Is kidney injury from Cyclophosphamide reversible?

Reversible. Typical onset: Hyponatremia within hours; cystitis acute..

How should kidney function be monitored during Cyclophosphamide therapy?

Serum sodium at baseline and within 24-48 h after high-dose IV cyclophosphamide, watching for acute dilutional hyponatremia/SIADH, especially when large hypotonic fluid volumes are co-administered for cystitis prophylaxis; Strict intake/output and daily weights during and after high-dose infusions to detect water retention before symptomatic hyponatremia develops; Urinalysis/urine dipstick for hematuria during and after therapy as an early sign of acrolein-mediated hemorrhagic cystitis; Serum creatinine/electrolytes and, in high tumor-burden hematologic disease, tumor lysis labs (K, phosphate, uric acid) around initial dosing; Symptom review for headache, nausea, confusion or seizures that may signal acute hyponatremia.

How can kidney injury from Cyclophosphamide be prevented?

Use isotonic rather than hypotonic fluids Mesna + hydration for cystitis

Who is at higher risk of kidney injury from Cyclophosphamide?

High-dose IV regimens; Concurrent hypotonic fluids.

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Printable monograph

Oxazaphosphorine alkylator

Cyclophosphamide

Cytoxan · Cyclo

Oxazaphosphorine alkylator · approved 1959 · 8 citations · FAERS AKI reporting ROR 2.20 (95% CI 2.12–2.29, 2,763 AKI reports)

Recent· through 2023

Deeply sourced8/9 · 7 signals

Met: 8 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 49y)
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 water-retainer — a vasopressin-independent drive to hold on to free water.

MildOxazaphosphorine alkylator

LymphomaBreastAutoimmune diseaseConditioning

§01

Signature kidney injury

Signature lesion

SIADH / Hyponatremia

Representative incidence52%

Dose-related hyponatremia (not reliably quantified); hemorrhagic cystitis ~5–20%, lower with mesna prophylaxis. Reported rate: hyponatremia in 52% — 69 adults who received high-dose cyclophosphamide therapy at a single center 2010-2014 (retrospective cohort (Bonella 2017, PMID 29890094).Source: Bonella et al., Rev Fac Cien Med Univ Nac Cordoba 2017

Onset & rechallenge

Time to injuryHyperacute (<24 h)

Hyponatremia within hours of dosing; cystitis is acute.

Distilled from: “Hyponatremia within hours; cystitis acute.”

Long-term outlook & thresholds

Renal recoveryUsually reversible

Both renal manifestations are acute and self-limited: the dilutional hyponatremia resolves with fluid restriction and sodium correction as the drug clears, and hemorrhagic cystitis settles with mesna, hydration and bladder irrigation. Unlike ifosfamide, cyclophosphamide is not a driver of chronic tubulopathy or CKD — it is the less urotoxic of the two oxazaphosphorines.PMID 9415661 (opens PubMed in a new tab)

Early-detection biomarkers

Serum sodium (with paired serum + urine osmolality) — SIADH-type dilutional hyponatremia (vasopressin-independent collecting-duct free-water retention). The signature injury is acute hyponatremia within hours of high-dose infusion; serial sodium with a low serum osmolality against an inappropriately concentrated urine flags water intoxication early — important because large hydration volumes are co-administered for bladder protection.PMID 4607502 (opens PubMed in a new tab)
Urinalysis — microscopic + dipstick hematuria — Acrolein hemorrhagic cystitis. Microscopic and dipstick urinalysis is the established bedside monitor for cyclophosphamide bladder toxicity — red cells precede gross hematuria and trigger mesna/hydration escalation; the randomized BMT-conditioning trial tracked patients exactly this way.PMID 1941060 (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

Host risk modifiers

Germline / pharmacogenomic variants that shift an individual's risk of this agent's kidney injury. Research-grade — not routine clinical testing.

