In a new study, researchers characterized the incidence of, and some patterns related to, acute kidney injury (AKI) in patients with non-Hodgkin lymphoma (NHL) after 1 month following chimeric antigen receptor T-cell (CAR-T) therapy. They reported their findings in the Mayo Clinic Proceedings.
“Approximately 1 in 6 patients who receive CAR-T therapy for resistant NHL develop AKI in the first month after infusion,” the research team explained in their report.
In this retrospective, single-center analysis conducted at Mayo Clinic in Rochester, Minnesota, the researchers studied the records of adult patients with aggressive NHL who had been treated with axicabtagene ciloleucel between June 2016 and November 2020. Follow-up had spanned 1 month after undergoing CAR-T therapy.
The researchers had goals of identifying the incidence of AKI and possible risk factors for its development after CAR-T therapy. An increase of at least 1.5-fold, compared with baseline, in the serum creatinine concentration was used to define post-CAR-T AKI. The baseline period was considered the day on which a patient underwent CAR-T infusion.
There were 83 patients evaluated in the analysis, of whom 14 (17%), experienced AKI in the follow-up period. By 1 month after CAR-T infusion, 71% of the AKI events were considered resolved.
Several factors were identified as significantly associated with development of AKI during the follow-up period. Among baseline clinical laboratory factors, this included a relatively lower estimated glomerular filtration rate (eGFR) at baseline in patients who developed AKI (median eGFR of 80.4 mL/min/1.73 m2), compared with that of patients who did not develop AKI (median eGFR of 93.5 mL/min/1.73 m2; P =.047).
Compared with patients who did not develop AKI, greater increases from baseline to peak serum lactate dehydrogenase level were seen in the group with AKI during follow-up, in terms of both median absolute change (P =.011) and median percentage change (P =.010). Increased peak uric acid (P =.015) and peak creatine kinase (P =.016) concentrations during the follow-up period were more prevalent in the group with incident AKI. Significant differences during follow-up were also seen in serum bicarbonate nadir (P =.042) and blood urea nitrogen peak (P =.011) concentrations in patients with or without AKI.
Receipt of intravenous contrast medium or other nephrotoxic agents (P =.012) and receipt of allopurinol/rasburicase prophylaxis (P =.020) were also more common in the group with incident AKI. Additionally, higher rates of usage of corticosteroids (P =.028), a higher total corticosteroid dose (P =.013), and higher numbers of tocilizumab doses (P =.005) showed significant associations with incident AKI.
“Patients with high tumor burden receiving larger doses of corticosteroids or tocilizumab should be closely monitored for development of AKI,” the researchers concluded. They also noted several factors may be useful for guiding identification of patients at elevated AKI risk and early use of supportive measures.
Disclosures: Some authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of disclosures.
Farooqi N, Sy-Go JPT, Miao J, et al. Incidence and risk factors for acute kidney injury after chimeric antigen receptor T-cell therapy. Mayo Clin Proc. 2022;97(7):1294-1304. doi:10.1016/j.mayocp.2022.05.018