Is kidney injury from Azacitidine reversible?

Reversible. Typical onset: During treatment cycles (days to weeks)..

How should kidney function be monitored during Azacitidine therapy?

Serum bicarbonate, BUN and creatinine before each cycle; Serum potassium and phosphate each cycle; Urinalysis for glucosuria/proteinuria if tubular dysfunction is suspected.

How can kidney injury from Azacitidine be prevented?

Reduce or delay the next cycle for unexplained renal dysfunction or worsening acidosis

Who is at higher risk of kidney injury from Azacitidine?

Higher cumulative dose; Pre-existing chronic kidney disease; Volume depletion; Concomitant nephrotoxins.

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Printable monograph

Hypomethylating agent

Azacitidine

Vidaza · Aza

Hypomethylating agent · approved 2004 · 8 citations · FAERS AKI reporting ROR 1.68 (95% CI 1.51–1.87, 358 AKI reports)

Recent· through 2024

Deeply sourced8/9 · 7 signals

Met: 8 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 23y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2024
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 agent that, at higher exposures, blunts the proximal tubule into a Fanconi-like acidosis.

ModerateHypomethylating agent

Myelodysplastic syndromesAcute myeloid leukemiaChronic myelomonocytic leukemia

§01

Signature kidney injury

Signature lesion

Fanconi Syndrome

Proximal tubular dysfunction (proximal/type 2 renal tubular acidosis, polyuria, and glucose/amino-acid/electrolyte wasting) was described with higher-dose azacitidine; with current low-dose subcutaneous/IV regimens overt AKI is uncommon and renal incidence is not well quantified (case-level).Source: Kintzel, Drug Saf 2001

Onset & rechallenge

Time to injuryAcute (~1–7 days)

During treatment cycles, days to weeks after starting.

Distilled from: “During treatment cycles (days to weeks).”

Long-term outlook & thresholds

Renal recoveryUsually reversible

Proximal tubular dysfunction (type 2 RTA / Fanconi-like syndrome) typically improves after dose reduction or discontinuation; the label triggers a 50% next-cycle reduction for unexplained bicarbonate <20 mEq/L or a BUN/creatinine rise, with resumption only after recovery.PMID 11219485 (opens PubMed in a new tab)

Cumulative-dose threshold

No validated numeric cumulative-dose threshold; the tubular-acidosis signal is exposure-dependent and derives largely from older higher-dose regimens.

Proximal (type 2) renal tubular acidosis and a Fanconi-like syndrome (bicarbonaturia, normoglycemic glucosuria, phosphate/potassium wasting) — uncommon with current low-dose subcutaneous/IV dosing.PMID 11219485 (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

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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.

Fanconi Syndrome#1 · Signatureno population incidence denominator
The characteristic renal lesion is a proximal (type 2) RTA / Fanconi-like tubulopathy (higher-dose exposure); quantitatively uncommon (case-level) with modern low-dose regimens PMID 29114374 (opens PubMed in a new tab)
Acute Tubular NecrosisSecondaryqualitative — no citable incidence
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.
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).
Pseudo-AKISecondaryqualitative — no citable incidence
The great mimic — a rise in creatinine from blocked tubular secretion (OCT2/MATE), NOT true injury. The GFR is intact; confirm with cystatin C before stopping effective therapy.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityModerate

ReversibilityReversible

Evidence8 citations

Nephron map

Proximal TubuleBulk reabsorption + drug uptake (OCT2, OATs)

Distal Tubule / Collecting Duct

Fanconi Syndrome

Global failure of proximal tubule reabsorption — glucosuria, phosphaturia and acidosis, classically from ifosfamide.

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Kidney injury

Mechanism of kidney injury

Direct proximal tubular epithelial toxicity impairs the apical/basolateral transport machinery (sodium-bicarbonate cotransport, sodium-glucose and sodium-amino-acid cotransport), producing a proximal (type 2) renal tubular acidosis and a Fanconi-like syndrome with bicarbonaturia, glucosuria, aminoaciduria and phosphate/potassium wasting. With heavier exposure, tubular cell injury can progress to acute tubular necrosis. Because azacitidine is incorporated into RNA of metabolically active, mitochondria-rich proximal tubular cells, energy-dependent reabsorption is preferentially disrupted.

Clinical presentation

Non-anion-gap (hyperchloremic) metabolic acidosis with an inappropriately alkaline urine pH for the degree of acidemia, polyuria, normoglycemic glucosuria, hypokalemia and hypophosphatemia; bland urinalysis aside from glucosuria. Creatinine rises in more severe cases.

