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.
24signature agents
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.
Moderate· 16Mild· 8
Agents’ overall reversibility
Partially reversible· 2Variable· 5Reversible· 17
Agents’ onset window
How soon each agent’s kidney toxicity typically appears — a whole-drug tempo, not specific to this lesion.
Hyperacute (<24 h)· 1Acute (days)· 1Subacute (weeks)· 16Delayed (weeks–months)· 2Variable· 4
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