§The Master Atlas

The full nephrotoxic catalog

Every one of the 290+ agents, organized by era — from established agents to the newest approvals and trial-stage investigational drugs. Profiled agents open to a full citation-grounded page.

Established195Recent61Frontier42Investigational1

Open the searchable explorer

Frontier and investigational entries are catalog-level — their renal signals are extrapolated from drug class and remain pending full citation-grounded profiles.

Injury signatures by agent count

Prerenal / Hemodynamic AKI167

Electrolyte Disturbance148

Acute Tubular Necrosis75

Glomerular Injury / Proteinuria59

Crystal / Obstructive Nephropathy46

Thrombotic Microangiopathy44

Hypertension38

Pseudo-AKI33

Acute Interstitial Nephritis30

SIADH / Hyponatremia24

Hemorrhagic Cystitis15

Chronic Interstitial Nephropathy12

Fanconi Syndrome11

Renal Cysts2

Severity

Severe13

Moderate135

Mild142

Reversibility

Often irreversible6

Partially reversible39

Variable43

Reversible202

Figure 1Toxicity landscape

The toxicity landscape

Every profiled agent placed by approval year and graded severity, colored by its signature kidney injury. Filter by signature; tap a dot to open its profile.

290 agents · 1949–2026

Severe

Moderate

Mild

1950

1960

1970

1980

1990

2000

2010

2020

Figure 2Class × injury matrix

The toxicity matrix

Every drug family against every kidney-injury signature — each mark's size encodes how strongly the injury tracks with the class: the share of that family's agents exhibiting it. A near-full block means the lesion is near-universal in the class; a small mark means only a handful. Hover or focus a mark to preview its agents; click to keep them listed.

association15%50%100%

Drug-class family by kidney-injury signature. Each cell sizes with the share of that family’s agents documented to cause the injury; select a cell to list them.
	ATN	AIN	TMA	GLOM	LYTE	FANC	XTAL	HTN	PRE	SIADH	CYST	PSEUDO	RCYST	CIN
Antibody-drug conjugates
Bispecifics / T-cell engagers
Checkpoint inhibitors
CAR-T cell therapy
Radiopharmaceuticals
Platinum agents
Alkylating agents
Antimetabolites
Antitumor antibiotics
Topoisomerase inhibitors
Anti-angiogenic (VEGF)
Microtubule inhibitors
mTOR inhibitors
EGFR / HER2 inhibitors
ALK / ROS1 / MET / TRK inhibitors
BCR-ABL inhibitors
BRAF / MEK inhibitors
BTK inhibitors
PI3K / AKT inhibitors
CDK4/6 inhibitors
FGFR inhibitors
Other kinase inhibitors
Hormonal / endocrine
Bisphosphonates & bone
Cytokines & enzymes
Monoclonal antibodies (other)
Other targeted agents

Figure 3Strongest FAERS renal signals

Acute-kidney-injury reporting disproportionality in openFDA FAERS, ranked by 95% CI lower bound. A reporting signal is a pharmacovigilance flag, not incidence. Agents with fewer than 50 FAERS reports are excluded — an odds ratio built on one or two can top a robustness ranking without being robust. A further 8 clear that floor but carry no acute-kidney-injury report at all, so there is no odds ratio to plot: absence from this forest is “queried, nothing there”, not a low signal.

SortShow25 of 215 agents

Lifileucel: reporting odds ratio 12.48 (95% CI 8.064–19.309), 22 acute-kidney-injury reports — significant
Trabectedin: reporting odds ratio 6.12 (95% CI 5.006–7.49), 99 acute-kidney-injury reports — significant
Pemetrexed: reporting odds ratio 4.89 (95% CI 4.622–5.165), 1,299 acute-kidney-injury reports — significant
Sirolimus: reporting odds ratio 4.6 (95% CI 4.177–5.059), 434 acute-kidney-injury reports — significant
Tagraxofusp: reporting odds ratio 6.33 (95% CI 4.164–9.609), 23 acute-kidney-injury reports — significant
Idecabtagene vicleucel: reporting odds ratio 5.47 (95% CI 4.089–7.326), 47 acute-kidney-injury reports — significant
Carfilzomib: reporting odds ratio 4.34 (95% CI 4.056–4.647), 862 acute-kidney-injury reports — significant
Cobimetinib: reporting odds ratio 4.47 (95% CI 3.778–5.297), 139 acute-kidney-injury reports — significant
Interleukin-2 (high-dose): reporting odds ratio 4.95 (95% CI 3.65–6.708), 43 acute-kidney-injury reports — significant
Clofarabine: reporting odds ratio 4.48 (95% CI 3.54–5.662), 72 acute-kidney-injury reports — significant
Inavolisib: reporting odds ratio 5.39 (95% CI 3.449–8.43), 20 acute-kidney-injury reports — significant
Adagrasib: reporting odds ratio 4.79 (95% CI 3.437–6.681), 36 acute-kidney-injury reports — significant
Cisplatin: reporting odds ratio 3.39 (95% CI 3.236–3.549), 1,863 acute-kidney-injury reports — significant
Isatuximab: reporting odds ratio 3.79 (95% CI 3.221–4.452), 151 acute-kidney-injury reports — significant
Pembrolizumab: reporting odds ratio 3.31 (95% CI 3.18–3.448), 2,447 acute-kidney-injury reports — significant
Fludarabine: reporting odds ratio 3.26 (95% CI 3.048–3.479), 906 acute-kidney-injury reports — significant
Melphalan: reporting odds ratio 3.3 (95% CI 3.039–3.582), 586 acute-kidney-injury reports — significant
Carboplatin: reporting odds ratio 2.94 (95% CI 2.824–3.053), 2,626 acute-kidney-injury reports — significant
Encorafenib: reporting odds ratio 3.17 (95% CI 2.777–3.622), 223 acute-kidney-injury reports — significant
Binimetinib: reporting odds ratio 3.19 (95% CI 2.752–3.708), 177 acute-kidney-injury reports — significant
Ifosfamide: reporting odds ratio 2.98 (95% CI 2.714–3.267), 459 acute-kidney-injury reports — significant
Zoledronic acid: reporting odds ratio 2.9 (95% CI 2.702–3.103), 825 acute-kidney-injury reports — significant
Cytarabine: reporting odds ratio 2.85 (95% CI 2.698–3.018), 1,260 acute-kidney-injury reports — significant
Thiotepa: reporting odds ratio 3.05 (95% CI 2.657–3.5), 207 acute-kidney-injury reports — significant
Ipilimumab: reporting odds ratio 2.84 (95% CI 2.651–3.033), 869 acute-kidney-injury reports — significant

Reporting odds ratio for acute kidney injury vs. all other FAERS reports (openFDA, as of 2026-10-01). A signal — oxblood, CI lower bound > 1 — reflects disproportionate reporting, not incidence or proven causation. Labels link to the drug profiles.

Figure 4Class → injury → nephron-segment flow

How each drug-class family distributes its kidney injury across the nephron. Ribbons are colored by the injury signature they carry — from the class that causes it (left), through the injury (center), to the nephron segment it strikes (right). Hover a node or ribbon to isolate a flow; ribbon width is the aggregated drug count.

