The Injury Atlas See it on the nephron Does the kidney recover? Cross-drug outcomesRepresentative per-agent hypertension incidence where a published figure is citable — open an agent's name for its profile and cited source, or hover its dot for the source inline. Agents without a citable figure are omitted; a tier without a number is not the same as a low number.
HTN
Hypertension
Raised blood pressure — archetypally on-target loss of endothelial nitric oxide from VEGF-pathway blockade, studied as a pharmacodynamic marker of drug exposure. Other agents raise it too: vascular effects of BCR-ABL, BTK and RET inhibitors and of copanlisib; abiraterone's mineralocorticoid excess; androgen suppression or blockade.
38agents
Where it strikes
Vasculature / Endothelium
Glomerular & peritubular capillaries
Glomerulus
Filtration barrier (podocytes + endothelium)
Agents’ overall severity
Each agent’s whole-drug severity grade, not the severity of this lesion specifically — an agent whose signature injury is elsewhere can still be graded severe here.
Severe· 2Moderate· 24Mild· 12
Agents’ overall reversibility
Partially reversible· 4Variable· 11Reversible· 23
Agents’ onset window
How soon each agent’s kidney toxicity typically appears — a whole-drug tempo, not specific to this lesion.
Hyperacute (<24 h)· 2Acute (days)· 2Subacute (weeks)· 20Delayed (weeks–months)· 5Variable· 9
Real-world reporting for this lesion
FAERS across all lesions →Agents with a disproportionate FAERS reporting signal for hypertension (reporting odds ratio with a 95% CI lower bound above 1) — a spontaneous-reporting signal, not incidence or proven causation. FAERS carries reporting and indication biases and has no denominator.
25Corroborated
Documented in the atlas profile and carrying a FAERS signal — the strongest claim the atlas makes.
6Documented, FAERS-silent
Documented in a profile with no reporting signal. Mostly expected: naming this lesion on a report can require a biopsy, and silence is not evidence against the literature.
14Not attributable
A real reporting signal that is not evidence for this drug-lesion pair: no MedDRA term names it, the naming subset asked alone came back flat, or the 2026-08 review attributed the reporting to the population, co-therapy, or class-level literature.
15Reported by name
The terms that name this lesion are disproportionate, but no profile documents it for that agent. Most are echoed by a sibling agent in the same class. Leads for review, never lesions the atlas claims.
5-FluorouracilAbirateroneArsenic trioxideAsciminibAtezolizumabAxitinibBevacizumabBicalutamideBrigatinibBusulfanCabozantinibCarfilzomibEnzalutamideErlotinibEverolimusFruquintinibIbandronateIbrutinibInterleukin-2 (high-dose)IrinotecanIsatuximabLanreotideLenvatinibLorlatinibMethotrexate (high-dose)NaxitamabNilotinibNintedanibNiraparibOctreotideOxaliplatinPaclitaxelPamidronatePazopanibPembrolizumabPenpulimabPexidartinibPonatinibPralsetinibRamucirumabRegorafenibRibociclibRipretinibRituximabSorafenibSunitinibTamoxifenTemsirolimusTrastuzumab emtansine (T-DM1)Tretinoin (ATRA)VandetanibVimseltinibZiv-afliberceptZoledronic acid
54 agents with a significant HTN reporting signal.
Management approach
Full framework →An expected effect (on-target with VEGF-pathway agents) — treat the blood pressure and usually continue the drug.
Drug-level levers
- Continue the agent if blood pressure is controlled (with VEGF-pathway agents, hypertension correlates with on-target activity).
- Hold for severe/refractory hypertension or a hypertensive emergency; resume once controlled.
- Dose-reduce for grade 3 hypertension not controlled on therapy.
Pharmacologic toolkit
- Antihypertensives — An ACE inhibitor/ARB (also helps any proteinuria) and/or a dihydropyridine calcium-channel blocker are common first choices; avoid non-dihydropyridine CCBs with CYP3A4-metabolized TKIs.
