What kind of kidney injury does Decitabine cause?

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

Is kidney injury from Decitabine reversible?

Reversible. Typical onset: Early after a treatment cycle (days) for tumor lysis; TMA over weeks..

How should kidney function be monitored during Decitabine therapy?

Uric acid, phosphate, potassium and calcium during early responding cycles; CBC with smear and LDH/haptoglobin if TMA is suspected; Serum creatinine through the first responding cycles.

How can kidney injury from Decitabine be prevented?

IV hydration to maintain brisk urine output Tumor lysis prophylaxis (allopurinol or rasburicase) in at-risk patients

Who is at higher risk of kidney injury from Decitabine?

High/proliferative tumor burden; Pre-existing renal impairment; Volume depletion; Hyperuricemia at baseline.

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Printable monograph

Hypomethylating agent

Decitabine

Dacogen · Decit

Hypomethylating agent · approved 2006 · 6 citations · FAERS AKI reporting ROR 1.74 (95% CI 1.36–2.22, 64 AKI reports)

Recent· through 2023

Deeply sourced7/9 · 6 signals

Met: 6 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 13y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Met: Current through 2023
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 hypomethylating cytidine analog whose marrow clearance can ignite tumor lysis and prerenal AKI.

MildHypomethylating agent

Myelodysplastic syndromesAcute myeloid leukemia

§01

Signature kidney injury

Signature lesion

Crystal / Obstructive Nephropathy

Tumor lysis syndrome with AKI is a recognized but uncommon complication when bulky/proliferative disease responds; renal incidence specific to decitabine is not well quantified (case-level). Rare biopsy-proven renal thrombotic microangiopathy has been reported.Source: Qin et al., Medicine (Baltimore) 2020 (TMA case); TLS reviews

Onset & rechallenge

Time to injuryVariable / unpredictable

Tumor-lysis AKI early (days) after a cycle; TMA over weeks.

Distilled from: “Early after a treatment cycle (days) for tumor lysis; TMA over weeks.”

§02

Renal toxicities, ranked

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

Crystal / Obstructive Nephropathy#1 · Signaturequalitative — no citable incidence
Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals.
Prerenal / Hemodynamic AKISecondaryqualitative — 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).
Thrombotic MicroangiopathySecondaryqualitative — no citable incidence
Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityMild

ReversibilityReversible

Evidence6 citations

Nephron map

Glomerulus

Vasculature / Endothelium

Distal Tubule / Collecting Duct

Tubular LumenThe urine flow path

Crystal / Obstructive Nephropathy

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

§03

Kidney injury

Mechanism of kidney injury

Rapid cytoreduction of responsive marrow releases uric acid, phosphate and potassium; intratubular uric-acid and calcium-phosphate precipitation, combined with volume depletion, produces obstructive/crystal-related and prerenal-ischemic AKI (tumor lysis nephropathy). Separately, rare biopsy-proven decitabine-associated thrombotic microangiopathy reflects endothelial injury with glomerular fibrin thrombi, crescents and tubular necrosis.

Clinical presentation

Hyperuricemia, hyperphosphatemia, hyperkalemia and a rising creatinine within days of a responding cycle in tumor lysis; in the rare TMA presentation, nephrotic-range proteinuria, hematuria, schistocytes/thrombocytopenia and AKI develop over weeks.

Management

Treat tumor lysis with aggressive hydration, rasburicase (preferred when urate is high or the patient is at high risk) or allopurinol, and correction of hyperkalemia/hyperphosphatemia; hold the drug and provide supportive care for AKI, with hemodialysis for refractory metabolic derangements. For suspected TMA, discontinue decitabine; reported cases recovered after withdrawal with supportive care (plasma exchange is generally not effective for drug-induced TMA).Lesion-level management framework

Risk factors

High/proliferative tumor burden
Pre-existing renal impairment
Volume depletion
Hyperuricemia at baseline

Prevention

IV hydration to maintain brisk urine output
Tumor lysis prophylaxis (allopurinol or rasburicase) in at-risk patients

Anticancer mechanism· how it treats cancer

Deoxycytidine analog phosphorylated to its triphosphate and incorporated directly into DNA, where it forms an irreversible covalent complex with DNA methyltransferase, causing enzyme depletion, genome-wide hypomethylation and reactivation of silenced tumor-suppressor genes; at higher concentrations it is also directly cytotoxic. Used for myelodysplastic syndromes and acute myeloid leukemia.

Note · Direct decitabine nephrotoxicity is case-level; the dominant renal risk is treatment-related tumor lysis rather than intrinsic tubular toxicity.