Drug-class family to injury signature — Platinum agents → Acute Tubular Necrosis · n=4
Drug-class family to injury signature — Platinum agents → Electrolyte Disturbance · n=3
Drug-class family to injury signature — Platinum agents → Prerenal / Hemodynamic AKI · n=1
Drug-class family to injury signature — Platinum agents → Hemorrhagic Cystitis · n=2
Drug-class family to injury signature — Platinum agents → Fanconi Syndrome · n=1
Drug-class family to injury signature — Platinum agents → SIADH / Hyponatremia · n=2
Drug-class family to injury signature — Platinum agents → Thrombotic Microangiopathy · n=1
Drug-class family to injury signature — Alkylating agents → Fanconi Syndrome · n=2
Drug-class family to injury signature — Alkylating agents → Acute Tubular Necrosis · n=8
Drug-class family to injury signature — Alkylating agents → Electrolyte Disturbance · n=12
Drug-class family to injury signature — Alkylating agents → Hemorrhagic Cystitis · n=3
Drug-class family to injury signature — Alkylating agents → SIADH / Hyponatremia · n=4
Drug-class family to injury signature — Alkylating agents → Chronic Interstitial Nephropathy · n=4
Drug-class family to injury signature — Alkylating agents → Thrombotic Microangiopathy · n=3
Drug-class family to injury signature — Alkylating agents → Crystal / Obstructive Nephropathy · n=3
Drug-class family to injury signature — Alkylating agents → Prerenal / Hemodynamic AKI · n=3
Drug-class family to injury signature — Antimetabolites → Crystal / Obstructive Nephropathy · n=10
Drug-class family to injury signature — Antimetabolites → Acute Tubular Necrosis · n=7
Drug-class family to injury signature — Antimetabolites → Chronic Interstitial Nephropathy · n=1
Drug-class family to injury signature — Antimetabolites → Electrolyte Disturbance · n=12
Drug-class family to injury signature — Antimetabolites → SIADH / Hyponatremia · n=3
Drug-class family to injury signature — Antimetabolites → Thrombotic Microangiopathy · n=7
Drug-class family to injury signature — Antimetabolites → Hypertension · n=1
Drug-class family to injury signature — Antimetabolites → Glomerular Injury / Proteinuria · n=2
Drug-class family to injury signature — Antimetabolites → Hemorrhagic Cystitis · n=1
Drug-class family to injury signature — Antimetabolites → Prerenal / Hemodynamic AKI · n=13
Drug-class family to injury signature — Antimetabolites → Fanconi Syndrome · n=1
Drug-class family to injury signature — Antimetabolites → Pseudo-AKI · n=1
Drug-class family to injury signature — Antitumor antibiotics → Thrombotic Microangiopathy · n=2
Drug-class family to injury signature — Antitumor antibiotics → Glomerular Injury / Proteinuria · n=2
Drug-class family to injury signature — Antitumor antibiotics → Hemorrhagic Cystitis · n=3
Drug-class family to injury signature — Antitumor antibiotics → Acute Tubular Necrosis · n=1
Drug-class family to injury signature — Antitumor antibiotics → Electrolyte Disturbance · n=4
Drug-class family to injury signature — Anti-angiogenic (VEGF) → Glomerular Injury / Proteinuria · n=15
Drug-class family to injury signature — Anti-angiogenic (VEGF) → Hypertension · n=15
Drug-class family to injury signature — Anti-angiogenic (VEGF) → Thrombotic Microangiopathy · n=10
Drug-class family to injury signature — Anti-angiogenic (VEGF) → Electrolyte Disturbance · n=2
Drug-class family to injury signature — mTOR inhibitors → Glomerular Injury / Proteinuria · n=4
Drug-class family to injury signature — mTOR inhibitors → Acute Tubular Necrosis · n=2
Drug-class family to injury signature — mTOR inhibitors → Thrombotic Microangiopathy · n=2
Drug-class family to injury signature — Monoclonal antibodies (other) → Electrolyte Disturbance · n=12
Drug-class family to injury signature — Monoclonal antibodies (other) → Glomerular Injury / Proteinuria · n=2
Drug-class family to injury signature — EGFR / HER2 inhibitors → SIADH / Hyponatremia · n=3
Drug-class family to injury signature — EGFR / HER2 inhibitors → Electrolyte Disturbance · n=7
Drug-class family to injury signature — EGFR / HER2 inhibitors → Pseudo-AKI · n=3
Drug-class family to injury signature — EGFR / HER2 inhibitors → Glomerular Injury / Proteinuria · n=2
Drug-class family to injury signature — EGFR / HER2 inhibitors → Acute Tubular Necrosis · n=3
Drug-class family to injury signature — EGFR / HER2 inhibitors → Prerenal / Hemodynamic AKI · n=7
Drug-class family to injury signature — EGFR / HER2 inhibitors → Thrombotic Microangiopathy · n=1
Drug-class family to injury signature — EGFR / HER2 inhibitors → Acute Interstitial Nephritis · n=1
Drug-class family to injury signature — EGFR / HER2 inhibitors → Hemorrhagic Cystitis · n=1
Drug-class family to injury signature — Checkpoint inhibitors → Acute Interstitial Nephritis · n=18
Drug-class family to injury signature — Checkpoint inhibitors → Glomerular Injury / Proteinuria · n=15
Drug-class family to injury signature — Checkpoint inhibitors → Electrolyte Disturbance · n=7
Drug-class family to injury signature — Checkpoint inhibitors → Hemorrhagic Cystitis · n=2
Drug-class family to injury signature — Checkpoint inhibitors → SIADH / Hyponatremia · n=2
Drug-class family to injury signature — CAR-T cell therapy → Prerenal / Hemodynamic AKI · n=5
Drug-class family to injury signature — CAR-T cell therapy → Acute Tubular Necrosis · n=4
Drug-class family to injury signature — CAR-T cell therapy → Crystal / Obstructive Nephropathy · n=4
Drug-class family to injury signature — Bispecifics / T-cell engagers → Prerenal / Hemodynamic AKI · n=12
Drug-class family to injury signature — Bispecifics / T-cell engagers → Acute Tubular Necrosis · n=6
Drug-class family to injury signature — Bispecifics / T-cell engagers → Crystal / Obstructive Nephropathy · n=7
Drug-class family to injury signature — Bispecifics / T-cell engagers → Electrolyte Disturbance · n=6
Drug-class family to injury signature — Antibody-drug conjugates → Acute Tubular Necrosis · n=7
Drug-class family to injury signature — Antibody-drug conjugates → Electrolyte Disturbance · n=9
Drug-class family to injury signature — Antibody-drug conjugates → Prerenal / Hemodynamic AKI · n=10
Drug-class family to injury signature — Antibody-drug conjugates → Acute Interstitial Nephritis · n=1
Drug-class family to injury signature — Antibody-drug conjugates → Fanconi Syndrome · n=1
Drug-class family to injury signature — Antibody-drug conjugates → Thrombotic Microangiopathy · n=1
Drug-class family to injury signature — Antibody-drug conjugates → Glomerular Injury / Proteinuria · n=3
Drug-class family to injury signature — Antibody-drug conjugates → Hypertension · n=1
Drug-class family to injury signature — Antibody-drug conjugates → Crystal / Obstructive Nephropathy · n=5
Drug-class family to injury signature — Monoclonal antibodies (other) → Prerenal / Hemodynamic AKI · n=12
Drug-class family to injury signature — Hormonal / endocrine → Prerenal / Hemodynamic AKI · n=8
Drug-class family to injury signature — Hormonal / endocrine → Pseudo-AKI · n=1
Drug-class family to injury signature — Other targeted agents → Thrombotic Microangiopathy · n=7
Drug-class family to injury signature — Other targeted agents → Acute Tubular Necrosis · n=12
Drug-class family to injury signature — Other targeted agents → Hypertension · n=3
Drug-class family to injury signature — Other targeted agents → Glomerular Injury / Proteinuria · n=3
Drug-class family to injury signature — Other targeted agents → Fanconi Syndrome · n=2
Drug-class family to injury signature — Other targeted agents → Prerenal / Hemodynamic AKI · n=29
Drug-class family to injury signature — Other targeted agents → Electrolyte Disturbance · n=22
Drug-class family to injury signature — Other targeted agents → Crystal / Obstructive Nephropathy · n=5
Drug-class family to injury signature — BCR-ABL inhibitors → Electrolyte Disturbance · n=1
Drug-class family to injury signature — BCR-ABL inhibitors → Fanconi Syndrome · n=1
Drug-class family to injury signature — BCR-ABL inhibitors → Acute Tubular Necrosis · n=1
Drug-class family to injury signature — BCR-ABL inhibitors → Glomerular Injury / Proteinuria · n=2
Drug-class family to injury signature — BCR-ABL inhibitors → Prerenal / Hemodynamic AKI · n=5
Drug-class family to injury signature — BCR-ABL inhibitors → Hypertension · n=3
Drug-class family to injury signature — BCR-ABL inhibitors → Thrombotic Microangiopathy · n=1
Drug-class family to injury signature — BCR-ABL inhibitors → Pseudo-AKI · n=2
Drug-class family to injury signature — ALK / ROS1 / MET / TRK inhibitors → Renal Cysts · n=2
Drug-class family to injury signature — ALK / ROS1 / MET / TRK inhibitors → Pseudo-AKI · n=12
Drug-class family to injury signature — ALK / ROS1 / MET / TRK inhibitors → Electrolyte Disturbance · n=2
Drug-class family to injury signature — ALK / ROS1 / MET / TRK inhibitors → Prerenal / Hemodynamic AKI · n=7
Drug-class family to injury signature — ALK / ROS1 / MET / TRK inhibitors → Hypertension · n=1
Drug-class family to injury signature — ALK / ROS1 / MET / TRK inhibitors → Glomerular Injury / Proteinuria · n=1
Drug-class family to injury signature — Other targeted agents → Pseudo-AKI · n=7
Drug-class family to injury signature — BRAF / MEK inhibitors → Acute Tubular Necrosis · n=7
Drug-class family to injury signature — BRAF / MEK inhibitors → Acute Interstitial Nephritis · n=5
Drug-class family to injury signature — BRAF / MEK inhibitors → Electrolyte Disturbance · n=6
Drug-class family to injury signature — BRAF / MEK inhibitors → Pseudo-AKI · n=1
Drug-class family to injury signature — BRAF / MEK inhibitors → Fanconi Syndrome · n=2
Drug-class family to injury signature — BRAF / MEK inhibitors → Prerenal / Hemodynamic AKI · n=7
Drug-class family to injury signature — FGFR inhibitors → Electrolyte Disturbance · n=4
Drug-class family to injury signature — Other kinase inhibitors → Hypertension · n=3
Drug-class family to injury signature — Other kinase inhibitors → Prerenal / Hemodynamic AKI · n=12
Drug-class family to injury signature — Other kinase inhibitors → Pseudo-AKI · n=4
Drug-class family to injury signature — Other kinase inhibitors → Glomerular Injury / Proteinuria · n=1
Drug-class family to injury signature — Other kinase inhibitors → SIADH / Hyponatremia · n=1
Drug-class family to injury signature — BTK inhibitors → Hypertension · n=2
Drug-class family to injury signature — BTK inhibitors → Prerenal / Hemodynamic AKI · n=4
Drug-class family to injury signature — BTK inhibitors → Glomerular Injury / Proteinuria · n=1
Drug-class family to injury signature — BTK inhibitors → Acute Tubular Necrosis · n=1
Drug-class family to injury signature — BTK inhibitors → Acute Interstitial Nephritis · n=1
Drug-class family to injury signature — BTK inhibitors → Crystal / Obstructive Nephropathy · n=3
Drug-class family to injury signature — BTK inhibitors → Electrolyte Disturbance · n=2
Drug-class family to injury signature — Monoclonal antibodies (other) → Crystal / Obstructive Nephropathy · n=2
Drug-class family to injury signature — Monoclonal antibodies (other) → Acute Tubular Necrosis · n=2
Drug-class family to injury signature — CDK4/6 inhibitors → Pseudo-AKI · n=3
Drug-class family to injury signature — CDK4/6 inhibitors → Prerenal / Hemodynamic AKI · n=3
Drug-class family to injury signature — CDK4/6 inhibitors → Electrolyte Disturbance · n=2
Drug-class family to injury signature — Topoisomerase inhibitors → Prerenal / Hemodynamic AKI · n=4
Drug-class family to injury signature — Topoisomerase inhibitors → Crystal / Obstructive Nephropathy · n=2
Drug-class family to injury signature — Topoisomerase inhibitors → Electrolyte Disturbance · n=3
Drug-class family to injury signature — Microtubule inhibitors → SIADH / Hyponatremia · n=4
Drug-class family to injury signature — Microtubule inhibitors → Electrolyte Disturbance · n=4
Drug-class family to injury signature — Microtubule inhibitors → Prerenal / Hemodynamic AKI · n=5
Drug-class family to injury signature — Microtubule inhibitors → Hemorrhagic Cystitis · n=3
Drug-class family to injury signature — Microtubule inhibitors → Glomerular Injury / Proteinuria · n=1
Drug-class family to injury signature — Microtubule inhibitors → Thrombotic Microangiopathy · n=1
Drug-class family to injury signature — Cytokines & enzymes → Prerenal / Hemodynamic AKI · n=4
Drug-class family to injury signature — Cytokines & enzymes → Glomerular Injury / Proteinuria · n=1
Drug-class family to injury signature — Cytokines & enzymes → Thrombotic Microangiopathy · n=1
Drug-class family to injury signature — Cytokines & enzymes → Electrolyte Disturbance · n=1
Drug-class family to injury signature — Cytokines & enzymes → SIADH / Hyponatremia · n=1
Drug-class family to injury signature — Bisphosphonates & bone → Acute Tubular Necrosis · n=2
Drug-class family to injury signature — Bisphosphonates & bone → Fanconi Syndrome · n=1
Drug-class family to injury signature — Bisphosphonates & bone → Glomerular Injury / Proteinuria · n=2
Drug-class family to injury signature — Bisphosphonates & bone → Electrolyte Disturbance · n=2
Drug-class family to injury signature — Hormonal / endocrine → Electrolyte Disturbance · n=7
Drug-class family to injury signature — Hormonal / endocrine → Hypertension · n=3
Drug-class family to injury signature — Hormonal / endocrine → SIADH / Hyponatremia · n=1
Drug-class family to injury signature — Monoclonal antibodies (other) → Acute Interstitial Nephritis · n=1
Drug-class family to injury signature — PI3K / AKT inhibitors → Prerenal / Hemodynamic AKI · n=5
Drug-class family to injury signature — PI3K / AKT inhibitors → Electrolyte Disturbance · n=4
Drug-class family to injury signature — Other kinase inhibitors → Electrolyte Disturbance · n=8
Drug-class family to injury signature — Other kinase inhibitors → Thrombotic Microangiopathy · n=1
Drug-class family to injury signature — Radiopharmaceuticals → Chronic Interstitial Nephropathy · n=3
Drug-class family to injury signature — Radiopharmaceuticals → Thrombotic Microangiopathy · n=1
Drug-class family to injury signature — Radiopharmaceuticals → Electrolyte Disturbance · n=3
Drug-class family to injury signature — Radiopharmaceuticals → Prerenal / Hemodynamic AKI · n=3
Drug-class family to injury signature — Radiopharmaceuticals → Crystal / Obstructive Nephropathy · n=1
Drug-class family to injury signature — Other targeted agents → SIADH / Hyponatremia · n=2
Drug-class family to injury signature — Cytokines & enzymes → Acute Tubular Necrosis · n=2
Drug-class family to injury signature — FGFR inhibitors → Crystal / Obstructive Nephropathy · n=1
Drug-class family to injury signature — CAR-T cell therapy → Electrolyte Disturbance · n=4
Drug-class family to injury signature — Antitumor antibiotics → Crystal / Obstructive Nephropathy · n=3
Drug-class family to injury signature — Antitumor antibiotics → Prerenal / Hemodynamic AKI · n=4
Drug-class family to injury signature — PI3K / AKT inhibitors → Acute Tubular Necrosis · n=1
Drug-class family to injury signature — PI3K / AKT inhibitors → Acute Interstitial Nephritis · n=2
Drug-class family to injury signature — PI3K / AKT inhibitors → Hypertension · n=1
Drug-class family to injury signature — Monoclonal antibodies (other) → Hypertension · n=2
Drug-class family to injury signature — Monoclonal antibodies (other) → Thrombotic Microangiopathy · n=1
Drug-class family to injury signature — Alkylating agents → Acute Interstitial Nephritis · n=1
Drug-class family to injury signature — Radiopharmaceuticals → Acute Tubular Necrosis · n=3
Drug-class family to injury signature — Hormonal / endocrine → Acute Interstitial Nephritis · n=1
Drug-class family to injury signature — Checkpoint inhibitors → Prerenal / Hemodynamic AKI · n=4
Drug-class family to injury signature — Checkpoint inhibitors → Thrombotic Microangiopathy · n=5
Drug-class family to injury signature — Checkpoint inhibitors → Hypertension · n=1
Drug-class family to injury signature — Checkpoint inhibitors → Acute Tubular Necrosis · n=3
Drug-class family to injury signature — Anti-angiogenic (VEGF) → Prerenal / Hemodynamic AKI · n=1
Drug-class family to injury signature — Checkpoint inhibitors → Chronic Interstitial Nephropathy · n=3
Drug-class family to injury signature — BRAF / MEK inhibitors → Chronic Interstitial Nephropathy · n=1
Drug-class family to injury signature — BRAF / MEK inhibitors → SIADH / Hyponatremia · n=1
Drug-class family to injury signature — BRAF / MEK inhibitors → Glomerular Injury / Proteinuria · n=1
Drug-class family to injury signature — BRAF / MEK inhibitors → Hypertension · n=1
Drug-class family to injury signature — mTOR inhibitors → Electrolyte Disturbance · n=2
Drug-class family to injury signature — Other kinase inhibitors → Acute Tubular Necrosis · n=1
Drug-class family to injury signature — Radiopharmaceuticals → Hypertension · n=1
Drug-class family to injury signature — Radiopharmaceuticals → Glomerular Injury / Proteinuria · n=1
Injury signature to nephron segment — Acute Tubular Necrosis → Proximal Tubule · n=77
Injury signature to nephron segment — Acute Tubular Necrosis → Distal Tubule / Collecting Duct · n=77
Injury signature to nephron segment — Electrolyte Disturbance → Distal Tubule / Collecting Duct · n=151
Injury signature to nephron segment — Hemorrhagic Cystitis → Bladder / Urothelium · n=15
Injury signature to nephron segment — Fanconi Syndrome → Proximal Tubule · n=11
Injury signature to nephron segment — SIADH / Hyponatremia → Distal Tubule / Collecting Duct · n=24
Injury signature to nephron segment — Thrombotic Microangiopathy → Vasculature / Endothelium · n=45
Injury signature to nephron segment — Thrombotic Microangiopathy → Glomerulus · n=45
Injury signature to nephron segment — Chronic Interstitial Nephropathy → Interstitium · n=12
Injury signature to nephron segment — Crystal / Obstructive Nephropathy → Tubular Lumen · n=46
Injury signature to nephron segment — Hypertension → Vasculature / Endothelium · n=38
Injury signature to nephron segment — Hypertension → Glomerulus · n=38
Injury signature to nephron segment — Glomerular Injury / Proteinuria → Glomerulus · n=59
Injury signature to nephron segment — Pseudo-AKI → Proximal Tubule · n=34
Injury signature to nephron segment — Acute Interstitial Nephritis → Interstitium · n=31
Injury signature to nephron segment — Renal Cysts → Distal Tubule / Collecting Duct · n=2

Ribbon width = aggregated drug count; one agent contributes to every injury signature it carries and to each nephron segment that injury strikes. Colors follow the injury taxonomy.

Figure 5Injury co-occurrence

The kidney-injury combinations that strike the same agent, ranked by how many agents carry each exact set. The dot column under each bar shows which injuries are in that combination — the multi-way overlaps a pairwise chord can only hint at. A set-size bar to the left of each injury row totals how often that injury appears across these combinations, for comparison against any single set.

Top 14 injury combinations among profiled agents · top bar = agents with exactly that set · connected dots = injuries in the combination · left set-size bar = total agents across these combinations carrying that injury (each agent counted once).

Figure 6Severity × reversibility

Every profiled agent placed by graded severity (x) against reversibility of injury (y), colored by signature lesion. Bubble area scales with FAERS report volume — a pharmacovigilance reporting-frequency proxy, not incidence; the many zero-report frontier agents render as small dots.

290 agents

Click a bubble to pin it below; click again (or the ×) to remove it. Bubble area ∝ FAERS total FAERS report volume (all reactions) above a minimum-size floor (zero-report agents stay visible) — a reporting-frequency proxy subject to notoriety and reporting bias, not an incidence estimate.

§ Cross-class synthesis

Class-effect nephrotoxicity

Where the kidney injury is a property of the whole drug class, not one agent — synthesized from the strongest evidence available for each class, which ranges from meta-analyses and RCTs down to case series where nothing stronger exists. References are ranked by study design, with journal impact factor (shown as IF≈, approximate) breaking ties — so the strongest, highest-impact evidence surfaces first. Expand a class for its renal signature and references.

Antibody-drug conjugates

AINATNFANC

4refs›

Nephrotoxicity from antibody-drug conjugates is driven chiefly by the cytotoxic payload rather than the antibody, with proximal-tubular handling/uptake of liberated MMAE (vedotin), SN-38 (sacituzumab govitecan), or deruxtecan producing acute tubular injury and, increasingly, biopsy-proven acute tubulointerstitial nephritis. The best-described agents are enfortumab vedotin (Nectin-4) and sacituzumab govitecan (TROP-2), where AKI/AIN and rare fatal renal events appear in registrational and real-world data; brentuximab vedotin has been linked to karyomegalic interstitial nephritis. Reported renal events are uncommon overall (low single-digit percent of serious events), but real-world FAERS disproportionality analyses flag AKI/interstitial nephritis as a class signal for bladder-cancer ADCs. Management is largely supportive (drug interruption/dose modification, exclusion of obstruction and other nephrotoxins) with corticosteroids and biopsy when AIN is suspected. Because severe cases can require dialysis, baseline and on-treatment renal monitoring with prompt nephrology referral is the prevention headline.

