What kind of kidney injury does Bicalutamide cause?

Acute Interstitial Nephritis — Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.

Is kidney injury from Bicalutamide reversible?

Reversible. Typical onset: If AIN occurs, typically subacute over weeks of exposure (idiosyncratic)..

How should kidney function be monitored during Bicalutamide therapy?

Liver function tests (hepatic metabolism/rare hepatotoxicity); PSA for treatment response; Urinalysis if AIN suspected.

How can kidney injury from Bicalutamide be prevented?

Review concomitant medications for additive AIN/nephrotoxicity risk

Who is at higher risk of kidney injury from Bicalutamide?

Idiosyncratic hypersensitivity predisposition (for rare AIN); Concurrent nephrotoxins or other AIN-associated drugs; Severe hepatic impairment (slower elimination — a hepatic, not renal, consideration).

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Printable monograph

Nonsteroidal antiandrogen

Bicalutamide

Casodex · Bical

Nonsteroidal antiandrogen · approved 1995 · 4 citations · FAERS AKI reporting ROR 1.75 (95% CI 1.51–2.01, 191 AKI reports)

Aging evidence· through 2020

Fairly sourced5/9 · 4 signals

Not met: 4 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 24y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Not met: Current through 2020
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.

Nonsteroidal antiandrogen for prostate cancer; largely kidney-neutral with no renal dose adjustment and only rare interstitial nephritis reports.

Mildestablished

Advanced prostate cancer (50 mg with an LHRH analog or surgical castration)Early (localized or locally advanced) nonmetastatic prostate cancer (150 mg monotherapy, regional)

§01

Signature kidney injury

Signature lesion

Acute Interstitial Nephritis

Bicalutamide is largely kidney-neutral. Pharmacokinetics are unaffected by renal impairment and no renal dose adjustment is required. Acute interstitial nephritis is, at most, a rare idiosyncratic case-report-level event; no meaningful incidence rate is established.Source: Cockshott et al., Clin Pharmacokinet 2004 (no renal dose adjustment; AIN rare/idiosyncratic)

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Idiosyncratic AIN, when it occurs, is typically subacute over weeks of exposure.

Distilled from: “If AIN occurs, typically subacute over weeks of exposure (idiosyncratic).”

§02

Renal toxicities, ranked

This agent's defining kidney lesion — its #1 signature. Cited incidence is shown where a citable figure exists; otherwise the tier stands qualitatively.

Acute Interstitial Nephritis#1 · Signaturequalitative — no citable incidence
Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.

§03

Kidney injury

Also documented as kidney-sparing

Bicalutamide — No direct renal injury. Hepatotoxicity (monitor LFTs).

The spared

Mechanism of kidney injury

Bicalutamide is cleared almost exclusively by hepatic metabolism (CYP-mediated oxidation of the (R)-enantiomer and glucuronidation), with little or no unchanged drug in urine, so it does not accumulate in renal impairment and lacks an intrinsic nephrotoxic pathway. Any acute interstitial nephritis would represent a rare, hypersensitivity-type idiosyncratic immune reaction rather than dose-dependent toxicity.

Clinical presentation

Renally asymptomatic in the vast majority. A rare AIN would present with subacute creatinine rise, possibly with pyuria, low-grade proteinuria, or hypersensitivity features. Antiandrogen pharmacologic effects (gynecomastia, breast tenderness, hot flushes) are common but non-renal.

Management

For suspected drug-induced AIN, discontinue bicalutamide and provide supportive care; corticosteroids may be considered per nephrology assessment in confirmed/biopsy-proven AIN. Otherwise no renal-specific management is required.Lesion-level management framework

Risk factors

Idiosyncratic hypersensitivity predisposition (for rare AIN)
Concurrent nephrotoxins or other AIN-associated drugs
Severe hepatic impairment (slower elimination — a hepatic, not renal, consideration)

Prevention

Review concomitant medications for additive AIN/nephrotoxicity risk

Anticancer mechanism· how it treats cancer

Bicalutamide is a nonsteroidal pure antiandrogen; its activity resides almost exclusively in the (R)-enantiomer, which competitively binds the androgen receptor and blocks androgen-driven transcription, inhibiting growth of androgen-dependent prostate cancer. It is used as monotherapy or combined with LHRH analogs/castration.

Note · Renal angle is reassuring: PK reviews explicitly show no effect of renal impairment on bicalutamide pharmacokinetics and no renal dose adjustment. AIN is rare/idiosyncratic and not quantified.

§04

Clinical depth

Renal dose adjustment

No dose adjustment for renal impairment. Dose with caution in severe hepatic impairment (slower (R)-enantiomer elimination).

