How should kidney function be monitored during Carfilzomib therapy?

Blood pressure at every visit (and home monitoring) - hypertension precedes/accompanies TMA; CBC, LDH, haptoglobin and peripheral smear for schistocytes, especially in the first cycles and on re-escalation; Serum creatinine and urine protein each cycle.

How can kidney injury from Carfilzomib be prevented?

Aggressive blood-pressure control before and during therapy Step-up dosing with dexamethasone premedication and adequate hydration on initiation/re-escalation

Who is at higher risk of kidney injury from Carfilzomib?

Pre-existing or treatment-emergent hypertension; Underlying myeloma renal disease; Volume status changes; Re-escalation after treatment breaks; Prior endothelial injury (e.g., post-transplant).

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Printable monograph

Proteasome inhibitor

Carfilzomib

Kyprolis · Carfil

Proteasome inhibitor · approved 2012 · 13 citations · FAERS AKI reporting ROR 4.34 (95% CI 4.06–4.65, 862 AKI reports)

Up to date· through 2025

Deeply sourced8/9 · 7 signals

Met: 13 citations
Met: 12+ references
Met: Accrued over 10+ years (span: 11y)
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 with a real renal signature — common AKI, thrombotic microangiopathy and hypertension in myeloma.

SevereProteasome inhibitor (second generation)

Multiple myeloma

§01

Signature kidney injury

Signature lesion

Thrombotic Microangiopathy

Representative incidence17%

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.Source: Fotiou et al., Blood Cancer J 2020 (114-patient cohort)

Onset & rechallenge

Time to injuryVariable / unpredictable

Often early (first cycles) but TMA can also appear later, including after a break and re-escalation.

Distilled from: “Variable — frequently early (first cycles), but TMA can also appear later, sometimes after a treatment break and re-escalation.”

RechallengeCase-by-case

TMA has recurred after a treatment break and re-escalation — reintroduce only with close monitoring.

Long-term outlook & thresholds

Renal recoveryOften partial recovery

Hematologic and renal recovery diverge, and the largest series (37 cases) is explicit that treatment did not drive either: TMA resolved in most patients (n = 34, 94%), yet 12 (44%) were still KDIGO stage 3 AKI at discharge — and of the patients given therapeutic plasma exchange (51%), corticosteroids (38%) or eculizumab (50%), "none of these treatments demonstrated a significant impact on outcomes". Stopping the drug is the intervention with a rationale; the rest is supportive.PMID 38658194 (opens PubMed in a new tab)

CKD trajectory.: In the 37-case French national TMA series, 44% were still KDIGO stage 3 AKI at discharge despite 94% TMA resolution - persistent CKD is common after carfilzomib-TMA.
Dialysis / RRT.: All cases in the largest series presented with AKI (stage 3 in 84%); dialysis is used to support severe TMA/AKI.

Early-detection biomarkers

Urine albumin / protein (albuminuria) — Glomerular / podocyte injury (FSGS variant). New or rising albuminuria/proteinuria is an early sign of carfilzomib endothelial/podocyte injury - albuminuria >1 g/day occurred in ~6% of a 114-patient cohort, with biopsy-proven FSGS implicating a shared endothelial/podocyte mechanism; check urine protein each cycle.PMID 33149167 (opens PubMed in a new tab)
MAHA panel - LDH, haptoglobin, platelet count and peripheral-smear schistocytes — Microangiopathic hemolysis from endothelial thrombotic microangiopathy. The hemolysis panel (elevated LDH, low haptoglobin, thrombocytopenia, schistocytes) is the earliest laboratory signature of carfilzomib-TMA - in pooled cases median presenting Hb was 8.3 g/dL and platelets 18 x10^9/L, with normal ADAMTS13; monitor from cycle 1 and on re-escalation.PMID 38728883 (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

Host risk modifiers

Germline / pharmacogenomic variants that shift an individual's risk of this agent's kidney injury. Research-grade — not routine clinical testing.

CFHR3-CFHR1CFHR3-CFHR1 deletion (delCFHR3-CFHR1, heterozygous/homozygous)
Germline deletion in the complement Factor H-related gene region increases susceptibility to carfilzomib-induced complement-mediated thrombotic microangiopathy (renal TMA/AKI); ~2.3-fold enrichment vs general population in carfilzomib-TMA patients. PMID 36849497 (opens PubMed in a new tab)
CFHAlternative complement pathway germline variants (CFH / CD46(MCP) / CFHR5)
Germline complement alternative-pathway dysregulation is enriched in myeloma patients who develop carfilzomib-induced TMA versus non-TMA controls, predisposing to complement-mediated renal endothelial injury (TMA/AKI). PMID 35743426 (opens PubMed in a new tab)

§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 · Signature5%PMID 33149167 (opens PubMed in a new tab)
TMA in ~5% (6/114) of a real-world RRMM cohort; other series report <1-5%
Acute Tubular NecrosisSecondary8.3%PMID 32382772 (opens PubMed in a new tab)
Grade 3-5 kidney toxicity 8.3% (21.3% any grade) in RCT meta-analysis, predominantly AKI
HypertensionSecondary13.2%PMID 33845729 (opens PubMed in a new tab)
All-grade hypertension 13.2%, high-grade 5.3% (45-trial meta-analysis)
Glomerular Injury / ProteinuriaRarequalitative — no citable incidence
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

17%incidence

SeveritySevere

ReversibilityPartially reversible

Evidence13 citations

Nephron map

GlomerulusFiltration barrier (podocytes + endothelium)

Vasculature / EndotheliumGlomerular & peritubular capillaries

Proximal Tubule

Distal Tubule / Collecting Duct

Thrombotic Microangiopathy

Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF.