CohortEnfortumab vedotin after PD-1 or PD-L1 inhibitors in cisplatin-ineligible patients with advanced urothelial carcinoma (EV-201): a multicentre, single-arm, phase 2 trial.Yu EY, et al. · Lancet OncolIF≈41.6 2021 · PMID 33991512Pivotal single-arm phase 2 trial (non-randomized) of enfortumab vedotin documenting treatment-related deaths including acute kidney injury and metabolic acidosis, establishing renal risk in the registrational dataset.PharmacovigilanceRisk Signals of Antibody-Drug Conjugates in Bladder Cancer: A Real-World FAERS Study.Liu et al. · Clin EpidemiolIF≈3.4 2025 · PMID 41341429Real-world FAERS disproportionality analysis of bladder-cancer ADCs (enfortumab vedotin/sacituzumab) identifying renal adverse-event risk signals including AKI/interstitial nephritis as a class signature.Case seriesSacituzumab-govitecan-induced severe acute tubulointerstitial nephritis requiring hemodialysis.Guarin G, et al. · BMC NephrolIF≈2.2 2024 · PMID 39522022Biopsy-proven severe acute tubulointerstitial nephritis from the TROP-2 ADC sacituzumab govitecan, demonstrating the AIN/payload mechanism and dialysis-requiring severity.Case seriesA case of karyomegalic interstitial nephritis without FAN1 mutations in the setting of brentuximab, ifosfamide, and carboplatin exposure.Leong M, et al. · BMC NephrolIF≈2.2 2024 · PMID 39543462Documents karyomegalic interstitial nephritis associated with brentuximab vedotin (CD30 MMAE-ADC) exposure, the characteristic chronic interstitial lesion linked to this agent.

Bispecifics / T-cell engagers

ATNPREAINGLOM

3refs›

Bispecific antibodies / T-cell engagers cause AKI predominantly through immune-activation toxicities that mirror CAR-T: cytokine release syndrome with hemodynamic compromise and inflammatory tubular injury, plus tumor lysis syndrome in bulky disease, yielding prerenal physiology and acute tubular injury with creatinine rise. A comparative cohort in relapsed/refractory myeloma found AKI is common after teclistamab and broadly similar in incidence to CAR-T, most cases mild and CRS-associated. Less commonly, biopsy-proven acute interstitial nephritis and CRS-driven podocytopathy/collapsing glomerulopathy (described with the bispecific blinatumomab and CAR-T) occur, the latter sometimes leaving residual CKD/proteinuria. Management centers on CRS control (tocilizumab, supportive care), TLS prophylaxis, and avoidance of concurrent nephrotoxins; AIN warrants biopsy and corticosteroids, with caution when combined with checkpoint inhibitors. Because most AKI is reversible CRS-related injury, early recognition and cytokine-directed therapy are the prevention headline.

CohortIncidence of acute kidney injury in relapsed and refractory multiple myeloma treated with teclistamab versus CAR-T cells.Charkviani M, et al. · Nephrol Dial TransplantIF≈4.8 2025 · PMID 39805729Comparative cohort quantifying AKI incidence after the BCMAxCD3 bispecific teclistamab versus CAR-T, establishing CRS-associated AKI as a class effect with rates comparable to cellular therapy.Case seriesSynergistic effect of teclistamab with PD-1 inhibition: a case of acute interstitial nephritis with dual immunotherapy.Mohan A, et al. · Clin Kidney JIF≈3.9 2024 · PMID 39974847Biopsy-proven acute interstitial nephritis attributable to the bispecific teclistamab (potentiated by PD-1 blockade), documenting AIN as a bispecific-associated lesion beyond CRS hemodynamics.Case seriesCollapsing Focal Segmental Glomerulosclerosis and Acute Kidney Injury Associated With Chimeric Antigen Receptor T-Cell (CAR-T) Therapy: A Case Report.Acharya R, et al. · Kidney MedIF≈3.4 2021 · PMID 34939018Describes CRS-driven collapsing glomerulopathy and AKI with T-cell-engaging therapy (blinatumomab/CAR-T), illustrating the cytokine-mediated podocytopathy/AKI mechanism shared across T-cell-engaging therapies.

Immune checkpoint inhibitors

AINCINATNGLOMLYTE

6refs›

Acute tubulointerstitial nephritis (ATIN/AIN) is the overwhelmingly dominant kidney irAE, found as the dominant lesion in roughly 90-93 percent of biopsied ICI-AKI cases and driven by loss of peripheral T-cell tolerance (often unmasking a reaction to a concurrent ATIN-causing drug such as a PPI or NSAID); glomerular lesions (minimal change, pauci-immune/IgA, podocytopathies) and electrolyte disturbances are rarer. Pooled real-world incidence of all-cause AKI during ICI therapy is about 14-16 percent, with ICI-specifically-attributable AKI nearer 3-5 percent; risk rises with lower baseline eGFR, PPI use, ipilimumab/combination regimens, and concurrent extra-renal irAEs. Median onset is roughly 14 weeks after initiation, presentation is typically subnephrotic proteinuria with pyuria, and most patients recover at least partially with corticosteroids; failure to recover predicts higher mortality. The management headline is to hold the ICI, discontinue offending co-medications, biopsy when feasible, and treat with steroids; rechallenge is possible but carries roughly a 20-25 percent risk of recurrent AKI.

Meta-analysisIncidence, mortality, and risk factors of acute kidney injury after immune checkpoint inhibitors: Systematic review and meta-analysis of real-world evidence.Xie W, Xiao S, Li X, et al. · Eur J Intern MedIF≈5.9 2023 · PMID 37263805Pooled 18 studies/12,111 patients giving overall AKI incidence 16.0 percent and ICI-attributable AKI 3.5 percent, a 51 percent increased death risk with AKI, and confirming PPI, ipilimumab, combination therapy and concurrent irAEs as risk factors.Meta-analysisAssociation of Proton Pump Inhibitor Use and Immune Checkpoint Inhibitor-Mediated Acute Kidney Injury: A Meta-Analysis and a Review of Related Outcomes.Mohan A, Krisanapan P, Tangpanithandee S, et al. · Am J NephrolIF≈4.6 2024 · PMID 38471492Meta-analysis of 14 studies/12,694 patients showing PPI use raises ICI-AKI odds ~1.84-fold and quantifying outcomes (67 percent renal recovery, 32 percent progression to CKD), supporting PPI avoidance as a modifiable prevention measure.Systematic reviewClinicopathological Features of Kidney Injury Related to Immune Checkpoint Inhibitors: A Systematic Review.Xu LY, Zhao HY, Yu XJ, et al. · J Clin MedIF≈3.0 2023 · PMID 36835884Largest biopsy-based synthesis (384 patients) confirming ATIN/AIN as the predominant pattern, with male sex, older age and PPI exposure linked to ATIN and glomerular injury linked to worse outcomes.CohortClinical Features and Outcomes of Immune Checkpoint Inhibitor-Associated AKI: A Multicenter Study.Cortazar FB, Kibbelaar ZA, Glezerman IG, et al. · J Am Soc NephrolIF≈13.6 2020 · PMID 31896554Landmark 138-patient multicenter cohort establishing that tubulointerstitial nephritis is the dominant lesion (93 percent of biopsies), defining risk factors (low eGFR, PPI, combination ICI), and quantifying recovery and ~23 percent recurrent-AKI rate on rechallenge.ReviewImmunotherapy in oncology and the kidneys: a clinical review of the evaluation and management of kidney immune-related adverse events.Rao Ullur A, Cote G, Pelletier K, Kitchlu A. · Clin Kidney JIF≈3.9 2023 · PMID 37261008Guideline-oriented clinical review of kidney irAEs detailing ATIN as the leading lesion plus emerging glomerular and electrolyte presentations, and evidence-based steroid treatment and rechallenge recommendations.ReviewImmune Checkpoint Inhibitor Nephrotoxicity: Update 2020.Gupta S, Cortazar FB, Riella LV, Leaf DE. · Kidney360IF≈3.2 2020 · PMID 35372904Authoritative onconephrology review proposing the definite/probable/possible ICI-AKI classification and summarizing incidence, risk factors, management, and rechallenge data.

CAR-T cell therapy

PREATNLYTEGLOM

5refs›

CAR-T-associated AKI is predominantly hemodynamic and largely reversible, arising from cytokine release syndrome (CRS)-driven vasodilation/hypoperfusion, tumor lysis syndrome, and capillary leak, with prerenal physiology and ischemic acute tubular injury being the usual lesions; transient proteinuria, electrolyte disorders (notably hypophosphatemia), and rare glomerular involvement are also described. Pooled and cohort incidence of AKI ranges from roughly 5 to 30 percent (meta-analytic estimate ~22 percent), most being KDIGO stage 1 and recovering with supportive care; only a minority require renal replacement therapy. Severe/higher-grade CRS and poor baseline performance status are the principal risk factors, and severe AKI predicts worse overall and disease-free survival plus progression to CKD. The management headline is prevention and prompt control of CRS (including tocilizumab), TLS prophylaxis, hemodynamic support, and avoidance of nephrotoxins.

Meta-analysisAcute kidney injury following chimeric antigen receptor T-cell therapy: Epidemiology, mechanism and prognosis.Yang Y, Luo K, Xu G. · Clin ImmunolIF≈7.2 2024 · PMID 38996858Systematic review/meta-analysis of 15 studies/694 patients establishing AKI incidence of 22 percent (mostly stage 1), CRS as the most common cause, low RRT requirement, and generally good renal recovery.CohortProspective evaluation of CAR-T cell therapy-related proteinuria and kidney dysfunction.Moncho-Frances F, Hernani R, Juan-Garcia I, et al. · Clin Kidney JIF≈3.9 2025 · PMID 41059413Prospective study of 63 patients documenting 19 percent AKI plus transient day-7 proteinuria and near-universal electrolyte disorders, linking inflammation-mediated tubular injury to CRS grade and IL-6.CohortAcute kidney injury in hematological patients treated with CAR-T cells: risk factors, clinical presentation and impact on outcomes.Russo E, Gambella M, Raiola AM, et al. · Sci RepIF≈3.8 2024 · PMID 39506012Cohort of 48 patients showing 29 percent AKI (mean onset day 6), independent association with severe CRS and poor performance status, and severe AKI predicting reduced survival plus CKD progression.ReviewNephrotoxicity in CAR-T Cell Therapy.Sadowski K, Ploch W, Downar A, et al. · Transplant Cell TherIF≈3.6 2025 · PMID 40107382Dedicated review of CAR-T nephrotoxicity covering incidence, CRS/TLS mechanisms, risk factors and biomarkers, product-specific differences, and safety of lymphodepletion in baseline AKI/CKD.ReviewAcute Kidney Injury Associated with Novel Anticancer Therapies: Immunotherapy.Karam S, Ali A, Fung W, et al. · Kidney360IF≈3.2 2025 · PMID 39992727Onconephrology review framing CAR-T kidney injury via CRS and immune effector cell-associated HLH alongside ICI-AIN, emphasizing prompt diagnosis and CRS-directed management.

Radiopharmaceuticals / radioligand therapy

ATNCINHTN

5refs›

In peptide-receptor radionuclide therapy and PSMA radioligand therapy, the kidney is a dose-limiting organ because filtered radiopeptides are reabsorbed and retained in proximal tubular cells, delivering chronic tubular radiation that produces a slowly progressive radiation nephropathy (tubular atrophy, interstitial fibrosis, vascular injury) manifesting as a sustained decline in creatinine clearance, often with hypertension, years after treatment. Long-term cohorts show median creatinine-clearance loss of roughly 3.8 percent/year with 177Lu-DOTATATE versus about 7.3 percent/year with the higher-energy 90Y-DOTATOC, with cumulative/per-cycle renal dose, prior nephrotoxic chemotherapy, hypertension, and diabetes as risk modifiers; in the pivotal NETTER-1 trial no excess renal toxicity was seen with amino-acid co-infusion. The cornerstone of prevention is co-infused positively charged amino acids (lysine/arginine) that competitively inhibit tubular reabsorption of the radiopeptide, supplemented by dosimetry-based dose limits and renal monitoring. 177Lu-PSMA agents carry comparatively lower renal dosimetry but warrant the same long-term surveillance.

RCTPhase 3 Trial of 177Lu-Dotatate for Midgut Neuroendocrine Tumors.Strosberg J, et al. · N Engl J MedIF≈96.2 2017 · PMID 28076709Pivotal NETTER-1 randomized trial of 177Lu-DOTATATE with renal-protective amino-acid co-infusion, the registrational renal-safety benchmark showing no excess nephrotoxicity.CohortProstate-Specific Membrane Antigen Radioligand Therapy Using 177Lu-PSMA I&T and 177Lu-PSMA-617 in Patients with Metastatic Castration-Resistant Prostate Cancer: Comparison of Safety, Biodistribution, and Dosimetry.Schuchardt C, et al. · J Nucl MedIF≈9.3 2022 · PMID 34887335Dosimetry/biodistribution study of 177Lu-PSMA agents characterizing renal radiation dose and safety, extending the radioligand nephropathy framework to PSMA-targeted therapy.CohortLong-term follow-up of renal function after peptide receptor radiation therapy with (90)Y-DOTA(0),Tyr(3)-octreotide and (177)Lu-DOTA(0),Tyr(3)-octreotate.Valkema R, et al. · J Nucl MedIF≈9.3 2005 · PMID 15653656Long-term cohort quantifying sustained creatinine-clearance decline after PRRT (median 3.8 percent/year for 177Lu vs 7.3 percent/year for 90Y) and identifying cumulative renal dose, hypertension, and diabetes as risk factors.CohortLong-term results of PRRT in advanced bronchopulmonary carcinoid.Mariniello A, et al. · Eur J Nucl Med Mol ImagingIF≈8.6 2016 · PMID 26392198Large long-term PRRT cohort showing mild/moderate renal-function decline (more frequent with 90Y-DOTATOC) and higher nephrotoxicity risk in patients with prior chemotherapy exposure.ReviewRenal toxicity of radiolabeled peptides and antibody fragments: mechanisms, impact on radionuclide therapy, and strategies for prevention.Vegt E, et al. · J Nucl MedIF≈9.3 2010 · PMID 20554737Landmark mechanistic review establishing proximal-tubular reabsorption/retention of radiopeptides as the basis of radiation nephropathy and amino-acid co-infusion as the principal renoprotective strategy.

Platinum agents

ATNLYTETMA

5refs›

Cisplatin is the prototypical nephrotoxin among platinum agents, producing dose-dependent proximal (S3 segment) tubular injury and acute tubular necrosis via cellular accumulation through OCT2/Ctr1 transporters, DNA damage, mitochondrial dysfunction, oxidative stress, and regulated necrosis/inflammation; clinically significant AKI affects roughly 20-40% of exposed patients and renal magnesium wasting with hypomagnesemia is characteristic and can persist. Repeated exposure drives CKD. The cornerstone of prevention is vigorous isotonic saline hydration; meta-analyses of observational data show magnesium supplementation during hydration roughly quarters the odds of cisplatin-induced AKI (OR ~0.22-0.24). Carboplatin is comparatively kidney-sparing (dosed by Calvert/AUC formula) and oxaliplatin is rarely nephrotoxic, with only sporadic ATN and immune hemolysis/TMA reports.

