What kind of kidney injury does Bortezomib cause?

Thrombotic Microangiopathy — Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF. Other reported patterns: Glomerular Injury / Proteinuria.

How should kidney function be monitored during Bortezomib therapy?

Serum creatinine and serum free light chains to track the (usually beneficial) renal response; CBC, LDH and haptoglobin if TMA is suspected; Urine protein for the rare glomerular microangiopathy; CBC each cycle (falling platelets/hemoglobin are usually the first clue to bortezomib-associated TMA).

How can kidney injury from Bortezomib be prevented?

Maintain hydration and manage myeloma renal drivers (light chains, calcium, volume)

Who is at higher risk of kidney injury from Bortezomib?

Underlying myeloma renal disease/MIDD; Pre-existing endothelial injury; Concurrent nephrotoxins.

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Printable monograph

Proteasome inhibitor

Bortezomib

Velcade · Bort

Proteasome inhibitor · approved 2003 · 7 citations · FAERS AKI reporting ROR 1.88 (95% CI 1.78–1.99, 1,204 AKI reports)

Up to date· through 2025

Deeply sourced7/9 · 6 signals

Met: 7 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 10y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
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.

The proteasome inhibitor that more often rescues the myeloma kidney than harms it — with rare TMA/glomerular injury.

ModerateProteasome inhibitor (first generation)

Multiple myelomaMantle cell lymphoma

§01

Signature kidney injury

Signature lesion

Thrombotic Microangiopathy

Bortezomib is generally renal-friendly and often improves renal function in myeloma by rapidly reducing light-chain-driven cast nephropathy; it requires no renal dose adjustment. Thrombotic microangiopathy and glomerular microangiopathy are rare, case-level events, and pharmacovigilance shows a far weaker TMA signal than carfilzomib.Source: Mizuno et al., CEN Case Rep 2021 (case); Deng et al., Support Care Cancer 2025 (FAERS)

Onset & rechallenge

Time to injuryVariable / unpredictable

Rare renal events can occur at any point, from weeks to several months after initiation.

Distilled from: “Rare adverse renal events can occur at any point during therapy, from weeks to several months after initiation; the beneficial light-chain reduction is often rapid.”

Long-term outlook & thresholds

Renal recoveryVariable

Bortezomib's dominant renal effect is recovery: it reverses light-chain cast nephropathy and often improves renal function in myeloma, needing no renal dose adjustment even on dialysis. The rare TMA and glomerular microangiopathy events are of variable reversibility and usually improve after drug cessation and supportive care.PMID 34680184 (opens PubMed in a new tab)

Early-detection biomarkers

Serum free light chains (sFLC) — The nephrotoxic light-chain burden driving myeloma cast nephropathy — bortezomib's target of benefit. A rapid fall in involved serum free light chains tracks bortezomib's beneficial renal response; the profile monitors sFLC to follow the usually favorable kidney course as cast nephropathy reverses.PMID 34680184 (opens PubMed in a new tab)
LDH, haptoglobin, platelet count and peripheral schistocytes (microangiopathic hemolysis panel) — Rare proteasome-inhibitor thrombotic microangiopathy. In proteasome-inhibitor-associated TMA the near-universal presentation is hemolytic anemia (~98%), thrombocytopenia (~97%) and AKI (~97%); check CBC, LDH and haptoglobin when TMA is suspected.PMID 39939437 (opens PubMed in a new tab)
Urine protein / albuminuria (uPCR or uACR) — Rare bortezomib glomerular microangiopathy. Rising, albumin-predominant proteinuria after starting bortezomib should prompt suspicion of glomerular microangiopathy even without systemic microangiopathic hemolysis, and warrants kidney biopsy.PMID 33909224 (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.

Thrombotic Microangiopathy#1 · Signaturequalitative — no citable incidence
Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF.
Glomerular Injury / ProteinuriaRarequalitative — no citable incidence
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.

§03

Kidney injury

Deep diveProteasome-inhibitor thrombotic microangiopathyWeeks into carfilzomib — often with an infection as the second hit — the microvascular endothelium tips into thrombotic microangiopathy: schistocytes and falling platelets, an acute kidney injury the drug set in motion, and an ADAMTS13 that comes back normal because this was never TTP.

