# Interleukin-6 in Natural and Pathophysiological Kidney Aging

## TL;DR

This paper reviews the role of interleukin-6 in kidney aging and related diseases, highlighting its impact on both natural and pathological processes.

## Contribution

The paper provides a comprehensive review of IL-6's role in kidney aging and its potential therapeutic implications.

## Key findings

- IL-6 is a key mediator of age-related kidney inflammation and disease.
- IL-6 inhibition may offer renoprotective benefits in certain kidney disorders.
- The role of IL-6 in kidney aging remains underexplored despite clinical interest in IL-6 inhibitors.

## Abstract

Kidney aging is receiving growing attention in middle- to high-income societies due to increasing longevity in general population. Chronic Kidney Disease (CKD) has been widely accepted as a major non-communicable human disease affecting over 10% of the adult population in industrialized countries. CKD is mainly caused by metabolic and cardiovascular disorders such as diabetes mellitus and hypertension, disproportionally affecting older people, whereas natural kidney aging is driven by age-dependent systemic and renal low-grade inflammation. Interleukin-6 (IL-6) is the key cytokine mediating age-related inflammation. At the same time, IL-6 has been implicated in the pathophysiology of cardiovascular and renal disorders as a major pro-inflammatory cytokine. Thereby, IL-6 is placed at the intersection between natural and pathophysiological kidney aging, and the latter accelerates systemic aging and substantially limits life quality and expectancy. Growing clinical availability of IL-6 inhibitors for treatment of autoimmune and autoinflammatory disorders demands clarification of potential renal consequences as well. Available data suggests that IL-6 inhibition may be renoprotective in some kidney disorders, but the setting of kidney aging has received only minor attention. The present review focuses on the known effects of IL-6 associated with natural or pathophysiological renal aging.