What kind of kidney injury does Venetoclax cause?

Crystal / Obstructive Nephropathy — Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals. Other reported patterns: Acute Tubular Necrosis, Prerenal / Hemodynamic AKI, Electrolyte Disturbance.

Is kidney injury from Venetoclax reversible?

Partially reversible. Typical onset: Acute — typically within hours to days of each dose-escalation step during the ramp-up..

How should kidney function be monitored during Venetoclax therapy?

TLS panel (uric acid, potassium, phosphate, calcium, creatinine) pre-dose, 6–8 h and 24 h after each ramp-up step; Strict intake/output and volume status during escalation; Continue intensified monitoring at each new dose level until 400 mg tolerated.

How can kidney injury from Venetoclax be prevented?

Mandatory weekly dose ramp-up (e.g., 20→50→100→200→400 mg over 5 weeks) Risk-stratified TLS prophylaxis by tumor burden: oral hydration (IV considered at medium and given at high burden) plus allopurinol at every tier, started 2–3 days before the first dose; at high burden, consider rasburicase if baseline uric acid is elevated Laboratory monitoring at and after each escalation (pre-dose, 6–8 h, 24 h) Inpatient admission with hydration for high-risk patients; consider pre-debulking (e.g., ibrutinib) to lower the TLS-risk category

Who is at higher risk of kidney injury from Venetoclax?

High tumor burden / bulky lymphadenopathy (≥5 cm) or high absolute lymphocyte count; High baseline LDH; Pre-existing CKD (reduced urate/phosphate clearance); Volume depletion; Inadequate ramp-up or prophylaxis.

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Printable monograph

BCL-2 inhibitor

Venetoclax

Venclexta · Veneto

BCL-2 inhibitor · approved 2016 · 12 citations · FAERS AKI reporting ROR 1.20 (95% CI 1.10–1.31, 534 AKI reports)

Up to date· through 2025

Deeply sourced9/9 · 8 signals

Met: 12 citations
Met: 12+ references
Met: Accrued over 10+ years (span: 17y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2025
Met: Real-world FAERS signal

Describes how this page is sourced, not how dangerous the drug is. Thinly sourced means fewer of the sourcing signals are met — not that the agent is kidney-safe. A rule-based summary, not a formal certainty appraisal.

A potent apoptosis inducer whose deep, rapid kill can crash the kidneys with tumor lysis — the mandated ramp-up exists for the kidney.

SevereBCL-2 inhibitor

CLL/SLLAcute myeloid leukemia (combinations)

§01

Signature kidney injury

Signature lesion

Crystal / Obstructive Nephropathy

Representative grade ≥3 incidence3.1%

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, grade 3/4 laboratory TLS fell to 3.1% (MURANO), with clinical TLS rarer still, and structured protocols can drive it near zero.Source: Seymour et al., NEJM 2018 (MURANO; 3.1% grade 3/4 lab TLS)

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Acute AKI within hours to days of each ramp-up dose-escalation step.

Distilled from: “Acute — typically within hours to days of each dose-escalation step during the ramp-up.”

Long-term outlook & thresholds

Renal recoveryVariable

The renal outcome is the tumor-lysis story. Under the mandated ramp-up and risk-stratified prophylaxis the lysis is contained: in the prospective real-world VeRVe cohort (239 CLL patients treated per label), clinical TLS occurred in 2.1% and none of those events was fatal or resulted in renal failure. An established oligoanuric TLS with crystal-driven AKI is a different trajectory — recovery then turns on how quickly the metabolic derangement is controlled, which is why the profile's management threshold for starting dialysis is deliberately low.PMID 38421404 (opens PubMed in a new tab)

Outcome marker.: In venetoclax/hypomethylating-agent AML induction the stakes of AKI are prognostic, not just renal: among 130 older patients, 38% developed AKI during the first cycle, its occurrence was associated with laboratory TLS, and it carried higher 30- and 60-day mortality and independently inferior overall survival (HR 1.86).PMID 41008838 (opens PubMed in a new tab)

Two different questions. Quick facts lists this agent's Reversibility as "Partially reversible" — this atlas's reading of the injury across its cited literature. The badge above is narrower: it classes only what the single outcome study cited here reported, which is why the two can differ without either being wrong.

