What kind of kidney injury does Cytarabine 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, SIADH / Hyponatremia.

Is kidney injury from Cytarabine reversible?

Reversible. Typical onset: Hours to days after initiating therapy in high-burden disease..

How should kidney function be monitored during Cytarabine therapy?

TLS panel (uric acid, K, phosphate, calcium, creatinine) frequently during induction; Neurologic/cerebellar exam with high-dose cytarabine, especially if renal function declines; Urine output and volume status.

How can kidney injury from Cytarabine be prevented?

TLS prophylaxis: aggressive hydration plus allopurinol or rasburicase by risk

Who is at higher risk of kidney injury from Cytarabine?

High tumor burden / high blast count; High baseline uric acid and LDH; Volume depletion and pre-existing renal impairment; Bulky/aggressive lymphoma (e.g., Burkitt).

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Printable monograph

Nucleoside analog

Cytarabine

Cytosar · AraC

Nucleoside analog · approved 1969 · 9 citations · FAERS AKI reporting ROR 2.85 (95% CI 2.70–3.02, 1,260 AKI reports)

Recent· through 2023

Deeply sourced8/9 · 7 signals

Met: 9 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 44y)
Met: Beyond single case reports
Met: High-impact journal
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.

The leukemia cornerstone whose renal danger comes from the tumor burden it melts away.

ModerateNucleoside analog antimetabolite

Acute myeloid leukemia (induction and high-dose consolidation)Acute lymphoblastic leukemiaLymphoma / CNS prophylaxis (intrathecal)

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Signature kidney injury

Signature lesion

Crystal / Obstructive Nephropathy

Intrinsic tubular nephrotoxicity is uncommon; the major renal risk is AKI from tumor lysis syndrome during leukemia/lymphoma cytoreduction, reported at case and series level including fatal TLS. Direct cytarabine-nephrotoxicity primary literature is genuinely sparse.Source: Seymour et al., Cancer 2002

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Hours to days after initiating therapy in high-burden disease.

Distilled from: “Hours to days after initiating therapy in high-burden disease.”

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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.

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).
SIADH / HyponatremiaRarequalitative — no citable incidence
One episode in a 1979 single-agent high-dose series; co-therapy and leukemic ADH production explain most reporting.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityModerate

ReversibilityReversible

Evidence9 citations

Nephron map

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.

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Kidney injury

Deep diveTumor lysis syndromeEffective therapy can kill a large, fast-dividing cancer so abruptly that the cells spill their contents into the blood — potassium, phosphate, and a flood of purines that becomes uric acid — and the two crystals that result, urate and calcium-phosphate, clog and poison the tubules: a metabolic emergency that is largely preventable with hydration, rasburicase, and, for venetoclax, a deliberately slow dose ramp-up.

Mechanism of kidney injury

Rapid leukemic/lymphoma cell kill releases uric acid, potassium and phosphate, producing tumor lysis syndrome with uric acid and calcium-phosphate crystal precipitation, intratubular obstruction and AKI; oliguria and electrolyte derangements dominate. High-dose cytarabine adds systemic toxicities (cerebellar, ocular, mucosal) but not characteristic tubular injury; renal clearance considerations modestly affect high-dose scheduling.

Clinical presentation

Hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia and rising creatinine at the start of cytoreductive therapy; oliguria in severe TLS.

Management

Treat established TLS with IV fluids, rasburicase, electrolyte correction and dialysis if needed (per the 2015 British/expert TLS guidance); supportive care for high-dose toxicities. TLS-related AKI is generally reversible with prompt management.Lesion-level management framework

Risk factors

High tumor burden / high blast count
High baseline uric acid and LDH
Volume depletion and pre-existing renal impairment
Bulky/aggressive lymphoma (e.g., Burkitt)

Prevention

TLS prophylaxis: aggressive hydration plus allopurinol or rasburicase by risk

Anticancer mechanism· how it treats cancer

Pyrimidine nucleoside analog phosphorylated to ara-CTP, which incorporates into DNA and inhibits DNA polymerase, halting S-phase replication. Cornerstone of acute myeloid leukemia induction/consolidation and used in lymphomas and CNS prophylaxis (intrathecal).

