Immunotherapies and renal injury

Immunotherapy has transformed the landscape of cancer treatment. The goal of immunotherapy is to boost host-protective anti-tumor immunity. Immune checkpoint inhibitor and chimeric antigen receptor T cell (CAR-T cell) therapy have revolutionized cancer care. However, immunotherapies can cause multiorgan dysfunction including acute kidney injury (AKI). Acute tubulointerstitial nephritis (ATIN), the most common cause of AKI associated with immune checkpoint inhibitors, is caused by the overactivation of the immune system due to cytotoxic T lymphocyte-associated antigen 4 and programmed cell death receptor 1/programmed cell death ligand 1 inhibition. Early institution of corticosteroids improves kidney outcomes in immune checkpoint inhibitor-associated ATIN. CAR-T therapy can also cause AKI, and the underlying mechanism for AKI is predominantly hemodynamic, leading to poor renal perfusion. CAR-T therapy-associated AKI tends to be mild and generally reversible with hemodynamic support. Several electrolyte abnormalities have also been reported with immunotherapies. Immunotherapies are highly effective, but their use can be associated with renal toxicities. Prompt recognition and management of renal toxicities are essential in improving outcomes. Future studies are needed to shed light on the pathogenesis and management of immunotherapy-related renal injury.