The Injury Atlas

PRE

Prerenal / Hemodynamic AKI

Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

139agents

Where it strikes

Vasculature / Endothelium

Glomerular & peritubular capillaries

See it on the nephron

Severity mix

Severe· 4Moderate· 49Mild· 86

Reversibility

Partially reversible· 6Variable· 18Reversible· 115

Signature offenders

98

Agents for which prerenal / hemodynamic aki is the defining renal lesion.

CAR-T Cell TherapyAcute — within the CRS window (first days–weeks).AKI ~5–33% across cohorts (commonly ~10–30%), mostly mild and reversible.Moderate Interleukin-2 (high-dose)Acute — during the treatment cycle.Oliguria / prerenal AKI is very common during therapy — almost universal at high dose — but reversible.Moderate BendamustineTLS within hours to days of the first cycle; TMA delayed and rare.Direct nephrotoxicity is uncommon; the principal renal risk is acute kidney injury from tumor lysis syndrome in high-burden disease, classically during the first cycle. TLS with renal failure is documented from the first reported case onward; TMA is rare and case-level.Moderate CytarabineHours to days after initiating therapy in high-burden disease.Intrinsic tubular nephrotoxicity is uncommon; the major renal risk is AKI from tumor lysis syndrome during leukemia/lymphoma cytoreduction, reported at case and series level including fatal TLS. Direct cytarabine-nephrotoxicity primary literature is genuinely sparse.Moderate FludarabineTLS within days of starting therapy; systemic toxicity accrues with impaired clearance.Direct nephrotoxicity is uncommon; the chief renal risks are tumor-lysis-syndrome AKI during cytoreduction and increased systemic toxicity when the renally cleared drug accumulates in renal impairment. About 60% of the active metabolite 2-F-ara-A is renally eliminated, so renal function directly drives exposure.Moderate ClofarabineEarly, typically within the first treatment cycle (days).A systemic inflammatory response syndrome (SIRS) / capillary-leak syndrome with associated AKI was reported in roughly 4% of treated children in the registration program; hypotension was among the most common grade 3 or greater adverse events in the pivotal phase II trial. Precise renal incidence is not well quantified and most AKI data are case-level.Moderate BlinatumomabEarly, typically during the first days of an infusion cycle (CRS) or with rapid tumor cytoreduction (TLS), concentrated around initiation and dose step-up.Acute kidney injury is predominantly secondary to cytokine release syndrome (CRS) and tumor lysis syndrome (TLS) rather than a direct drug effect; renal injury is described mainly at the case/series level and is not robustly quantified as a primary endpoint. By analogy to immune-effector-cell therapies, AKI is generally low-grade and rapidly reversible when the syndrome is controlled.Moderate TeclistamabEarly, concentrated around step-up (priming) dosing and the first full doses when CRS risk is highest (first days to weeks).Cytokine release syndrome is very common with teclistamab (about 72% of patients in the pivotal MajesTEC-1 trial, predominantly grade 1-2); CRS-associated acute kidney injury is an emerging, case-level signal superimposed on frequent baseline myeloma-related kidney disease, and is not separately well quantified.Moderate TalquetamabEarly, around step-up (priming) dosing and the initial full doses when CRS risk peaks.Cytokine release syndrome is common with talquetamab (about three-quarters of patients in MonumenTAL-1, predominantly grade 1-2); CRS-associated acute kidney injury is an emerging, case-level signal that is not separately well quantified, superimposed on frequent baseline myeloma kidney disease.Moderate ElranatamabEarly, concentrated around the two-step priming doses and the first full doses.Cytokine release syndrome is common with elranatamab (about 58% in the pivotal MagnetisMM-3 trial, largely grade 1-2 with the two-step priming regimen); CRS-associated acute kidney injury, and occasionally tumor-lysis-related injury, are emerging case-level signals that are not separately well quantified, superimposed on frequent myeloma kidney disease.Moderate MosunetuzumabEarly — during cycle 1 step-up dosing, coincident with CRS (first days to ~2 weeks).No direct tubular nephrotoxic signal. AKI is a downstream/case-level consequence of cytokine release syndrome (CRS, ~44% any-grade, almost all grade 1-2 and concentrated in cycle 1) and tumor lysis syndrome; renal-specific incidence is not quantified.Moderate EpcoritamabEarly — during cycle 1 step-up dosing with CRS.No direct tubular signal. AKI is case-level and downstream of CRS (~50% any-grade, predominantly grade 1-2 with subcutaneous step-up dosing) and tumor lysis; renal incidence is not separately quantified — emerging data.Moderate GlofitamabEarly — concentrated around cycle 1 step-up dosing and the first full dose.No direct tubular signal. AKI is case-level, downstream of CRS (~63% any-grade, grade >=3 in ~4% after obinutuzumab pretreatment and step-up dosing) and tumor lysis; renal incidence not separately quantified — emerging data.Moderate Sacituzumab govitecanVariable; prerenal AKI tracks with GI toxicity during treatment cycles.AKI is mainly prerenal, driven by the severe diarrhea/nausea and neutropenia that dominate the ASCENT safety profile; renal-specific incidence is not well quantified. A biopsy-proven severe acute tubulointerstitial nephritis requiring hemodialysis has also been reported (case-level).Moderate Gemtuzumab ozogamicinEarly — tumor lysis with induction; VOD typically within weeks, notably around hematopoietic stem-cell transplant.Direct nephrotoxicity is not a prominent signal. AKI is chiefly secondary to tumor lysis syndrome and to hepatic sinusoidal obstruction syndrome/veno-occlusive disease (VOD), the latter a recognized, sometimes fatal complication that produces hepatorenal-type AKI. Renal-specific incidence is not quantified.Moderate Inotuzumab ozogamicinEarly — tumor lysis during initial therapy; VOD typically peri-transplant.Direct nephrotoxicity is not a prominent signal. AKI is chiefly secondary to tumor lysis and to hepatic sinusoidal obstruction syndrome/veno-occlusive disease (VOD) — a notable, sometimes fatal complication, particularly around subsequent allogeneic stem-cell transplant. Renal-specific incidence is not quantified.Moderate IvosidenibDifferentiation syndrome typically days to weeks after starting therapy (median ~30 days); tumor lysis early during cytoreduction.Differentiation (IDH) syndrome is a recognized, potentially fatal complication — reported in roughly 10-19% of AML patients across IDH-inhibitor experience (e.g. ~10.4-11.7% with the IDH2 inhibitor enasidenib in pooled/phase 1-2 analyses) — and can drive AKI through capillary leak, fluid overload, hypotension, and inflammation; tumor lysis