Early-detection biomarkers

Laboratory tumor-lysis panel (phosphate, calcium, potassium, uric acid) — Laboratory TLS — the metabolic event that drives this agent's crystal-nephropathy AKI. The only agent-specific evidence tying the panel to a renal endpoint: among 130 older AML patients on venetoclax with a hypomethylating agent, 49 (38%) developed AKI during treatment and its occurrence was associated with laboratory TLS. Which analytes actually move has shifted under modern prophylaxis — in a 113-patient real-world AML series every TLS event was laboratory-only, driven by hyperphosphataemia (10) and hypocalcaemia (9) rather than urate (1) (Abernathy, PMID 35946111). The counterweight belongs here too: with the standard 5-week CLL ramp-up the yield is very low (laboratory TLS 1.8%, no clinical TLS, no antihyperuricaemic therapy in 55 patients), and those authors argue for reducing rather than intensifying monitoring in low-risk CLL (Huang, PMID 39556786).PMID 41008838 (opens PubMed in a new tab)
Absolute lymphocyte count 24 h after the dose — Rate of tumour-cell kill — how fast intracellular solute is being released. The only genuinely kinetic early-warning signal in this drug's literature: in 33 CLL patients undergoing rapid dose escalation after a BTK inhibitor, a fall in absolute lymphocyte count of 10 × 10³/µL from pre-dose to 24 h post-dose was associated with increased TLS risk (hazard ratio 1.32, P = .02) after controlling for dose level, and the authors conclude the rapidity of the ALC drop helps predict TLS. Hypothesis-generating only — n = 33, single centre, and a non-label rapid escalation in a proliferative post-BTKi population, never validated. In that cohort all five clinical TLS events were renal injury.PMID 33031541 (opens PubMed in a new tab)

Long-term outcome and threshold data distilled from the agent's cited literature — educational, not a substitute for the primary sources.

Recovery across agents

§02

Renal toxicities, ranked

This agent's kidney lesions ordered by prominence — the #1 signature lesion first, then secondary and rare patterns. Cited incidence is shown where a citable figure exists; otherwise the tier stands qualitatively.

Crystal / Obstructive Nephropathy#1 · Signature2.1%PMID 38421404 (opens PubMed in a new tab)
Clinical tumor-lysis syndrome (uric-acid load with AKI) in 2.1% and laboratory TLS in 6.3% of a prospective real-world CLL cohort (n=239) using the mandated venetoclax dose ramp-up (VeRVe).
Electrolyte DisturbanceSecondary6.3%PMID 38421404 (opens PubMed in a new tab)
Laboratory TLS — hyperkalemia / hyperphosphatemia / hyperuricemia — in 6.3% of the VeRVe real-world CLL cohort on venetoclax with ramp-up.
Acute Tubular NecrosisSecondaryqualitative — no citable incidence
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.
Prerenal / Hemodynamic AKIRarequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

3.1%grade ≥3 incidence

SeveritySevere

ReversibilityPartially reversible

Evidence12 citations

Nephron map

Vasculature / Endothelium

Proximal Tubule

Distal Tubule / Collecting Duct

Tubular LumenThe urine flow path

Crystal / Obstructive Nephropathy

Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals.

§03

Kidney injury

Deep diveTumor lysis syndromeEffective therapy can kill a large, fast-dividing cancer so abruptly that the cells spill their contents into the blood — potassium, phosphate, and a flood of purines that becomes uric acid — and the two crystals that result, urate and calcium-phosphate, clog and poison the tubules: a metabolic emergency that is largely preventable with hydration, rasburicase, and, for venetoclax, a deliberately slow dose ramp-up.

Mechanism of kidney injury

Rapid, synchronous apoptosis releases intracellular potassium, phosphate, and nucleic acids; nucleic acids are catabolized to uric acid. Uric acid and calcium-phosphate crystallize within distal tubules causing intratubular obstruction and crystal nephropathy, compounded by urate-driven afferent vasoconstriction and ischemic ATN — classic tumor-lysis AKI. The risk is exquisitely dose-step dependent, which is why the escalation schedule and prophylaxis are mandated.

Clinical presentation

Hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia and rising creatinine during ramp-up; oliguric AKI, cardiac arrhythmia and (historically) death in severe cases. Onset clusters within 24–72 h of each dose escalation step.

