025) although changes were not correlated (r=-0.10) with significant improvements in SpO (69.1%±4.5% vs 75.8%±3.8%; p=0.001).

DISCUSSION

Profound systemic hypoxia imposed by altitude does not result in greater post-exercise proteinuria than sea level. Losartan and acetazolamide may attenuate post-exercise proteinuria, however further research is warranted.

MeSH

Proteinuria, Altitude, Kidney, Exercise Test, Hypoxia, Orosomucoid, Losartan

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