can also occur with cytoreduction.Moderate EnasidenibDifferentiation syndrome typically days to weeks after starting (median onset ~30 days; reported range days to ~4–5 months).IDH-inhibitor differentiation syndrome (the main route to AKI) occurs in roughly 10% of enasidenib-treated AML patients (10.4% any-grade in a pooled trial analysis; ~7% grade ≥3 in the first-in-human study). Tumor lysis is a secondary risk. Direct tubular nephrotoxicity is not well quantified.Moderate Tretinoin (ATRA)Usually within the first 1–3 weeks of induction (bimodal: first week and third week).Differentiation (retinoic acid) syndrome — the main route to AKI — occurs in roughly 2–37% of APL patients depending on criteria and prophylaxis (commonly cited around 25%); acute renal failure is part of its defining end-organ spectrum.Moderate Arsenic trioxideDifferentiation syndrome within the first weeks of induction; QT/electrolyte effects throughout treatment.Differentiation syndrome (the main route to AKI) occurs in a substantial minority of APL patients; grade 3–4 renal toxicity in ATO-based regimens is uncommon in randomized data. Direct nephrotoxicity is not well quantified, but QT prolongation and electrolyte disturbances are frequent and clinically important.Moderate TagraxofuspTypically during the first treatment cycle, often within days of the first doses; recurrence in later cycles is uncommon with proactive monitoring.Capillary leak syndrome (CLS) is a boxed-warning toxicity occurring in ~19-21% of treated patients (grade >=3 in ~7%, with rare deaths) in the pivotal trial; the resulting hypotension, hypoalbuminemia, and fluid shifts can precipitate prerenal AKI and, with prolonged hypoperfusion, ischemic ATN. Renal-specific AKI incidence is not separately quantified.Moderate TarlatamabCRS typically within the first cycle, often after the first full (post-priming) doses; AKI tracks the CRS course.Cytokine release syndrome is the dominant on-target toxicity — common (majority of patients in early studies), mostly low-grade, and mitigated by step-up/priming dosing and inpatient monitoring of initial doses. AKI is principally a downstream consequence of CRS (hypotension, fever, capillary leak, volume shifts) rather than a direct tubular toxin; renal-specific incidence is not separately well quantified.Moderate RevumenibDuring early treatment as leukemic differentiation and lysis occur (first days–weeks).Differentiation syndrome and tumor lysis syndrome are recognized on-target risks identified during development (differentiation syndrome carries a boxed warning). Resulting AKI is hemodynamic (capillary leak, fluid shifts) and/or crystal/metabolic (TLS); renal-specific incidence is not separately well quantified. QTc prolongation is an additional class effect.Moderate CapivasertibEarly in therapy, tracking diarrhea/hyperglycemia (first cycles).Diarrhea and hyperglycemia are the characteristic on-target toxicities (diarrhea very common; hyperglycemia frequent, occasionally severe). AKI, when it occurs, is largely a downstream pre-renal consequence of diarrhea-related volume loss and osmotic/metabolic disturbance; direct renal incidence is not well quantified. Rash is common but not nephrotoxic.Moderate LifileucelAcute — within hours to days of high-dose IL-2 administration during the conditioning/expansion phase.AKI is common in the overall regimen but is driven by the high-dose IL-2 component (and lymphodepletion), not the TILs themselves. In the pooled C-144-01 experience renal/AKI events fell within the expected high-dose IL-2 toxicity spectrum; a clean drug-specific AKI rate for the TIL product alone is not established. By analogy to other adoptive cell therapies, AKI in the broader CAR-T literature runs 5-33%.Moderate ZiftomenibDifferentiation syndrome typically within the first weeks of therapy as blasts differentiate; QTc prolongation is also seen.Renal-specific data are not established. The class-defining serious toxicity is differentiation syndrome — reported in 12/83 (15%) of patients in the KOMET-001 phase 1 trial (with higher severity in KMT2A-rearranged patients, halting that cohort's enrolment) — which can cause capillary leak, fluid overload and AKI. Tumor-lysis risk accompanies rapid blast clearance. No drug-specific renal incidence is published.Moderate Denileukin diftitoxAcute, peri-infusion (first 1-2 cycles); generally not cumulative.Capillary-leak syndrome (CLS) occurred in ~20.3% (grade >=3 ~5.8%) in the 2024 denileukin diftitox-cxdl trial. With the original formulation hypoalbuminemia was very common (~79%, ~15% grade 3/4) and a vascular-leak syndrome occurred in roughly a quarter of patients. AKI here is prerenal/hemodynamic rather than a quantified direct renal injury rate.Moderate Idecabtagene vicleucelWithin the first 1-2 weeks (the CRS window).Published CAR-T AKI incidence runs roughly 5-30% across cohorts and is mostly mild (KDIGO stage 1); in one cohort any-grade AKI reached ~30% by day 100 with rapid recovery. Most AKI parallels cytokine-release syndrome (CRS) and reverses within ~30 days.Moderate Ciltacabtagene autoleucelAKI in the first 1-2 weeks; the movement disorder is delayed (weeks).CRS-associated AKI mirrors the BCMA CAR-T class (roughly 5-30% across cohorts, mostly mild) and generally reverses with supportive care. A distinct, non-renal signature toxicity is a delayed movement-and-neurocognitive (parkinsonism-like) syndrome.Moderate AlpelisibHyperglycemia typically within the first 1-2 weeks; prerenal AKI follows volume depletion or a hyperglycemic crisis.Hyperglycemia is essentially on-target and very common: any-grade hyperglycemia ~64% and grade 3/4 hyperglycemia ~36.6% in SOLAR-1, with diabetic ketoacidosis reported rarely in pharmacovigilance. The renal injury is secondary (osmotic diuresis/volume depletion or DKA) rather than a direct lesion; a discrete AKI incidence is not well quantified.Moderate GilteritinibDifferentiation syndrome from a few days up to ~3 months (often within the first month); TLS early; PRES variable.Differentiation syndrome (boxed warning) occurs in roughly 3% of treated patients and can cause capillary leak, fluid overload and renal dysfunction; tumor lysis and PRES are labeled risks. Discrete AKI incidence is not separately quantified and is largely a consequence of these syndromes.Moderate NeratinibDiarrhea characteristically within the first days-to-weeks; prerenal AKI follows uncontrolled fluid loss.Diarrhea is near-universal without prophylaxis: in ExteNET, grade 3 diarrhea occurred in ~40% without antidiarrheal prophylaxis, falling substantially with loperamide and dose-escalation strategies (CONTROL). The resulting volume-depletion prerenal AKI is not separately quantified.Moderate OlutasidenibDifferentiation syndrome within days to a few months (often early); tumor lysis early in treatment.Differentiation