Blinatumomab

T-cell activation drives release of IFN-gamma, TNF, and especially IL-6; CRS produces a hemodynamic, prerenal pattern (systemic vasodilation, capillary leak with intravascular volume depletion, and renal hypoperfusion) that, if sustained, progresses to ischemic acute tubular injury. In parallel, rapid lysis of a high leukemic burden causes tumor lysis syndrome—hyperuricemia, hyperphosphatemia with calcium-phosphate deposition, and uric-acid crystal/cast formation—producing intratubular obstruction and crystal/urate nephropathy.

Rising creatinine during CRS (fever, hypotension, hypoxia), often with the metabolic derangements of TLS (hyperkalemia, hyperphosphatemia, hyperuricemia, hypocalcemia); oliguria and volume overload in severe cases.

Early, typically during the first days of an infusion cycle (CRS) or with rapid tumor cytoreduction (TLS), concentrated around initiation and dose step-up.

Bispecific T-cell engager (BiTE) that simultaneously binds CD19 on B cells and CD3 on T cells, forming an immunologic synapse that redirects polyclonal cytotoxic T cells to lyse CD19-positive leukemic blasts independent of MHC or co-stimulation. Used in B-cell precursor acute lymphoblastic leukemia.

Treat CRS by grade (supportive care, corticosteroids, and tocilizumab for severe IL-6-driven CRS) and manage TLS aggressively (hydration, rasburicase for hyperuricemia, electrolyte correction, and renal replacement therapy for refractory hyperkalemia/hyperphosphatemia or oligoanuria). Interrupt blinatumomab for severe CRS; renal function generally recovers once the underlying syndrome is controlled.