Abstract
Immune checkpoint inhibitors are now approved for more than 50 indications, and increasing numbers of patients with advanced cancer are receiving immunotherapy. Immune-related adverse events that result from checkpoint inhibitors can affect any organ system. The most common kidney side effect is acute kidney injury, typically caused by acute interstitial nephritis. This review covers the most recent advances in immune checkpoint inhibitor-induced acute kidney injury. The review focuses on the differences between checkpoint inhibitor classes in causing acute kidney injury and differentiating immune checkpoint inhibitor-induced kidney damage from other causes of acute kidney injury. We describe the appropriate use of a kidney biopsy in the diagnosis of acute kidney injury and highlight the need for identification of noninvasive diagnostic and predictive biomarkers of immune checkpoint inhibitor-induced acute kidney injury. In the treatment section, approaches to corticosteroid use and the risks and benefits of rechallenging patients who experience acute kidney injury are debated. We also clarify the long-term adverse effects of immune checkpoint inhibitors on kidney function and the risk of chronic kidney disease in cancer survivors.
Highlights
Immune checkpoint inhibitors (ICIs) are considered standard of care in the management of many advanced cancers
We describe the appropriate use of a kidney biopsy in the diagnosis of acute kidney injury and highlight the need for identification of non-invasive diagnostic and predictive biomarkers of immune checkpoint inhibitor-induced acute kidney injury
Acute kidney injury (AKI) after ICIs was noted in early case reports with acute tubulo-interstitial nephritis (AIN) as the most common pattern of injury.[4,5,6]
Summary
Immune checkpoint inhibitors (ICIs) are considered standard of care in the management of many advanced cancers. Another important clue while evaluating the cause of AKI in a patient receiving ICIs is the occurrence of non-renal immune related adverse events.[19] A patient concurrently or recently diagnosed with ICI-induced rash, colitis, myocarditis, or thyroiditis, for example is more likely to have an immune related adverse event in another organ such as the Journal Pre-proof kidney Such patients have a propensity to develop activated T-cells against autoantigens and the intensity threshold for an immune response against self-tissue has already been reached. Additional stains to confirm ICI-induced AKI may Journal Pre-proof be used to confirm association with ICIs – positive staining of tubular epithelial cells for PD-L1 has been shown to help differentiate PD-1-related AIN from other AIN.[45] the clinical utility has not been validated and larger studies are needed before the PD-L1 stain can be recommended for this purpose.
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