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Clinical depth

Renal dose adjustment

Standard-dose cytarabine needs little renal adjustment; for HIGH-dose cytarabine, reduced renal function (and age) increase the risk of neurotoxicity (cerebellar) so dose reduction is advised when creatinine/CrCl worsens. Renal handling is a high-dose neurotoxicity concern more than a nephrotoxicity one.

Dialyzability & ESKD dosing

Cytarabine is rapidly deaminated to inactive ara-U with a short half-life; it is not primarily managed by dialysis, though dialysis is used to treat TLS-related renal failure and electrolyte derangements.

Differential diagnosis

TLS-AKI (hyperuricemia, hyperphosphatemia, hyperkalemia, oliguria after cytoreduction) vs prerenal azotemia (volume-responsive) vs leukemic renal infiltration. With high-dose cytarabine, distinguish renal-function-driven cerebellar neurotoxicity from CNS disease - the kidney shapes neurotoxicity risk more than it manifests injury.

Monitoring

TLS panel (uric acid, K, phosphate, calcium, creatinine) frequently during induction
Neurologic/cerebellar exam with high-dose cytarabine, especially if renal function declines
Urine output and volume status

Key trials & series

Seymour Cancer 2002 (cisplatin-fludarabine-cytarabine salvage) - cytarabine-containing regimen with fatal TLS
KDIGO onco-nephrology controversies conference (Malyszko Kidney Int 2020) - AKI/TLS in hematologic malignancy
British/expert TLS management guidance (rasburicase, hydration)

Clinical pearls

The renal threat is the tumor, not the drug: anticipate and prophylax TLS at induction in high-burden AML/lymphoma.
With HIGH-dose cytarabine, a falling CrCl is a cerebellar-toxicity red flag - reduce dose and examine for nystagmus/ataxia.
Rasburicase plus hydration is the workhorse for cytarabine-era TLS-AKI, which is usually reversible.
A single-agent high-dose cytarabine series recorded one SIADH episode (1979); most SIADH in cytarabine regimens belongs to vincristine/cyclophosphamide partners or leukemic ADH production.

Beyond the kidney — non-renal toxicities· 4 organ systems

Class-level context for the major non-renal toxicities of the Nucleoside analog class.

Gastrointestinal

Diarrhea, colitis, mucositis, perforation

Mucositis and diarrhea

Hepatic / Liver

Transaminitis, hepatitis, VOD/SOS

Transaminitis (methotrexate)

Hematologic

Cytopenias, thrombosis, TMA

Myelosuppression

Pulmonary

Pneumonitis, ILD, effusions, hypertension

Methotrexate / gemcitabine pneumonitis

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References

7 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

7 references · 1979–2023 · 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.

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.

CaseB · ModerateAcute tumor lysis syndrome and treatment response in patients treated for refractory chronic lymphocytic leukemia with short-course, high-dose cytosine arabinoside, cisplatin, and etoposide.McCroskey RD et al. · Cancer 1990 · PMID 2369709Small case series in which high-dose cytarabine-based therapy triggered acute tumor lysis syndrome with renal compromise (one death from acute tumor lysis), a volume-depletion/urate hemodynamic mechanism of AKI managed with hydration and forced diuresis.CaseC · LimitedAcute rhabdomyolysis as a complication of cytarabine chemotherapy for acute myeloid leukemia: case report and review of literature.Truica CI et al. · Am J Hematol 2002 · PMID 12210815AML patient developed fulminant cytarabine-induced rhabdomyolysis complicated by acute renal failure requiring hemodialysis, a myoglobinuric/hemodynamic mechanism of AKI directly attributed to cytarabine.

