What kind of kidney injury does Thalidomide 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 Thalidomide therapy?

Uric acid, potassium, phosphate, calcium, creatinine at initiation in high-burden disease; Heart rate (bradycardia); Signs/symptoms of VTE.

How can kidney injury from Thalidomide be prevented?

Tumor-lysis prophylaxis (hydration, allopurinol or rasburicase) when indicated VTE prophylaxis per regimen

Who is at higher risk of kidney injury from Thalidomide?

High tumor burden; Pre-existing renal impairment; Volume depletion; Bradycardia / reduced perfusion; concurrent rate-slowing or hypotensive drugs.

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Printable monograph

Immunomodulatory drug (IMiD)

Thalidomide

Thalomid · THAL

Immunomodulatory drug (IMiD) · approved 2006 · 6 citations

Dated evidence· through 2017

Fairly sourced4/9 · 4 signals

Met: 6 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 9y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Not met: Current through 2017
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.

The original IMiD, whose kidney risk is dominated by tumor lysis and reduced perfusion rather than direct nephrotoxicity.

MildImmunomodulatory drug (IMiD)

Multiple myelomaErythema nodosum leprosum

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Thalidomide is not a direct nephrotoxin; the principal renal hazard is tumor lysis syndrome, which is uncommon in myeloma and reported at the case level. Sinus bradycardia is a recognized dose-related non-renal effect that, with the drug’s sedative/hypotensive properties, can compound prerenal physiology. Venous thromboembolism is the other dominant class toxicity.Source: Chang et al., Chang Gung Med J 2011

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Tumor lysis within days of initiation in high-burden disease.

Distilled from: “Tumor lysis within days of initiation in high-burden disease; bradycardia over weeks of dosing.”

§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

Evidence6 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

Kidney injury is largely indirect: effective cytoreduction precipitates tumor lysis with hyperuricemia and hyperphosphatemia, producing urate/calcium-phosphate intratubular crystal deposition and a prerenal/AKI picture. Drug-induced bradycardia, sedation, and hypotension can reduce renal perfusion; thromboembolic events can rarely involve the renal vasculature.

Clinical presentation

Stable renal function in most patients; TLS presents with hyperuricemia, hyperkalemia, hyperphosphatemia, and rising creatinine. Bradycardia, constipation, somnolence, and peripheral neuropathy are characteristic non-renal effects.

Management

Manage tumor lysis with isotonic hydration, rasburicase/allopurinol, and electrolyte correction; address bradycardia/hypotension to preserve renal perfusion. Direct dose-limiting nephrotoxicity is not characteristic of thalidomide.Lesion-level management framework

Risk factors

High tumor burden
Pre-existing renal impairment
Volume depletion
Bradycardia / reduced perfusion; concurrent rate-slowing or hypotensive drugs

Prevention

Tumor-lysis prophylaxis (hydration, allopurinol or rasburicase) when indicated
VTE prophylaxis per regimen

Anticancer mechanism· how it treats cancer

Parent immunomodulatory drug that binds cereblon, inhibits angiogenesis (VEGF/bFGF), modulates cytokines (suppresses TNF-alpha), and co-stimulates T/NK cells. Used in multiple myeloma and erythema nodosum leprosum.

Note · Tumor lysis, bradycardia, and VTE are the salient issues; thalidomide itself is not a classic direct nephrotoxin.

§04

Clinical depth

Renal dose adjustment

No specific renal dose adjustment is mandated (thalidomide is poorly renally cleared, eliminated largely by non-enzymatic hydrolysis); use cautiously and titrate to tolerance in advanced CKD. Dose on dialysis days after the session.

Dialyzability & ESKD dosing

Not significantly dialyzed in routine practice; no supplemental dosing required. Give after hemodialysis on dialysis days.

Differential diagnosis

As with the other IMiDs, separate TLS crystal nephropathy from prerenal azotemia and myeloma cast nephropathy; bradycardia-related hypoperfusion should be considered when AKI accompanies a low heart rate.