Management

Hold or reduce dose for unexplained renal dysfunction or worsening acidosis. Replace bicarbonate, potassium and phosphate; remove concurrent nephrotoxins. Tubular dysfunction typically improves after dose reduction or discontinuation. Before dose-reducing for an isolated creatinine bump, confirm a true GFR fall: azacitidine can also produce a pseudo-AKI in which it blocks tubular creatinine secretion so serum creatinine rises while cystatin C / measured GFR is preserved — checking cystatin C avoids needlessly cutting an effective therapy.Lesion-level management framework

Risk factors

Higher cumulative dose
Pre-existing chronic kidney disease
Volume depletion
Concomitant nephrotoxins

Prevention

Reduce or delay the next cycle for unexplained renal dysfunction or worsening acidosis

Anticancer mechanism· how it treats cancer

Pyrimidine (cytidine) analog incorporated into RNA (the majority) and, after reduction, into DNA. Once in DNA it forms an irreversible covalent adduct with DNA methyltransferase, depleting the enzyme and producing genome-wide hypomethylation that reverses aberrant promoter silencing and restores tumor-suppressor expression. Standard therapy for myelodysplastic syndromes (MDS), acute myeloid leukemia and chronic myelomonocytic leukemia.

Note · Classic tubular-acidosis signal derives largely from older higher-dose data; modern low-dose renal toxicity is case-level. Kidney injury in MDS patients is frequently disease- or vasculitis-related rather than drug-induced, which matters for attribution. Azacitidine pseudo-AKI — an isolated creatinine rise from inhibited tubular creatinine secretion with a preserved true GFR — is reported as an ASN Kidney Week abstract (listed under this agent's non-PubMed conference reports).

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Clinical depth

Renal dose adjustment

No starting-dose adjustment is required for baseline renal impairment, but the label mandates a 50% dose reduction of the next cycle if unexplained serum bicarbonate <20 mEq/L or a rise in BUN/creatinine occurs, with resumption only after recovery to baseline. Use with caution and closer monitoring in CKD.

Dialyzability & ESKD dosing

Azacitidine and its metabolites are partly renally cleared; specific hemodialysis removal data are limited. It is given to dialysis patients in practice with careful monitoring, but no validated supplemental dosing exists.

Differential diagnosis

Differentiate drug-induced proximal RTA/Fanconi (normoglycemic glucosuria, hypophosphatemia, low-molecular-weight proteinuria) from MDS-associated kidney disease (often a pauci-immune or ANCA-associated vasculitis with active urine sediment and hematuria) and from prerenal azotemia (bland sediment, FeNa <1%). A kidney biopsy is warranted when MDS-related glomerulonephritis is suspected.

Monitoring

Serum bicarbonate, BUN and creatinine before each cycle
Serum potassium and phosphate each cycle
Urinalysis for glucosuria/proteinuria if tubular dysfunction is suspected

Key trials & series

AZA-001 survival trial (Lancet Oncol 2009) — established azacitidine in higher-risk MDS (renal effects were uncommon at standard dosing)
Historical high-dose azacitidine experience underlying the tubular-acidosis signal

Clinical pearls

Think proximal RTA, not glomerular disease — the hallmark is a normal-anion-gap acidosis with glucosuria despite euglycemia.
Much of the AKI in azacitidine-treated MDS patients is from the underlying disease (vasculitis), so biopsy before blaming the drug.
The label gives an explicit bicarbonate threshold (<20 mEq/L) that triggers a 50% dose reduction.

§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 · 2001–2024 · 1 since 2022

Primary (non–case-report) references per year — a proxy for how actively the agent's renal literature is accruing. Recent years are highlighted. Reflects curation depth, not a systematic bibliometric count.

Case reports — ranked by strength· 2

Single-patient and small-series reports, graded by evidentiary strength — A Strong (biopsy-proven plus a series and/or positive rechallenge), B Moderate, and C Limited (a single clinically-diagnosed case). Strongest first. Grades are inferred automatically from each report's abstract and journal — a heuristic ranking aid, not a formal quality appraisal.

CaseC · LimitedReversible renal impairment after administration of a single dose of Azacitidine.Villanueva Sánchez E et al. · Med Clin (Barc) 2024 · PMID 38423943Case report of acute, reversible renal impairment (acute kidney injury) developing after a single dose of azacitidine, resolving on withdrawal.CaseC · LimitedVenetoclax with Azacitidine Induced Tumor Lysis Syndrome in an Elderly Patient with Acute Myeloid Leukemia: A Case Report.Kim M et al. · Electrolyte Blood Press 2021 · PMID 35003285Case report of tumor lysis syndrome with attendant electrolyte derangement and acute kidney injury after venetoclax plus azacitidine in a low-burden AML patient.

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.

