Creatinine rise; emerging data.

Diarrhea-driven prerenal AKI.

Mild reversible creatinine rises only; dose-limiting toxicities are neurologic and GI; renal data confounded by cisplatin.

Predominantly hepatobiliary elimination; renal clearance minor, kidney risk mainly tumor lysis in AML; reduce dose in organ impairment.

Differentiation syndrome; QT prolongation.

Renal tubular acidosis and rare AKI.

Creatinine rise; rhabdomyolysis reports.

Renally excreted (~2/3 in urine); half-life rises exponentially below CrCl 25-35 — exposure/clearance issue amplifying pulmonary toxicity, not a direct nephrotoxin.

CRS and tumor lysis → AKI.

Tubulointerstitial AKI; vemurafenib strongest.

CRS-driven prerenal AKI and tumor lysis.

Kidney-sparing; GFR-dosed by the Calvert formula.

AKI, TMA and hypertension — a hot myeloma signal.

CRS-driven AKI; delayed neurotoxicity.

Proximal tubular ATN + magnesium wasting; the archetype.

Capillary-leak / SIRS-like AKI and tumor lysis.

Real-world AKI signal with BRAF partners.

2025 TROP2 ADC; renal signal theoretical, extrapolated from the ADC class.

CRS and tumor lysis — emerging.

Differentiation syndrome and tumor lysis.

Class tubular signal; usually mild.

Emerging AKI and electrolyte signals in urothelial cancer.

Rare minimal-change disease and AKI.

Class delayed cumulative tubulointerstitial/ATN; usually mild; acute signal often really cisplatin.

Lower renal risk than zoledronate.

Tumor lysis, hypertension and AKI.

CRS-driven AKI and tumor lysis in myeloma.

Chloroacetaldehyde → Fanconi syndrome.

Fluid retention; rare Fanconi and AKI.

Renally cleared; AKI and rare Fanconi/TMA.

2024 cellular therapy; high-dose IL-2 conditioning → capillary leak AKI.

Rhabdomyolysis risk in small-cell lung cancer.

Tumor lysis in bulky lymphoma is the main renal hazard; modern topical gel has no detectable systemic absorption.

Delivers melphalan intracellularly; BRIDGE supports a reduced 30 mg dose in moderate renal impairment.

Crystal nephropathy; glucarpidase rescue.

Diarrhea-driven prerenal AKI; QT prolongation.

Podocyte injury → proteinuria and FSGS.

Second-gen platinum with reduced renal toxicity vs cisplatin.

Water-soluble nitrosourea; renal risk inferred at class level; cumulative delayed tubulointerstitial injury; DLT is myelosuppression.

High tumor-lysis risk in CLL.

Least nephrotoxic platinum; rare immune hemolysis.

Rare AKI; pancreatitis- and thrombosis-mediated.

Cumulative tubular toxicity, RTA and nephrogenic DI.

Renally cleared; dose-related acute kidney injury.

Cumulative tubular ATN; hypocalcemia is an on-target antiresorptive effect.

Antifolate with MTX-like renal handling.

Classic cytotoxic with recognized renal/urological complications; AKI usually multifactorial; hypersensitivity AIN possible.

Renally cleared antifolate; exposure ~doubles in renal impairment; forerunner CB3717 withdrawn for crystal nephrotoxicity.

Tumor lysis with bulky disease; treats some GN.

Diarrhea-driven prerenal AKI; emerging direct signals.

Renally excreted; dominant toxicity is reversible myelosuppression; caution in renal impairment.

Proteinuria, cast nephropathy, delayed graft recovery.

Elevated CK / rhabdomyolysis → pigment nephropathy.

Newer agent; renal data emerging.

Classic proximal tubular toxin → Fanconi and dose-limiting AKI.

Renally excreted, so caution in renal impairment; myelosuppression is the dominant toxicity.

Capillary-leak syndrome → AKI.

CRS-related AKI — emerging.

2024 small-cell lung BiTE; CRS-driven AKI risk.

CRS-associated AKI in myeloma — emerging signal.

Rhabdomyolysis → pigment nephropathy; hepatotoxicity.

Emerging AKI/proteinuria reports — under-published.

Differentiation syndrome → capillary leak and AKI.

Major tumor lysis syndrome risk on ramp-up.

Toxic ATN, infusion-rate dependent.