Meta-analysisPrevention of Cisplatin-Induced Acute Kidney Injury: A Systematic Review and Meta-Analysis.Hamroun A, et al. · DrugsIF≈13.0 2019 · PMID 31429065Systematic review across 51 studies and 21 prevention methods finding magnesium supplementation significantly nephroprotective (OR 0.24) and documenting 20-40% AKI incidence.Meta-analysisA systematic review for prevention of cisplatin-induced nephrotoxicity using different hydration protocols and meta-analysis for magnesium hydrate supplementation.Li J, et al. · Clin Exp NephrolIF≈2.0 2023 · PMID 37530867Confirms hydration as the prevention backbone and that magnesium supplementation during hydration protects against cisplatin nephrotoxicity (OR 0.22).CohortIncidence and risk factors for acute kidney injury in head and neck cancer patients treated with concurrent chemoradiation with high-dose cisplatin.van der Vorst MJDL, et al. · BMC CancerIF≈3.4 2019 · PMID 31703649Prospective cohort (n=124) documenting KDIGO-defined AKI in 69% with high-dose cisplatin and persistent long-term renal impairment.ReviewCisplatin nephrotoxicity: new insights and therapeutic implications.Tang C, et al. · Nat Rev NephrolIF≈28.6 2023 · PMID 36229672Authoritative mechanistic review establishing cisplatin proximal tubular ATN pathways (DNA damage, mitochondrial injury, regulated necrosis, inflammation) and the AKI-to-CKD transition.ReviewCisplatin nephrotoxicity: mechanisms and renoprotective strategies.Pabla N, Dong Z. · Kidney IntIF≈14.8 2008 · PMID 18272962Landmark mechanistic review on tubular cell death signaling, inflammation and renoprotective approaches in cisplatin nephrotoxicity.

Alkylating agents

FANCATNSIADHTMA

4refs›

Ifosfamide is the dominant nephrotoxin in this class, causing chloroacetaldehyde-mediated proximal tubular injury with a Fanconi-type tubulopathy (hypophosphatemia, glucosuria, low-molecular-weight proteinuria, renal tubular acidosis) plus reduced GFR; biopsies show ATN with proximal tubular vacuolization and mitochondrial damage resembling tenofovir toxicity, and injury can be irreversible, sometimes progressing to dialysis-dependent CKD months after therapy. Risk rises with high cumulative dose, young age, unilateral nephrectomy, and concomitant cisplatin. Cyclophosphamide characteristically causes hyponatremia from water retention (an SIAD/nephrogenic antidiuresis mechanism) during high-dose hydration and hemorrhagic cystitis (acrolein), the latter mitigated by mesna and hydration. High-dose conditioning regimens contribute to transplant-associated TMA and sinusoidal obstruction syndrome.

Systematic reviewLate effects of chemotherapeutic agents on renal function in childhood cancer survivors: a review of the literature.O'Sullivan D. · Ir J Med SciIF≈2.0 2017 · PMID 27339643Literature review quantifying ifosfamide nephrotoxicity (1-50%) and platinum-associated hypomagnesemia in childhood cancer survivors.CohortUnilateral nephrectomy and cisplatin as risk factors of ifosfamide-induced nephrotoxicity: analysis of 120 patients.Rossi R, et al. · J Clin OncolIF≈42.1 1994 · PMID 8270973Pediatric cohort (n=120) defining dose-dependent proximal tubulopathy/Fanconi syndrome and identifying unilateral nephrectomy and cisplatin as key risk factors.Case series[Ifosphamide nephrotoxicity].Ensergueix G, Karras A. · Nephrol TherIF≈0.8 2018 · PMID 29606257Multicenter series of 34 adults showing renal failure in over 80% and Fanconi syndrome in two-thirds, with biopsy ATN/mitochondrial injury and frequent progression to CKD/dialysis.ReviewPathophysiology of Drug-Induced Hyponatremia.Kim GH. · J Clin MedIF≈3.0 2022 · PMID 36233678Mechanistic review identifying cyclophosphamide (and ifosfamide/vincristine) as causes of hyponatremia via SIADH/nephrogenic antidiuresis with AQP2 upregulation.

Antimetabolites

TMAXTALATNLYTE

5refs›

Antimetabolites cause two distinct renal syndromes. Gemcitabine is a leading cause of drug-induced thrombotic microangiopathy: a dose/duration-related endothelial injury (often complement-associated on biopsy) presenting with microangiopathic hemolytic anemia, thrombocytopenia, new/worsening hypertension and renal failure, with reported incidence from roughly 0.015% to 2.7% and high mortality; management centers on drug withdrawal, supportive care, and selective use of plasma exchange, eculizumab, or rituximab. High-dose methotrexate causes crystalline tubular obstruction and direct tubular toxicity with AKI and delayed drug clearance; prevention relies on volume expansion, urinary alkalinization, and leucovorin, and established AKI with elevated MTX levels is rescued with glucarpidase per consensus thresholds. Pemetrexed causes a slowly reversible/irreversible proximal tubular toxicity (acute tubular damage, interstitial fibrosis) that can force discontinuation.

Systematic reviewDrug-induced thrombotic microangiopathy: An updated review of causative drugs, pathophysiology, and management.Mazzierli T, et al. · Front PharmacolIF≈4.4 2023 · PMID 36699080Comprehensive DITMA review showing gemcitabine among major causes with prominent capillary complement deposition and outlining drug-withdrawal/plasma-exchange/anti-complement management.GuidelineConsensus Guideline for Use of Glucarpidase in Patients with High-Dose Methotrexate Induced Acute Kidney Injury and Delayed Methotrexate Clearance.Ramsey LB, et al. · OncologistIF≈5.2 2018 · PMID 29079637Expert consensus defining methotrexate-concentration/creatinine thresholds and timing for glucarpidase rescue in HDMTX-induced AKI.Case seriesMicroangiopathy associated with gemcitabine: a drug interaction with nab-paclitaxel? A case series and literature review.Allard J, et al. · Eur J Clin PharmacolIF≈3.4 2022 · PMID 35507073Case series describing gemcitabine-TMA (anemia, thrombocytopenia, renal failure) and a potential nab-paclitaxel interaction raising incidence.Case seriesGemcitabine-related thrombotic microangiopathy: a single-centre retrospective series.Leal F, et al. · J ChemotherapyIF≈2.4 2014 · PMID 24091354Single-center series confirming gemcitabine-TMA as an underdiagnosed, high-mortality complication.Case seriesPemetrexed-induced acute kidney failure following irreversible renal damage: two case reports and literature review.Zattera T, et al. · J NephropatholIF≈1.0 2017 · PMID 28491851Biopsy-supported cases establishing pemetrexed proximal tubular injury/interstitial damage with poorly reversible AKI.

Antitumor antibiotics (anthracyclines)

TMAGLOM

4refs›

Among antitumor antibiotics, mitomycin C is the classic cause of cancer chemotherapy-associated hemolytic-uremic syndrome/thrombotic microangiopathy: a cumulative dose-related endothelial injury producing microangiopathic hemolytic anemia, thrombocytopenia and renal failure, with characteristic glomerular capillary and arteriolar thrombosis on biopsy and historically high mortality. Recognition mandates drug cessation, since re-exposure precipitates recurrence; the role of plasma exchange is uncertain. The anthracycline doxorubicin (adriamycin) is best known experimentally as the standard rodent model of podocyte injury and focal segmental glomerulosclerosis (proteinuria, glomerulosclerosis, tubulointerstitial fibrosis); clinically, anthracycline nephrotoxicity is uncommon but TMA and glomerular injury have been reported.

Systematic reviewDrug-induced thrombotic microangiopathy: An updated review of causative drugs, pathophysiology, and management.Mazzierli T, et al. · Front PharmacolIF≈4.4 2023 · PMID 36699080Updated DITMA review situating mitomycin among dose-related TMA agents and detailing pathophysiology and management.Case seriesMitomycin-induced hemolytic-uremic syndrome.Proia AD, et al. · Arch Pathol Lab MedIF≈6.1 1984 · PMID 6210069Classic clinicopathologic series establishing mitomycin C as a cause of HUS/TMA with glomerular and arteriolar thrombosis and high lethality.ReviewDrug-associated thrombotic thrombocytopenic purpura-hemolytic uremic syndrome.Medina PJ, Sipols JM, George JN. · Curr Opin HematolIF≈2.8 2001 · PMID 11604563Landmark review framing mitomycin C as the prototype of dose-related (toxic) drug-associated TTP-HUS and the imperative to avoid re-exposure.ReviewAdriamycin nephropathy: a model of focal segmental glomerulosclerosis.Lee VWS, Harris DCH. · Nephrology (Carlton)IF≈2.0 2011 · PMID 21175974Definitive review of doxorubicin (adriamycin) as the rodent FSGS model: podocyte injury, glomerulosclerosis, tubulointerstitial fibrosis and genetic susceptibility.

Anti-angiogenic (VEGF/VEGFR)

HTNGLOMTMAATN

5refs›

VEGF/VEGFR blockade produces a stereotyped class effect of dose-dependent hypertension plus proteinuria, driven by loss of glomerular endothelial-podocyte VEGF signaling, nitric-oxide depletion, and downregulation of nephrin. The dominant biopsy lesion with direct VEGF-ligand inhibitors (bevacizumab, aflibercept) is renal-limited thrombotic microangiopathy (endotheliosis), while glomerulopathies (minimal change/FSGS-like) are more typical of the receptor TKIs. In pooled RCT meta-analyses, bevacizumab raises the relative risk of proteinuria roughly 1.4 to 2.2-fold and of hypertension about 3 to 7.5-fold in a dose-dependent manner, with grade 3 or higher events in single-digit percentages. Management centers on blood-pressure control (RAAS blockade preferred), proteinuria surveillance, and drug interruption for nephrotic-range proteinuria, TMA, or severe hypertension; most events are reversible on withdrawal.

The renal lesion is set by where the podocyte→VEGF-A→glomerular endothelial VEGFR2 axis is interrupted. Sequestering the ligand (anti-VEGF-A monoclonal antibody, VEGF-trap) produces renal-limited thrombotic microangiopathy with glomerular endotheliosis; blocking the receptor — extracellularly (anti-VEGFR2 antibody) or at the intracellular kinase site (multi-kinase VEGFR TKIs) — drives the antiangiogenic hypertension–proteinuria signature, with the TKIs additionally producing FSGS-like / minimal-change glomerulopathy. Select a blockade node below.

◆ Mechanism schematic

The glomerular VEGF axis — where the barrier fails

Podocyte-derived VEGF-A signals paracrine onto glomerular endothelial VEGFR2, maintaining the fenestrated endothelium and the filtration barrier. Select a blockade node — where the axis is interrupted decides the lesion.

Direct ligand inhibitors

Renal-limited TMA / glomerular endotheliosis

Receptor blockade

Hypertension; TKIs → FSGS-like / minimal-change

Intact barrier: podocyte VEGF-A holds the endothelial fenestrae open and nephrin at the slit diaphragm. Select a node to trace how blockade at that level injures the barrier.

After the class-effects vegf review. Node → lesion mapping per Estrada et al., J Am Soc Nephrol 2019 (PMID 30642877); hypertension / proteinuria relative-risk magnitudes per Zhu et al. 2007 (PMID 17261421) and Ye & Chen 2013 (PMID 23543268). Educational — not medical advice.

Meta-analysisRisks of proteinuria and hypertension with bevacizumab, an antibody against vascular endothelial growth factor: systematic review and meta-analysis.Zhu X, Wu S, Dahut WL, Parikh CR · Am J Kidney DisIF≈9.4 2007 · PMID 17261421Landmark meta-analysis quantifying the dose-dependent relative risk of proteinuria (RR 1.4-2.2) and hypertension (RR 3.0-7.5) with bevacizumab across RCTs.Meta-analysisBevacizumab in the treatment of ovarian cancer: a meta-analysis from four phase III randomized controlled trials.Ye Q, Chen HL · Arch Gynecol ObstetIF≈2.1 2013 · PMID 23543268Phase III RCT meta-analysis confirming significantly increased hypertension (OR 4.6) and proteinuria (OR 4.9) as a reproducible class effect.ReviewNephrotoxicity induced by intravitreal vascular endothelial growth factor inhibitors: emerging evidence.Hanna RM, Barsoum M, Arman F, et al. · Kidney IntIF≈14.8 2019 · PMID 31229276Establishes the renal injury phenotype (accelerated hypertension, proteinuria, glomerular disease, TMA) even from systemic absorption of anti-VEGF agents.ReviewTherapeutic Inhibition of VEGF Signaling and Associated Nephrotoxicities.Estrada CC, Maldonado A, Mallipattu SK · J Am Soc NephrolIF≈13.6 2019 · PMID 30642877Authoritative mechanistic review mapping each inhibition node to its lesion: direct VEGFA inhibition to renal TMA, receptor-TKIs to FSGS/minimal change, mTOR to podocyte injury.Review[Nephrotoxicity of anti-angiogenesis drugs].Grechukhina KS, Chebotareva NV, Krasnova TN · Ter ArkhIF≈0.8 2020 · PMID 33346501Reviews the clinical-morphologic spectrum of antiangiogenic nephropathy, noting thrombotic microangiopathy of renal vessels as the most common histologic finding.

Kinase inhibitors (TKIs)

HTNGLOMPSEUDOLYTETMA

5refs›

VEGFR-targeting TKIs (sunitinib, sorafenib, pazopanib, cabozantinib) share the antiangiogenic class signature of hypertension and proteinuria, with glomerular lesions (FSGS-like, minimal change) and occasional TMA; cabozantinib carries among the highest hypertension risk (all-grade RR ~5.5). Distinct from true nephrotoxicity, many targeted agents (TKIs, CDK4/6 inhibitors, MET inhibitors) inhibit the renal cationic transporters OCT2 and MATE1/2-K, blocking tubular creatinine secretion and producing a reversible, asymptomatic serum-creatinine rise (pseudo-AKI) with preserved measured GFR. Electrolyte disturbances and, with certain agents, benign renal cysts also occur. The management headline is to confirm true injury with cystatin-C or measured GFR before dose-reducing for an isolated creatinine bump, while genuinely controlling hypertension and monitoring proteinuria.