syndrome (boxed warning) occurred in ~14% of patients (grade >=3 ~9%, with rare fatality) in the pivotal cohort; tumor lysis is a labeled risk. Discrete AKI incidence is not separately quantified and is largely consequent on these syndromes.Moderate Loncastuximab tesirineEdema/effusions accumulate over cycles; prerenal changes track the fluid shifts.Edema and effusions (pleural, pericardial, peritoneal) are characteristic PBD-payload toxicities and were common in LOTIS-2; the resulting fluid shifts and AKI are not separately quantified. Tumor lysis is an additional consideration in responding lymphoma.Moderate DinutuximabInfusion-associated and acute — pain, capillary leak and blood-pressure swings occur during/around each infusion.Severe neuropathic pain is near-universal, and capillary-leak syndrome and hypertension are common, sometimes severe, infusion-associated toxicities (driven partly by concurrent IL-2). The resulting fluid shifts and prerenal AKI are managed proactively but not separately quantified.Moderate TebentafuspEarly — first 1–3 weekly doses, coinciding with peak CRS.Cytokine release syndrome is very common early in treatment and, with the associated hypotension, is the principal mechanism of acute kidney injury; severe sepsis-like CRS with hypotension has been reported. The pivotal phase 3 trial established CRS, hypotension and rash as defining toxicities, mitigated by weekly step-up dosing. A dedicated tebentafusp renal/AKI study does not exist; renal injury is inferred from the CRS literature.Moderate ZolbetuximabAround infusions, especially the first cycles, tracking the nausea/vomiting peak.Direct nephrotoxicity is not a recognized feature. The defining, dose-limiting toxicity in the pivotal SPOTLIGHT and GLOW trials is severe nausea and vomiting (an on-target effect on gastric mucosa), which can cause volume depletion and prerenal acute kidney injury. A quantified renal-injury rate is not reported; the renal risk is mechanistic/indirect.Moderate CatumaxomabCytokine-release symptoms within hours of each intraperitoneal infusion; any prerenal AKI follows the inflammatory/volume insult.No characteristic intrinsic nephrotoxicity. The dominant treatment-related toxicity is cytokine-release-related (pyrexia, nausea, vomiting, chills, fatigue) plus intraperitoneal-administration effects (abdominal pain); transient transaminase rises and lymphopenia are common but usually clinically minor. Cytokine release with fever, GI losses, and large-volume ascites/paracentesis creates a setting for prerenal/hemodynamic AKI rather than a direct renal lesion. Drug-specific renal incidence is not quantified.Moderate DacarbazineVariable; hepatic VOD typically days to weeks after exposure.Direct nephrotoxicity is minimal and not well quantified; the notable vascular toxicity is hepatic veno-occlusive disease / sinusoidal obstruction (now recognized as not rare), with renal effects largely secondary to severe systemic illness, hepatic injury or volume loss.Mild CapecitabineAcute, during cycles with GI toxicity; TMA delayed and rare.Intrinsic nephrotoxicity is uncommon; the main renal issue is prerenal AKI from drug-induced diarrhea and volume depletion. Renal impairment increases toxicity - in the PK study, all patients with severe impairment (CrCl <30) had grade 3-4 adverse events - so labeling mandates dose adjustment by creatinine clearance and contraindicates severe impairment.Mild DecitabineEarly after a treatment cycle (days) for tumor lysis; TMA over weeks.Tumor lysis syndrome with AKI is a recognized but uncommon complication when bulky/proliferative disease responds; renal incidence specific to decitabine is not well quantified (case-level). Rare biopsy-proven renal thrombotic microangiopathy has been reported.Mild HydroxyureaVery early (within 12-24 hours of high-dose treatment).Acute tumor lysis syndrome from hydroxyurea is rare and reported at case level, almost exclusively with high-dose cytoreduction of leukemias carrying a high blast burden. Standard-dose hydroxyurea is not characteristically nephrotoxic.Mild NelarabineEarly after treatment initiation (days).Tumor lysis syndrome with attendant AKI is a labeled risk when bulky T-ALL responds rapidly; drug-specific renal incidence is not well quantified (case-level). The dose-limiting and most feared toxicity is neurologic, not renal.Mild AfatinibDays to weeks after starting therapy, tracking with the onset and severity of diarrhea (often within the first cycles).Diarrhea is very common with afatinib (the dominant class toxicity, all-grade in the large majority and grade >=3 in roughly 10-15% in LUX-Lung trials), and the consequent dehydration can precipitate prerenal AKI. Pharmacovigilance data identify afatinib as carrying the strongest renal-failure/AKI signal among EGFR agents, frequently co-reported with diarrhea; trial-based renal incidence is not separately quantified.Mild Brentuximab vedotinEarly — tumor lysis in the first cycle(s) of bulky disease.Direct nephrotoxicity is minimal. Tumor lysis syndrome occurs at low rates (<=5% in anaplastic large-cell lymphoma experience) and is the principal pathway to AKI/electrolyte disturbance; renal-specific incidence is not quantified.Mild Polatuzumab vedotinEarly — tumor lysis during initial cycles of bulky disease.Renal data are limited; direct nephrotoxicity is not a prominent trial signal. AKI is case-level and chiefly tumor-lysis- or volume-mediated. Renal-specific incidence is not quantified.Mild Belantamab mafodotinVariable; renal events reported during prolonged therapy. Ocular toxicity is often detectable within the first cycles.Renal-specific data are emerging and sparse; direct nephrotoxicity is not an established signal. In myeloma, AKI more often reflects the underlying disease (cast nephropathy, hypercalcemia, volume status) than the ADC. A case of focal segmental glomerulosclerosis after belantamab mafodotin (confounded by severe COVID-19) has been reported. The defining toxicity is ocular keratopathy (71-77% in DREAMM-2).Mild Mirvetuximab soravtansineVariable; tracks with GI toxicity during treatment cycles.Direct nephrotoxicity is not a prominent trial signal; ocular (keratopathy/blurred vision, ~50% any-grade across pooled trials) and GI/fatigue toxicities dominate. AKI is case-level and chiefly volume-mediated (GI toxicity). Renal-specific incidence is not quantified.Mild PomalidomideTumor lysis typically within days of starting therapy in high-burden disease.Pomalidomide pharmacokinetics are not substantially altered by renal impairment - it is extensively metabolized hepatically, with <5% renal excretion of unchanged drug - and pooled trial data show a similar safety profile and dosing across renal-function subgroups, including dialysis. The principal renal hazard is tumor lysis syndrome (TLS), which is uncommon and case-level