GSTM1functional (non-null) GSTM1, combined with CYP2C9 normal-function genotype
In children receiving cyclophosphamide-based myeloablative conditioning before allogeneic HSCT, carrying functional alleles at both GSTM1 and CYP2C9 was associated with ~4.8-fold higher risk of hemorrhagic cystitis (HR 4.8, 95% CI 1.3-18.4, p=0.02) vs dysfunctional/null genotypes, supporting pre-emptive genotyping to guide uroprotective prophylaxis. PMID 28744217 (opens PubMed in a new tab)

§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.

SIADH / Hyponatremia#1 · Signatureno population incidence denominator
SIADH with hyponatremia is a recognized complication of high-dose cyclophosphamide (direct collecting-duct water retention); described at case/mechanistic level with no cohort incidence denominator. PMID 10864220 (opens PubMed in a new tab)
Hemorrhagic CystitisSecondary2.7%PMID 21337321 (opens PubMed in a new tab)
Hemorrhagic cystitis in 22/805 (2.7%) cyclophosphamide-treated systemic necrotizing vasculitis patients over 4,230 patient-years; risk driven by cumulative dose and oral (vs IV) administration. Higher and dose-limiting in high-dose/conditioning settings without mesna.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

52%incidence

SeverityMild

ReversibilityReversible

Evidence8 citations

Nephron map

Distal Tubule / Collecting DuctFine-tuning of Na, K, Mg, acid & water

Bladder / Urothelium

SIADH / Hyponatremia

Inappropriate water retention at the collecting duct — high-dose cyclophosphamide.

§03

Kidney injury

Deep diveDrug-induced SIADH: the sodium falls and the tumour takes the blameHyponatremia is the commonest electrolyte disorder in oncology and its commonest explanation is the cancer itself — which is exactly why a drug that impairs free-water excretion can go on being given for months while the sodium is treated as a feature of the disease.

Mechanism of kidney injury

Thought to up-regulate aquaporin-2 in the collecting duct independent of vasopressin (shown in rat studies), retaining free water — dangerous because large hydration volumes are co-administered to protect the bladder. The acrolein metabolite causes hemorrhagic cystitis.

Clinical presentation

Acute hyponatremia within hours of high-dose infusion, low serum osmolality with inappropriately concentrated urine; hematuria from cystitis.

Management

Careful fluid management and sodium correction; mesna, hydration and bladder irrigation for cystitis.Lesion-level management framework

Risk factors

High-dose IV regimens
Concurrent hypotonic fluids

Prevention

Use isotonic rather than hypotonic fluids
Mesna + hydration for cystitis

Anticancer mechanism· how it treats cancer

Prodrug converted to phosphoramide mustard, cross-linking DNA. Lymphomas, breast cancer, autoimmune disease and transplant conditioning.

Note · Less urotoxic than ifosfamide.

§04

Clinical depth

Renal dose adjustment

Cyclophosphamide itself is not classically considered intrinsically nephrotoxic and the FDA label does not specify creatinine-clearance-based cutpoints; however, parent drug and active metabolites are partly renally cleared, so clinical practice and onco-nephrology references suggest dose attenuation (often roughly 25% reduction) for severe impairment (CrCl <10-25 mL/min) and caution in advanced CKD to limit accumulation and exaggerated toxicity. Adequate hydration with high IV doses is the key renal-safety measure, more so than empiric dose cuts.

Dialyzability & ESKD dosing

Cyclophosphamide and its metabolites are appreciably dialyzable (the parent is a small, water-soluble, minimally protein-bound molecule), with reported clearance during hemodialysis; on HD days it is conventionally administered after dialysis, or dosing is timed to avoid removing drug before it is bioactivated. Data are limited and largely pharmacokinetic/case-level rather than from prospective ESKD dosing studies.

