Immune Checkpoint Inhibitor-Induced Renal Toxicity
Summary
Immune checkpoint inhibitors (ICIs) have transformed oncology by unleashing antitumour T-cell responses through blockade of inhibitory pathways such as cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) and programmed cell death protein 1/programmed death-ligand 1 (PD-1/PD-L1). Despite durable cancer control, ICIs can provoke immune-related adverse events (irAEs) affecting multiple organs, including the kidneys. Renal toxicity typically presents as acute kidney injury (AKI), most often due to acute interstitial nephritis (AIN) characterised by inflammatory cell infiltration of the tubulointerstitial compartment. Less common manifestations include acute tubular necrosis, glomerulonephritis and renal tubular acidosis. Clinical onset ranges from weeks to months after ICI initiation and may coincide with extrarenal irAEs. Diagnosis relies on monitoring serum creatinine, urine analysis and, in uncertain cases, renal biopsy. Emerging non-invasive biomarkers such as urinary chemokines aim to facilitate early detection. Management requires prompt cessation of ICIs in moderate to severe cases and initiation of immunosuppression, usually corticosteroids, with consideration of therapy rechallenge in selected patients. Understanding risk factors, mechanistic pathways and optimal diagnostic algorithms is critical to balance effective cancer therapy against potentially serious renal complications.
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Immune Checkpoint Inhibitor-Induced Renal Toxicity publication trend
The graph below shows the total number of articles in immune checkpoint inhibitor-induced renal toxicity across all publications each year (not limited to Nature Index journals).
Technical terms
Immune checkpoint inhibitor: Monoclonal antibody that blocks inhibitory receptors on T cells (e.g. CTLA-4, PD-1), enhancing antitumour immunity.
Acute kidney injury (AKI): Sudden decline in renal function indicated by rapid rise in serum creatinine and/or reduced urine output.
Acute interstitial nephritis (AIN): Immune-mediated inflammation of the renal interstitium and tubules, often presenting with AKI.
Biomarker: Measurable substance used to detect or monitor physiological or pathological processes.
Programmed cell death protein 1 (PD-1): Inhibitory receptor on T cells that modulates immune responses upon ligand binding.
Cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4): Inhibitory receptor on T cells that downregulates early immune activation.
References
- Immune checkpoint inhibitors induce acute interstitial nephritis in mice with increased urinary MCP1 and PD-1 glomerular expression. Journal of Translational Medicine (2024).
- Incidence and risk factors of acute kidney injury in cancer patients treated with immune checkpoint inhibitors: a systematic review and meta-analysis. Frontiers in Immunology (2023).
- Nephrotoxicity in the Age of Immune Checkpoint Inhibitors: Mechanisms, Diagnosis, and Management. International Journal of Molecular Sciences (2023).
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