When to biopsy
Not indicated for isolated hypertension.
Monitoring
- · Home and clinic blood pressure, especially in the first cycles
- · Urine protein
Educational use only. Educational synthesis of the published literature — not a treatment protocol, dosing guide, or medical advice. Regimens and agents shown are illustrative of what the literature describes; verify against current guidelines (ASON / KDIGO / ASCO / NCCN) and individualize to the patient. Using this site creates no clinician–patient relationship.
What the guidelines say
All guidelines →Society and consensus recommendations that speak to hypertension.
Each recommendation below is this atlas's faithful summary of the source, not a quotation from it — follow the PubMed link for the wording the society published. Summaries may be superseded; consult the current full text and individualize to the patient.
KDIGOManagement of Blood Pressure in Patients With Chronic Kidney Disease Not Receiving Dialysis: Synopsis of the 2021 KDIGO Clinical Practice GuidelineAnn Intern Med 2021 · PMID 34152826Recommends standardized office BP measurement and a target systolic BP <120 mm Hg for most CKD patients, with RAAS inhibitors first-line when albuminuria is present — the BP-management basis for anti-VEGF/TKI-induced hypertension and proteinuria.ESC2022 ESC Guidelines on cardio-oncology developed in collaboration with the European Hematology Association (EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS)Eur Heart J 2022 · PMID 36017568For VEGF/VEGFR inhibitors, perform baseline cardiovascular risk assessment, monitor blood pressure (weekly during the first cycle, then regularly) and treat to a target <140/90 mmHg with ACE inhibitors/ARBs and dihydropyridine calcium-channel blockers; manage VEGFi-associated hypertension and proteinuria with interruption/dose modification when severe.ESCEuropean Society of Cardiology quality indicators for the prevention and management of cancer therapy-related cardiovascular toxicity in cancer treatmentEur Heart J Qual Care Clin Outcomes 2022 · PMID 36316010Adherence quality indicators require documented baseline cardiovascular risk assessment and structured monitoring of cardiovascular complications (including hypertension) during cancer therapy such as VEGF-pathway inhibitors.UK Consensus PanelUsing bevacizumab to treat metastatic cancer: UK consensus guidelinesBr J Hosp Med (Lond) 2010 · PMID 21135762Assess and monitor blood pressure and proteinuria during bevacizumab therapy; treat emergent hypertension to standard targets and interrupt/discontinue the drug for uncontrolled hypertension, nephrotic-range proteinuria or other severe vascular toxicity.
Cited incidence across agents
Where the literature gives a representative hypertension figure, the agents ranked highest first. Hover a dot for its cited note.
Offending agents
Signature offenders
24Agents for which hypertension is the defining renal lesion.
VEGFR Tyrosine Kinase InhibitorsHypertension within days–weeks; proteinuria over weeks–months.Hypertension ~17–50%; proteinuria 8–73% across agents (the cited review's ranges; it reports no single pooled proteinuria rate).ModerateRamucirumabWithin the first one to two cycles (weeks).Hypertension and proteinuria are common class effects; nephrotic syndrome is a less frequent but reported event, sometimes after only 1-2 doses and typically accompanied by hypertension.ModerateZiv-afliberceptWithin weeks to a few months of therapy.Hypertension and proteinuria are common class effects; in the registrational VELOUR trial, grade 3-4 hypertension and proteinuria were more frequent with aflibercept plus FOLFIRI than with FOLFIRI alone. Nephrotic-range proteinuria and renal thrombotic microangiopathy are documented, including with the ophthalmic formulation, indicating a direct VEGF-trap mechanism. A meta-analysis of 15 trials (4,451 patients) put the summary all-grade hypertension incidence at 42.4%.ModerateLenvatinibWithin the first weeks of therapy (hypertension early; proteinuria over weeks).Hypertension is among the most common adverse events; in the SELECT thyroid-cancer trial hypertension occurred in