Mechanism of kidney injury

Net renal effect is usually beneficial via rapid suppression of nephrotoxic free light chains, mitigating intratubular cast nephropathy. Rarely, endothelial injury produces a systemic thrombotic microangiopathy or a localized glomerular microangiopathy (proposed via VEGF/NF-κB-related endothelial perturbation), with proteinuria and AKI even in the absence of systemic MAHA.

Clinical presentation

Usually stable or improving renal function in myeloma. Rare TMA: microangiopathic hemolysis, thrombocytopenia, AKI. Rare glomerular microangiopathy: increasing (often albumin-predominant) proteinuria with AKI and biopsy-confirmed endothelial injury, sometimes alongside monoclonal immunoglobulin deposition disease.

Management

For TMA/glomerular microangiopathy, hold/discontinue, provide supportive care and obtain nephrology evaluation (kidney biopsy for unexplained proteinuria/AKI); otherwise continue with standard myeloma renal management, leveraging bortezomib's light-chain-lowering benefit.Lesion-level management framework

Risk factors

Underlying myeloma renal disease/MIDD
Pre-existing endothelial injury
Concurrent nephrotoxins

Prevention

Maintain hydration and manage myeloma renal drivers (light chains, calcium, volume)

Anticancer mechanism· how it treats cancer

Reversible (boronate) inhibitor of the chymotrypsin-like activity of the 20S proteasome, causing accumulation of misfolded proteins, NF-κB pathway modulation and apoptosis in myeloma cells. A backbone of multiple myeloma therapy and used in mantle cell lymphoma.

§04

Clinical depth

Renal dose adjustment

No renal dose adjustment required at any level of renal function, including dialysis (bortezomib is hepatically metabolized via CYP-mediated deboronation). This renal-sparing profile is a key reason it anchors regimens for myeloma with kidney involvement.

Dialyzability & ESKD dosing

Not appreciably dialyzed; on dialysis days, administer after the HD session per label. No supplemental dose required.

Differential diagnosis

In a bortezomib-treated myeloma patient, rising creatinine is far more often cast nephropathy/myeloma activity (improving with treatment) than drug toxicity. Reserve a drug-TMA/microangiopathy diagnosis for hemolysis/thrombocytopenia or new heavy proteinuria with supportive biopsy, and exclude MIDD and amyloid.

Monitoring

Serum creatinine and serum free light chains to track the (usually beneficial) renal response
CBC, LDH and haptoglobin if TMA is suspected
Urine protein for the rare glomerular microangiopathy
CBC each cycle (falling platelets/hemoglobin are usually the first clue to bortezomib-associated TMA)

Key trials & series

Mizuno CEN Case Rep 2021 (biopsy-proven glomerular microangiopathy)
Deng Support Care Cancer 2025 (FAERS PI-TMA; bortezomib weaker signal than carfilzomib)

Clinical pearls

Bortezomib usually helps the myeloma kidney - it lowers nephrotoxic light chains and needs no renal dose adjustment, including on dialysis.
Contrast with carfilzomib: bortezomib's TMA signal is real but rare and much weaker.
New heavy proteinuria on bortezomib warrants biopsy - glomerular microangiopathy and MIDD are on the differential.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Thrombotic Microangiopathy Glomerular Injury / Proteinuria

Beyond the kidney — non-renal toxicities· 3 organ systems

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

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

Peripheral neuropathy (bortezomib)

Cardiac

Cardiomyopathy, QT, ischemia, myocarditis

Heart failure / hypertension (carfilzomib)

Hematologic

Cytopenias, thrombosis, TMA

Thrombocytopenia

§05

References

5 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

5 references · 2015–2025 · 1 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· 2

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.

CaseB · ModerateProteasome inhibitor associated thrombotic microangiopathy.Yui JC et al. · Am J Hematol 2016 · PMID 27286661Multicenter case series of 11 myeloma patients developing thrombotic microangiopathy with proteasome inhibitors including bortezomib, with renal impairment (median creatinine 3.12 mg/dL) and resolution on drug withdrawal.CaseC · LimitedUnique Presentation of Bortezomib-Associated Thrombotic Microangiopathy Responsive to Therapeutic Plasma Exchange and Eculizumab Therapy.Sterner RC et al. · Hematol Rep 2022 · PMID 35466182Case report of a multiple myeloma patient who developed bortezomib-associated thrombotic microangiopathy four months after initiating therapy, responding to plasma exchange and eculizumab.