Management

Aggressive IV hydration, rasburicase for hyperuricemia, correct hyperkalemia/hyperphosphatemia/hypocalcemia, and hold venetoclax. Initiate renal replacement therapy early for refractory hyperkalemia, severe hyperphosphatemia/uremia or oliguria — the threshold is lower than usual because cell breakdown is ongoing.Lesion-level management framework

Risk factors

High tumor burden / bulky lymphadenopathy (≥5 cm) or high absolute lymphocyte count
High baseline LDH
Pre-existing CKD (reduced urate/phosphate clearance)
Volume depletion
Inadequate ramp-up or prophylaxis

Prevention

Mandatory weekly dose ramp-up (e.g., 20→50→100→200→400 mg over 5 weeks)
Risk-stratified TLS prophylaxis by tumor burden: oral hydration (IV considered at medium and given at high burden) plus allopurinol at every tier, started 2–3 days before the first dose; at high burden, consider rasburicase if baseline uric acid is elevated
Laboratory monitoring at and after each escalation (pre-dose, 6–8 h, 24 h)
Inpatient admission with hydration for high-risk patients; consider pre-debulking (e.g., ibrutinib) to lower the TLS-risk category

Anticancer mechanism· how it treats cancer

Selective BH3-mimetic inhibitor of the anti-apoptotic protein BCL-2; it displaces pro-apoptotic effectors (BIM/BAX/BAK) to restore mitochondrial apoptosis in malignant cells, producing deep, rapid remissions in CLL/SLL and (with azacitidine/low-dose cytarabine) in AML.

Note · TLS risk is dose-ramp dependent and largely mitigated by the mandated escalation and prophylaxis schedule — the ramp-up protocol is, in effect, a nephroprotective regimen. Pre-treatment debulking shifts patients to a lower TLS-risk category.

§04

Clinical depth

Renal dose adjustment

No dose adjustment for mild, moderate OR severe renal impairment (CrCl >=15 mL/min) — venetoclax is hepatically (CYP3A) cleared and does not accumulate renally, and the label makes that recommendation across all three bands rather than stopping at moderate. The renal number that changes management is a tumor-lysis threshold, not a clearance one: CrCl <80 mL/min calls for more intensive TLS prophylaxis and monitoring when starting treatment, because reduced clearance of urate and phosphate magnifies TLS risk. Below CrCl 15 and on dialysis the label makes no recommendation and data are limited.

Dialyzability & ESKD dosing

Not meaningfully dialyzed — highly protein-bound (>99%), hepatically (CYP3A) metabolized small molecule with negligible renal excretion. Dialysis is used to treat TLS metabolic complications, not to remove the drug.

Differential diagnosis

Tumor-lysis AKI (hyperuricemia + hyperphosphatemia + hyperkalemia + hypocalcemia, urate/phosphate crystals) vs prerenal azotemia of hydration deficit vs contrast or other nephrotoxins. The temporal lock to ramp-up steps is the giveaway.

Monitoring

TLS panel (uric acid, potassium, phosphate, calcium, creatinine) pre-dose, 6–8 h and 24 h after each ramp-up step
Strict intake/output and volume status during escalation
Continue intensified monitoring at each new dose level until 400 mg tolerated

Key trials & series

Roberts et al., NEJM 2015 — pivotal R/R CLL phase 1 (clinical TLS including a death drove the mandated ramp-up)
Seymour et al., NEJM 2018 — MURANO (venetoclax-rituximab; 3.1% grade 3/4 laboratory TLS)
Al-Sawaf et al., Lancet Oncol 2020 — CLL14 (fixed-duration venetoclax-obinutuzumab frontline)

Clinical pearls

The 5-week ramp-up and prophylaxis schedule is fundamentally a kidney-protection protocol — never skip dose escalation or TLS labs.
TLS risk scales with tumor bulk and baseline renal function; debulking (e.g., with ibrutinib) can downgrade the risk category before venetoclax.
In venetoclax TLS, start renal replacement therapy at a lower threshold than usual because ongoing apoptosis keeps releasing potassium and phosphate.

Beyond the kidney — non-renal toxicities· 2 organ systems

Class-level context for the major non-renal toxicities of the BCL-2 inhibitor class.

Hematologic

Cytopenias, thrombosis, TMA

Neutropenia

Immune / Infusion

CRS, infusion reactions, irAEs, anaphylaxis

Tumor-lysis-driven systemic effects

§05

References

9 primary references — trials, cohorts, mechanism, and reviews. Single-patient case reports are listed separately below, graded by strength. Citation metadata via PubMed / NLM.