in myeloma.Mild ThalidomideTumor lysis within days of initiation in high-burden disease; bradycardia over weeks of dosing.Thalidomide is not a direct nephrotoxin; the principal renal hazard is tumor lysis syndrome, which is uncommon in myeloma and reported at the case level. Sinus bradycardia is a recognized dose-related non-renal effect that, with the drug’s sedative/hypotensive properties, can compound prerenal physiology. Venous thromboembolism is the other dominant class toxicity.Mild NilotinibVascular events accrue over months to years of therapy.Nilotinib carries a recognized risk of arterial occlusive events and metabolic effects (dysglycemia, hyperlipidemia), but direct renal toxicity is limited; in comparative CML cohorts nilotinib generally did not cause significant eGFR decline relative to imatinib. Any kidney impact is largely mediated through vascular disease and perfusion rather than intrinsic nephrotoxicity.Mild OlaparibCreatinine rise within weeks of starting therapy; reverses on discontinuation.Olaparib commonly causes a reversible, dose-dependent rise in serum creatinine. In a 66-patient study, median creatinine rose ~14% (and creatinine-based eGFR fell ~13%) on treatment, while cystatin C and cystatin C-based eGFR were unchanged - indicating no true GFR decline. Thrombotic microangiopathy is a rare, case-level event for the PARP-inhibitor class.Mild RucaparibWithin the first weeks of treatment.Early reversible serum-creatinine elevation is common and partly drug-specific: rucaparib is a recognized inhibitor of renal cation transporters, and a pooled meta-analysis found markedly higher odds of creatinine rise vs placebo across the class, but grade >=3 renal events were rare (<1%).Mild TalazoparibThe pharmacokinetic effect is present from initiation in patients with reduced renal function; cytopenias accrue over the first cycles.Renal clearance is a major elimination route (~two-thirds of dose), so exposure rises with declining renal function: dedicated PK studies show higher AUC and more myelosuppression in moderate-severe impairment, mandating dose reduction. Class-level mild creatinine elevation may occur; severe intrinsic nephrotoxicity is uncommon.Mild BinimetinibWeeks into therapy.Clinically significant intrinsic nephrotoxicity is uncommon; modest creatinine elevations occur and CK elevation is a recognized MEK-class effect. In COLUMBUS, grade 3-4 blood-CK increase occurred in ~7% with encorafenib plus binimetinib; rare rhabdomyolysis can secondarily threaten the kidney.Mild SelumetinibVariable; adverse events can appear after prolonged dosing.Long-term pediatric trial data (SPRINT, up to ~5 years) show a manageable safety profile with no new safety signals; significant nephrotoxicity is not prominent, with creatinine changes generally modest. CK elevation is a recognized MEK-class laboratory effect.Mild SotorasibWhen AKI occurs, it is acute during the first weeks–months of therapy, typically tracking GI toxicity.Clinically significant nephrotoxicity is uncommon and case-level in humans (the dominant on-target/off-tumor toxicity is hepatotoxicity). Proximal tubular toxicity is prominent in rats via a reactive mercapturate-pathway metabolite. Human renal incidence is not well quantified.Mild AdagrasibEarly — within the first weeks of therapy.Renal effects are usually mild: a creatinine rise (partly from inhibited tubular creatinine secretion) plus prerenal AKI from GI losses. The KRYSTAL-1 registrational program reported renal-related lab changes; a dedicated PubMed-indexed pseudo-AKI/albuminuria study for adagrasib does not yet exist, so the precise incidence is unquantified.Mild BelzutifanAnemia and hypoxia develop over the first weeks of therapy.Anemia is the most common on-target adverse event (the leading grade 3 event in pivotal trials) and hypoxia is frequent. Direct nephrotoxicity is not a prominent or well-quantified signal; renal function changes mostly reflect underlying RCC/nephrectomy status.Mild ZanubrutinibTumor lysis early (first cycle); otherwise renal function typically stable.Direct nephrotoxicity is not a prominent signal. Cardiovascular toxicity (atrial fibrillation, hypertension) is lower than ibrutinib in pooled and head-to-head (ASPEN, ALPINE) analyses. Tumor lysis can occur with rapid cytoreduction of bulky CLL/lymphoma; renal events are case-level and not well quantified.Mild DaratumumabTumor lysis (if any) early; renal benefit accrues over treatment as paraprotein/free light chains fall.Direct nephrotoxicity is uncommon; tumor lysis can occur with high tumor burden. Crucially, daratumumab-based regimens IMPROVE outcomes (PFS, and OS in relapsed disease) in myeloma patients with renal insufficiency, including dialysis-dependent patients, and can drive renal recovery.Mild IsatuximabTumor lysis (if any) early; renal benefit over the treatment course.Direct nephrotoxicity is uncommon; tumor lysis can occur with high tumor burden. In the ICARIA-MM and IKEMA renal-impairment subgroups, isatuximab regimens remained effective and produced renal responses; real-world data show inferior PFS with eGFR <60 but persistent benefit.Mild IrinotecanAcute cholinergic diarrhea within hours of infusion; delayed diarrhea after ~24 hours and over subsequent days, with AKI following cumulative volume loss.Direct nephrotoxicity is not a recognized feature; the principal renal risk is prerenal AKI from severe early (cholinergic) and delayed diarrhea with volume depletion. Severe (grade 3-4) irinotecan toxicity, mostly diarrhea/neutropenia, occurs in roughly a quarter to a third of patients and is enriched in UGT1A1 poor metabolizers. AKI incidence specifically attributable to irinotecan is not well quantified.Mild TopotecanExposure-related hematologic toxicity manifests across treatment cycles; prerenal AKI follows intercurrent volume loss.Topotecan is substantially renally cleared, so impaired kidney function increases drug exposure and myelosuppression risk; pharmacokinetic studies show topotecan AUC rises ~109% (moderate) and ~174% (severe impairment), supporting dose reduction. Direct topotecan-induced nephrotoxicity is not a recognized signal, and drug-attributable AKI incidence is not well quantified.Mild EtoposideTLS typically within hours to a few days of starting cytotoxic therapy in sensitive tumors; exposure-related myelosuppression accrues over cycles.Etoposide is renally cleared (~30-40% as unchanged drug, so dose-adjust in renal impairment) and is a frequent component of regimens for bulky, rapidly proliferating tumors that can trigger tumor lysis syndrome (TLS). Direct etoposide nephrotoxicity is not a recognized signal; TLS-related AKI risk depends on tumor burden and tumor type rather than a per-drug rate.Mild PaclitaxelInfusion reactions occur during or shortly after administration (typically first/second exposure); any