Inflammation: A Key Contributor to the Genesis and Progression of Chronic Kidney Disease

Abstract

It has become apparent that inflammation and inflammatory reactions can evoke renal injury and promote chronic kidney disease (CKD) progression. Under physiological condition, intrarenal vascular distribution is heterogeneous, and medulla is hypoxic. To avoid energy deprivation in the low pO2 regions of the kidney, an array of hormones, autocoids, and vasoactive substances, including medullipin, prostaglandins, endothelins, nitric oxide, angiotensin II, kinins, and adenosine, tonically regulates the microvasculature to ensure a perfect match of the microcirculation (O2 supply) and renal tubules (O2 demand). Inflammation, systemic or intrarenal, not only can abolish the microvascular response to its regulators, but also induces an array of tubular toxins, including reactive oxygen species, leading to tubular injury, nephron dropout, and onset of CKD. Positive acid balance, electrolyte alterations, and intestinal dysbiosis can perpetuate CKD progression. Understanding the role of inflammation in the genesis and progression of CKD will foster the development of strategies to prevent and treat the underlying inflammation and improve CKD outcomes.