Catumaxomab

Catumaxomab's renal risk is hemodynamic and indirect. By cross-linking tumor cells, T cells, and Fc-receptor-bearing accessory cells, it triggers a brisk cytokine release (TNF-alpha, IL-6, IFN-gamma), producing fever, vomiting, and a systemic inflammatory/vasodilatory state; combined with the fluid shifts of malignant ascites and therapeutic paracentesis, this can cause volume depletion and renal hypoperfusion — a prerenal acute kidney injury pattern — and contribute to electrolyte disturbance. There is no described direct tubular, glomerular, or crystal toxicity from the antibody itself. Management is supportive and hemodynamic.

Cytokine-release symptoms (fever, chills, nausea, vomiting) and abdominal pain after intraperitoneal dosing; if AKI develops it is typically prerenal — oliguria with a bland sediment, responsive to volume — in the context of fever, GI losses, and ascites management. Transient transaminitis and lymphopenia are expected and usually benign.

Cytokine-release symptoms within hours of each intraperitoneal infusion; any prerenal AKI follows the inflammatory/volume insult.

Trifunctional rat/mouse hybrid bispecific antibody binding EpCAM on tumor cells and CD3 on T cells, while its intact Fc region engages Fc-gamma-receptor-positive accessory immune cells (macrophages, NK cells, dendritic cells). This tri-cell complex drives potent T-cell- and accessory-cell-mediated tumor killing. Administered intraperitoneally for malignant ascites due to EpCAM-positive tumors.

Supportive: treat fever and GI losses, restore volume for prerenal AKI, and correct electrolytes. The antibody requires no renal dose adjustment; manage the hemodynamic/inflammatory insult and the underlying ascites.