prerenal AKI follows the hemodynamic instability.Paclitaxel has low direct nephrotoxicity. Hypersensitivity/infusion reactions - historically attributed to the Cremophor EL (polyoxyethylated castor oil) vehicle via complement activation, with newer evidence for IgE-mediated reactions - and associated fluid shifts can transiently compromise renal perfusion, but structural kidney injury is uncommon and not well quantified.Mild DocetaxelFluid retention develops cumulatively (often after several cycles / cumulative dose); hypersensitivity reactions occur during infusion.Docetaxel has low direct renal toxicity. Its characteristic fluid-retention syndrome (peripheral edema, effusions, weight gain) reflects increased capillary permeability rather than tubular injury; AKI directly attributable to docetaxel is uncommon and not well quantified, and the drug has been used successfully even in kidney-transplant recipients.Mild CabazitaxelAKI follows intercurrent gastrointestinal or infectious complications during treatment cycles.Cabazitaxel has low direct nephrotoxicity; AKI is uncommon and, when it occurs, is usually mediated by gastrointestinal losses (diarrhea, occurring in a substantial minority), neutropenic sepsis, or hemodynamic instability rather than direct tubular toxicity. In real-world safety data, grade >=3 diarrhea and febrile neutropenia each occur in roughly 5% of patients. A drug-specific renal AKI rate is not well established.Mild EribulinExposure-related toxicity accrues across cycles; prerenal AKI follows volume loss.Eribulin is not a recognized direct nephrotoxin. Pharmacokinetic study shows reduced clearance and ~1.5-fold higher exposure with moderate-to-severe renal impairment, supporting dose adjustment; any AKI is generally prerenal and not well quantified.Mild AsparaginaseLinked to intercurrent complications during induction/intensification therapy.Direct asparaginase nephrotoxicity is uncommon; classic toxicities are hypersensitivity (up to ~30% with E. coli-derived enzyme), pancreatitis, hepatic dysfunction, hyperammonemia, and coagulopathy/thrombosis. When AKI occurs it is typically secondary to pancreatitis, hemodynamic instability, or thrombotic complications rather than a direct tubular toxin, and is not well quantified.Mild PirtobrutinibEarly after initiation in high-burden disease (first cycle); TLS is usually a single early event.Direct nephrotoxicity is not characteristic. Tumor lysis syndrome is an identified risk when rapidly debulking high-burden lymphoid malignancy; renal-specific incidence is low and not well quantified. BTK inhibitors as a class are also associated with hypertension and bleeding/atrial fibrillation (non-renal).Mild ZanidatamabVariable; tied to GI/volume events during treatment cycles rather than a fixed latency.No drug-specific nephrotoxicity rate is established. In HERIZON-BTC-01 the dominant toxicities were diarrhea and infusion reactions; any AKI is expected to be largely prerenal/volume-mediated (diarrhea, reduced intake) or related to the underlying biliary obstruction, rather than a direct tubular effect.Mild TovorafenibNot well defined; any change emerges during ongoing therapy rather than at a fixed onset.No established intrinsic nephrotoxicity. In FIREFLY-1 the prominent toxicities were hair-color change, rash, anemia and fatigue; renal events were not a defining signal, and any creatinine elevation is described qualitatively rather than as a quantified AKI rate.Mild ImetelstatAny tumor-lysis-type risk would be early after initiation; otherwise no defined renal onset.No established direct nephrotoxicity. In IMerge the dominant toxicities were cytopenias (thrombocytopenia, neutropenia); renal injury was not a defining adverse event. Tumor-lysis-type metabolic risk is theoretical and most relevant with high disease burden, not a quantified rate in lower-risk MDS.Mild MirdametinibNot well defined; edema and any creatinine changes evolve during ongoing therapy.No established intrinsic nephrotoxicity. Across MEK-inhibitor experience (including the NF106 mirdametinib trial) the characteristic toxicities are rash, edema, diarrhea and CK elevation; renal events are not a defining signal and any creatinine change is qualitative rather than a quantified AKI rate.Mild RuxolitinibAny tumor-lysis risk is early (first cycles); withdrawal syndrome occurs within days of stopping; otherwise no defined renal onset.No established intrinsic nephrotoxicity. Over a decade of safety data show cytopenias and infections (including opportunistic) as the dominant toxicities. Renal concerns are indirect: rare tumor-lysis at treatment initiation in bulky myelofibrosis, the need for dose reduction in renal impairment, and a recognized ruxolitinib-withdrawal syndrome on abrupt cessation — rather than direct tubular injury.Mild MomelotinibAny tumor-lysis risk is early; otherwise no defined renal onset.No established intrinsic nephrotoxicity. As a JAK-inhibitor-class agent, dominant toxicities are hematologic (thrombocytopenia), infection, and (notably) peripheral neuropathy; renal injury is not a defining signal. Tumor-lysis at initiation and prerenal factors are the indirect renal considerations.Mild QuizartinibHighest around induction (tumor lysis, neutropenic sepsis); ongoing electrolyte monitoring through therapy.No established intrinsic nephrotoxicity. In QuANTUM-First the dominant grade 3-4 events were febrile neutropenia, hypokalemia and pneumonia; QT prolongation is a hallmark. Renal injury is indirect — tumor-lysis at induction, sepsis/cytopenia-related prerenal/ischemic AKI, and electrolyte derangements. AKI is common in AML induction generally (KDIGO-defined rates are high in cohort studies), but a quizartinib-attributable rate is not defined.Mild CasdatifanNot established; class anemia/hypoxia effects emerge during ongoing therapy.Renal-specific data are not established. By analogy to the first-in-class HIF-2α inhibitor belzutifan, expected on-target effects include anemia (belzutifan: ~27-90% across trials) and hypoxia, plus possible fluid retention/edema; these are class effects rather than direct nephron injury. No casdatifan-specific renal incidence is published.Mild Ibritumomab tiuxetanTLS is early (hours to days); cytopenias are delayed (weeks).Direct renal radiation toxicity is essentially negligible — yttrium-90 is a pure beta-emitter and the kidney is not a critical organ on dosimetry; the dose-limiting toxicity is delayed myelosuppression. The renal hazard is indirect tumor lysis syndrome (TLS) in bulky/high-burden disease; a drug-specific TLS rate is not well quantified and is rare.Mild Radium-223 dichlorideGI effects early; hematologic nadir over weeks. No characteristic renal onset.Direct renal toxicity is minimal and not a recognized feature; renal labs are typically unaffected. The dominant toxicities