Meta-analysisIncidence and risk of hypertension associated with cabozantinib in cancer patients: a systematic review and meta-analysis.Zhang X, Shao Y, Wang K · Expert Rev Clin PharmacolIF≈3.7 2016 · PMID 27181268Meta-analysis showing VEGFR-TKI hypertension is a quantifiable class effect (cabozantinib all-grade RR 5.48), exceeding several other approved VEGFR-TKIs.ReviewTherapeutic Inhibition of VEGF Signaling and Associated Nephrotoxicities.Estrada CC, Maldonado A, Mallipattu SK · J Am Soc NephrolIF≈13.6 2019 · PMID 30642877Documents that VEGFR tyrosine-kinase inhibition is preferentially associated with glomerulopathies (minimal change disease, FSGS) versus TMA from direct ligand inhibition.ReviewRenal Toxicities of Targeted Therapies.Abbas A, Mirza MM, Ganti AK, Tendulkar K · Target OncolIF≈4.5 2015 · PMID 25922090Class-wide review cataloging TKI-associated hypertension, proteinuria, electrolyte derangements, and acute/chronic renal failure with management strategies.ReviewTargeted Cancer Therapies Causing Elevations in Serum Creatinine Through Tubular Secretion Inhibition: A Case Report and Review of the Literature.Mach T, Qi A, Bouganim N, Trinh E · Can J Kidney Health DisIF≈2.2 2022 · PMID 35756332Reviews pseudo-AKI across TKIs, CDK4/6, PARP, and MET inhibitors and advocates cystatin-C/measured GFR to avoid unnecessary biopsy or dose changes.MechanisticTucatinib Inhibits Renal Transporters OCT2 and MATE Without Impacting Renal Function in Healthy Subjects.Topletz-Erickson AR, Lee AJ, Mayor JG, et al. · J Clin PharmacolIF≈2.4 2020 · PMID 32989831Phase 1 mechanistic study proving a kinase inhibitor raises serum creatinine by blocking OCT2/MATE-mediated tubular creatinine secretion while measured GFR stays normal (pseudo-AKI).

Hormonal / endocrine agents

HTNLYTE

3refs›

The signature renal-relevant toxicity of abiraterone is iatrogenic mineralocorticoid excess: CYP17 blockade upstream of cortisol drives a compensatory ACTH-mediated rise in deoxycorticosterone and corticosterone, producing hypertension, hypokalemia, and fluid retention; co-administered corticosteroids (prednisone) or mineralocorticoid antagonists (eplerenone/spironolactone) mitigate this. In pivotal RCTs and meta-analysis, abiraterone significantly increases hypokalemia (OR ~3.1) and fluid retention (OR ~1.4), with the magnitude amplified when control patients receive no steroid and in hormone-sensitive (versus castration-resistant) disease. The management headline is to monitor potassium and blood pressure on abiraterone, give the protective steroid, and use mineralocorticoid-receptor antagonists for breakthrough mineralocorticoid effects.

Meta-analysisAssociation between RCT methodology and disease indication with mineralocorticoid-related toxicity for patients receiving abiraterone acetate for advanced prostate cancer: A meta-analysis of RCTs.Hall ME, Padgett WJ, Klaassen Z, et al. · Clin Genitourin CancerIF≈2.3 2023 · PMID 37236862Meta-analysis of 6 RCTs quantifying abiraterone hypokalemia (OR 3.10) and fluid retention (OR 1.41) and showing modulation by concurrent steroid and disease indication.RCTAbiraterone and increased survival in metastatic prostate cancer.de Bono JS, Logothetis CJ, Molina A, et al. · N Engl J MedIF≈96.2 2011 · PMID 21612468Pivotal COU-AA-301 phase III RCT establishing survival benefit and the characteristic mineralocorticoid-excess adverse events (fluid retention, hypertension, hypokalemia).ReviewAbiraterone acetate: a promising drug for the treatment of castration-resistant prostate cancer.Agarwal N, Hutson TE, Vogelzang NJ, Sonpavde G · Future OncolIF≈3.0 2010 · PMID 20465382Explains the secondary mineralocorticoid-excess mechanism (compensatory deoxycorticosterone/corticosterone rise) and management with eplerenone or low-dose corticosteroids.

Bisphosphonates & bone-targeted

ATNGLOMLYTE

5refs›

Nitrogen-containing IV bisphosphonates show drug-specific renal injury patterns: zoledronic acid characteristically causes dose- and infusion-rate-dependent acute tubular necrosis (proximal tubular toxicity), whereas pamidronate — especially at supratherapeutic doses — causes collapsing focal segmental glomerulosclerosis with podocyte injury and nephrotic-range proteinuria (the landmark Markowitz clinicopathologic series). Risk rises with rapid infusion, higher/cumulative dose, dehydration, and pre-existing CKD; the zoledronate program required protocol amendments (longer infusion, dose reduction) due to renal toxicity. The RANKL-antibody denosumab spares the kidney of these lesions but causes clinically important hypocalcemia, making it the preferred bone-targeted agent in renal impairment. The prevention headline is to keep the recommended dose and a 15-minute or longer infusion, ensure hydration, hold for renal deterioration, and monitor calcium with denosumab.

RCTDenosumab and bone-metastasis-free survival in men with castration-resistant prostate cancer: results of a phase 3, randomised, placebo-controlled trial.Smith MR, Saad F, Coleman R, et al. · LancetIF≈98.4 2011 · PMID 22093187Large phase 3 RCT of the RANKL antibody denosumab establishing hypocalcemia and osteonecrosis of the jaw as its signature toxicities (versus bisphosphonate tubular injury).Case seriesCollapsing focal segmental glomerulosclerosis following treatment with high-dose pamidronate.Markowitz GS, Appel GB, Fine PL, et al. · J Am Soc NephrolIF≈13.6 2001 · PMID 11373339The landmark clinicopathologic series establishing pamidronate as the first drug-associated cause of collapsing FSGS, with dose-dependent podocyte and tubular toxicity.ReviewApproval summary for zoledronic acid for treatment of multiple myeloma and cancer bone metastases.Ibrahim A, Scher N, Williams G, et al. · Clin Cancer ResIF≈10.0 2003 · PMID 12855610FDA approval summary documenting that zoledronate phase III trials were amended twice for renal toxicity, mandating 15-minute infusion and dose reduction.ReviewCollapsing glomerulopathy.Schwimmer JA, Markowitz GS, Valeri A, Appel GB · Semin NephrolIF≈2.8 2003 · PMID 12704581Authoritative review of collapsing glomerulopathy that incorporates pamidronate among recognized secondary causes and describes the podocyte-injury pathogenesis.MechanisticAcute renal effects of intravenous bisphosphonates in the rat.Pfister T, Atzpodien E, Bohrmann B, Bauss F · Basic Clin Pharmacol ToxicolIF≈2.9 2005 · PMID 16364053Controlled animal study localizing IV bisphosphonate (zoledronate/ibandronate) injury to the proximal convoluted tubule with tubular degeneration/necrosis (ATN mechanism).

Cytokines & enzymes

PREATNGLOMTMALYTE

4refs›

This class causes hemodynamic and immune-mediated kidney injury distinct from cytotoxic nephrotoxins. High-dose IL-2 (aldesleukin) produces a capillary-leak/vascular-leak syndrome with hypotension, oliguria, weight gain and prerenal azotemia; in the pivotal 199-patient series creatinine rose in nearly all patients (peaking ~2.7 mg/dL) but reversed completely off-therapy with no long-term intrinsic damage, so management is supportive hemodynamic/fluid optimization. Interferons (alpha, beta, gamma) are associated with collapsing FSGS presenting as acute renal failure and nephrotic-range proteinuria, typically in patients carrying APOL1 high-risk alleles and marked by endothelial tubuloreticular inclusions on biopsy; rarer interferon-associated thrombotic microangiopathy also occurs, and the headline intervention is prompt drug discontinuation. Asparaginase contributes occasional electrolyte and tubular disturbances. Recognizing the reversible hemodynamic pattern of IL-2 versus the discontinue-the-drug imperative of interferon collapsing glomerulopathy is the key clinical distinction.

CohortInnate immunity pathways regulate the nephropathy gene Apolipoprotein L1.Nichols B, Jog P, Lee JH, et al. · Kidney IntIF≈14.8 2015 · PMID 25100047Mechanistic study with a clinical cohort of interferon-induced collapsing FSGS patients all carrying the APOL1 high-risk genotype, showing interferon upregulates APOL1 and explaining the gene-drug interaction.Case seriesRenal dysfunction associated with the administration of high-dose interleukin-2 in 199 consecutive patients with metastatic melanoma or renal carcinoma.Guleria AS, Yang JC, Topalian SL, et al. · J Clin OncolIF≈42.1 1994 · PMID 7989949Pivotal 199-patient series defining high-dose IL-2 renal toxicity as transient hemodynamic dysfunction that reverses fully off-therapy without long-term damage.Case seriesTreatment with IFN-{alpha}, -{beta}, or -{gamma} is associated with collapsing focal segmental glomerulosclerosis.Markowitz GS, Nasr SH, Stokes MB, D'Agati VD. · Clin J Am Soc NephrolIF≈8.5 2010 · PMID 20203164Landmark 11-case biopsy series establishing interferon (all three classes) as a cause of collapsing FSGS with acute renal failure, nephrotic proteinuria, and improvement after IFN discontinuation.ReviewRecombinant interleukin-2.Bruton JK, Koeller JM. · PharmacotherapyIF≈2.9 1994 · PMID 7885967Review documenting that high-dose IL-2 dose-limiting toxicities include hypotension, weight gain and oliguria that are reversible on discontinuation, and that low-dose regimens reduce this toxicity.

Established

Historic backbone agents with well-characterized nephrotoxicity.

195

Adrenolytic1

Mitotane

Lysodren

Profile

Indirect: hypoadrenalism drives hyponatremia/prerenal; cisplatin nephrotoxicity in EDP-M.

LYTEPRE

Moderate

ALK TKI4

Alectinib

Alecensa

Profile

Creatinine rise via reduced tubular secretion.

PSEUDOPRE

Mild

Brigatinib

Alunbrig

Profile

Creatinine elevation; usually benign.

PSEUDOPREHTN

Mild

Ceritinib

Zykadia

Profile

GI-driven prerenal AKI.

PREPSEUDO

Mild

Lorlatinib

Lorbrena

Profile

Edema and metabolic effects.

PSEUDOPREGLOM

Mild

ALK/ROS1/MET TKI1

Crizotinib

Xalkori

Profile

Reversible creatinine rise and renal cysts.

RCYSTPSEUDOLYTE

Mild

Alkylating agent (methylmelamine)1

Altretamine (hexamethylmelamine)

Hexalen

Profile

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

PRE

Mild

Alkylating agent (nitrogen mustard)2

Chlorambucil

Leukeran

Profile

Minimal direct nephrotoxicity; rare drug-associated SIADH/hyponatremia is the kidney-relevant signal.

SIADHLYTE

Mild

Mechlorethamine

Mustargen

Profile

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

LYTEXTAL

Moderate

Alkylator6

Bendamustine

Treanda

Profile

Tumor lysis-mediated AKI is the principal risk; TMA is rare.

XTALTMALYTE

Moderate

Busulfan

Myleran

Profile

Conditioning-regimen TMA risk.

TMA

Moderate

Dacarbazine

DTIC

Profile

Rare hepatic veno-occlusive disease; minimal direct renal injury.

PRE

Mild

Melphalan

Alkeran

Profile

SIADH in high-dose myeloma conditioning; renally cleared.

SIADHLYTE

Mild

Temozolomide

Temodar

Profile

Occasional SIADH; generally renally well tolerated.

SIADHLYTE

Mild

Thiotepa

Tepadina

Profile

Hemorrhagic cystitis; renally cleared.

CYST

Mild

Androgen-receptor inhibitor1

Enzalutamide

Xtandi

Profile

Hypertension; rare electrolyte effects.

HTNLYTE

Mild

Anthracenedione1

Mitoxantrone

Novantrone

Profile

Tumor lysis; low direct renal toxicity.

XTALLYTEPRE

Mild

Anthracycline2

Doxorubicin

Adriamycin

Profile

Experimental podocyte model; clinical proteinuria rare.

GLOMTMACYST

Mild

Idarubicin

Idamycin

Profile

Tumor lysis in acute leukemia.

XTALLYTEPRE

Mild

Anti-CD20 antibody2

Obinutuzumab

Gazyva

Profile

High tumor-lysis risk in CLL.

XTALATNPRE

Moderate

Rituximab

Rituxan

Profile

Tumor lysis with bulky disease; treats some GN.

XTALATNPRE

Moderate

Anti-CD38 antibody2

Daratumumab

Darzalex

Profile

Tumor lysis; usable in renal impairment.

PRELYTE

Mild

Isatuximab

Sarclisa

Profile

Tumor lysis in myeloma.

PRELYTE

Mild

Anti-EGFR antibody3

Cetuximab

Erbitux

Profile

TRPM6 magnesium wasting.

LYTEGLOM

Mild

Necitumumab

Portrazza

Profile

Severe hypomagnesemia, class effect.

LYTE

Moderate

Panitumumab

Vectibix

Profile

TRPM6 magnesium wasting — heavier than cetuximab.

LYTEGLOM

Mild

Anti-GD2 antibody1

Dinutuximab

Unituxin

Profile

Capillary-leak syndrome, hypertension and severe pain in neuroblastoma.

PREHTNTMA

Moderate

Anti-PD-1 antibody2

Cemiplimab

Libtayo

Profile

ICI-associated AIN.

AINGLOM

Moderate

Dostarlimab

Jemperli

Profile

ICI-associated AIN.

AINGLOM

Moderate

Anti-PD-L1 antibody3

Atezolizumab

Tecentriq

Profile

Interstitial nephritis; rare glomerular disease.

AINGLOMCYST

Moderate

Avelumab

Bavencio

Profile

ICI-associated AIN.

AINGLOM

Moderate

Durvalumab

Imfinzi

Profile

ICI-associated AIN.

AINGLOM

Moderate

Anti-RANKL antibody1

Denosumab

Xgeva

Profile

Severe hypocalcemia in low GFR; not directly nephrotoxic.

LYTE

Moderate

Anti-SLAMF7 mAb1

Elotuzumab

Empliciti

Profile

Kidney-neutral antibody; unchanged PK in severe impairment and dialysis; no renal dose adjustment.

PRE

Mild

Anti-VEGF antibody1

Bevacizumab

Avastin

Profile

Proteinuria, hypertension, glomerular TMA.

GLOMHTNTMA

Moderate

Anti-VEGFR2 antibody1

Ramucirumab

Cyramza

Profile

Hypertension and proteinuria, class effect.

HTNGLOMTMA

Moderate

Antibody-drug conjugate (BCMA/MMAF)1

Belantamab mafodotin

Blenrep

Profile

Myeloma ADC; renal data emerging.

GLOM

Mild

Antibody-drug conjugate (CD22/calicheamicin)1

Inotuzumab ozogamicin

Besponsa

Profile

Tumor lysis and VOD in ALL.

PRELYTEXTAL

Moderate

Antibody-drug conjugate (CD30/MMAE)1

Brentuximab vedotin

Adcetris

Profile

Tumor lysis in lymphoma.

