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Oxidative Stress in the Kidney: Proximal Tubule Disorders

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Abstract

Redox changes initiate various cellular signals in the cells, and the redox environment can determine if a cell will proliferate, differentiate, or die. Imbalance of the redox status such as during oxidative stress can trigger a series of events, leading to cellular dysfunction. Reactive oxygen species (ROS) are increasingly considered as being involved in the initiation and progression of chronic renal disease. The proximal tubule is a major site of ROS production, due to its high transport activity supported by an oxygen consuming metabolism. Various congenital and acquired renal disorders induce ROS in proximal tubule cells (PTC), which are characterized by their capacity for receptor-mediated endocytosis of albumin. Recent studies suggest that albumin exerts a dual effect on the proximal tubule. In physiological conditions, endocytosis of albumin is a survival factor, protecting the cells against oxidant injury. In case of glomerular proteinuria, exposure of the PTC to an excess of albumin induces oxidative stress and causes renal injury. Furthermore, defects in the receptor-mediated endocytic uptake of albumin are also related to a state of increased oxidative stress, causing tubulointerstitial fibrosis and renal failure. In this chapter, we review available evidence about the nature of stimuli and initial events involved in ROS generation and antioxidant mechanisms in PTC.

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Terryn, S., Devuyst, O. (2011). Oxidative Stress in the Kidney: Proximal Tubule Disorders. In: Miyata, T., Eckardt, KU., Nangaku, M. (eds) Studies on Renal Disorders. Oxidative Stress in Applied Basic Research and Clinical Practice. Humana Press. https://doi.org/10.1007/978-1-60761-857-7_10

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