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.

Highlights

  • Chronic kidney disease (CKD) is a worldwide public health problem

  • The same group has subsequently shown that global activation of hypoxia inducible factor (HIF)-1α in all tubules ameliorated inflammation and fibrosis (Kobayashi et al, 2012). These results suggest that the outcomes of HIF activation are cell-specific, context-specific and timing-dependent in CKD (Yu et al, 2012b)

  • An increasing number of experimental and clinical studies indicate that renal tissue hypoxia, resulting from mismatch between oxygen delivery and consumption is a major contributor to CKD progression

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Summary

Introduction

Chronic kidney disease (CKD) is a worldwide public health problem. Besides its impact on health, CKD and end-stage renal disease (ESRD) require substantial healthcare resources (Honeycutt et al, 2013). Numerous studies have elucidated the underlying mechanisms of CKD and identified new therapeutic targets, but success in clinical translation has been limited. Imbalance between oxygen delivery and consumption leading to tissue hypoxia has been recognized as an important contributor to CKD development and progression (Fine et al, 1998; Norman and Fine, 2006; O’Connor, 2006; Mimura and Nangaku, 2010). The aim of this review is to discuss the role of renal oxygenation (oxygen delivery, consumption and tissue oxygen tension) in CKD progression and potential therapeutic options based on recent literature

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