Evidence accrual

9 references · 2008–2025 · 4 since 2023

Primary (non–case-report) references per year — a proxy for how actively the agent's renal literature is accruing. Recent years are highlighted. Reflects curation depth, not a systematic bibliometric count.

Case reports — ranked by strength· 3

Single-patient and small-series reports, graded by evidentiary strength — A Strong (biopsy-proven plus a series and/or positive rechallenge), B Moderate, and C Limited (a single clinically-diagnosed case). Strongest first. Grades are inferred automatically from each report's abstract and journal — a heuristic ranking aid, not a formal quality appraisal.

CaseC · Limited[Complete and Prolonged Remission after a Single Dose of Venetocalx in a Patient with Acute Myeloid Leukemia (AML) Who Experienced Tumor Lysis Syndrome (TLS): Case Report].Porges T et al. · Harefuah 2025 · PMID 41445209Venetoclax induced severe clinical tumor lysis syndrome requiring dialysis in an AML patient, a manifestation of acute crystal/obstructive nephropathy and AKI.CaseC · LimitedTumor Lysis Syndrome with Venetoclax/Carfilzomib/Dexamethasone for Relapsed/Refractory Multiple Myeloma: A Case Report.Fankhauser R et al. · Reports (MDPI) 2024 · PMID 40757710Venetoclax-based therapy precipitated tumor lysis syndrome with subsequent renal failure in a multiple myeloma patient, illustrating uric-acid/crystal-mediated obstructive nephropathy.CaseC · LimitedTumor Lysis Syndrome Caused by Unrecognized Richter's Transformation of Chronic Lymphocytic Leukemia: Treatment With Venetoclax for Suspected Disease Progression.Chango Azanza JJ et al. · Cureus 2020 · PMID 32550064Venetoclax triggered clinical tumor lysis syndrome requiring hospitalization in transformed CLL, reflecting the drug's signature uric-acid crystal/obstructive renal injury.

FDA label — boxed warning & renal dosing· renal impairment

Quoted verbatim from this agent's current FDA label (May 2026) — not paraphrased or interpreted. Full label on DailyMed .

Renal impairment — from the label

Due to the increased risk of TLS, patients with reduced renal function (CLcr <80 mL/min, calculated by Cockcroft-Gault formula) require more intensive prophylaxis and monitoring to reduce the risk of TLS when initiating treatment with VENCLEXTA [see Dosage and Administration ( 2.1 , 2.2 , 2.3 , 2.4 ) and Warnings and Precautions ( 5.1 )] . No dose adjustment is recommended for patients with mild, moderate or severe renal impairment (CLcr ≥15 mL/min) [see Clinical Pharmacology ( 12.3 )] .

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 61,220 of them for this agent. Nobody counts the patients who were fine, so none of these numbers is an incidence, a risk, or a rate: they describe what gets reported, shaped by a drug's fame, its indication, and who was watching. How these numbers work.

Reporting odds ratio (ROR) — is kidney injury named in this agent's reports more often than in every other drug's? Above 1 means yes, disproportionately.
Renal phenotypes — the same question asked separately for each kind of kidney injury, so the ratios differ from the overall one and from each other.
Outcomes — a share of this agent's own reports, not of patients: how many were filed as involving a death or a hospitalization. Not a case-fatality rate.

FAERS reported renal phenotypes· 1 signal

Only significant signals appear (95% CI lower bound above 1) — a phenotype missing here was tested and did not reach significance, except Prerenal / Hemodynamic AKI, Pseudo-AKI, Renal Cysts, Chronic Interstitial Nephropathy — outside the clinician-reviewed MedDRA term map, never queried — and ATN and AIN, queried but biopsy-bound: real cases are filed as generic “acute kidney injury”, so their absence is not a negative. As of 2026-10-01.

What reporting says about this profile's documented lesions

Electrolyte Disturbancecorroborated · ROR 1.65 — on the terms that name the lesion (ROR 2.01)
Crystal / Obstructive NephropathyNo disproportionate reporting — This phenotype IS reportable and this agent has enough reports, yet the reporting is not disproportionate — the one genuinely informative negative of the four.
Acute Tubular NecrosisNot measurable in reporting — Reporters cannot reliably name this lesion, so its absence from FAERS is expected and is not evidence against the documented injury.
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Electrolyte Disturbance

ROR 1.6595% CI 1.54–1.76· 911 reports

FAERS outcomes & reporting trend· 28.3% of reports w/ death · 38.7% w/ hospitalization

28.3%

Reported with a death outcome

17,332 of 61,220 reports

38.7%

Reported with hospitalization

23,668 of 61,220 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 6 systems · 61,220 reports

Bars rank systems by summed reaction-term mentions (a report counts once per term it names) — an ordinal “more vs less reported” cue, not a tally of distinct reports. Renal & urinary first. As of 2026-10-01.