about 68% (grade >=3 ~42%) and proteinuria in roughly 31%. In KEYNOTE-B61 (lenvatinib plus pembrolizumab) grade 3-4 hypertension occurred in ~23%. Proteinuria is a frequent renal AE with lenvatinib.ModerateCabozantinibWithin weeks of starting therapy.Hypertension and proteinuria are common; in pivotal RCC trials (e.g., METEOR, CABOSUN) hypertension was among the most frequent adverse events with grade >=3 rates around 15-28%. Cabozantinib is one of the TKIs most often associated with proteinuria, with case reports of nephrotic syndrome. Reported rate: grade >=3 hypertension in 15% — Adults with advanced/metastatic clear-cell renal cell carcinoma previously treated with >=1 VEGFR tyrosine-kinase… (Choueiri 2016, PMID 27279544).ModerateRegorafenibWithin the first weeks of therapy.Hypertension is common and frequently grade 3. Pooling 3,813 patients across the cardiovascular-event literature puts all-grade hypertension at 36.8% (95% CI 29.8-43.8%) and high-grade at 9.9% (7.4-12.4%), against controls a relative risk of 4.10 all-grade and 5.82 high-grade. An earlier, smaller meta-analysis of 1,069 patients from five trials (750 on regorafenib) ran higher at 44.4% (30.8-59.0%) all-grade and 12.5% (5.2-27.1%) high-grade, with wider intervals; the CORRECT trial itself reported about 28% (grade 3 ~7%). Proteinuria also occurs as a VEGF-pathway class effect, but is not separately quantified for this agent.ModerateVandetanibWithin the first weeks of therapy.In the pivotal phase III ZETA trial, any-grade hypertension occurred in about 32% of vandetanib-treated patients versus 5% with placebo; proteinuria occurs as an antiangiogenic class effect.ModerateTivozanibWithin the first weeks of therapy.In the phase III TIVO-3 trial, hypertension was the most common grade 3-4 treatment-related adverse event, occurring in about 20% of tivozanib-treated patients; proteinuria occurs as a VEGFR class effect but is comparatively less prominent.ModeratePonatinibHypertension 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.ModerateSelpercatinibHypertension 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. Reported rate: grade >=3 hypertension in 19.7% — 837 patients with RET-activated advanced/metastatic solid tumors receiving selpercatinib monotherapy (20 mg QD to 240… (Raez 2024, PMID 39471424).ModerateIbrutinibHypertension 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.ModerateFruquintinibWithin weeks of starting therapy (hypertension often earliest).Hypertension and proteinuria are characteristic VEGFR-TKI class effects; in the FRESCO-2 safety analysis hypertension was the most frequent treatment-related adverse event of special interest, occurring in 28.9% of fruquintinib-treated patients all-grade and 10.7% at grade ≥3, with proteinuria also reported (1.3% of patients required a dose reduction for it). Renal-specific TMA is rare but described across the VEGF-inhibitor class.ModerateCopanlisibAcute and infusion-bound — within hours of each dose, resolving within ~24 h.On monotherapy (CHRONOS-1), transient on-infusion-day hypertension occurs in 29.6% all-grade (grade 3 23.9%), and hyperglycemia in 50.0% all-grade (grade 3 33.1%, grade 4 7.0%); with rituximab (CHRONOS-3) the grade 3-4 rates are higher — hypertension 40% and hyperglycemia 56%. Both peak within hours of the infusion and largely resolve by the next day. Sustained renal injury is uncommon.ModerateSunitinibHypertension typically appears early (within the first treatment cycle/weeks); proteinuria develops over weeks to months, and biopsy-proven TMA in case series presented on average around 2 years (range ~7-36 months) into therapy.In a systematic review/meta-analysis of 4,999 patients across 13 trials, all-grade hypertension occurred in ~21.6% and high-grade hypertension in ~6.8% of sunitinib-treated patients, with a significantly increased risk of renal dysfunction versus controls (RR ~1.36); risk varied by tumor type and dosing schedule. Proteinuria is common but less consistently quantified, and severe glomerular lesions (thrombotic microangiopathy, nephrotic-range proteinuria) are reported mainly at the case-series level. Reported