PRELYTEXTAL

Mild

Antibody-drug conjugate (CD33/calicheamicin)1

Gemtuzumab ozogamicin

Mylotarg

Profile

Tumor lysis and veno-occlusive disease.

PRELYTEXTAL

Moderate

Antibody-drug conjugate (CD79b/MMAE)1

Polatuzumab vedotin

Polivy

Profile

Tumor lysis; emerging renal data.

PRELYTEXTAL

Mild

Antibody-drug conjugate (FRα/DM4)1

Mirvetuximab soravtansine

Elahere

Profile

Ocular toxicity dominates; renal involvement indirect/case-level (GI volume loss).

PRE

Mild

Antibody-drug conjugate (HER2/DM1)1

Trastuzumab emtansine (T-DM1)

Kadcyla

Profile

Rare nodular regenerative TMA-like signals.

TMAGLOMHTN

Moderate

Antibody-drug conjugate (HER2/DXd)1

Trastuzumab deruxtecan

Enhertu

Profile

Emerging AKI/proteinuria reports — under-published.

ATNFANCLYTE

Moderate

Antibody-drug conjugate (Nectin-4/MMAE)1

Enfortumab vedotin

Padcev

Profile

Emerging AKI and electrolyte signals in urothelial cancer.

ATNLYTEPRE

Moderate

Antibody-drug conjugate (Trop-2/SN-38)1

Sacituzumab govitecan

Trodelvy

Profile

Diarrhea-driven prerenal AKI; emerging direct signals.

PREAINATN

Moderate

Antifolate3

Methotrexate (high-dose)

Trexall

Profile

Crystal nephropathy; glucarpidase rescue.

XTALATN

Moderate

Pemetrexed

Alimta

Profile

Cumulative chronic tubulointerstitial injury; RTA and nephrogenic DI.

CINATNLYTE

Moderate

Pralatrexate

Folotyn

Profile

Antifolate with MTX-like renal handling.

XTALATN

Moderate

Antifolate (TS inhibitor)1

Raltitrexed

Tomudex

Profile

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

ATNXTAL

Moderate

Antimetabolite (oral 5-FU prodrug)3

Carmofur (HCFU)

Mifurol

Profile

Lipophilic oral 5-FU prodrug (Japan); class-level renal risk; hallmark toxicity is leukoencephalopathy not nephropathy.

TMALYTEPRE

Moderate

Doxifluridine

Furtulon

Profile

5'-DFUR prodrug; class-level TMA risk plus a real renal-clearance component warranting caution in renal impairment.

TMALYTEPRE

Moderate

Tegafur-uracil (UFT)

UFT

Profile

Oral tegafur+uracil; rare fluoropyrimidine-class TMA/HUS (often with mitomycin C), otherwise kidney-sparing.

TMALYTEPRE

Severe

Antineoplastic metal salt1

Gallium nitrate

Ganite

Profile

Dose-limiting acute tubular necrosis; potentiated by dehydration and concurrent nephrotoxins.

ATNPRELYTE

Moderate

Antitumor antibiotic4

Bleomycin

Blenoxane

Profile

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

PRE

Mild

Dactinomycin (actinomycin D)

Cosmegen

Profile

Renal risk indirect via tumor lysis in chemosensitive pediatric tumors; hepatic veno-occlusive disease is the signature organ toxicity.

LYTEPREXTAL

Moderate

Mitomycin C

Mutamycin

Profile

Prototype dose-dependent TMA.

TMAGLOMCYST

Severe

Plicamycin (mithramycin)

Mithracin

Profile

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

ATNLYTE

Moderate

BCL-2 inhibitor1

Venetoclax

Venclexta

Profile

Major tumor lysis syndrome risk on ramp-up.

XTALATNPRE

Severe

BCR-ABL TKI5

Bosutinib

Bosulif

Profile

Reversible eGFR decline.

PSEUDOPRE

Mild

Dasatinib

Sprycel

Profile

Nephrotic-range proteinuria — a notable signal.

GLOM

Moderate

Imatinib

Gleevec

Profile

Fluid retention; rare Fanconi and AKI.

LYTEFANCATN

Mild

Nilotinib

Tasigna

Profile

eGFR decline over time.

PRE

Mild

Ponatinib

Iclusig

Profile

Vascular toxicity and hypertension.

HTNPRETMA

Moderate

Bispecific (BCMA×CD3)2

Elranatamab

Elrexfio

Profile

CRS and tumor lysis — emerging.

PREATNXTAL

Moderate

Teclistamab

Tecvayli

Profile

CRS-associated AKI in myeloma — emerging signal.

PREATN

Moderate

Bispecific (CD20×CD3)3

Epcoritamab

Epkinly

Profile

CRS and tumor lysis — emerging.

PRELYTEXTAL

Moderate

Glofitamab

Columvi

Profile

CRS and tumor lysis — emerging.

PRELYTEXTAL

Moderate

Mosunetuzumab

Lunsumio

Profile

CRS and tumor lysis in lymphoma.

PRELYTEXTAL

Moderate

Bispecific (GPRC5D×CD3)1

Talquetamab

Talvey

Profile

CRS-related AKI — emerging.

PREATN

Moderate

Bisphosphonate3

Ibandronate

Boniva

Profile

Lower renal risk than zoledronate.

ATNLYTEGLOM

Mild

Pamidronate

Aredia

Profile

Collapsing FSGS — first drug ever linked.

GLOM

Severe

Zoledronic acid

Zometa

Profile

Toxic ATN, infusion-rate dependent.

ATNFANC

Moderate

BiTE (CD19×CD3)1

Blinatumomab

Blincyto

Profile

CRS and tumor lysis → AKI.

PREATNXTAL

Moderate

Bone-seeking radiopharmaceutical1

Strontium-89 chloride

Metastron

Profile

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

LYTEPRE

Moderate

Bone-seeking radiopharmaceutical (153Sm-EDTMP)1

Samarium-153 lexidronam

Quadramet

Profile

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

ATN

Moderate

BRAF inhibitor3

Dabrafenib

Tafinlar

Profile

Milder than vemurafenib; pyrexia-driven AKI, rare granulomatous AIN, hyponatremia.

AINPRELYTE

Mild

Encorafenib

Braftovi

Profile

Class tubular signal; usually mild.

ATNAIN

Mild

Vemurafenib

Zelboraf

Profile

Strongest renal offender of the BRAF/MEK class: proximal tubular injury/Fanconi and early AKI.

ATNFANCLYTE

Moderate

BRAF/MEK inhibitor1

BRAF / MEK inhibitors (vemurafenib · dabrafenib · trametinib)

Profile

Tubulointerstitial AKI; vemurafenib strongest.

ATNAINLYTE

Mild

BTK inhibitor3

Acalabrutinib

Calquence

Profile

Tumor lysis; lower hypertension than ibrutinib.

HTNPREXTAL

Mild

Ibrutinib

Imbruvica

Profile

Tumor lysis, hypertension and AKI.

HTNPREGLOM

Moderate

Zanubrutinib

Brukinsa

Profile

Tumor lysis in CLL/lymphoma.

PRELYTEXTAL

Mild

CAR-T cell therapy1

CAR-T cell therapy

Kymriah · Yescarta

Profile

CRS-driven prerenal AKI and tumor lysis.

PREATNXTAL

Moderate

CDK4/6 inhibitor3

Abemaciclib

Verzenio

Profile

Benign creatinine rise via tubular secretion block.

PSEUDOPRE

Mild

Palbociclib

Ibrance

Profile

Generally renally well tolerated.

PSEUDOPRELYTE

Mild

Ribociclib

Kisqali

Profile

Creatinine rise; QT prolongation.

PSEUDOPRELYTE

Mild

CTLA-4 checkpoint inhibitor1

Ipilimumab

Yervoy

Profile

CTLA-4 inhibitor; immune (often granulomatous) interstitial nephritis.

AINCINGLOM

Severe

CYP17 inhibitor1

Abiraterone

Zytiga

Profile

Mineralocorticoid excess: hypokalemia, hypertension, edema.

LYTEHTN

Moderate

Cytokine2

Interferon-α

Intron A

Profile

Collapsing FSGS in APOL1 carriers.

GLOMTMA

Severe

Interleukin-2 (high-dose)

Proleukin

Profile

Capillary-leak prerenal AKI.

PRELYTESIADH

Moderate

Differentiating agent1

Arsenic trioxide

Trisenox

Profile

Differentiation syndrome; QT prolongation.

PREATNLYTE

Moderate

EGFR TKI4

Afatinib

Gilotrif

Profile

Diarrhea-driven prerenal AKI.

PREATNLYTE

Mild

Erlotinib

Tarceva

Profile

Rare minimal-change disease and AKI.

GLOMATNPRE

Mild

Gefitinib

Iressa

Profile

Rare nephrotic syndrome.

GLOMAINCYST

Mild

Osimertinib

Tagrisso

Profile

Hyponatremia and occasional AKI.

SIADHLYTEPSEUDO

Mild

Enzyme1

Asparaginase

Elspar

Profile

Rare AKI; pancreatitis-mediated.

PRE

Mild

Enzyme (asparaginase)1

Pegaspargase

Oncaspar

Profile

Rare AKI; pancreatitis- and thrombosis-mediated.

PREATN

Mild

FGFR inhibitor3

Erdafitinib

Balversa

Profile

Hyperphosphatemia is an on-target class effect.

LYTE

Moderate

Futibatinib

Lytgobi

Profile

Hyperphosphatemia, class effect.

LYTE

Moderate

Pemigatinib

Pemazyre

Profile

Hyperphosphatemia; nephrocalcinosis risk.

LYTE

Moderate

GnRH agonist1

Leuprolide

Lupron

Profile

Metabolic syndrome; indirect renal risk.

HTN

Mild

Hedgehog (SMO) inhibitor1

Vismodegib

Erivedge

Profile

Muscle spasms; hyponatremia reported.

SIADHLYTE

Mild

HIF-2α inhibitor1

Belzutifan

Welireg

Profile

Anemia/hypoxia; emerging renal profile in VHL/RCC.

PRE

Mild

Hormonal–alkylating conjugate1

Estramustine

Emcyt

Profile

Fluid retention, edema and thromboembolism.

PRE

Mild

Hydrazine alkylating agent1

Procarbazine

Matulane

Profile

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

ATNAIN

Moderate

Hypomethylating agent2

Azacitidine

Vidaza

Profile

Proximal (type 2) RTA / Fanconi-like tubulopathy; overt AKI uncommon.

FANCATNLYTE

Moderate

Decitabine

Dacogen

Profile

Tumor lysis in MDS/AML.

XTALPRELYTE

Mild

IDH1 inhibitor1

Ivosidenib

Tibsovo

Profile

Differentiation syndrome → AKI; tumor lysis.

PRELYTEATN

Moderate

IDH2 inhibitor1

Enasidenib

Idhifa

Profile

Differentiation syndrome and tumor lysis.

PREATNLYTE

Moderate

IL-3 immunotoxin1

Tagraxofusp

Elzonris

Profile

Capillary-leak syndrome → AKI.

PREATN

Moderate

Immune checkpoint inhibitor1

Checkpoint inhibitors (pembrolizumab · nivolumab · ipilimumab)

Profile

Acute interstitial nephritis with long latency.

AINGLOMLYTE

Moderate

Immunomodulatory drug (IMiD)3

Lenalidomide

Revlimid

Profile

Renally cleared; AKI and rare Fanconi/TMA.

ATNFANCTMA

Moderate

Pomalidomide

Pomalyst

Profile

Tumor lysis; usable in renal impairment.

PRELYTEXTAL

Mild

Thalidomide

Thalomid

Profile

Tumor lysis and bradycardia.

PRELYTEXTAL

Mild

KRAS G12C inhibitor2

Adagrasib

Krazati

Profile

Creatinine rise; emerging data.

PREGLOMPSEUDO

Mild

Sotorasib

Lumakras

Profile

Newer agent; renal data emerging.

PREATN

Mild

MEK inhibitor4

Binimetinib

Mektovi

Profile

Creatinine rise; rhabdomyolysis reports.

ATNPRE

Mild

Cobimetinib

Cotellic

Profile

Real-world AKI signal with BRAF partners.

ATNAIN

Mild

Selumetinib

Koselugo

Profile

Creatinine rise in neurofibromatosis.

PRELYTE

Mild

Trametinib

Mekinist

Profile

MEK inhibitor; hypertension, proteinuria, and combination-therapy AKI.

PREAINGLOM

Moderate

MET inhibitor2

Capmatinib

Tabrecta

Profile

Reversible creatinine rise and edema.

PSEUDOPRE

Mild

Tepotinib

Tepmetko

Profile

Creatinine rise and peripheral edema.

PSEUDOPRE

Mild

Microtubule inhibitor1

Eribulin

Halaven

Profile

Reduced clearance in renal impairment.

PRE

Mild

mTOR inhibitor4

Everolimus

Afinitor

Profile

Podocyte injury with proteinuria/FSGS; occasional thrombotic microangiopathy.

GLOMTMALYTE

Moderate

mTOR inhibitors (everolimus · temsirolimus)

Profile

Podocyte injury → proteinuria and FSGS.

GLOMATNTMA

Mild

Sirolimus

Rapamune

Profile

Proteinuria, cast nephropathy, delayed graft recovery.

GLOMATN

Moderate

Temsirolimus

Torisel

Profile

Proteinuria and glomerular effects; less firmly quantified than everolimus.

GLOMLYTE

Mild

Nitrosourea (alkylating)2

Fotemustine

Muphoran

Profile

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

CINATNLYTE

Moderate

Nimustine (ACNU)

Nidran

Profile

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

CINATNLYTE

Moderate

Nitrosourea alkylator3

Carmustine (BCNU)

BiCNU

Profile

Delayed interstitial fibrosis with high cumulative dose.

CINTMA

Moderate

Lomustine (CCNU)

Gleostine

Profile

Cumulative interstitial nephritis and CKD.

CIN

Moderate

Streptozocin

Zanosar

Profile

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

FANCATNLYTE

Severe

Nonsteroidal antiandrogen1

Bicalutamide

Casodex

Profile

Hepatically cleared, kidney-neutral, no renal dose adjustment; only rare idiosyncratic interstitial nephritis.

AIN

Mild

Nucleoside analog2

Cytarabine

Cytosar

Profile

Tumor lysis in leukemia; high-dose toxicity.

XTALPRELYTE

Moderate

Gemcitabine

Gemzar

Profile

Dose-cumulative thrombotic microangiopathy.

TMAHTNGLOM

Severe

Oral fluoropyrimidine + TP inhibitor1

Trifluridine/tipiracil

Lonsurf

Profile

Tipiracil is renally cleared; reduced GFR raises exposure and early severe neutropenia; dose-reduce in renal impairment.