Disproportionality (acute kidney injury):ROR 1.2095% CI 1.10–1.31· 534 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Blood & lymphatic

Neutropenia3,427Febrile Neutropenia3,114Platelet Count Decreased2,824Myelosuppression2,662White Blood Cell Count Decreased2,290

Immune / infection

Pneumonia2,672Infection1,984Covid-191,655Sepsis1,334

General / constitutional

Pyrexia2,765Fatigue2,637Asthenia1,783

Gastrointestinal

Diarrhoea2,374Nausea2,130

Cardiac

Atrial Fibrillation1,179

Metabolic & electrolyte

Tumour Lysis Syndrome1,145

Guidelines & consensus· 13

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.

General onco-nephrology references

ADQIThe nephrotoxic effects of anti-cancer therapies: consensus report of the 34th Acute Disease Quality Initiative workgroupNat Rev Nephrol 2026 · PMID 41361704Provides expert-based statements (modified Delphi) on preventing and managing cisplatin/platinum-associated AKI, including isotonic IV hydration, attention to volume status and concomitant nephrotoxins, and incorporates evidence that IV magnesium supplementation may reduce cisplatin-associated AKI; emphasizes risk stratification and standardized AKI definitions.SIRMSIRM-SIN-AIOM: appropriateness criteria for evaluation and prevention of renal damage in the patient undergoing contrast medium examinations-consensus statements from Italian College of Radiology (SIRM), Italian College of Nephrology (SIN) and Italian Association of Medical Oncology (AIOM)Radiol Med 2022 · PMID 35303246Recommends eGFR-based renal risk assessment and pre/post-contrast isotonic saline or sodium bicarbonate hydration; advises maintaining a 5-7 day interval between iodinated contrast administration and cisplatin in cancer patients to reduce additive nephrotoxicity.KDIGOKDIGO Controversies Conference on onco-nephrology: understanding kidney impairment and solid-organ malignancies, and managing kidney cancerKidney Int 2020 · PMID 33126977Identifies platinum compounds (especially cisplatin) as leading cytotoxic causes of acute tubular injury, AKI, and electrolyte/magnesium wasting; calls for interdisciplinary onco-nephrology care, accurate GFR estimation, and individualized drug dosing in patients with reduced kidney function.KDIGOKDIGO Controversies Conference on onco-nephrology: kidney disease in hematological malignancies and the burden of cancer after kidney transplantationKidney Int 2020 · PMID 33276867Addresses chemotherapy-associated AKI/CKD in hematologic cancer, GFR estimation and chemotherapy dosing in patients with reduced kidney function, and management priorities and research gaps for onco-nephrology care.ADDIKDIntegrating International Consensus Guidelines for Anticancer Drug Dosing in Kidney Dysfunction (ADDIKD) into everyday practiceEClinicalMedicine 2025 · PMID 40290844Provides GRADE-based, drug-specific dose-adjustment recommendations for anticancer agents in kidney dysfunction (illustrated for methotrexate, cisplatin, carboplatin and nivolumab); the recommendations build on Part 1's standardised CKD-EPI eGFR assessment rather than Cockcroft-Gault creatinine clearance.ADDIKDAligning kidney function assessment in patients with cancer to global practices in internal medicineEClinicalMedicine 2025 · PMID 40290845Three consensus recommendations: assess kidney function by GFR (measured GFR or CKD-EPI eGFR), classify it using KDIGO categories, and use this uniform approach to dose anticancer drugs — moving cancer medicine away from Cockcroft-Gault estimated creatinine clearance.ADDIKDA methodology for determining dosing recommendations for anticancer drugs in patients with reduced kidney functionEClinicalMedicine 2025 · PMID 40290846Establishes that, where RCT evidence is lacking, anticancer drug dosing recommendations in kidney dysfunction should be derived by critically appraising observational literature via GRADE combined with structured international multidisciplinary consensus voting.KDIGODiagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1)Crit Care 2013 · PMID 23394211Defines/stages AKI by serum creatinine and urine output; emphasizes avoiding nephrotoxins, maintaining euvolemia/perfusion, dose-adjusting drugs to kidney function, and monitoring high-risk patients — the framework applied to nephrotoxic anti-cancer agents.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknownsKidney Int 2024 · PMID 38519239Evaluate and risk-stratify CKD, manage to delay progression and its complications, and practise explicit medication management and drug stewardship — the framework the atlas's G1–G5 eGFR banding and every renal dose-adjustment recommendation sit inside. Because the guideline excludes dialysis and transplant recipients by its own statement of scope, its recommendations do not carry to those settings, where this atlas's dialyzability and post-transplant guidance rests on other sources.KDIGOExecutive summary of the KDIGO 2021 Guideline for the Management of Glomerular DiseasesKidney Int 2021 · PMID 34556300Provides the staging/treatment framework for drug-associated glomerular lesions (e.g., bisphosphonate- and interferon-related collapsing FSGS, VEGF-inhibitor podocytopathy/proteinuria), including immunosuppression and supportive RAAS-blockade strategies.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of ANCA-Associated VasculitisKidney Int 2024 · PMID 38388147Updates immunosuppressive induction (rituximab/cyclophosphamide), incorporates avacopan and lower-dose or glucocorticoid-sparing regimens — the management framework for drug- and checkpoint-inhibitor-associated ANCA/pauci-immune glomerulonephritis.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of Lupus NephritisKidney Int 2024 · PMID 38182299Updates first-line lupus nephritis therapy to combination immunosuppression with the addition of belimumab or a calcineurin inhibitor (voclosporin) — informs management of immune-complex/lupus-like glomerulonephritis encountered with immunotherapy.KDIGOExecutive summary of the KDIGO 2025 Clinical Practice Guideline for the Management of Immunoglobulin A Nephropathy (IgAN) and Immunoglobulin A Vasculitis (IgAV)Kidney Int 2025 · PMID 40975525Encourages liberal kidney biopsy and stricter proteinuria control (<0.5 g/d, ideally <0.3 g/d) with RAAS blockers, SGLT2 inhibitors, and targeted-release budesonide — the framework for IgA-dominant glomerular lesions, including those triggered by immune-modulating cancer therapy.