§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.Appears in 1 documented synergy combination

Mechanism of kidney injury

Endothelial injury — likely from proteasome-inhibition-induced loss of endothelial homeostasis and a complement-amplified response — drives a thrombotic microangiopathy with microvascular thrombosis, microangiopathic hemolysis, thrombocytopenia and AKI; renal biopsy in the cohort showed FSGS in some albuminuric patients, implicating a shared endothelial/podocyte mechanism. Carfilzomib also causes hypertension that compounds renal risk, and underlying myeloma kidney disease frequently coexists. Direct tubular (ATN) injury can also occur.

Clinical presentation

AKI with new or worsening hypertension; in TMA, microangiopathic hemolytic anemia (schistocytes, elevated LDH, low haptoglobin), thrombocytopenia and rising creatinine, sometimes requiring dialysis; in the podocytopathy variant, new albuminuria/proteinuria with relatively preserved or modestly reduced GFR. Onset is often abrupt, within the first cycles.

Management

Hold/discontinue carfilzomib at first suspicion of TMA; supportive AKI care and aggressive hypertension control; plasma exchange and complement inhibition (e.g., eculizumab) have been used successfully in reported carfilzomib-TMA cases; dialysis if severe. Outcome data diverge by cohort and endpoint: across the published PI-TMA case literature, drug cessation plus supportive care (with PLEX/HD/eculizumab as needed) was associated with improved hematologic outcomes in 96.3% and renal outcomes in 93.3% (60 published cases), but published cases are selected for recovery — in the largest unselected series (37 cases, French national TMA reference center) TMA resolved in 94% while 44% still had KDIGO stage 3 AKI at discharge. Counsel on that split: hematologic resolution is the rule, renal sequelae are frequent.Lesion-level management framework

Risk factors

Pre-existing or treatment-emergent hypertension
Underlying myeloma renal disease
Volume status changes
Re-escalation after treatment breaks
Prior endothelial injury (e.g., post-transplant)

Prevention

Aggressive blood-pressure control before and during therapy
Step-up dosing with dexamethasone premedication and adequate hydration on initiation/re-escalation

Anticancer mechanism· how it treats cancer

Irreversible (epoxyketone) inhibitor of the chymotrypsin-like activity of the 20S proteasome, causing accumulation of misfolded/ubiquitinated proteins, ER stress and apoptosis in myeloma cells. Used in relapsed/refractory multiple myeloma.

Note · TMA is the headline serious lesion; AKI, albuminuria/FSGS and hypertension are individually common. Reported TMA-rate figures are trial-specific.

§04

Clinical depth

Renal dose adjustment

Per label no starting-dose adjustment is required across renal function including dialysis (carfilzomib is rapidly metabolized by peptidase/epoxide hydrolase, not renally cleared); however, given the high rate of renal events, monitor closely and hold for TMA/AKI rather than adjusting prophylactically.

Dialyzability & ESKD dosing

On hemodialysis days, administer carfilzomib after the HD session (per label) for theoretical dialytic clearance; the parent drug is largely cleared by non-renal metabolism. Dialysis is otherwise used to support TMA/AKI.

Differential diagnosis

Separate carfilzomib-TMA (MAHA, thrombocytopenia, schistocytes, normal ADAMTS13) from TTP (severe ADAMTS13 deficiency), from atypical HUS, and from myeloma-related kidney disease (cast nephropathy, light chains). The combination of new hypertension + AKI + hemolysis on carfilzomib is the classic trigger to stop the drug and work up TMA.

Monitoring

Blood pressure at every visit (and home monitoring) - hypertension precedes/accompanies TMA
CBC, LDH, haptoglobin and peripheral smear for schistocytes, especially in the first cycles and on re-escalation
Serum creatinine and urine protein each cycle

Key trials & series

CARDAMON (Camilleri Br J Haematol 2021; TMA rate and mitigation)
Fotiou Blood Cancer J 2020 (114-patient renal-toxicity cohort, ~17% renal events)
Deng Support Care Cancer 2025 (FAERS PI-TMA pharmacovigilance, carfilzomib dominant)

Clinical pearls

Carfilzomib has the strongest renal/TMA signature of the proteasome inhibitors - new hypertension plus AKI plus hemolysis means stop the drug and check a smear and ADAMTS13.
Renal events are common (~17% in cohort data), early and unpredictable - monitor from cycle 1.
Re-escalation after a treatment break is a recognized trigger for TMA.

