What kind of kidney injury does Pomalidomide cause?

Prerenal / Hemodynamic AKI — Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome. Other reported patterns: Electrolyte Disturbance, Crystal / Obstructive Nephropathy.

How should kidney function be monitored during Pomalidomide therapy?

Uric acid, potassium, phosphate, calcium, and creatinine at initiation in high-burden disease; CBC at least monthly.

How can kidney injury from Pomalidomide be prevented?

Risk-stratify for TLS and give prophylaxis: hydration plus allopurinol (intermediate risk) or rasburicase (high risk) Maintain adequate hydration; avoid urine alkalinization (promotes calcium-phosphate deposition)

Who is at higher risk of kidney injury from Pomalidomide?

High tumor burden / rapidly proliferative disease; Pre-existing renal impairment; Volume depletion; Elevated baseline uric acid or LDH.

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Printable monograph

Immunomodulatory drug (IMiD)

Pomalidomide

Pomalyst · POM

Immunomodulatory drug (IMiD) · approved 2013 · 7 citations

Up to date· through 2025

Deeply sourced7/9 · 6 signals

Met: 7 citations
Not 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
Not 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 later-generation IMiD usable across renal impairment, with tumor lysis as the main kidney risk.

MildImmunomodulatory drug (IMiD)

Multiple myeloma (relapsed/refractory)Kaposi sarcoma

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Pomalidomide pharmacokinetics are not substantially altered by renal impairment - it is extensively metabolized hepatically, with <5% renal excretion of unchanged drug - and pooled trial data show a similar safety profile and dosing through moderate renal impairment (CrCl 30 to <60). Dialysis patients are the exception - the label reports about 38% higher AUC and 64% more serious adverse events there, with a reduced starting dose given after the session. The principal renal hazard is tumor lysis syndrome (TLS), which is uncommon and case-level in myeloma.Source: Siegel et al., Leuk Lymphoma 2016 (pooled renal-impairment analysis)

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Tumor lysis typically within days of starting therapy in high-burden disease.

Distilled from: “Tumor lysis typically within days of starting therapy in high-burden disease.”

§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.

Prerenal / Hemodynamic AKI#1 · Signaturequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Electrolyte DisturbanceSecondaryqualitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).
Crystal / Obstructive NephropathySecondaryqualitative — no citable incidence
Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityMild

ReversibilityReversible

Evidence7 citations

Nephron map

Vasculature / Endothelium

Distal Tubule / Collecting Duct

Tubular Lumen

Prerenal / Hemodynamic AKI

Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

§03

Kidney injury

Mechanism of kidney injury

Direct nephrotoxicity is minimal; kidney injury is predominantly indirect. Rapid tumor cell death releases uric acid, potassium, and phosphate; uric-acid and calcium-phosphate crystals precipitate within distal tubules (intratubular obstruction) and hyperuricemia causes a prerenal/crystal-nephropathy AKI, particularly with high tumor burden or volume depletion.

Clinical presentation

Most patients maintain stable renal function. TLS presents with hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and rising creatinine within days of starting therapy; oliguria can develop with crystal obstruction.

Management

Treat established TLS with aggressive isotonic hydration, rasburicase for hyperuricemia, and electrolyte correction; dialysis for refractory hyperkalemia, hyperphosphatemia, or oligoanuric AKI. Because pomalidomide is hepatically metabolized, it is generally usable in renal impairment without major PK-based dose change, though clinical monitoring remains important.Lesion-level management framework

Risk factors

High tumor burden / rapidly proliferative disease
Pre-existing renal impairment
Volume depletion
Elevated baseline uric acid or LDH

Prevention

Risk-stratify for TLS and give prophylaxis: hydration plus allopurinol (intermediate risk) or rasburicase (high risk)
Maintain adequate hydration; avoid urine alkalinization (promotes calcium-phosphate deposition)

Anticancer mechanism· how it treats cancer

Third-generation cereblon-binding immunomodulatory drug that degrades IKZF1/IKZF3, with antimyeloma, anti-angiogenic, and T/NK-cell immunostimulatory activity. Used in relapsed/refractory multiple myeloma, usually with dexamethasone, and in Kaposi sarcoma.

Note · Distinguished from lenalidomide by usability in renal impairment. Direct nephrotoxicity is not a defining feature; tumor lysis is the key renal concern.

§04

Clinical depth

Renal dose adjustment

No starting-dose change is required for renal impairment short of dialysis (extensive hepatic metabolism). For severe renal impairment REQUIRING DIALYSIS the label directs a reduced starting dose: 3 mg daily in multiple myeloma, 4 mg daily in Kaposi sarcoma, since AUC rises about 38% and the rate of serious adverse events about 64% relative to normal renal function. On hemodialysis days give the dose after the session completes, because exposure falls significantly during dialysis. Reduce dose for hepatic impairment and for hematologic toxicity.

Dialyzability & ESKD dosing

Exposure falls significantly during hemodialysis, which is why the daily dose is given after the session rather than before it — not because the drug is unaffected by dialysis. Patients on dialysis also start lower (3 mg daily in multiple myeloma, 4 mg in Kaposi sarcoma), since AUC runs about 38% higher and serious adverse events about 64% more frequent than with normal renal function.

Differential diagnosis

Distinguish TLS-related crystal nephropathy (hyperuricemia, hyperphosphatemia, urate/calcium-phosphate crystals) from prerenal azotemia (volume responsive) and from myeloma cast nephropathy (paraprotein, free light chains). The metabolic profile and timing within days of cytoreduction identify TLS.

