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Review
. 2017 Jun 28:8:385.
doi: 10.3389/fphys.2017.00385. eCollection 2017.

Renal Oxygenation in the Pathophysiology of Chronic Kidney Disease

Affiliations
Review

Renal Oxygenation in the Pathophysiology of Chronic Kidney Disease

Zhi Zhao Liu et al. Front Physiol. .

Abstract

Chronic kidney disease (CKD) is a significant health problem associated with high morbidity and mortality. Despite significant research into various pathways involved in the pathophysiology of CKD, the therapeutic options are limited in diabetes and hypertension induced CKD to blood pressure control, hyperglycemia management (in diabetic nephropathy) and reduction of proteinuria, mainly with renin-angiotensin blockade therapy. Recently, renal oxygenation in pathophysiology of CKD progression has received a lot of interest. Several advances have been made in our understanding of the determinants and regulators of renal oxygenation in normal and diseased kidneys. The goal of this review is to discuss the alterations in renal oxygenation (delivery, consumption and tissue oxygen tension) in pre-clinical and clinical studies in diabetic and hypertensive CKD along with the underlying mechanisms and potential therapeutic options.

Keywords: AMPK; chronic kidney disease pathophysiology; hypoxia; hypoxia inducible factor (HIF); renal oxygen consumption.

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Figures

Figure 1
Figure 1
Schematic describing pathophysiology for the development of CKD in diabetes and hypertension (see text for details).

References

    1. Aukland K., Krog J. (1960). Renal oxygen tension. Nature 188:671. 10.1038/188671a0 - DOI - PubMed
    1. Babickova J., Klinkhammer B. M., Buhl E. M., Djudjaj S., Hoss M., Heymann F., et al. . (2017). Regardless of etiology, progressive renal disease causes ultrastructural and functional alterations of peritubular capillaries. Kidney Int. 91, 70–85. 10.1016/j.kint.2016.07.038 - DOI - PubMed
    1. Bel R., Coolen B. F., Nederveen A. J., Potters W. V., Verberne H. J., Vogt L., et al. . (2016). Magnetic resonance imaging–derived renal oxygenation and perfusion during continuous, steady-state angiotensin-II infusion in healthy humans. J. Am. Heart Assoc. 5:e003185. 10.1161/JAHA.115.003185 - DOI - PMC - PubMed
    1. Blantz R. C., Deng A., Miracle C. M., Thomson S. C. (2007). Regulation of kidney function and metabolism: a question of supply and demand. Trans. Am. Clin. Climatol. Assoc. 118, 23–43. - PMC - PubMed
    1. Bohle A., Mackensen-Haen S., Wehrmann M. (1996). Significance of postglomerular capillaries in the pathogenesis of chronic renal failure. Kidney Blood Press. Res. 19, 191–195. 10.1159/000174072 - DOI - PubMed