PRE

Moderate

Oxazaphosphorine alkylator2

Cyclophosphamide

Cytoxan

Profile

Vasopressin-independent hyponatremia; hemorrhagic cystitis.

SIADHCYST

Mild

Ifosfamide

Ifex

Profile

Chloroacetaldehyde → Fanconi syndrome.

FANCATNLYTE

Severe

PARP inhibitor4

Niraparib

Zejula

Profile

Hypertension and creatinine rise.

HTNPSEUDO

Mild

Olaparib

Lynparza

Profile

Benign creatinine rise via OCT2/MATE inhibition.

PSEUDOTMA

Mild

Rucaparib

Rubraca

Profile

Transporter-mediated creatinine rise.

PSEUDO

Mild

Talazoparib

Talzenna

Profile

Renally cleared; creatinine rise.

PSEUDO

Mild

PD-1 checkpoint inhibitor2

Nivolumab

Opdivo

Profile

PD-1 inhibitor; ICI acute interstitial nephritis is the prototype.

AINCINGLOM

Moderate

Pembrolizumab

Keytruda

Profile

PD-1 inhibitor; ICI interstitial nephritis, varied glomerular lesions.

AINCINGLOM

Moderate

PI3Kδ inhibitor1

Idelalisib

Zydelig

Profile

Immune-mediated colitis → volume-depletion prerenal AKI; transaminitis.

PREAIN

Mild

Platinum agent4

Carboplatin

Paraplatin

Profile

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

ATNLYTECYST

Mild

Cisplatin

Platinol

Profile

Proximal tubular ATN + magnesium wasting; the archetype.

ATNLYTEPRE

Severe

Nedaplatin

Aqupla

Profile

Second-gen platinum with reduced renal toxicity vs cisplatin.

ATNLYTE

Moderate

Oxaliplatin

Eloxatin

Profile

Least nephrotoxic platinum; rare immune hemolysis.

TMAATN

Mild

Podophyllotoxin (topo II)1

Teniposide

Vumon

Profile

Highly protein-bound, low renal clearance (~10-25% urinary); renal relevance is PK/exposure not direct injury; not dialyzable.

LYTEPRE

Mild

Proteasome inhibitor3

Bortezomib

Velcade

Profile

Rare TMA; reverses myeloma cast nephropathy.

TMAGLOM

Moderate

Carfilzomib

Kyprolis

Profile

AKI, TMA and hypertension — a hot myeloma signal.

TMAATNHTN

Severe

Ixazomib

Ninlaro

Profile

Rare TMA reports.

TMA

Moderate

Purine analog4

Cladribine

Leustatin

Profile

Tumor lysis; high-dose nephrotoxicity.

XTALPRELYTE

Mild

Clofarabine

Clolar

Profile

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

PREATNGLOM

Moderate

Fludarabine

Fludara

Profile

Tumor lysis; accumulates in renal impairment.

XTALPRELYTE

Moderate

Nelarabine

Arranon

Profile

Tumor lysis in T-ALL.

XTALPRELYTE

Mild

Purine analog (ADA inhibitor)1

Pentostatin

Nipent

Profile

Renally cleared; dose-related acute kidney injury.

ATNLYTESIADH

Moderate

Pyrimidine analog1

5-Fluorouracil

Adrucil

Profile

Rare TMA, esp. with mitomycin; mostly renally safe.

TMAPRE

Mild

Pyrimidine analog (oral 5-FU)1

Capecitabine

Xeloda

Profile

Diarrhea-driven prerenal AKI; dose-adjust for CrCl.

PRETMA

Mild

Radioimmunotherapy (Y-90 anti-CD20)1

Ibritumomab tiuxetan

Zevalin

Profile

Yttrium-90 radioimmunotherapy; tumor lysis with bulky lymphoma.

PREXTALLYTE

Mild

Radiopharmaceutical (alpha-emitter)1

Radium-223 dichloride

Xofigo

Profile

Bone-seeking alpha emitter; minimal direct renal toxicity.

PRE

Mild

Recombinant TNF-α (cytokine)1

Tasonermin

Beromun

Profile

Isolated-limb-perfusion agent; systemic leakage → SIRS/hypotension → prerenal AKI.

PREATN

Moderate

RET inhibitor2

Pralsetinib

Gavreto

Profile

Hypertension; rare AKI.

HTNPREPSEUDO

Mild

Selpercatinib

Retevmo

Profile

Hypertension and creatinine rise.

HTNPREPSEUDO

Moderate

Retinoid (differentiating agent)1

Tretinoin (ATRA)

Vesanoid

Profile

Differentiation syndrome → capillary leak and AKI.

PREATN

Moderate

Ribonucleotide reductase inhibitor1

Hydroxyurea

Hydrea

Profile

Tumor lysis in myeloproliferative disease.

XTALPRELYTE

Mild

SERM1

Tamoxifen

Nolvadex

Profile

Hypercalcemia flare; rare hyponatremia.

SIADHLYTEPRE

Mild

Somatostatin analog2

Lanreotide

Somatuline

Profile

Kidney-neutral (CLARINET: diarrhea dominant); increased exposure in renal impairment.

LYTEPRE

Mild

Octreotide

Sandostatin

Profile

Kidney-neutral/possibly renoprotective; renally cleared, caution in severe CKD/dialysis.

LYTEPRE

Mild

Taxane3

Cabazitaxel

Jevtana

Profile

Rare AKI; mostly GI-mediated.

PRECYST

Mild

Docetaxel

Taxotere

Profile

Fluid retention; low direct renal toxicity.

PRECYSTTMA

Mild

Paclitaxel

Taxol

Profile

Low direct nephrotoxicity; vehicle reactions.

PRECYSTGLOM

Mild

Topoisomerase I inhibitor2

Irinotecan

Camptosar

Profile

Diarrhea-driven prerenal AKI.

PRE

Mild

Topotecan

Hycamtin

Profile

Renally cleared; dose-adjust for CrCl.

PRE

Mild

Topoisomerase II inhibitor1

Etoposide

Etopophos

Profile

Tumor lysis; renally cleared.

XTALPRELYTE

Mild

Topoisomerase II inhibitor (acridine)1

Amsacrine

Amsidine

Profile

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

LYTEXTAL

Moderate

Trifunctional bispecific (EpCAM×CD3)1

Catumaxomab

Removab

Profile

Intraperitoneal; cytokine-release- and ascites/paracentesis-driven prerenal AKI; withdrawn (EU) 2017.

PRELYTE

Moderate

VEGF trap1

Ziv-aflibercept

Zaltrap

Profile

Hypertension and proteinuria like bevacizumab.

HTNGLOMTMA

Moderate

VEGFR TKI8

Axitinib

Inlyta

Profile

Potent VEGFR-TKI; hypertension and proteinuria dominate.

HTNGLOMTMA

Moderate

Lenvatinib

Lenvima

Profile

Highest-ranked TKI for hypertension; proteinuria.

HTNGLOM

Moderate

Pazopanib

Votrient

Profile

VEGFR-TKI; hypertension, proteinuria, TMA.

GLOMHTNTMA

Moderate

Regorafenib

Stivarga

Profile

Hypertension and proteinuria.

HTNGLOM

Moderate

Sorafenib

Nexavar

Profile

Anti-angiogenic hypertension and proteinuria; occasional TMA.

HTNGLOMTMA

Moderate

Sunitinib

Sutent

Profile

VEGFR-TKI; hypertension and proteinuria, TMA reported.

HTNGLOMTMA

Moderate

Tivozanib

Fotivda

Profile

Hypertension and proteinuria in RCC.

HTNGLOM

Moderate

VEGFR TKIs (sunitinib · sorafenib · pazopanib · axitinib)

Profile

Hypertension as an on-target marker; proteinuria.

HTNGLOMTMA

Moderate

VEGFR/EGFR/RET TKI1

Vandetanib

Caprelsa

Profile

Hypertension; QT prolongation.

HTNGLOMLYTE

Moderate

VEGFR/FGFR/PDGFR TKI1

Nintedanib

Ofev

Profile

Proteinuria and rare TMA.

HTNTMAGLOM

Mild

VEGFR/MET TKI1

Cabozantinib

Cabometyx

Profile

Hypertension and proteinuria; nephrotic case reports.

HTNGLOM

Moderate

Vinca alkaloid4

Vinblastine

Velban

Profile

SIADH and rare Raynaud/vascular events.

SIADHLYTE

Mild

Vincristine

Oncovin

Profile

SIADH → hyponatremia.

SIADHLYTE

Mild

Vinflunine

Javlor

Profile

Used because of renal impairment (cisplatin-unfit urothelial); CrCl-based dose bands; watch SIADH/hyponatremia.

LYTEPRESIADH

Mild

Vinorelbine

Navelbine

Profile

SIADH reports.

SIADHLYTE

Mild

Recent

Approvals of the last several years with maturing renal data.

AKT inhibitor1

Capivasertib

Truqap

Profile

2023 breast-cancer AKT inhibitor; AKI with diarrhea/hyperglycemia.

PRELYTE

Moderate

Androgen receptor inhibitor (ARSI)1

Darolutamide

Nubeqa

Profile

Not nephrotoxic; exposure rises in severe renal impairment, so consider dose adaptation.

LYTEPRE

Mild

Anti-CCR4 antibody1

Mogamulizumab

Poteligeo

Profile

Tumor lysis and rare AKI; cutaneous T-cell lymphoma.

PRELYTE

Mild

Anti-CD19 antibody1

Tafasitamab

Monjuvi

Profile

Tumor lysis and infusion reactions in lymphoma.

PRELYTE

Mild

Anti-GD2 antibody1

Naxitamab

Danyelza

Profile

Anti-GD2 antibody; infusion-related hypertension and prerenal AKI.

PREHTN

Moderate

Antibody-drug conjugate (CD19/PBD)1

Loncastuximab tesirine

Zynlonta

Profile

Capillary-leak-type edema, effusions and AKI.

PRELYTE

Moderate

Antibody-drug conjugate (tissue factor/MMAE)1

Tisotumab vedotin

Tivdak

Profile

Ocular/bleeding toxicity dominates; renal involvement essentially unreported.

PRE

Mild

BCMA-directed CAR T-cell therapy1

Anitocabtagene autoleucel

AKI mainly via CRS-related hemodynamic/prerenal injury; rare minimal change disease reported post-BCMA CAR-T.

PRE

Moderaterecent

BCR-ABL STAMP inhibitor1

Asciminib

Scemblix

Profile

Hypertension and pancreatitis; allosteric BCR-ABL inhibitor.

HTNPRE

Mild

BCR-ABL1 tyrosine kinase inhibitor (3rd generation)1

Olverembatinib

Olverembatinib (HQP1351)

Profile

Potent T315I-active TKI with a largely renal-sparing profile

GLOMPREHTN

Mild

Bispecific T-cell engager (DLL3-directed BiTE)1

Tarlatamab

Imdelltra

Profile

Tumor lysis syndrome with initial dosing may cause urate/phosphate crystal nephropathy and AKI

PREATN

Severe

CD19 CAR-T cell therapy1

Lisocabtagene maraleucel

Breyanzi

Profile

CRS-driven prerenal AKI and tumor-lysis crystal nephropathy in the first weeks; low severe-CRS rate softens the renal burden.

PREATNXTAL

Moderate

CSF1R inhibitor1

Pexidartinib

Turalio

Profile

Boxed hepatotoxicity; secondary renal effects.

PRE

Mild

CSF1R tyrosine kinase inhibitor1

Vimseltinib

Romvimza

Profile

A clean-kidney targeted TKI — watch the CPK, not the nephron.

PSEUDOPRE

Mild

EGFR exon20 TKI1

Mobocertinib

Exkivity

Profile

Diarrhea-driven prerenal AKI; QT prolongation.

PREATNLYTE

Mild

EGFR tyrosine kinase inhibitor1

Furmonertinib

Class-effect hypothesis: EGFR TKIs may cause electrolyte wasting (hypomagnesemia); no direct renal toxicity data in titles

LYTE

Mildrecent

EZH2 inhibitor1

Tazemetostat

Tazverik

Profile

Tumor lysis; generally low direct renal toxicity.

PRELYTE

Mild

FAK inhibitor1

Defactinib

No direct nephrotoxicity signal in titles; FAK biology renal-relevant but drug-specific injury unestablished

LYTE

Mildrecent

FGFR inhibitor1

Infigratinib

Truseltiq

Profile

Hyperphosphatemia — on-target FGFR class effect; nephrocalcinosis risk.

LYTEXTAL

Moderate

FLT3 / multikinase inhibitor1

Midostaurin

Rydapt

Profile

Tumor lysis, edema and QT in AML/mastocytosis.

PRELYTE

Mild

FLT3 inhibitor2

Gilteritinib

Xospata

Profile

Differentiation syndrome, tumor lysis and PRES in AML.

PRELYTE

Moderate

Quizartinib

Vanflyta

Profile

2023 AML FLT3 inhibitor; tumor lysis and QT.

PRELYTE

Mild

Gamma-secretase inhibitor1

Nirogacestat

Ogsiveo

Profile

2023 desmoid-tumor agent; phosphate/electrolyte disturbance.

LYTEFANC

Mild

Hedgehog (SMO) inhibitor2

Glasdegib

Daurismo

Profile

QT prolongation and muscle spasms; AML.

PRELYTE

Mild

Sonidegib

Odomzo

Profile

Elevated CK / rhabdomyolysis → pigment nephropathy.

ATN

Mild

HER2 / pan-EGFR TKI1

Neratinib

Nerlynx

Profile

Severe diarrhea → prerenal AKI; loperamide prophylaxis.

PRELYTE

Moderate

HER2 TKI1

Tucatinib

Tukysa

Profile

Benign creatinine rise via tubular secretion inhibition.

PSEUDO

Mild

HER2-directed antibody-drug conjugate (MMAE)1

Disitamab vedotin

MMAE payload ADC; renal signal not clearly established in titles—drug used for urothelial/bladder cancer; possible tubular injury

ATN

Mildrecent

Immunotoxin (anti-CD22 PE38)1

Moxetumomab pasudotox

Lumoxiti

Profile

Boxed warning for capillary-leak syndrome and hemolytic-uremic syndrome / TMA.

TMAPRE

Severe

JAK/ACVR1 inhibitor1

Momelotinib

Ojjaara

Profile

2023 myelofibrosis JAK inhibitor.

PSEUDOPRE

Mild

JAK1/2 inhibitor1

Ruxolitinib

Jakafi

Profile

Tumor lysis in myelofibrosis; renally adjusted.

PRELYTETMA

Mild

JAK2 inhibitor1

Fedratinib

Inrebic

Profile

JAK2 inhibitor; GI-loss prerenal azotemia and electrolyte disturbance.

LYTEPRE

Mild

KIT / PDGFRA inhibitor1

Avapritinib

Ayvakit

Profile

Edema, intracranial bleeding and cognitive effects.