Monitoring

Uric acid, potassium, phosphate, calcium, creatinine at initiation in high-burden disease
Heart rate (bradycardia)
Signs/symptoms of VTE

Key trials & series

Coiffier et al. evidence-based TLS guidelines (class management)

Clinical pearls

Thalidomide is not a classic tubular nephrotoxin - watch for tumor lysis, bradycardia, and VTE instead.
Bradycardia plus hypotension can produce prerenal AKI; reassess perfusion before blaming intrinsic injury.

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. Citation metadata via PubMed / NLM.

Evidence accrual

6 references · 2008–2017 · 3 since 2015

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.

FDA label — boxed warning & renal dosing· boxed warning

Quoted verbatim from this agent's current FDA label (Mar 2023) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: EMBRYO-FETAL TOXICITY AND VENOUS THROMBOEMBOLISM WARNING: EMBRYO-FETAL TOXICITY AND VENOUS THROMBOEMBOLISM See full prescribing information for complete boxed warning. EMBRYO -FETAL TOXICITY • If THALOMID is taken during pregnancy, it can cause severe birth defects or embryo-fetal death. THALOMID should never be used by females who are pregnant or who could be pregnant while taking the drug. Even a single dose [1 capsule (regardless of strength)] taken by a pregnant woman during her pregnancy can cause severe birth defects. • Pregnancy must be excluded before start of treatment. Prevent pregnancy thereafter by the use of two reliable methods of contraception. ( 5.1 , 8.3 ) THALOMID is only available through a restricted distribution program, the THALOMID REMS ® program ( 5.2 ). VENOUS THROMBOEMBOLISM • Significant increased risk of deep vein thrombosis (DVT) and pulmonary embolism (PE) in patients with multiple myeloma receiving THALOMID with dexamethasone ( 5.3 ). EMBRYO-FETAL TOXICITY If THALOMID is taken during pregnancy, it can cause severe birth defects or embryo-fetal death. THALOMID should never be used by females who are pregnant or who could become pregnant while taking the drug. Even a single dose [1 capsule (regardless of strength)] taken by a pregnant woman during her pregnancy can cause severe birth defects. Because of this toxicity and in an effort to…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 36,497 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· 5 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

Electrolyte Disturbancecorroborated · ROR 1.93 — on the terms that name the lesion (ROR 1.58)
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
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.

Thrombotic Microangiopathy

ROR 2.1295% CI 1.64–2.75· 57 reports

Glomerular Injury / Proteinuria

ROR 2.0095% CI 1.65–2.43· 101 reports

Electrolyte Disturbance

ROR 1.9395% CI 1.78–2.08· 634 reports

SIADH / Hyponatremia

ROR 1.5395% CI 1.34–1.75· 214 reports

Hemorrhagic Cystitis

ROR 1.3695% CI 1.17–1.59· 164 reports

FAERS outcomes & reporting trend· 33.3% of reports w/ death · 29.1% w/ hospitalization

33.3%

Reported with a death outcome

12,158 of 36,497 reports

29.1%

Reported with hospitalization

10,618 of 36,497 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 36,497 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 0.6695% CI 0.57–0.76· 175 AKI reports ·AKI is reported less often than for other drugs (CI entirely below 1) — no disproportionate signal.

Renal & urinary

Renal Failure781

General / constitutional

Fatigue1,410Asthenia1,021Pyrexia960Fall656Pain605

Immune / infection

Pneumonia1,713Sepsis818Infection783

Blood & lymphatic

Anaemia1,022Thrombocytopenia879Neutropenia835

Gastrointestinal

Constipation995Nausea865Diarrhoea832

Nervous system

Neuropathy Peripheral1,823Dizziness756

Respiratory

Dyspnoea991Pulmonary Embolism655

Vascular

Deep Vein Thrombosis843

Skin

Rash680

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 Thalidomide 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

Pomalidomide

Pomalyst · Immunomodulatory drug (IMiD)

Profile

Tumor lysis; usable in renal impairment.

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 Thalidomide 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 Thalidomide’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 Thalidomide; 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 141 clinical records among all 200 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.