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

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 · 2014–2025 · 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· 4

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 · LimitedDelayed Onset of Thrombotic Microangiopathy (TMA) upon Prolonged Carfilzomib Therapy in Multiple Myeloma: A Case Report and Comprehensive Review.Ceglédi A et al. · Pharmaceuticals (Basel) 2024 · PMID 39770564Rare delayed-onset TMA with acute kidney injury, oliguria and complement activation arising 11 months into carfilzomib therapy, resolving after drug withdrawal and plasmapheresis.CaseC · LimitedCarfilzomib‐Induced Thrombotic Microangiopathy—Two Case Reports.Attucci I et al. · Cancer Rep (Hoboken) 2024 · PMID 39390755Two multiple myeloma patients on carfilzomib developed DI-TMA (2.2% incidence in 91 treated patients) with AKI requiring dialysis; both improved rapidly on eculizumab with discontinuation of hemodialysis. Includes denominator and literature review of 75 prior cases.CaseC · LimitedCarfilzomib-Associated Thrombotic Microangiopathy in a Multiple Myeloma Patient: Complement Genetic Alterations Impact and Eculizumab Therapy.Lopes J et al. · Cureus 2025 · PMID 40895697Carfilzomib-associated TMA with dialysis-requiring acute kidney injury and underlying complement gene variants (CFHR3-CFHR1 deletion), with full renal recovery after eculizumab.CaseC · LimitedCarfilzomib-induced thrombotic microangiopathy (TMA) refractory to eculizumab: A case report and literature review.Meseha M et al. · Ann Hematol 2024 · PMID 39191958Relapsed multiple myeloma patient developed carfilzomib-induced TMA refractory to eculizumab and supportive care, progressing to encephalopathy and refractory GI bleeding and transition to comfort care. Illustrates a fatal/refractory phenotype of PI-induced TMA.

Conference abstracts & journal reports· 1 non-PubMed

Non-PubMed sources — conference abstracts (e.g. ASN Kidney Week, badged Abstract) and case reports from non-indexed field journals (e.g. Journal of Onco-Nephrology, badged Journal). Included for completeness; weigh below peer-reviewed PubMed citations.

AbstractCarfilzomib-Induced Thrombotic Microangiopathy: Rapid Renal Recovery with Eculizumab TherapyAbu Amer N, Lahav M, Vaisman A, Volkov A, Beckerman P · ASN Kidney Week 2025 2025 · Abstract TH-PO0209Carfilzomib (proteasome inhibitor) TMA that had progressed to dialysis-dependence achieved hematologic normalization and renal recovery on eculizumab, with dialysis discontinued within eight weeks — supporting complement blockade for severe proteasome-inhibitor TMA.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 28,118 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· 3 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 29.54
Hypertensioncorroborated · ROR 1.94 — on the terms that name the lesion (ROR 2.68)
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.
Glomerular Injury / ProteinuriaNo 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.

Thrombotic Microangiopathy

ROR 29.5495% CI 27.16–32.12· 579 reports

Hypertension

ROR 1.9495% CI 1.82–2.06· 983 reports

Electrolyte Disturbance

ROR 1.9395% CI 1.77–2.11· 490 reports

FAERS outcomes & reporting trend· 15.6% of reports w/ death · 33.5% w/ hospitalization

15.6%

Reported with a death outcome

4,377 of 28,118 reports

33.5%

Reported with hospitalization

9,417 of 28,118 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 28,118 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 4.3495% CI 4.06–4.65· 862 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Renal & urinary

Acute Kidney Injury862Renal Failure465

Blood & lymphatic

Thrombocytopenia1,543Anaemia1,117Neutropenia1,114Platelet Count Decreased600Pancytopenia447

General / constitutional

Fatigue1,542Pyrexia1,167Asthenia710

Immune / infection

Pneumonia1,389Infection676Sepsis597Covid-19489

Gastrointestinal

Diarrhoea1,123Nausea1,082Vomiting534

Respiratory

Dyspnoea1,117

Vascular

Hypertension714

Nervous system

Neuropathy Peripheral693

Cardiac

Cardiac Failure568

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 Carfilzomib 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 · 72% phenotype match

Bortezomib

Velcade · Proteasome inhibitor

Profile

Rare TMA; reverses myeloma cast nephropathy.

TMAGLOM

Moderate#2 · 71% phenotype match

Ziv-aflibercept

Zaltrap · VEGF trap

Profile

Hypertension and proteinuria like bevacizumab.

HTNGLOMTMA

Moderate#3 · 60% phenotype match

Bevacizumab

Avastin · Anti-VEGF antibody

Profile

Proteinuria, hypertension, glomerular TMA.

GLOMHTNTMA

Moderate#4 · 60% phenotype match

Ramucirumab

Cyramza · Anti-VEGFR2 antibody

Profile

Hypertension and proteinuria, class effect.

HTNGLOMTMA

Moderate#5 · 60% phenotype match

VEGFR TKIs (sunitinib · sorafenib · pazopanib · axitinib)

VEGFR TKI

Profile

Hypertension as an on-target marker; proteinuria.

HTNGLOMTMA

Moderate#6 · 60% phenotype match

Compare Carfilzomib 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 Carfilzomib’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 Carfilzomib; 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 64 clinical records among all 79 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.