Differential diagnosis

Cyclophosphamide-associated hyponatremia is typically acute, transient, and tightly time-locked to a high-dose IV infusion (often within hours), reflecting a direct distal-nephron/ADH-potentiating water-retention effect compounded by the large fluid loads given for cystitis prophylaxis — distinguish it from chronic SIADH of malignancy, vincristine/other-drug SIADH, and true hypovolemic hyponatremia. Hematuria here is hemorrhagic cystitis (lower urinary tract, acrolein-driven, dysmorphic-RBC-poor, often with clots) rather than a glomerular or tubular parenchymal lesion; contrast with ifosfamide, which more characteristically causes proximal tubulopathy/Fanconi syndrome.

Monitoring

Serum sodium at baseline and within 24-48 h after high-dose IV cyclophosphamide, watching for acute dilutional hyponatremia/SIADH, especially when large hypotonic fluid volumes are co-administered for cystitis prophylaxis
Strict intake/output and daily weights during and after high-dose infusions to detect water retention before symptomatic hyponatremia develops
Urinalysis/urine dipstick for hematuria during and after therapy as an early sign of acrolein-mediated hemorrhagic cystitis
Serum creatinine/electrolytes and, in high tumor-burden hematologic disease, tumor lysis labs (K, phosphate, uric acid) around initial dosing
Symptom review for headache, nausea, confusion or seizures that may signal acute hyponatremia

Key trials & series

CYCLOPS (Ann Rheum Dis/JAMA 2009, de Groot) — pulse vs daily oral cyclophosphamide in ANCA vasculitis; lower cumulative dose with pulse dosing, relevant to cumulative-exposure toxicity including bladder
Euro-Lupus Nephritis Trial (Houssiau, Arthritis Rheum 2002) — low-dose vs high-dose IV cyclophosphamide in lupus nephritis showed equivalent renal efficacy with reduced cumulative exposure/toxicity

Clinical pearls

The dominant 'renal' signature is acute, dose-dependent hyponatremia/SIADH after high-dose IV cyclophosphamide — give isotonic rather than hypotonic fluids and avoid overhydration with free water to prevent symptomatic, occasionally seizure-inducing, water intoxication.
Hemorrhagic cystitis is caused by the metabolite acrolein concentrating in urine, not by parenchymal kidney injury; prevent it with mesna (which detoxifies acrolein in the bladder) plus aggressive hydration and frequent voiding.
Unlike its analog ifosfamide, cyclophosphamide rarely causes proximal tubular dysfunction or Fanconi syndrome — overt parenchymal nephrotoxicity is uncommon and the agent is generally regarded as mild for the kidney at standard doses.
The hyponatremia is usually self-limited as the drug clears; management is fluid restriction and isotonic-fluid correction rather than chronic SIADH therapy, with attention to avoiding overly rapid sodium correction.
Cumulative dose drives long-term urologic risk (chronic cystitis, fibrosis, and bladder malignancy), so dose-sparing regimens (e.g., pulse IV or Euro-Lupus low-dose protocols) reduce toxicity without sacrificing efficacy in autoimmune indications.

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

Class-level context for the major non-renal toxicities of the Oxazaphosphorine alkylator class.

Hematologic

Cytopenias, thrombosis, TMA

Myelosuppression; secondary malignancy risk

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

Ifosfamide encephalopathy (chloroacetaldehyde)

Cardiac

Cardiomyopathy, QT, ischemia, myocarditis

High-dose cyclophosphamide cardiotoxicity

§05

References

5 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

5 references · 1974–2017 · 2 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.

Case reports — ranked by strength· 3

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 · LimitedCyclophosphamide-induced symptomatic hyponatraemia.Bruining DM et al. · Neth J Med 2011 · PMID 21527808Severe symptomatic hyponatremia with seizure following adjuvant cyclophosphamide-containing chemotherapy, a rare life-threatening SIADH-type complication.CaseC · LimitedWater intoxication following moderate-dose intravenous cyclophosphamide.Bressler RB et al. · Arch Intern Med 1985 · PMID 3977522First report of water intoxication/impaired free-water excretion after moderate-dose IV cyclophosphamide, with renal insufficiency identified as a risk factor.CaseC · LimitedLow-Dose Cyclophosphamide Associated With Hyponatremia and Hepatotoxicity.DeChiara JR et al. · Cureus 2023 · PMID 37849582Case of cyclophosphamide-induced symptomatic hyponatremia attributed to nephrogenic syndrome of inappropriate antidiuresis (water toxicity), even at low dose.

