PD-1 阻断在结外 NK/T 细胞淋巴瘤中诱导的免疫介导 IgA 肾病

A man in his early fifties was diagnosed with extranodal natural killer/T-cell lymphoma involving the nasal cavity and cervical lymph nodes. At the time of diagnosis, renal function was entirely normal. He was started on first-line combination therapy consisting of a PD-1 monoclonal antibody, pegaspargase, the histone deacetylase inhibitor chidamide, and systemic corticosteroids, with an early and favorable clinical response of the lymphoma.

However, prior to the second treatment cycle, routine laboratory evaluation revealed new-onset proteinuria accompanied by a rising serum creatinine level. Subsequent renal biopsy demonstrated IgA-dominant immune complex deposition with crescent formation, consistent with rapidly progressive IgA glomerulonephritis. The immune checkpoint inhibitor was promptly discontinued, and high-dose corticosteroid therapy was initiated, followed by cyclophosphamide. Renal function showed partial but meaningful improvement. Given the renal toxicity, systemic immunotherapy was withheld, and the lymphoma was subsequently managed successfully with radiotherapy alone.

At twelve months of follow-up, the patient remained in complete oncologic remission, with markedly improved renal parameters. This case highlights a rare presentation of rapidly progressive IgA nephropathy associated with PD-1 blockade in extranodal NK/T-cell lymphoma, a relationship that remains insufficiently characterized in current literature.

It emphasizes the importance of close and regular monitoring of renal function and urinalysis during immunotherapy. Early recognition of renal involvement, together with timely discontinuation of the immune checkpoint inhibitor and appropriate immunosuppressive treatment, may preserve kidney function while still allowing effective control of the underlying malignancy.