FDA label — boxed warning & renal dosing· renal impairment

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

Renal impairment — from the label

No starting dosage adjustment of bortezomib is recommended for patients with renal impairment. In patients requiring dialysis, bortezomib should be administered after the dialysis procedure [see Clinical Pharmacology ( 12.3 )] .

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 88,913 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· 6 signals

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

Thrombotic Microangiopathycorroborated · ROR 4.62
Glomerular Injury / Proteinuriacorroborated · ROR 1.97 — on the terms that name the lesion (ROR 1.8)

Thrombotic Microangiopathy

ROR 4.6295% CI 4.12–5.18· 298 reports

Electrolyte Disturbance

ROR 2.6495% CI 2.53–2.76· 2,095 reports

SIADH / Hyponatremia

ROR 2.2795% CI 2.11–2.43· 766 reports

Acute Tubular Necrosis

ROR 2.1595% CI 1.74–2.65· 89 reports

Glomerular Injury / Proteinuria

ROR 1.9795% CI 1.74–2.24· 242 reports

Hemorrhagic Cystitis

ROR 1.1895% CI 1.06–1.31· 347 reports

FAERS outcomes & reporting trend· 15.8% of reports w/ death · 31.9% w/ hospitalization

15.8%

Reported with a death outcome

14,068 of 88,913 reports

31.9%

Reported with hospitalization

28,334 of 88,913 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 88,913 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 1.8895% CI 1.78–1.99· 1,204 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

Thrombocytopenia3,709Neutropenia2,717Anaemia2,703Platelet Count Decreased2,174Febrile Neutropenia1,412

Gastrointestinal

Diarrhoea5,183Nausea3,115Constipation2,201Vomiting1,816

General / constitutional

Fatigue4,550Pyrexia2,866Asthenia2,216

Nervous system

Neuropathy Peripheral6,473Dizziness1,541

Immune / infection

Pneumonia4,069Sepsis1,799Infection1,621

Skin

Rash2,444

Respiratory

Dyspnoea2,095

Vascular

Hypotension1,500

Metabolic & electrolyte

Decreased Appetite1,431

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 Bortezomib 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

Trastuzumab emtansine (T-DM1)

Kadcyla · Antibody-drug conjugate (HER2/DM1)

Profile

Rare nodular regenerative TMA-like signals.

TMAGLOMHTN

Moderate#1 · 73% phenotype match

Carfilzomib

Kyprolis · Proteasome inhibitor

Profile

AKI, TMA and hypertension — a hot myeloma signal.

TMAATNHTN

Severe#2 · 71% phenotype match

Busulfan

Myleran · Alkylator

Profile

Conditioning-regimen TMA risk.

TMA

Moderate#3 · 65% phenotype match

Ixazomib

Ninlaro · Proteasome inhibitor

Profile

Rare TMA reports.

TMA

Moderate#4 · 65% phenotype match

Ziv-aflibercept

Zaltrap · VEGF trap

Profile

Hypertension and proteinuria like bevacizumab.

HTNGLOMTMA

Moderate#5 · 62% phenotype match

Bevacizumab

Avastin · Anti-VEGF antibody

Profile

Proteinuria, hypertension, glomerular TMA.

GLOMHTNTMA

Moderate#6 · 62% phenotype match

Compare Bortezomib 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.

Who studies this

The leading contributors to Bortezomib’s clinical kidney literature on PubMed, ranked by a blend of publication volume and citation impact — filtered toward clinical work via the PubMed Humans heading and clinical publication types (trials, cohorts, case reports, guidelines, reviews). Names link to that author’s work on Bortezomib; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.

Ranked by a 50/50 blend of publication volume and a position-weighted, capped Relative Citation Ratio (NIH iCite) on this agent’s renal literature; the citation count shown is the raw total, not the ranking score — counted over the 243 clinical records among the 300 most-relevant of 577 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.