Bendamustine
Treanda · Alkylator
Tumor lysis-mediated AKI is the principal risk; TMA is rare.
PRETMALYTE
ModerateOpen →
CAR-T cell therapy
CAR-T Cell Therapy
Kymriah · Yescarta · CAR-T
Cytokine storm reaches the kidney — AKI riding the wave of CRS.
ModerateCellular immunotherapy · approved 2017
B-cell lymphomaALLMultiple myeloma
Signature kidney injury
Prerenal / Hemodynamic AKI
Representative incidence20%
AKI ~5–33% across cohorts (commonly ~10–30%), mostly mild and reversible.
Source: Gutgarts et al., Biol Blood Marrow Transplant 2020; Kanbay et al., Clin Kidney J 2024
Toxicity fingerprint
Tap a signature to trace where it strikes the nephron.
0%incidence
SeverityModerate
ReversibilityReversible
Evidence0 refs
Nephron map
Vasculature / EndotheliumGlomerular & peritubular capillaries
Proximal Tubule
Distal Tubule / Collecting Duct
Tubular Lumen
Prerenal / Hemodynamic AKI
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Mechanism of kidney injury
Predominantly secondary to cytokine release syndrome — capillary leak and hemodynamic compromise cause prerenal AKI/ATN — compounded by tumor lysis syndrome, lymphodepleting conditioning, nephrotoxic antibiotics and sepsis.
Clinical presentation
AKI during or after CRS (fever, hypotension), often with electrolyte derangements and concurrent tumor-lysis labs.
Onset
Acute — within the CRS window (first days–weeks).
Reversibility
Reversible
Anticancer mechanism
Autologous T cells engineered to target a tumor antigen (e.g. CD19). B-cell lymphomas, leukemias and myeloma.
Management
Treat CRS, supportive AKI care, manage tumor lysis, dialysis if needed.
Risk factors
- Grade ≥3 CRS
- Lower baseline GFR
- High tumor burden / elevated LDH
- IV contrast
Prevention
- Tumor-lysis prophylaxis
- Hydration
- CRS management (tocilizumab/steroids)
- Avoid nephrotoxins
Note · A newer modality; incidence data are still maturing.
Where it strikes
Nephron segments
Vasculature / Endothelium
Glomerular & peritubular capillaries
Proximal Tubule
Bulk reabsorption + drug uptake (OCT2, OATs)
Tubular Lumen
The urine flow path
Injury signatures
Prerenal / Hemodynamic AKIAcute Tubular NecrosisCrystal / Obstructive Nephropathy
Beyond the kidney
Class-level context for the major non-renal toxicities of car-t cell therapys.
Immune / Infusion
CRS, infusion reactions, irAEs, anaphylaxis
- Cytokine release syndrome
Neurologic
Neuropathy, encephalopathy, ICANS, PRES
- ICANS / neurotoxicity
Hematologic
Cytopenias, thrombosis, TMA
- Cytopenias, hypogammaglobulinemia
Evidence
5 peer-reviewed references. Citation metadata via PubMed / NLM.
LandmarkAcute Kidney Injury after CAR-T Cell Therapy: Low Incidence and Rapid Recovery.Gutgarts V et al. · Biol Blood Marrow Transplant 2020 · PMID 32088364Foundational incidence study: 30% any-grade AKI by day 100, mostly mild.PMIDPredictors and implications of renal injury after CD19 chimeric antigen receptor T-cell therapy.Boardman AP et al. · Haematologica 2025 · PMID 39568416Large cohort plus FDA analysis linking AKI to CRS and worse survival.PMIDAcute kidney injury following CAR-T cell therapy: a nephrologist's perspective.Kanbay M et al. · Clin Kidney J 2024 · PMID 39781479Comprehensive review (incidence 5–33%, CRS, TLS, management).PMIDAcute kidney injury after CAR-T cell infusion.Rousseau A et al. · Bull Cancer 2024 · PMID 36220698Details CRS-related hypoperfusion, cytokine injury and tumor lysis.PMIDAcute Kidney Injury in Cancer Immunotherapy Recipients.Joseph A et al. · Cells 2022 · PMID 36552755Cross-class review of CAR-T and checkpoint-inhibitor AKI.
Related agents
Other agents sharing the same signature kidney injury.