PRELYTE

Mild

KIT switch-control inhibitor1

Ripretinib

Qinlock

Profile

Hypertension and alopecia in GIST.

HTN

Mild

Marine alkylating agent2

Lurbinectedin

Zepzelca

Profile

Rhabdomyolysis risk in small-cell lung cancer.

ATNLYTEXTAL

Mild

Trabectedin

Yondelis

Profile

Rhabdomyolysis → pigment nephropathy; hepatotoxicity.

ATNLYTE

Moderate

Mutant IDH1/2 inhibitor1

Vorasidenib

Voranigo

Profile

A brain-penetrant IDH inhibitor whose kidney footprint is a benign creatinine bump, not true AKI.

PSEUDOPRE

Mild

Non-covalent BTK inhibitor1

Pirtobrutinib

Jaypirca

Profile

2023 BTK inhibitor; tumor lysis risk.

XTALPRELYTE

Mild

Oral selective estrogen-receptor degrader (SERD)1

Elacestrant

Orserdu

Profile

2023 oral SERD; nausea-dominant, minimal intrinsic nephrotoxicity.

PRE

Mild

Pan-PI3K inhibitor1

Copanlisib

Aliqopa

Profile

Transient infusion-related hypertension and hyperglycemia.

HTN

Moderate

PARP inhibitor1

saruparib

PARP inhibitors may raise serum creatinine via tubular transporter inhibition without true GFR loss

PSEUDO

Mildrecent

PD-1 immune checkpoint inhibitor4

Penpulimab

Penpulimab (AK105)

Profile

Fc-silent PD-1 blocker for nasopharyngeal carcinoma — class-typical, infrequent immune interstitial nephritis

AINATNLYTE

Moderate

Retifanlimab

Zynyz

Profile

PD-1 blockade — kidney injury is immune-mediated interstitial nephritis, not direct tubular toxicity.

AINLYTEPRE

Moderate

Tislelizumab

Tevimbra

Profile

A PD-1 blocker whose kidney risk is the class-typical rare immune-mediated interstitial nephritis.

AINPRETMA

Moderate

Toripalimab

Loqtorzi

Profile

First FDA-approved drug for nasopharyngeal carcinoma; renal risk is class-typical immune-mediated interstitial nephritis.

AINLYTEGLOM

Moderate

PD-1/CTLA-4 bispecific immune checkpoint inhibitor1

Cadonilimab

Immune-related acute tubulointerstitial nephritis; ICI-class effect, may co-occur with ureteritis/cystitis

AIN

Moderaterecent

PD-L1 immune checkpoint inhibitor2

Cosibelimab

Unloxcyt

Profile

PD-L1 blockade for cutaneous SCC — watch for late immune interstitial nephritis

AINGLOMLYTE

Moderate

Sugemalimab

Cejemly

Profile

A full-length anti-PD-L1 antibody whose kidney is its immune system: rare but real autoimmune interstitial nephritis.

AINATNLYTE

Moderate

Peptide-conjugated alkylator1

Melphalan flufenamide (melflufen)

Pepaxto

Profile

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

ATNLYTE

Moderate

PI3Kα inhibitor1

Alpelisib

Piqray

Profile

Severe hyperglycemia (on-target) → osmotic diuresis and prerenal AKI risk.

PRELYTEATN

Moderate

PI3Kδ/γ inhibitor1

Duvelisib

Copiktra

Profile

Colitis and diarrhea → prerenal AKI.

PREAIN

Mild

Radioligand therapy (alpha-emitter)1

Actinium 225 PSMA

PSMA-expressing proximal tubules concentrate 225Ac ligand; alpha radiation risks tubular injury/CKD

ATN

Moderaterecent

Radioligand therapy (PRRT)1

Lutetium-177 Dotatate

Lutathera

Profile

Peptide receptor radionuclide therapy; proximal tubular radiation nephropathy is dose-limiting — amino-acid co-infusion is renoprotective.

CINTMA

Moderate

Radiopharmaceutical (¹³¹I-MIBG)1

Iobenguane I-131

Azedra

Profile

¹³¹I-MIBG radioligand; catecholamine hypertension and radiation tubular injury.

ATNCINHTN

Mild

RAS(ON) multi-selective inhibitor1

daraxonrasib

No specific nephrotoxicity signal in available titles; renal effects unknown, monitor electrolytes empirically

LYTE

Mildrecent

ROS1/TRK TKI1

Repotrectinib

Augtyro

Profile

2023 ROS1 inhibitor; creatinine rise via secretion block.

PSEUDO

Mild

Thrombopoietin receptor agonist1

promacta

Rare AKI reported; possible thrombotic microangiopathy in ITP patient on eltrombopag; mechanism uncertain, needs review

TMA

Moderaterecent

TRK inhibitor1

Larotrectinib

Vitrakvi

Profile

Mild creatinine rise; generally well tolerated.

PSEUDO

Mild

TRK/ROS1 TKI1

Entrectinib

Rozlytrek

Profile

Creatinine rise via reduced tubular secretion.

PSEUDO

Mild

VEGFR TKI1

Fruquintinib

Fruzaqla

Profile

2023 colorectal VEGFR-TKI; hypertension and proteinuria, class effect.

HTNGLOMTMA

Moderate

XPO1 (nuclear export) inhibitor1

Selinexor

Xpovio

Profile

Hyponatremia is common and dose-limiting.

SIADHLYTEPRE

Moderate

Frontier

Just-arrived agents — renal signals often extrapolated from class.

ALK TKI1

Ensartinib

Ensacove

Profile

ALK TKI carrying the crizotinib-class renal signature: benign creatinine rise and possible renal cysts.

PSEUDORCYSTLYTE

Mild

Anti-Claudin-18.2 monoclonal antibody1

Zolbetuximab

Vyloy

Profile

2024 gastric mAb; severe on-target nausea/vomiting → volume-depletion prerenal AKI.

PRE

Moderate

Antibody-drug conjugate (TROP2/DXd)1

Datopotamab deruxtecan (Dato-DXd)

Datroway

Profile

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

ATNGLOM

Moderate

BCL-2 inhibitor1

Sonrotoclax

Beqalzi

Profile

2026 second-gen BCL-2 inhibitor, more potent than venetoclax; tumor-lysis AKI is the class risk, managed with mandated dose ramp-up.

XTALLYTEPRE

Severe

BCMA CAR-T cell therapy2

Ciltacabtagene autoleucel

Carvykti

Profile

CRS-driven AKI; delayed neurotoxicity.

PREATNLYTE

Moderate

Idecabtagene vicleucel

Abecma

Profile

CRS-driven AKI and tumor lysis in myeloma.

PREATNLYTE

Moderate

BCMA×CD3 bispecific T-cell engager1

Linvoseltamab

Lynozyfic

Profile

T-cell redirection, not tubular poison — AKI rides on cytokine release, not the drug itself.

PREXTALLYTE

Mild

Bispecific (CD20×CD3)1

Odronextamab

Ordspono

Profile

CD20×CD3 bispecific; tumor-lysis urate crystal nephropathy with CRS.

XTALPRELYTE

Moderate

Bispecific T-cell engager (gp100×CD3 ImmTAC)1

Tebentafusp

Kimmtrak

Profile

CRS-driven hypotension → prerenal AKI early in dosing; uveal melanoma.

PRE

Moderate

c-Met ADC (MMAE)1

Telisotuzumab vedotin (Teliso-V)

Emrelis

Profile

c-Met MMAE antibody-drug conjugate; proximal tubular ATN risk extrapolated from the ADC/MMAE class.

ATNLYTE

Moderate

CD123 antibody-drug conjugate1

Pivekimab sunirine

Decnupaz

Profile

2026 CD123 ADC for BPDCN; renal risk indirect — TLS in the CD123+ disease plus the CD123-class capillary-leak concern; its own dose-limiting toxicity was reversible VOD.

PREXTALLYTE

Moderate

CD19 CAR-T cell therapy1

Obecabtagene autoleucel (Obe-cel)

Aucatzyl

Profile

CD19 CAR-T for adult B-ALL; CRS- and tumor-lysis-associated AKI, with notably lower high-grade CRS.

PRELYTE

Moderate

Cereblon E3 ligase modulator (CELMoD)1

Iberdomide

Zenbexus

Profile

2026 first-in-class CELMoD; no attributable lesion (renal impairment 11% vs 8% on the comparator arm) but exposure rises 1.8x below eGFR 30 off dialysis.

PRE

Mild

EGFR exon20 TKI1

Sunvozertinib

Zegfrovy

Profile

2025 EGFR exon20 TKI; renal magnesium wasting (SIADH-pattern hyponatremia possible).

LYTESIADHPRE

Mild

EGFR TKI (3rd-gen)1

Lazertinib

Lazcluze

Profile

2024 EGFR TKI; hyponatremia like osimertinib.

SIADHLYTE

Mild

EGFR-MET bispecific antibody1

Amivantamab

Rybrevant

Profile

EGFR-mediated electrolyte (magnesium) wasting; an emerging acute interstitial nephritis signal is also clinician-flagged.

LYTEAIN

Moderate

HER2 bispecific antibody1

Zanidatamab

Ziihera

Profile

2024 biliary-tract HER2 bispecific; renal data emerging.

PRELYTE

Mild

HER2 TKI1

Zongertinib

Hernexeos

Profile

HER2 exon20 TKI (2025); creatinine rise likely a secretion artifact.

PSEUDOPRE

Mild

HER2/EGFR TKI1

Sevabertinib

Hyrnuo

Profile

2025 reversible HER2/EGFR TKI; profuse diarrhea (84-91%) → prerenal AKI, plus EGFR-pathway renal magnesium wasting.

PRELYTE

Mild

HER2×HER3 bispecific antibody1

Zenocutuzumab

Bizengri

Profile

2024 NRG1-fusion bispecific; mostly grade 1-2 AEs — at most diarrhea-related prerenal risk, no CRS/TLS mechanism.

PRELYTE

Mild

IDH1 inhibitor1

Olutasidenib

Rezlidhi

Profile

Differentiation syndrome and tumor lysis in AML.

PRELYTE

Moderate

Imipridone (ONC201; DRD2/ClpP)1

Dordaviprone

Modeyso

Profile

2025 imipridone for H3 K27M glioma; renally well tolerated — QT prolongation, not nephrotoxicity, is the safety focus.

PRE

Mild

Immune checkpoint inhibitor (anti-LAG-3)1

Relatlimab

Opdualag

Profile

2022 LAG-3 inhibitor (with nivolumab); class immune-mediated AIN, amplified by combination ICI.

AIN

Moderate

Immunotoxin (IL-2–diphtheria)1

Denileukin diftitox

Lymphir

Profile

Capillary-leak syndrome → prerenal AKI.

PRE

Moderate

JAK2/ACVR1 inhibitor1

Pacritinib

Vonjo

Profile

JAK2/ACVR1 inhibitor; diarrhea-driven prerenal AKI and electrolyte loss.

PRELYTEATN

Moderate

MAGE-A4 TCR-T cell therapy1

Afamitresgene autoleucel (Afami-cel)

Tecelra

Profile

First TCR-T cell therapy for a solid tumor; CRS-associated hemodynamic AKI.

PRELYTE

Moderate

MEK inhibitor1

Mirdametinib

Gomekli

Profile

2025 NF1 MEK inhibitor; creatinine rise and edema.

PRELYTE

Mild

Menin inhibitor2

Revumenib

Revuforj

Profile

2024 leukemia agent; differentiation syndrome and tumor lysis.

PRELYTEXTAL

Moderate

Ziftomenib

Komzifti

Profile

2025 NPM1-mutated AML menin inhibitor; differentiation syndrome and tumor lysis.

PRELYTE

Moderate

Oral selective estrogen-receptor degrader (SERD)1

Imlunestrant

Inluriyo

Profile

2025 brain-penetrant oral SERD; renally benign — the only wrinkle is the benign abemaciclib creatinine rise in the combo.

PSEUDOPRE

Mild

Pan-PI3K inhibitor1

Gedatolisib

Revtorpyk

Profile

2026 IV pan-PI3K + mTORC1/2 (breast); on-target hyperglycemia and low-grade Na/K/Mg drift — creatinine up 14% vs 8% control, grade 3-4 rare.

LYTEPRE

Mild

PD-1 x VEGF bispecific antibody1

Ivonescimab

AK112 (Akeso/Summit)

Profile

Two nephrotoxic pathways in one molecule: VEGF-blockade glomerular injury plus checkpoint-inhibitor interstitial nephritis.

GLOMHTNAIN

Moderate

PI3Kα inhibitor1

Inavolisib

Itovebi

Profile

PI3Kα inhibitor whose renal-relevant toxicity is on-target hyperglycemia and electrolyte shifts, not a kidney lesion.

LYTE

Moderate

PROTAC estrogen-receptor degrader1

Vepdegestrant

Veppanu

Profile

2026 first PROTAC ER degrader; no meaningful intrinsic renal signal.

PRE

Mild

Radioligand therapy (PSMA)1

Lutetium-177 PSMA-617 (vipivotide)

Pluvicto

Profile

PSMA-targeted radioligand for prostate cancer; renal radiation exposure and xerostomia.

CINLYTE

Moderate

RAF/MEK inhibitor1

Avutometinib

Avmapki (co-packaged with defactinib as Avmapki Fakzynja)

Profile

RAF/MEK clamp; CK elevation/rhabdomyolysis and tubular electrolyte wasting.

LYTEATNPRE

Moderate

ROS1 TKI1

Taletrectinib

Ibtrozi

Profile

Next-gen ROS1 TKI; benign transporter-mediated creatinine rise (pseudo-AKI), not true GFR loss.

PSEUDO

Mild

ROS1-selective TKI1

Zidesamtinib

Jideytro

Profile

2026 TRK-sparing ROS1 TKI; no creatinine abnormality reached the label's >=20% lab-table cutoff — unlike the class's benign pseudo-AKI rise. Renally quiet so far.

PRE

Mild

Selective glucocorticoid-receptor antagonist1

Relacorilant

Lifyorli

Profile

2026 GR antagonist (ovarian); hypokalemia via cortisol/mineralocorticoid receptor — the mifepristone effect, blunted by GR-selectivity.

LYTEHTN

Mild

Telomerase inhibitor1

Imetelstat

Rytelo

Profile

2024 MDS agent; tumor lysis risk.

PRELYTE

Mild

Tumor-infiltrating lymphocyte (TIL) therapy1

Lifileucel

Amtagvi

Profile

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

PREATNLYTE

Moderate

Type II pan-RAF (BRAF) inhibitor1

Tovorafenib

Ojemda

Profile

2024 pediatric glioma RAF inhibitor; creatinine rise.

PRE

Mild

Investigational

Trial-stage agents with predicted, not yet established, profiles.

HIF-2α inhibitor (investigational)1

Casdatifan

Profile

Trial-stage RCC HIF-2α inhibitor; renal profile being defined.

PRE

Mild