AbstractAzacitidine Inhibition of Creatinine Tubular Secretion: A Case ReportASN Kidney Week 2019 2019 · Abstract TH-PO150Episodic serum-creatinine rises on azacitidine that did not track with cystatin C, indicating blocked tubular creatinine secretion (pseudo-AKI) rather than a true GFR fall — a useful counterpoint to azacitidine's better-known proximal tubulopathy.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 29,498 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

Fanconi Syndromecorroborated · ROR 2.78 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
Electrolyte Disturbancecorroborated · ROR 1.85 — on the terms that name the lesion (ROR 2.31)
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.
Pseudo-AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Fanconi Syndrome

ROR 2.7895% CI 1.79–4.32· 20 reports

Electrolyte Disturbance

ROR 1.8595% CI 1.70–2.03· 494 reports

Thrombotic Microangiopathy

ROR 1.7995% CI 1.31–2.46· 39 reports

SIADH / Hyponatremia

ROR 1.6695% CI 1.43–1.91· 187 reports

Hemorrhagic Cystitis

ROR 1.5595% CI 1.32–1.82· 151 reports

FAERS outcomes & reporting trend· 36.5% of reports w/ death · 43.5% w/ hospitalization

36.5%

Reported with a death outcome

10,778 of 29,498 reports

43.5%

Reported with hospitalization

12,837 of 29,498 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 4 systems · 29,498 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 1.6895% CI 1.51–1.87· 358 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 Neutropenia2,963Neutropenia1,916Myelosuppression1,609Thrombocytopenia1,540Anaemia1,346

Immune / infection

Pneumonia2,000Sepsis1,258Infection1,116Septic Shock610

General / constitutional

Pyrexia1,659Fatigue762Asthenia616

Gastrointestinal

Nausea1,022Diarrhoea882Vomiting639

Guidelines & consensus· 18

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.TLS Expert PanelGuidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based reviewJ Clin Oncol 2008 · PMID 18509186Prevention is the best management: hydration plus prophylactic rasburicase for high-risk patients, hydration plus allopurinol or rasburicase for intermediate-risk, and monitoring for low-risk; for established TLS add aggressive hydration and diuresis plus allopurinol or rasburicase for hyperuricemia. Urinary alkalinization is NOT recommended.TLS Consensus PanelRecommendations for the evaluation of risk and prophylaxis of tumour lysis syndrome (TLS) in adults and children with malignant diseases: an expert TLS panel consensusBr J Haematol 2010 · PMID 20331465Stratify each patient as low/intermediate/high TLS risk using tumor type, bulk/stage, proliferation rate, baseline laboratory TLS, and renal impairment/involvement, then match prophylaxis intensity (monitoring vs allopurinol vs rasburicase) to the assigned risk level.BCSHGuidelines for the management of tumour lysis syndrome in adults and children with haematological malignancies on behalf of the British Committee for Standards in HaematologyBr J Haematol 2015 · PMID 25876990Risk-adapted prophylaxis and management of TLS in haematological malignancy: hydration with allopurinol for lower-risk and rasburicase for high-risk patients, with monitoring of electrolytes and renal function to prevent and treat AKI.Cairo-BishopTumour lysis syndrome: new therapeutic strategies and classificationBr J Haematol 2004 · PMID 15384972Defines the Cairo-Bishop criteria distinguishing laboratory TLS (>=2 metabolic abnormalities: hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia within 3 days before to 7 days after therapy) from clinical TLS (laboratory TLS plus AKI, cardiac arrhythmia, or seizure), with a severity grading scheme adopted by subsequent guidelines.

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 Azacitidine 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 deruxtecan

Enhertu · Antibody-drug conjugate (HER2/DXd)

Profile

Emerging AKI/proteinuria reports — under-published.

ATNFANCLYTE

Moderate#1 · 77% phenotype match

Imatinib

Gleevec · BCR-ABL TKI

Profile

Fluid retention; rare Fanconi and AKI.

LYTEFANCATN

Mild#2 · 72% phenotype match

Streptozocin

Zanosar · Nitrosourea alkylator

Profile

Classic proximal tubular toxin → Fanconi and dose-limiting AKI.

FANCATNLYTE

Severe#3 · 72% phenotype match

Pentostatin

Nipent · Purine analog (ADA inhibitor)

Profile

Renally cleared; dose-related acute kidney injury.

ATNLYTESIADH

Moderate#4 · 71% phenotype match

Nedaplatin

Aqupla · Platinum agent

Profile

Second-gen platinum with reduced renal toxicity vs cisplatin.

ATNLYTE

Moderate#5 · 65% phenotype match

Zoledronic acid

Zometa · Bisphosphonate

Profile

Toxic ATN, infusion-rate dependent.

ATNFANC

Moderate#6 · 65% phenotype match

Compare Azacitidine 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.

Who studies this

The leading contributors to Azacitidine’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 Azacitidine; 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 16 clinical records among all 21 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.