Where Venetoclax sits in nephrotoxicity space — each dot is an anti-cancer agent, positioned so neighbors share a kidney-injury phenotype. Its 6 closest are filled and lead to a numbered marker, matching the numbered cards below.

Position is a 2-D projection (MDS) of each agent's injury signature, nephron target, severity, and class, so two dots can sit close on the page while differing on an axis the projection flattened — the numbered ranking is computed from the full metric, not from the distance you see. Open the full map.

Phenotype-similar agents· the numbered markers on the map above

Sonrotoclax

Beqalzi · BCL-2 inhibitor

Profile

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

XTALLYTEPRE

Severe#1 · 85% phenotype match

Obinutuzumab

Gazyva · Anti-CD20 antibody

Profile

High tumor-lysis risk in CLL.

XTALATNPRE

Moderate#2 · 84% phenotype match

Rituximab

Rituxan · Anti-CD20 antibody

Profile

Tumor lysis with bulky disease; treats some GN.

XTALATNPRE

Moderate#3 · 84% phenotype match

Odronextamab

Ordspono · Bispecific (CD20×CD3)

Profile

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

XTALPRELYTE

Moderate#4 · 80% phenotype match

Pivekimab sunirine

Decnupaz · CD123 antibody-drug conjugate

Profile

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

PREXTALLYTE

Moderate#5 · 80% phenotype match

Arsenic trioxide

Trisenox · Differentiating agent

Profile

Differentiation syndrome; QT prolongation.

PREATNLYTE

Moderate#6 · 75% phenotype match

Compare Venetoclax with its nearest agents

Nearest agents by kidney-injury phenotype (shared injuries, nephron target, severity, class) — a similarity approximation, not a claim of shared drug identity or mechanism.

Kidney risk across Other targeted agents

Same-class agents ordered by their documented kidney-injury profile — atlas severity, an acute-kidney-injury FAERS signal, and how many injury types each is documented to cause. Agents nearer the top carry the lighter documented renal profile.

A comparison of documented kidney-injury data within one drug class — not a substitution recommendation. Efficacy, indication, and non-renal toxicity differ between these agents and are out of scope here. Educational only, not medical advice.