figures are class-consistent with other VEGF-pathway inhibitors.ModerateAxitinibHypertension typically emerges early, frequently within days to the first few weeks of starting therapy. Proteinuria tends to develop over weeks of continued exposure and is dose-related. Severe glomerular lesions (TMA, nephrotic syndrome) are usually later and more variable in timing.Hypertension is the dominant and best-quantified renal-relevant signal. In the randomized phase III AXIS trial, treatment-emergent all-causality hypertension occurred in 40.4% of axitinib-treated patients (vs 29.0% with sorafenib), with grade 3 hypertension in 15.3% and grade 4 in 0.3%. A real-world VEGFR-TKI cohort in metastatic RCC similarly found hypertension to be the single most common anti-angiogenesis-related adverse event (about 48.6% in TKI-naive patients across the class). Proteinuria is the next most common renal effect; across the VEGF-inhibitor class mild/asymptomatic proteinuria is reported in roughly 21% to 63% of patients, with heavy (nephrotic-range) proteinuria in up to about 6.5% of RCC patients, and axitinib-specific proteinuria rates have been higher in some populations (e.g., Japanese cohorts). Thrombotic microangiopathy and other glomerular lesions (FSGS-like injury, podocytopathy, hyaline occlusive glomerular microangiopathy) are reported at the severe, biopsy-level end of the spectrum but are not precisely quantified for axitinib specifically.ModerateSorafenibHypertension typically emerges within the first few weeks of treatment; proteinuria develops over weeks to months of continued exposure. Nephrotic syndrome and thrombotic microangiopathy are variable, generally appearing after weeks to months but occasionally sooner.Hypertension is the dominant renal-vascular signal: a systematic review/meta-analysis of 9 trials (4,599 patients) reported an all-grade incidence of 23.4% (95% CI 16.0-32.9%) and high-grade (grade 3-4) incidence of 5.7% (Wu 2008), and a larger meta-analysis of 93 trials (20,494 patients) gave concordant figures of 21.3% all-grade and 5.9% high-grade, with higher rates in renal-cell and thyroid cancer and rising incidence with longer treatment duration (Yang 2017). Proteinuria is a VEGF-pathway class effect: across VEGF-signaling inhibitors mild/asymptomatic proteinuria is reported in roughly 21-63% and heavy (nephrotic-range) proteinuria in up to about 6.5% of renal-cell carcinoma patients (Izzedine 2009); drug-specific quantitative proteinuria data for sorafenib alone are more limited. Nephrotic-range proteinuria and renal-limited thrombotic microangiopathy are documented but uncommon.ModerateNintedanibOver months of therapy in reported cases.Renal effects are uncommon; proteinuria and rare biopsy-proven renal thrombotic microangiopathy have been reported, consistent with VEGF-pathway inhibition. Renal incidence is not well quantified (case-level), and much of the published renal experience comes from pulmonary-fibrosis rather than oncology cohorts.MildNiraparibHypertension typically emerges within the first weeks to months of therapy.Hypertension is a 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%.MildPralsetinibHypertension within the first weeks to months.Hypertension is among the more common grade >=3 treatment-related adverse events (about 11% in the ARROW NSCLC cohort); clinically significant intrinsic AKI is rare.MildAcalabrutinibTumor 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. Tumor lysis is the principal route to AKI; direct nephrotoxicity is case-level.MildEnzalutamideHypertension emerges over weeks to months of therapy.Hypertension is the dominant renovascular signal. A 2024 JAMA Oncology meta-analysis of androgen-receptor signaling inhibitors found a markedly increased risk of grade ≥3 hypertension (relative risk ~2.25); an earlier meta-analysis showed the same for enzalutamide specifically. Direct intrinsic kidney injury is uncommon; rare hyponatremia appears mainly in combination regimens. Reported rate: hypertension in 11.9% — Pooled analysis of 7 randomized clinical trials of enzalutamide in prostate cancer, 7347 patients (Zhu 2019, PMID 