are gastrointestinal (diarrhea, nausea) and myelosuppression. Any AKI is essentially always attributable to other causes (obstruction, dehydration, concomitant nephrotoxins).Mild CladribineTumor-lysis AKI is acute (24-72 h); high-dose sensorimotor neuropathy is delayed (weeks).At standard hairy-cell-leukemia doses cladribine is renally quiet; clinically significant nephrotoxicity is uncommon and dose-related, worst at historical high investigational doses. The dominant renal hazard is tumor lysis syndrome in bulky/leukocytotic disease, reported at the case level rather than as a population incidence.Mild PegaspargaseToxicities cluster during induction/first doses; AKI is usually reversible with treatment of the underlying thrombosis or pancreatitis.Direct nephrotoxicity is not recognized; AKI is indirect and uncommon. For context, symptomatic thrombosis occurs in ~1.5-5% of children and is higher (~5-10%+) in adults/adolescents-and-young-adults, and clinical pancreatitis in ~5-10%. A drug-specific AKI incidence is not quantified (it is a downstream complication, not a tracked endpoint).Mild MobocertinibDiarrhea early (within the first week); AKI follows. Prerenal AKI is typically reversible with early volume repletion and diarrhea control.Diarrhea is near-universal: any-grade ~83% (up to ~93% pooled), grade >=3 ~20-21%, with median onset ~5 days. AKI is predominantly prerenal; a real-world cohort reported grade >=3 renal failure in ~6%. Precise drug-attributable AKI and QT rates are not robustly quantified beyond class warnings.Mild MitoxantroneTumor lysis hours to days post-infusion.Direct nephrotoxicity is low and not quantified; the principal renal risk is tumor lysis syndrome when used in bulky/rapidly proliferating hematologic malignancies. Benign blue-green discoloration of urine/sclera is expected (the anthracenedione chromophore), not injury.Mild IdarubicinHours to days after starting induction.Minimal intrinsic nephrotoxicity; the dominant renal threat is tumor lysis syndrome in acute leukemia. In one inv(16) AML induction cohort tumor-lysis AKI occurred in ~6%, with some requiring hemodialysis; a general drug-specific AKI rate is not quantified.Mild EstramustineEdema/VTE within weeks to the first 2 months.Renal injury is hemodynamic/prerenal rather than a quantified direct rate. The dominant safety liability is venous (and arterial/cardiovascular) thromboembolism with fluid retention/edema; in randomized data the majority of cardiovascular complications occurred within the first year.Mild IdelalisibDiarrhea/colitis often delayed — a median of several months into therapy; transaminitis is typically earlier (first weeks).Severe immune-mediated diarrhea/colitis occurs in roughly 14-20% (grade 3+) and transaminitis is common; secondary prerenal AKI from volume loss is not separately quantified. Direct renal lesions are rare.Mild DuvelisibDiarrhea/colitis often after several months; rash and transaminitis can appear earlier.Diarrhea/colitis is common (any-grade ~50%, grade 3+ roughly 15-20% in DUO); the resulting volume-depletion prerenal AKI is not separately tabulated. Direct nephrotoxicity is uncommon.Mild GlasdegibMuscle spasms and QT changes within early cycles; prerenal/electrolyte issues track intercurrent illness and intake.Muscle spasms, QT prolongation, cytopenias, edema, nausea and mucositis are the labeled toxicities; the FDA notes a use limitation in severe renal impairment (a renal-impairment trial was a post-marketing requirement). Direct nephrotoxicity is not a defined signal, and AKI is largely secondary (dehydration, sepsis, tumor lysis).Mild MidostaurinTumor lysis early in induction; prerenal/electrolyte issues track intercurrent illness; edema across treatment.Given with intensive chemotherapy, the dominant toxicities are cytopenias, nausea/vomiting, mucositis, edema and QT changes; tumor lysis is a treatment-related (largely chemotherapy-driven) hazard. A midostaurin-specific direct nephrotoxicity is not described, and AKI is multifactorial (volume loss, sepsis, TLS).Mild AvapritinibEdema and cognitive effects across treatment; GI-related prerenal changes track intercurrent toxicity.Edema (periorbital/peripheral) is very common, and intracranial hemorrhage and cognitive/CNS effects are notable labeled toxicities; nausea/diarrhea contribute to volume shifts. Direct nephrotoxicity is not a defined signal and AKI, when it occurs, is secondary (fluid shifts, GI losses, mastocytosis mediator release).Mild PexidartinibHepatotoxicity can occur early (often within the first 1-2 months) or later; secondary renal effects track the severity of the systemic/hepatic illness.The defining toxicity is serious, sometimes cholestatic, hepatotoxicity (boxed warning, REMS program); hair-color change, fatigue and GI effects are common. Direct nephrotoxicity is not a recognized signal, and renal effects are secondary (dehydration during illness, hepatorenal physiology in severe liver injury).Mild TazemetostatTumor lysis, if it occurs, is early after response; prerenal effects track intercurrent GI toxicity.Tazemetostat is generally well tolerated with low direct organ toxicity; the noted boxed risk is secondary T-cell lymphoma/myeloid malignancy. Tumor lysis is an uncommon, treatment-related concern in responding lymphoma. A discrete AKI rate is not quantified and direct nephrotoxicity is low.Mild TafasitamabInfusion reactions early (first cycle); tumor lysis early in responders.Infusion-related reactions occur early (largely first cycle) and cytopenias are common; tumor lysis is an uncommon, treatment-related concern in responding lymphoma. Direct nephrotoxicity is not a recognized signal and AKI is secondary.Mild MogamulizumabInfusion reactions early; rash over weeks; tumor lysis early in responders.Drug rash and infusion reactions are characteristic; tumor lysis occurred in roughly 2-3% in some series. AKI is rare and largely secondary to tumor lysis or volume shifts; a discrete AKI incidence is not well quantified.Mild Tisotumab vedotinNot characterized for renal events; any prerenal AKI would track volume depletion (days).Direct nephrotoxicity is not a recognized signal. In the pivotal innovaTV 301 and innovaTV 204 trials the defining toxicities were ocular (conjunctivitis, dry eye, keratitis), bleeding/epistaxis and peripheral neuropathy; a quantified renal-injury rate was not reported. Renal involvement, if any, is indirect/case-level.Mild ElacestrantNot characterized for renal events; any prerenal AKI would track GI toxicity.Direct nephrotoxicity is not a recognized feature. In the pivotal phase 3 EMERALD trial the dominant toxicities were nausea, fatigue, vomiting and decreased appetite; a discrete renal-injury rate was not reported. Any renal involvement is best understood as indirect/case-level (e.g., volume depletion from GI toxicity).Mild

