Inflammation and kidney stones: cause and effect?

This short review is intended to highlight the potential role of inflammation as a key pathological driver, rather than a mere consequence, of nephrolithiasis. Although there is clearly a strong likelihood that the relationship is bidirectional, and that kidney stone-triggered inflammation can establish a vicious cycle of tissue injury and stone formation.

These consist of data from both recent preclinical and clinical studies demonstrating the importance of inflammation in models of stone disease and in kidney tissue from patients with nephrolithiasis, and as a potential driver of disease recurrence and a suitable treatment target. In particular, the role of immune cells and their relationship to the NLRP3 inflammasome is becoming clearer, as well as the potential contribution to tissue injury and stone formation of the pro-inflammatory cytokines interleukin-1β and interleukin-18.

This concept is not new and raises the possibility that targeting inflammation directly may prove to be a novel and suitable means of treatment for at least some types of kidney stone, and in certain clinical settings, both acutely and as prevention, especially in those patients experiencing recurrent stone episodes and/or who have a well defined metabolic cause such as uric acid or calcium oxalate stones.