§04

Clinical depth

Renal dose adjustment

No formal renal dose adjustment is established in the label; decitabine is largely metabolized by deamination (cytidine deaminase) rather than renal excretion. Use caution in significant renal impairment given limited data and monitor renal function closely.

Dialyzability & ESKD dosing

Not well characterized; the short plasma half-life and rapid deamination limit the rationale for dialytic dosing. Hemodialysis is used to treat AKI/metabolic complications, not to adjust drug levels.

Differential diagnosis

Separate tumor lysis nephropathy (urate/phosphate surge, uric-acid:creatinine >1, calcium-phosphate or urate crystals) from decitabine-associated TMA (microangiopathic hemolysis, thrombocytopenia, schistocytes, biopsy fibrin thrombi) and from prerenal azotemia. In MDS, also consider disease-related glomerulonephritis.

Monitoring

Uric acid, phosphate, potassium and calcium during early responding cycles
CBC with smear and LDH/haptoglobin if TMA is suspected
Serum creatinine through the first responding cycles

Key trials & series

Decitabine phase III MDS registration trial (Kantarjian, Cancer 2006)
Qin et al. biopsy-proven decitabine-associated renal TMA case (Medicine 2020)

Clinical pearls

The chief renal hazard of a hypomethylating agent is the tumor lysis it can precipitate when bulky disease responds, not the molecule itself.
Rasburicase is preferred over allopurinol when baseline uric acid is high or G6PD status is normal and risk is high.
A microangiopathic picture (low platelets, schistocytes, LDH) after weeks of therapy should prompt drug discontinuation rather than plasma exchange.

§05

References

6 primary references — trials, cohorts, mechanism, and reviews. Citation metadata via PubMed / NLM.

Evidence accrual

6 references · 2010–2023 · 1 since 2021

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.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 5,106 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 4.79
Electrolyte Disturbancecorroborated · ROR 1.91 — on the terms that name the lesion (ROR 3.56)
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.
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Thrombotic Microangiopathy

ROR 4.7995% CI 3.02–7.62· 18 reports

Acute Tubular Necrosis

ROR 2.5195% CI 1.13–5.59· 6 reports

Electrolyte Disturbance

ROR 1.9195% CI 1.54–2.35· 88 reports

FAERS outcomes & reporting trend· 26% of reports w/ death · 36.6% w/ hospitalization

26%

Reported with a death outcome

1,330 of 5,106 reports

36.6%

Reported with hospitalization

1,871 of 5,106 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 5 systems · 5,106 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 1.7495% CI 1.36–2.22· 64 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

Febrile Neutropenia492Myelosuppression382Neutropenia329Thrombocytopenia267Platelet Count Decreased257

Immune / infection

Pneumonia355Sepsis226Infection210

General / constitutional

Pyrexia303Fatigue252Asthenia171

Gastrointestinal

Nausea241Diarrhoea170

Respiratory

Dyspnoea140Respiratory Failure122

Guidelines & consensus· 14

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.

ADQIConventional cytotoxic chemotherapy-associated nephrotoxicity: consensus report of the 34th Acute Disease Quality Initiative (ADQI) WorkgroupKidney Int 2026 · PMID 41881107Cisplatin is identified as a leading cytotoxic nephrotoxin; the workgroup details preventive measures (adequate isotonic hydration, correction of volume depletion, avoidance of concurrent nephrotoxins, attention to electrolyte/magnesium wasting) and management of cisplatin-associated AKI, with a research agenda for knowledge gaps.

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 Decitabine 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

Hydroxyurea

Hydrea · Ribonucleotide reductase inhibitor

Profile

Tumor lysis in myeloproliferative disease.

XTALPRELYTE

Mild#1 · 88% phenotype match

Nelarabine

Arranon · Purine analog

Profile

Tumor lysis in T-ALL.

XTALPRELYTE

Mild#2 · 88% phenotype match

Cladribine

Leustatin · Purine analog

Profile

Tumor lysis; high-dose nephrotoxicity.

XTALPRELYTE

Mild#3 · 88% phenotype match

Fludarabine

Fludara · Purine analog

Profile

Tumor lysis; accumulates in renal impairment.

XTALPRELYTE

Moderate#4 · 83% phenotype match

Etoposide

Etopophos · Topoisomerase II inhibitor

Profile

Tumor lysis; renally cleared.

XTALPRELYTE

Mild#5 · 77% phenotype match

Pomalidomide

Pomalyst · Immunomodulatory drug (IMiD)

Profile

Tumor lysis; usable in renal impairment.

PRELYTEXTAL

Mild#6 · 77% phenotype match

Compare Decitabine 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 Antimetabolites

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.