Also associated

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Agents that cause prerenal / hemodynamic aki as a secondary pattern alongside a different signature lesion.

CisplatinAcute — creatinine peaks ~day 4–7; magnesium wasting can persist for months.AKI in ~20–35% per cycle (classic teaching: ~1 in 3). Hypomagnesemia in 40–100%.Severe VenetoclaxAcute — typically within hours to days of each dose-escalation step during the ramp-up.Tumor lysis syndrome is the defining renal risk, concentrated during the weekly dose ramp-up. Early-development unmitigated dosing caused fatal TLS; with the mandated 5-week ramp-up and risk-stratified prophylaxis, clinical TLS fell to ~3% (e.g., grade 3/4 laboratory TLS 3.1% in MURANO), and structured protocols can drive it near zero.Severe Moxetumomab pasudotoxCycle-related: CLS within the first days of a cycle; HUS often during/after cycles 2-3.Boxed warning for capillary-leak syndrome (CLS) and hemolytic-uremic syndrome (HUS)/TMA. In the pivotal phase 3 trial HUS occurred in ~7.5% and CLS in ~5%; reviews cite roughly 9% each. Fatal CLS has been reported (in a pediatric ALL case).Severe Tegafur-uracil (UFT)Variable; TMA/HUS typically emerges after weeks to months of cumulative exposure.Direct renal injury from UFT is rare and largely class-level. Fluoropyrimidine-associated thrombotic microangiopathy / hemolytic-uremic syndrome is a rare, mostly case-report-level event, frequently in combination regimens (e.g., with mitomycin C). No reliable drug-specific incidence rate is established.Severe Enfortumab vedotinVariable; tubular/prerenal AKI tracks with intercurrent GI toxicity, and hyperglycemic-AKI events are often reported after the second or third dose.Renal injury is not a prominent or well-quantified trial signal, and EV is notably usable across the spectrum of renal function (including eGFR <30). When AKI occurs it spans prerenal (GI-toxicity dehydration), hyperglycemia/DKA-associated, and case-level tubular (ATN) patterns. In EV-201 cohort 2, three of 89 patients had treatment-related deaths within 30 days (one each from AKI, metabolic acidosis and multi-organ dysfunction), underscoring a real but uncommon acute renal-metabolic risk.Moderate PonatinibHypertension can emerge early; arterial occlusive events accrue over months, with dose reduction mitigating risk.Ponatinib carries a black-box warning for arterial occlusive and thrombotic events and has the highest cardiovascular event rate among CML TKIs (about 41% in one comparative cohort; cumulative arterial occlusive events ~31% over 5 years in the PACE trial). Treatment-emergent hypertension is common; renal injury is largely a downstream consequence of hypertension and vascular disease.Moderate SelpercatinibHypertension within the first weeks to months; creatinine changes early.Hypertension is among the most common adverse events in LIBRETTO-001 (a frequent grade >=3 event), and a reversible serum-creatinine increase is also recognized. A single-center hereditary-MTC series found hypertension in ~26% on selective RET inhibitors.Moderate IbrutinibHypertension develops over weeks–months (can be early); tumor lysis is early (first cycle); glomerular/interstitial lesions are case-level over weeks to months.New or worsened hypertension is common (~26% in a real-world CLL cohort comparing it with acalabrutinib; higher with longer follow-up). AKI at CLL presentation and with tumor lysis is well described. Drug-attributable AKI from interstitial nephritis or glomerular endotheliosis is case-level.Moderate RituximabAcute — typically within hours to a few days of the first infusion.Clinical tumor lysis with the first cycle is uncommon with modern prophylaxis (~1% clinical TLS in a real-world fractionated-rituximab aggressive-B-NHL series), but risk rises sharply with bulky disease, high LDH and Burkitt histology.Moderate ObinutuzumabAcute — within hours to days of the first (split) dose.Carries a notably high tumor-lysis risk in CLL — among the highest of the anti-CD20 agents — particularly with the first (split) infusion in high-burden disease (the CLL11 trial enrolled patients with CrCl 30–69 mL/min and saw higher infusion reactions/TLS). Direct nephrotoxicity is case-level.Moderate SelinexorEarly — within the first cycle/few weeks; front-loaded.Hyponatremia is common and dose-limiting. In STORM it occurred in ~22% of patients and was predominantly grade >=3 — the most common grade >=3 non-hematologic toxicity. In BOSTON any-grade hyponatremia affected roughly a third of the selinexor arm (grade 3-4 ~8-9%); in SADAL grade 3-4 hyponatremia occurred in ~8%.Moderate Dactinomycin (actinomycin D)TLS within hours to days of initiating effective chemotherapy; VOD typically within the first weeks of treatment.Direct nephrotoxicity is not an established feature of dactinomycin. The clinically relevant renal risk is tumor lysis syndrome (TLS) when used against bulky, chemosensitive pediatric tumors; precise incidence attributable to dactinomycin alone is not quantified, as it is given in multi-agent regimens.Moderate DoxifluridineVariable; class-level TMA typically after prolonged cumulative exposure.No drug-specific nephrotoxicity incidence is established. Renal risk is inferred at the fluoropyrimidine-class level (rare TMA/HUS); direct doxifluridine renal injury reports are sparse.Moderate Carmofur (HCFU)Variable; class-level TMA after cumulative exposure.No established drug-specific renal incidence. Renal risk is class-level (rare fluoropyrimidine TMA/HUS). Carmofur's characteristic serious toxicity is leukoencephalopathy, not nephrotoxicity.Moderate MitotaneAdrenal insufficiency and its electrolyte/volume consequences develop over weeks of therapy as adrenolytic effect accrues; cisplatin-associated AKI in EDP-M is acute, within days of chemotherapy cycles.Intrinsic mitotane nephrotoxicity is not characteristically quantified. Clinically important renal events are indirect (adrenal insufficiency-related electrolyte/volume disturbance) or attributable to co-administered cisplatin in EDP-M; incidence not reliably enumerated for mitotane alone.Moderate 5-FluorouracilTMA often delayed (weeks to months); prerenal effects acute with GI toxicity.Intrinsic nephrotoxicity is low; the recognized vascular renal complication is thrombotic microangiopathy/hemolytic-uremic syndrome, classically with mitomycin C, with 5-FU as a frequent co-agent. In TTP/HUS series the most common antecedent chemotherapy is mitomycin C plus 5-FU.Mild BosutinibDevelops over months of therapy; time to grade 3b eGFR is shortest with later-line use.Long-term bosutinib is associated with a gradual, generally reversible decline in eGFR. In a long-term analysis, renal adverse events occurred in roughly 6-13% across lines of therapy, and a notable fraction reached grade 3b or worse eGFR (<45 mL/min/1.73 m2), with many recovering on follow-up; the pattern resembles the eGFR decline seen with imatinib.Mild CrizotinibCreatinine rise often within weeks and reverses on discontinuation; cysts develop and grow over months.Crizotinib commonly causes a reversible rise in serum creatinine and is distinctively associated with the development and progression of complex renal cysts. Peripheral edema and electrolyte disturbances (including hypophosphatemia and hypokalemia) are reported. In real-world ALK-inhibitor cohorts, creatinine-based AKI/CKD events are frequent but mostly mild and reversible; frank kidney failure is uncommon.Mild AlectinibCreatinine rise within weeks of starting therapy (mean eGFR declines over the first 90 days); reverses after discontinuation.Alectinib is associated with creatinine elevations that are usually benign. In a real-world ALK-inhibitor cohort, alectinib was the most-used agent (91 of 191 treatments) and creatinine-based AKI/CKD events were frequent (10% AKI within 90 days, 14% CKD at 1 year) but mostly mild and reversible, with few treatment changes attributed to AKI and none requiring dialysis.Mild BrigatinibCreatinine changes typically emerge within weeks and tend to reverse on discontinuation.As an ALK inhibitor, brigatinib is associated with creatinine elevations that are generally benign. In a real-world ALK-inhibitor cohort, creatinine-based AKI/CKD events occurred but were mostly mild and reversible across agents including brigatinib; class reviews note elevated creatinine, occasional edema, and rare electrolyte disturbances. A distinct, early-onset pulmonary event (within the first week) is a separate non-renal class concern.Mild LorlatinibMetabolic effects and edema appear within weeks of starting therapy.Lorlatinib is characterized by prominent metabolic effects - hypercholesterolemia and hypertriglyceridemia occur in the majority of patients (the leading grade 3/4 toxicity in the CROWN trial) - plus peripheral