Monitoring

Uric acid, potassium, phosphate, calcium, and creatinine at initiation in high-burden disease
CBC at least monthly

Key trials & series

Siegel et al. pooled analysis of pomalidomide-dexamethasone across renal-impairment subgroups
Coiffier et al. evidence-based TLS management guidelines

Clinical pearls

Pomalidomide is the IMiD of choice in significant renal impairment - no dose change short of dialysis, unlike lenalidomide; dialysis patients start lower (3 mg in myeloma, 4 mg in Kaposi sarcoma) and take the dose after the session.
The kidney risk is the disease response (tumor lysis), not the drug itself - prophylax high-burden patients.
Avoid urinary alkalinization in TLS; it favors calcium-phosphate precipitation.

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

Class-level context for the major non-renal toxicities of the Immunomodulatory drug (IMiD) class.

Vascular

Hypertension, VTE/ATE, bleeding, aneurysm

Venous thromboembolism

Hematologic

Cytopenias, thrombosis, TMA

Myelosuppression

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

Neuropathy (thalidomide)

§05

References

6 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

6 references · 2008–2025 · 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· 1

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 · LimitedA case of acute kidney injury from crystal nephropathy secondary to pomalidomide and levofloxacin use.Baird P et al. · J Oncol Pharm Pract 2016 · PMID 25591868Onconephrology case report of acute kidney injury attributed to crystal nephropathy developing during pomalidomide (plus levofloxacin) therapy.

FDA label — boxed warning & renal dosing· boxed warning · renal impairment

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

Boxed warning

WARNING: EMBRYO-FETAL TOXICITY and VENOUS AND ARTERIAL THROMBOEMBOLISM Embryo-Fetal Toxicity Pomalidomide capsules are contraindicated in pregnancy. Pomalidomide capsules are a thalidomide analogue. Thalidomide is a known human teratogen that causes severe birth defects or embryo-fetal death. In females of reproductive potential, obtain 2 negative pregnancy tests before starting pomalidomide capsules treatment. Females of reproductive potential must use 2 forms of contraception or continuously abstain from heterosexual sex during and for 4 weeks after stopping pomalidomide capsules treatment [see Contraindications (4), Warnings and Precautions (5.1) and Use in Specific Populations (8.1, 8.3)]. Pomalidomide capsules are only available through a restricted distribution program called PS-Pomalidomide REMS [see Warnings and Precautions (5.2)]. Information about PS-Pomalidomide REMS is available at www.PS-PomalidomideREMS.com or by calling the REMS Call Center at 1-888-423-5436. Venous and Arterial Thromboembolism Deep venous thrombosis (DVT), pulmonary embolism (PE), myocardial infarction, and stroke occur in patients with multiple myeloma treated with pomalidomide capsules. Prophylactic antithrombotic measures were employed in clinical trials. Thromboprophylaxis is recommended, and the choice of regimen should be based on assessment of the patient's underlying risk factors [ see…

Renal impairment — from the label

In patients with severe renal impairment requiring dialysis, the AUC of pomalidomide increased by 38% and the rate of SAE increased by 64% relative to patients with normal renal function; therefore, starting dose adjustment is recommended. For patients with severe renal impairment requiring dialysis, administer pomalidomide capsules after the completion of hemodialysis on dialysis days because exposure of pomalidomide could be significantly decreased during dialysis [see Dosage and Administration (2.7) and Clinical Pharmacology (12.3)].

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 102,194 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.
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 outcomes & reporting trend· 13.7% of reports w/ death · 26.7% w/ hospitalization

13.7%

Reported with a death outcome

14,025 of 102,194 reports

26.7%

Reported with hospitalization

27,241 of 102,194 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 102,194 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 0.9395% CI 0.86–1.00· 692 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

General / constitutional

Fatigue7,499Asthenia2,684Pyrexia1,933Peripheral Swelling1,891Fall1,731

Blood & lymphatic

White Blood Cell Count Decreased3,664Neutropenia3,342Platelet Count Decreased1,746Anaemia1,706

Immune / infection

Pneumonia6,314Covid-191,840Nasopharyngitis1,672

Gastrointestinal

Diarrhoea3,909Constipation2,668Nausea2,565

Nervous system

Neuropathy Peripheral2,669Dizziness2,254

Skin

Rash3,064

Respiratory

Dyspnoea2,846

Musculoskeletal

Muscle Spasms1,529

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 Pomalidomide 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

Thalidomide

Thalomid · Immunomodulatory drug (IMiD)

Profile

Tumor lysis and bradycardia.

PRELYTEXTAL

Mild#1 · 100% phenotype match

Etoposide

Etopophos · Topoisomerase II inhibitor

Profile

Tumor lysis; renally cleared.

XTALPRELYTE

Mild#2 · 89% phenotype match

Hydroxyurea

Hydrea · Ribonucleotide reductase inhibitor

Profile

Tumor lysis in myeloproliferative disease.

XTALPRELYTE

Mild#3 · 89% phenotype match

Nelarabine

Arranon · Purine analog

Profile

Tumor lysis in T-ALL.

XTALPRELYTE

Mild#4 · 89% phenotype match

Cladribine

Leustatin · Purine analog

Profile

Tumor lysis; high-dose nephrotoxicity.

XTALPRELYTE

Mild#5 · 89% phenotype match

Ibritumomab tiuxetan

Zevalin · Radioimmunotherapy (Y-90 anti-CD20)

Profile

Yttrium-90 radioimmunotherapy; tumor lysis with bulky lymphoma.

PREXTALLYTE

Mild#6 · 88% phenotype match

Compare Pomalidomide 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 Pomalidomide’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 Pomalidomide; 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 30 clinical records among all 35 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.