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Pronounced kidney hypoxia precedes albuminuria in type 1 diabetic mice
Linkoping Univ, Dept Med & Hlth Sci, Linkoping, Sweden.;Linkoping Univ, Ctr Med Image Sci & Visualizat, Linkoping, Sweden..
Linkoping Univ, Dept Med & Hlth Sci, Linkoping, Sweden..
Geisel Sch Med Dartmouth, EPR Ctr Study Viable Syst, Dept Radiol, Hanover, NH USA..
Linkoping Univ, Dept Med & Hlth Sci, Linkoping, Sweden.;Linkoping Univ, Ctr Med Image Sci & Visualizat, Linkoping, Sweden.;Linkoping Univ, Dept Radiol Norrkoping, Linkoping, Sweden..
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2016 (English)In: AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, ISSN 1931-857X, Vol. 310, no 9, F807-F809 p.Article in journal (Refereed) PublishedText
Abstract [en]

Intrarenal tissue hypoxia has been proposed as a unifying mechanism for the development of chronic kidney disease, including diabetic nephropathy. However, hypoxia has to be present before the onset of kidney disease to be the causal mechanism. To establish whether hypoxia precedes the onset of diabetic nephropathy, we implemented a minimally invasive electron paramagnetic resonance oximetry technique using implanted oxygen sensing probes for repetitive measurements of in vivo kidney tissue oxygen tensions in mice. Kidney cortex oxygen tensions were measured before and up to 15 days after the induction of insulinopenic diabetes in male mice and compared with normoglycemic controls. On day 16, urinary albumin excretions and conscious glomerular filtration rates were determined to define the temporal relationship between intrarenal hypoxia and disease development. Diabetic mice developed pronounced intrarenal hypoxia 3 days after the induction of diabetes, which persisted throughout the study period. On day 16, diabetic mice had glomerular hyperfiltration, but normal urinary albumin excretion. In conclusion, intrarenal tissue hypoxia in diabetes precedes albuminuria thereby being a plausible cause for the onset and progression of diabetic nephropathy.

Place, publisher, year, edition, pages
2016. Vol. 310, no 9, F807-F809 p.
Keyword [en]
diabetic nephropathy, kidney tissue oxygen tensions, intrarenal hypoxia
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-297275DOI: 10.1152/ajprenal.00049.2016ISI: 000375115700001PubMedID: 26936871OAI: oai:DiVA.org:uu-297275DiVA: diva2:941886
Funder
Swedish Research CouncilSwedish Heart Lung FoundationSwedish Diabetes Association
Available from: 2016-06-23 Created: 2016-06-22 Last updated: 2016-06-23Bibliographically approved

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Palm, Fredrik
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