edema. Direct renal toxicity is limited and, like other ALK inhibitors, creatinine elevations are generally mild and reversible. Renal effects are not well quantified specifically for lorlatinib.Mild CeritinibPrerenal AKI can occur whenever GI toxicity causes significant fluid loss, often early in therapy.Ceritinib causes frequent gastrointestinal toxicity (nausea, vomiting, diarrhea in the majority of patients), which can lead to volume depletion and prerenal AKI; as an ALK inhibitor it can also produce generally mild, reversible creatinine elevations. The prerenal AKI risk is largely a downstream effect of GI losses and is not precisely quantified.Mild NiraparibHypertension typically emerges within the first weeks to months of therapy.Hypertension is a characteristic, class-distinctive adverse event: a FAERS pharmacovigilance plus RCT meta-analysis estimated ~16.9% any-grade hypertension, disproportionately higher with niraparib than other PARP inhibitors. A small reversible serum-creatinine rise is also seen across the class (pooled OR for creatinine elevation ~5 vs placebo), but grade >=3 nephrotoxicity is <1%.Mild PralsetinibHypertension within the first weeks to months.Hypertension is among the more common grade >=3 treatment-related adverse events (about 11% grade >=3 in the ARROW NSCLC cohort); clinically significant intrinsic AKI is rare.Mild CapmatinibEarly — within the first cycles.Increased blood creatinine is a common treatment-related adverse event (~21% in GEOMETRY mono-1; higher in some Asian subsets), and peripheral edema is the single most common adverse event (~47%); most events are grade 1-2 and reversible.Mild TepotinibEarly — within the first cycles.Blood creatinine increase and peripheral edema are the main treatment-related adverse events in the VISION program; both are common and generally mild to moderate and manageable, rarely leading to discontinuation.Mild AcalabrutinibTumor lysis early (first cycle); hypertension over weeks–months.Hypertension occurs but is less frequent than with ibrutinib (~15% vs ~26% in a matched real-world cohort; ELEVATE-RR confirmed lower hypertension and atrial fibrillation head-to-head). One single-center cardio-oncology cohort still found ~49% new/worsened hypertension by sensitive criteria, so it is not negligible. Tumor lysis is the principal route to AKI; direct nephrotoxicity is case-level.Mild AbemaciclibEarly — within the first weeks (median onset ~3 weeks), stable thereafter, reversible on discontinuation.A benign serum-creatinine rise occurs in roughly one-fifth of patients (~20% in a single-center series; a class effect across CDK4/6 inhibitors), almost always grade 1–2 and without true GFR loss. In a dedicated CDK4/6-inhibitor cohort, ~73% of creatinine rises were confirmed pseudo-AKI by cystatin C–based eGFR.Mild PalbociclibOften within the first 1-2 cycles (median onset roughly 30-35 days); creatinine plateaus and reverses after dose hold or discontinuation.A reversible rise in serum creatinine is common, but true structural kidney injury is uncommon. CDK4/6 inhibitors block the proximal-tubule transporters that secrete creatinine, producing a 'pseudo-AKI' picture. In a single-centre cohort, 17.5% of palbociclib-treated patients met creatinine-based AKI criteria, and when cystatin C was available, 73% of those events proved to be pseudo-AKI rather than a true GFR decline.Mild RibociclibFirst cycles (median onset roughly 6 weeks for the creatinine signal); reversible on hold or discontinuation. QTc effects are dose- and concentration-dependent and seen early.Like other CDK4/6 inhibitors, ribociclib produces a frequent, reversible creatinine rise via inhibition of tubular creatinine secretion (pseudo-AKI ~14% in a class-effect analysis); clinically meaningful structural AKI is uncommon. A retrospective cohort of palbociclib/ribociclib patients found a >=20% creatinine-clearance decline in about 23%.Mild RepotrectinibEarly after initiation; stable thereafter (a step change, not a progressive decline).An apparent rise in serum creatinine is described that often reflects inhibition of tubular creatinine secretion rather than a true fall in GFR (pseudo-AKI). Genuine intrinsic nephrotoxicity is not a characteristic feature and is not well quantified. This pattern is increasingly recognized across kinase inhibitors (e.g., ALK TKIs, where most creatinine-based eGFR changes do not require treatment change).Mild SunvozertinibElectrolyte changes can appear within the first weeks to months of therapy; hypomagnesemia risk rises with treatment duration.No established AKI rate. As with the EGFR-inhibitor class, the renal-relevant signal is electrolyte disturbance — particularly hypomagnesemia (renal Mg wasting) and diarrhea-driven losses, with a hyponatremia/SIADH-like pattern possible — rather than structural nephron injury. WU-KONG6 reported diarrhea and skin/EGFR-pathway toxicities as dominant; renal-specific events are not quantified.Mild TucatinibWithin the first weeks of therapy; plateaus and is fully reversible within days of discontinuation.A mild creatinine increase is common and expected, but it reflects inhibition of tubular creatinine secretion (a 'pseudo-AKI' artifact) rather than true GFR loss. Dedicated transporter/PK studies show tucatinib inhibits renal OCT2 and MATE1/MATE2-K without changing iohexol-measured GFR.Mild EntrectinibWithin the first weeks of therapy; reversible on discontinuation.A mild blood-creatinine increase is recognized and is attributed to reduced tubular creatinine secretion rather than true GFR decline (a pseudo-AKI pattern). It is typically modest, early and reversible; a meaningful structural-AKI rate is not established.Mild ZongertinibNot established; any creatinine change would emerge during early therapy by class analogy.Renal data are not established. In Beamion LUNG-1 the toxicity profile was mainly low-grade (diarrhea, rash) with no drug-related interstitial lung disease; renal events were not a defining signal. By analogy to other HER2/TKI agents (tucatinib), any creatinine rise is most likely a benign tubular-secretion (pseudo-AKI) effect rather than true injury.Mild BleomycinPharmacokinetic accumulation is immediate in renal impairment; clinical (pulmonary) toxicity is cumulative over weeks to months.Bleomycin is not a classic direct nephrotoxin; the actionable renal issue is exposure-driven. Roughly two-thirds of a dose is cleared renally, and terminal half-life rises exponentially once creatinine clearance falls below ~25-35 mL/min, magnifying systemic (especially pulmonary) toxicity. Direct kidney injury is not well quantified and is largely confounded by co-administered cisplatin.Mild VinflunineElectrolyte/prerenal effects can appear within days of a cycle; PK accumulation in renal impairment is immediate but mitigated by protocol dose reduction.No strong direct nephrotoxic signal. Vinflunine is given to renally impaired, cisplatin-unfit patients with a defined dose-reduction schema, and tolerability in renal impairment mirrors that of patients with normal renal function once dose-banded. SIADH/hyponatremia is a class-level vinca-alkaloid effect rather than a quantified vinflunine-specific rate.Mild TeniposideNo characteristic renal onset; pharmacokinetic exposure effects are immediate but clinically modest.Minimal direct nephrotoxicity. Teniposide is highly protein-bound with low renal clearance (only ~10-25% of a dose is recovered in urine versus a larger fraction for etoposide), so the kidney is a minor elimination route and direct renal injury is not a characteristic toxicity. Renal relevance is pharmacokinetic/exposure-related and not quantified as a discrete nephrotoxicity rate.Mild OctreotideNot applicable for intrinsic injury; pharmacokinetic accumulation in renal failure is gradual.No characteristic intrinsic nephrotoxicity; octreotide is generally considered kidney-neutral. Renal events are rare, indirect, and not reliably quantified. Mild electrolyte disturbances are uncommon and not well enumerated.Mild LanreotideNot applicable for intrinsic injury; exposure rises gradually in renal impairment.No characteristic intrinsic nephrotoxicity; lanreotide is generally kidney-neutral. Renal adverse events are not a defining feature and are not reliably quantified; mild electrolyte effects are uncommon.Mild DarolutamideNot applicable for intrinsic injury; exposure differences in renal impairment are present from initiation and steady state (reached in ~2 days).No characteristic intrinsic nephrotoxicity. In ARAMIS, rates of adverse events including hypertension were similar to placebo. Renal-relevant findings are pharmacokinetic (increased exposure in severe renal impairment); intrinsic renal injury incidence not meaningfully quantified.Mild

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