31557062).MildLeuprolideMonths to years (metabolic/cardiovascular and skeletal).No characteristic direct nephrotoxicity. Androgen-deprivation therapy is associated with metabolic syndrome, insulin resistance, dyslipidemia and increased cardiovascular disease, which raise long-term renovascular risk; a systematic review/meta-analysis confirms excess cardiovascular events with androgen-pathway therapy, and preclinical models show GnRH-agonist-induced metabolic syndrome and atherosclerosis. Reported rate: hypertension in 14.6% — 137 subjects with advanced prostate cancer indicated for androgen ablation, receiving leuprolide mesylate subcutaneous… (Shore 2020, PMID 30941562).MildAsciminibHypertension can emerge across treatment; pancreatitis often early.Hypertension and pancreatitis (with amylase/lipase elevations) are recognized toxicities; thrombocytopenia/neutropenia are common. In first-line use (ASC4FIRST), hypertension occurred more frequently with asciminib than comparator TKIs — all-grade 10.5%, grade >=3 5.5%. Asciminib has a cleaner overall profile than prior TKIs, and direct nephrotoxicity is not a defined signal — renal effects are largely hypertension-mediated.MildRipretinibHypertension can develop within early cycles and persist.Hypertension is the recognized renal-relevant toxicity: in the INVICTUS phase 3 trial (n=85), grade 3-4 hypertension occurred in 3 patients (4%) — the second most common grade 3-4 treatment-related event after lipase increase — alongside alopecia, palmar-plantar erythrodysesthesia, fatigue and myalgia. Direct nephrotoxicity is not a defined signal; renal effects are hypertension-mediated.Mild
Also associated
14Agents that cause hypertension as a secondary pattern alongside a different signature lesion.
GemcitabineDelayed — months of cumulative exposure.Estimates span three orders of magnitude by ascertainment. The only figure with a real denominator is the manufacturer safety-database review: 12 cases against 78,800 patient exposures, a crude 0.015% (range 0.008–0.078%). The product characteristics give 0.01%. Against that, a single center reported 2.7% — four of its five cases on nab-paclitaxel/gemcitabine, where a pharmacokinetic interaction is suspected. Historically high mortality: of 23 cases with reported outcome in the literature tally, 11 died within a few weeks, death directly attributed to HUS in two.SevereCarfilzomibVariable — frequently early (first cycles), but TMA can also appear later, sometimes after a treatment break and re-escalation.Renal complications are common and a recognized class concern: in a 114-patient real-world cohort, ~17% had carfilzomib-attributable renal events (TMA ~5%, albuminuria >1 g/day ~6%, otherwise-unexplained grade >=3 AKI ~5%), occurring mostly early and unpredictably. On the prospective CARDAMON trial 8 patients experienced TMA (6 of 8 hypertensive at presentation, 7 of 8 with AKI); after a protocol amendment adding aggressive hypertension management, carfilzomib step-up dosing at the start of maintenance and dexamethasone premedication, the rate fell from 4.2 to 1.6 events per 1,000 patient-cycles with no further maintenance events. Pharmacovigilance (FAERS) shows carfilzomib carries by far the strongest TMA signal among proteasome inhibitors.SevereBevacizumabWeeks to months; dose-dependent.In a 72-trial meta-analysis (21,902 bevacizumab cases vs 20,608 controls), all-grade proteinuria was 18% (95% CI 11.7–26.6%) and high-grade 2.4% (1.8–3.2%); all-grade hypertension was 25.3% (21.5–29.5%). Relative to controls the risk ratios were 3.37 for all-grade and 5.49 for high-grade proteinuria. A separate 16-trial meta-analysis put high-grade proteinuria at 2.2% and nephrotic syndrome at RR 7.78, with renal cell carcinoma carrying the highest cumulative incidence (10.2%).ModerateTrastuzumab emtansine (T-DM1)Variable; reported after initiation, over weeks to months of therapy.Renal toxicity is rare and case-level. FDA adverse-event analyses flagged renal events with trastuzumab-based therapy, and biopsy-proven cases (collapsing focal segmental glomerulosclerosis; TMA-like microvascular injury) have been reported. Incidence