FDA label — boxed warning & renal dosing· renal impairment

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

Renal impairment — from the label

Monitor for toxicity in patients with moderate and severe renal impairment. ( 8.6 , 12.3 )

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 176,004 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· 8 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

Hemorrhagic Cystitiscorroborated · ROR 3.64 — on the terms that name the lesion (ROR 46.43)
SIADH / Hyponatremiacorroborated · ROR 2.35 — on the terms that name the lesion (ROR 4.7)

Thrombotic Microangiopathy

ROR 9.8895% CI 9.31–10.48· 1,187 reports

Hemorrhagic Cystitis

ROR 3.6495% CI 3.49–3.81· 2,056 reports

Glomerular Injury / Proteinuria

ROR 3.5595% CI 3.32–3.80· 846 reports

SIADH / Hyponatremia

ROR 2.3595% CI 2.24–2.48· 1,565 reports

Electrolyte Disturbance

ROR 2.2195% CI 2.14–2.29· 3,477 reports

Fanconi Syndrome

ROR 2.0295% CI 1.63–2.50· 86 reports

Acute Tubular Necrosis

ROR 1.8895% CI 1.60–2.21· 154 reports

Acute Interstitial Nephritis

ROR 1.5295% CI 1.34–1.73· 238 reports

FAERS outcomes & reporting trend· 20.3% of reports w/ death · 36.2% w/ hospitalization

20.3%

Reported with a death outcome

35,641 of 176,004 reports

36.2%

Reported with hospitalization

63,682 of 176,004 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 6 systems · 176,004 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 2.2095% CI 2.12–2.29· 2,763 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 Neutropenia14,530Neutropenia10,580Thrombocytopenia6,525Anaemia6,149Myelosuppression4,374

Immune / infection

Pneumonia6,669Sepsis5,730Infection4,649Cytokine Release Syndrome3,746

Gastrointestinal

Nausea6,252Diarrhoea5,490Vomiting4,912Mucosal Inflammation3,569

General / constitutional

Pyrexia9,243Fatigue4,227Asthenia3,148

Respiratory

Dyspnoea3,811

Nervous system

Neuropathy Peripheral3,476

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 Cyclophosphamide 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

Thiotepa

Tepadina · Alkylator

Profile

Hemorrhagic cystitis; renally cleared.

CYST

Mild#1 · 65% phenotype match

Melphalan

Alkeran · Alkylator

Profile

SIADH in high-dose myeloma conditioning; renally cleared.

SIADHLYTE

Mild#2 · 56% phenotype match

Temozolomide

Temodar · Alkylator

Profile

Occasional SIADH; generally renally well tolerated.

SIADHLYTE

Mild#3 · 56% phenotype match

Chlorambucil

Leukeran · Alkylating agent (nitrogen mustard)

Profile

Minimal direct nephrotoxicity; rare drug-associated SIADH/hyponatremia is the kidney-relevant signal.

SIADHLYTE

Mild#4 · 54% phenotype match

Vinblastine

Velban · Vinca alkaloid

Profile

SIADH and rare Raynaud/vascular events.

SIADHLYTE

Mild#5 · 46% phenotype match

Vincristine

Oncovin · Vinca alkaloid

Profile

SIADH → hyponatremia.

SIADHLYTE

Mild#6 · 46% phenotype match

Compare Cyclophosphamide 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 Alkylating 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 Cyclophosphamide’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 Cyclophosphamide; 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 204 clinical records among the 300 most-relevant of 4,449 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.