FDA label — boxed warning & renal dosing· boxed warning

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

Boxed warning

WARNING Only physicians experienced in cancer chemotherapy should use Cytarabine Injection. For induction therapy patients should be treated in a facility with laboratory and supportive resources sufficient to monitor drug tolerance and protect and maintain a patient compromised by drug toxicity. The main toxic effect of cytarabine is bone marrow suppression with leukopenia, thrombocytopenia and anemia. Less serious toxicity includes nausea, vomiting, diarrhea and abdominal pain, oral ulceration and hepatic dysfunction. The physician must judge possible benefit to the patient against known toxic effects of this drug in considering the advisability of therapy with cytarabine. Before making this judgment or beginning treatment, the physician should be familiar with the following text.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 61,947 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· 7 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 2.42 — on the terms that name the lesion (ROR 2.65)
SIADH / Hyponatremiacorroborated · ROR 2.09 — on the terms that name the lesion (ROR 4.31)
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 4.8695% CI 4.25–5.55· 219 reports

Acute Tubular Necrosis

ROR 2.8195% CI 2.25–3.49· 81 reports

Hemorrhagic Cystitis

ROR 2.5795% CI 2.35–2.80· 520 reports

Electrolyte Disturbance

ROR 2.4295% CI 2.29–2.56· 1,345 reports

SIADH / Hyponatremia

ROR 2.0995% CI 1.91–2.29· 494 reports

Acute Interstitial Nephritis

ROR 1.5095% CI 1.21–1.86· 83 reports

Glomerular Injury / Proteinuria

ROR 1.2295% CI 1.01–1.48· 105 reports

FAERS outcomes & reporting trend· 23.2% of reports w/ death · 40.2% w/ hospitalization

23.2%

Reported with a death outcome

14,387 of 61,947 reports

40.2%

Reported with hospitalization

24,916 of 61,947 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 61,947 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 2.8595% CI 2.70–3.02· 1,260 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 Injury1,260

Blood & lymphatic

Febrile Neutropenia8,130Neutropenia3,748Thrombocytopenia3,017Myelosuppression2,322Pancytopenia2,189

Immune / infection

Sepsis3,082Pneumonia2,492Septic Shock1,948Infection1,916

Gastrointestinal

Nausea1,907Mucosal Inflammation1,827Diarrhoea1,821Vomiting1,761

General / constitutional

Pyrexia4,380

Vascular

Hypotension1,486

Respiratory

Respiratory Failure1,299

Nervous system

Headache1,071

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 Cytarabine 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

Fludarabine

Fludara · Purine analog

Profile

Tumor lysis; accumulates in renal impairment.

XTALPRELYTE

Moderate#1 · 88% phenotype match

Hydroxyurea

Hydrea · Ribonucleotide reductase inhibitor

Profile

Tumor lysis in myeloproliferative disease.

XTALPRELYTE

Mild#2 · 83% phenotype match

Nelarabine

Arranon · Purine analog

Profile

Tumor lysis in T-ALL.

XTALPRELYTE

Mild#3 · 83% phenotype match

Cladribine

Leustatin · Purine analog

Profile

Tumor lysis; high-dose nephrotoxicity.

XTALPRELYTE

Mild#4 · 82% phenotype match

Decitabine

Dacogen · Hypomethylating agent

Profile

Tumor lysis in MDS/AML.

XTALPRELYTE

Mild#5 · 75% phenotype match

Dactinomycin (actinomycin D)

Cosmegen · Antitumor antibiotic

Profile

Renal risk indirect via tumor lysis in chemosensitive pediatric tumors; hepatic veno-occlusive disease is the signature organ toxicity.

LYTEPREXTAL

Moderate#6 · 75% phenotype match

Compare Cytarabine 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 Cytarabine’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 Cytarabine; 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 52 clinical records among all 102 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.