is not quantified.ModerateAbirateroneWithin the first weeks of therapy; recurs if glucocorticoid coverage is inadequate or interrupted.Mineralocorticoid-excess effects are common: in COU-AA-301 fluid retention, hypertension and hypokalemia were all more frequent than with placebo-prednisone. Severe (grade 3–4) hypokalemia, occasionally to 1.7–2.1 mEq/L, is reported even with concomitant prednisone. Meta-analysis confirms an increased relative risk of hypertension. A single-center retrospective cohort of 79 patients reported renal events in 63.3% of abiraterone-treated patients — AKI in 30.4%, half of whom progressed to chronic kidney disease (Pujol-Pujol 2025). Reported rate: grade >=3 hypokalemia in 12% — 597 men with newly diagnosed high-risk metastatic castration-sensitive prostate cancer randomized to abiraterone… (Fizazi 2019, PMID 30987939).ModerateDinutuximabInfusion-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.ModerateIvonescimabVEGF-pathway proteinuria/hypertension typically within the first weeks-to-cycles; checkpoint-inhibitor AIN usually delayed, often 8-16 weeks (range days to >1 year).Renal-specific data are immature for this newly approved agent; no dedicated nephrotoxicity series exists. In registrational trials, grade >=3 VEGF-related adverse events (a class category encompassing proteinuria, hypertension, and hemorrhage) occurred in roughly 3% of patients (HARMONi-A: 5/161, 3.1%) — against 4/161 (2.5%) in the chemotherapy-alone arm of the same trial, a one-patient difference that is not separable from background. Grade >=3 immune-related adverse events (the checkpoint-inhibitor category that includes AIN) occurred in ~6-9% across trials, though kidney-specific irAE rates were not separately tabulated. Clinically significant AKI was uncommon.ModeratePazopanibProteinuria and hypertension typically emerge within weeks to a few months of starting therapy; TMA case reports describe onset within the first weeks to ~2 months.Proteinuria is common but usually low-grade, and reported any-grade rates span roughly 15% to 80% depending on the population and how proteinuria was ascertained. In a pooled secondary analysis of two phase III trials of pazopanib or sunitinib in metastatic RCC (n=1392, Sorich 2016), any-grade proteinuria occurred in 15.0% and grade 3/4 in 3.7% — a trial adverse-event figure covering both agents, not a pazopanib-specific rate. In a single-center first-line mRCC cohort, proteinuria was reported in 80% of the pazopanib-treated patients (Land 2016), most grade 1-2 and managed with continued monitoring at the same dose. Assume proteinuria is the expectation rather than the exception on pazopanib and schedule urine protein monitoring accordingly. Hypertension is one of the most frequent class effects, with severe (grade 3-4) hypertension a recognized class risk. Thrombotic microangiopathy is rare and largely case-level; biopsy-proven renal-limited and systemic TMA/TTP-like presentations have been reported.ModerateTrametinibVariable. Pyrexia-associated AKI tends to appear early, tracking the febrile syndrome that often begins within the first weeks to few months of dabrafenib/trametinib. The rare biopsy-proven interstitial nephritis and glomerulonephritis cases have presented later — generally around 2 to 6 months into therapy.The renal signal from trametinib itself is modest. In an FDA Adverse Event Reporting System (FAERS) disproportionality analysis, trametinib carried a statistically significant but low acute-kidney-injury reporting odds ratio of 1.32 (95% CI 1.11-1.56) — well below vemurafenib's — and at mean steady-state plasma concentrations trametinib produced no measurable cytotoxicity in cultured proximal-tubular, glomerular endothelial or glomerular epithelial cells (Sanagawa, Anticancer Drugs 2021). Most of the quantified AKI burden comes from combination use: in a single-center retrospective cohort of 199 patients receiving dabrafenib/trametinib, 42 (21%) met an AKI definition (1.5x creatinine rise) within 12 months, and roughly a quarter of those episodes (about 5% of the whole cohort) occurred during a treatment-induced pyrexia syndrome (Seethapathy, Nephrol Dial Transplant 2022). Biopsy-proven interstitial nephritis and glomerular lesions are rare and reported only as individual cases; kidney impairment was rarely reported in the pivotal monotherapy trial.ModerateNaxitamabAcute and infusion-locked — hypotension, hypertension, and the rest of the infusion-reaction complex begin within minutes to a few hours of starting the infusion and are most pronounced during the early cycles; significant infusion-related events become rare after the first few treatment cycles.Frank acute kidney injury is not a systematically reported endpoint for naxitamab and no validated AKI incidence figure exists; the renal-relevant risk is hemodynamic rather than a direct nephrotoxic lesion. The closest quantitative anchor comes from the pivotal single-arm phase 2 Trial 201 (NCT03363373), where naxitamab-related grade 3 adverse events were dominated by hypotension in 58% and pain in 54% of patients — the infusion-reaction physiology that can transiently compromise renal perfusion. Pharmacovigilance corroborates the signal: in an FDA Adverse Event Reporting System analysis of anti-GD2 antibodies, hypotension, hypertension, urticaria, and capillary-leakage syndrome were among the most frequent and strongest naxitamab-associated signals. Because these figures describe hemodynamic events (not measured creatinine-defined AKI), the numeric AKI rate is left unquantified.ModerateBrigatinibCreatinine 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.MildOlverembatinibVariable; proteinuria and hypertension, when they occur with multi-kinase TKIs, typically emerge over weeks to months of therapy.Renal-specific data are sparse. In the Chinese phase 1/2 program (n=165) proteinuria was among the common treatment-related adverse events, though grade and exact rate were not separately quantified; clinically significant AKI was not a prominent signal. Direct nephrotoxicity appears low overall.MildIobenguane I-131Biphasic — modest, often transient creatinine changes within weeks of a therapeutic dose; the characteristic radiation nephropathy is delayed, typically appearing 6-12 months or later after cumulative renal irradiation, sometimes years out.Reported renal toxicity is uncommon and usually low-grade. In a dosimetry-guided high-activity 131I-MIBG cohort, 3 of 14 patients (21%) had transient grade 1 renal toxicity (Maric 2023, small single-center series using conventional 131I-MIBG). In the registrational high-specific-activity trial (Azedra, n=68 dosed), renal failure was not among the most common treatment-emergent events — nausea, myelosuppression and fatigue dominated — and clinically significant (grade >=3) nephrotoxicity was rare. The kidney concern is driven less by acute events than by the delayed, cumulative absorbed radiation dose, so headline incidence figures come from small cohorts and should be read as low-grade signal rather than a robust rate.MildRelacorilantElectrolyte shifts, if they develop, track cumulative cortisol/MR activation over the treatment course rather than a single dose, and are typically detected on routine chemistry monitoring during cycles rather than as an acute event.No discrete drug-specific incidence of relacorilant acute kidney injury is published; in the registrational phase 3 ROSELLA trial (Olawaiye, Lancet 2025; n=381) the adverse-event profile with relacorilant plus nab-paclitaxel was similar to nab-paclitaxel alone after adjusting for exposure, and no new safety signals were reported. The renal-relevant concern is electrolyte, specifically hypokalemia, inferred from the pharmacology of GR antagonism rather than from a large observed AKI signal. The precedent is mifepristone, a non-selective GR/PR antagonist, where blocking cortisol's own receptor allowed cortisol to activate the mineralocorticoid receptor and produce clinically significant, spironolactone-responsive hypokalemia (Chu, J Clin Endocrinol Metab 2001). Relacorilant is a selective GR antagonist designed to reduce this and other off-target effects, so the hypokalemia risk is expected to be milder — a monitoring point, not a dominant toxicity.Mild