Pathophysiology of Tubulointerstitial Nephritis

Abstract

Acute tubulointerstitial nephritis (ATIN) encompasses a wide range of kidney disease. It represents the final common pathophysiological pathway from a variety of diverse insults leading to sterile cellular infiltrate, interstitial fibrosis and tubular atrophy. In this article, we approach the development of ATIN from an immunological lens and explore how it relates to epithelial cell healing and fibrosis. The role of intrinsic and extrinsic insults such as damage associated molecular patterns and pathogen associated molecular patterns and their activation of deleterious inflammatory pathways are also discussed. Additionally, specific drug, metabolic and environmental causes and mechanisms are reviewed. While ATIN is an expansive topic, taking this approach to study kidney inflammation, healing and fibrosis will provide a uniform scaffold for understanding this complex and diverse set of diseases.