Dialyzability & ESKD dosing

Not expected to be meaningfully dialyzable given high protein binding and hepatic clearance; not clinically relevant to dosing.

Differential diagnosis

Distinguish rare AIN from other causes of AKI in prostate-cancer patients: obstructive uropathy (bladder outlet/ureteral obstruction), prerenal azotemia, and concurrent nephrotoxic medications.

Monitoring

Liver function tests (hepatic metabolism/rare hepatotoxicity)
PSA for treatment response
Urinalysis if AIN suspected

Key trials & series

Casodex dose-ranging and pharmacokinetic studies (PMID 9471040, PMID 8560674) show efficacy with no effect on renal function and no renal-impairment effect on PK; PMID 15509184 is the definitive clinical pharmacokinetics/metabolism review.

Clinical pearls

Think drug-induced AIN only as a rare, idiosyncratic event — and rule out obstruction first in a prostate-cancer patient with rising creatinine.

Where it strikes· nephron segments & injury signatures

Nephron segments

Interstitium

Supporting tissue around the tubules

Injury signatures

Acute Interstitial Nephritis

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

Class-level context for the major non-renal toxicities of the Nonsteroidal antiandrogen class.

Cardiac

Cardiomyopathy, QT, ischemia, myocarditis

QT, hypertension, fluid retention

Musculoskeletal

Myalgia, myositis, rhabdomyolysis, ONJ

Bone loss, fatigue, hot flashes

Hepatic / Liver

Transaminitis, hepatitis, VOD/SOS

Transaminitis (abiraterone)

§05

References

3 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

3 references · 1996–2004 · 1 since 2002

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· 1

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 · ModerateSuccessful recovery from multiple organ failure associated with bicalutamide and leuprorelin acetate for prostate cancer.Saito S · Urol Case Rep 2020 · PMID 31934548Combined androgen blockade with bicalutamide caused acute kidney injury requiring hemodialysis, with renal biopsy revealing drug-induced tubulointerstitial nephritis (acute interstitial nephritis).

FDA label — boxed warning & renal dosing· renal impairment

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

Renal impairment — from the label

Renal impairment (as measured by creatinine clearance) had no significant effect on the elimination of total bicalutamide or the active R-enantiomer.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 15,150 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

Acute Interstitial NephritisNot measurable in reporting — Reporters cannot reliably name this lesion, so its absence from FAERS is expected and is not evidence against the documented injury.

Fanconi Syndrome

ROR 7.8895% CI 5.47–11.36· 29 reports

Hemorrhagic Cystitis

ROR 6.5895% CI 5.89–7.35· 322 reports

Crystal / Obstructive Nephropathy

ROR 3.7695% CI 3.20–4.42· 150 reports

Electrolyte Disturbance

ROR 2.7295% CI 2.45–3.01· 369 reports

Glomerular Injury / Proteinuria

ROR 2.1095% CI 1.56–2.82· 44 reports

SIADH / Hyponatremia

ROR 1.9395% CI 1.60–2.33· 112 reports

Hypertension

ROR 1.7195% CI 1.56–1.88· 471 reports

FAERS outcomes & reporting trend· 17.9% of reports w/ death · 36% w/ hospitalization

17.9%

Reported with a death outcome

2,714 of 15,150 reports

36%

Reported with hospitalization

5,460 of 15,150 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 10 systems · 15,150 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 1.7595% CI 1.51–2.01· 191 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

General / constitutional

Fatigue1,328Asthenia809Fall423Pain412Back Pain400

Gastrointestinal

Nausea563Diarrhoea528Constipation376

Respiratory

Dyspnoea541Interstitial Lung Disease366

Vascular

Hot Flush793

Nervous system

Dizziness582

Metabolic & electrolyte

Decreased Appetite513

Blood & lymphatic

Anaemia500

Immune / infection

Pneumonia392

Musculoskeletal

Arthralgia378

Psychiatric

Confusional State311

Guidelines & consensus· 13

Each recommendation below is this atlas's faithful summary of the source, not a quotation from it — follow the PubMed link for the wording the society published. Summaries may be superseded; consult the current full text and individualize to the patient.

General onco-nephrology references

ADQIThe nephrotoxic effects of anti-cancer therapies: consensus report of the 34th Acute Disease Quality Initiative workgroupNat Rev Nephrol 2026 · PMID 41361704Provides expert-based statements (modified Delphi) on preventing and managing cisplatin/platinum-associated AKI, including isotonic IV hydration, attention to volume status and concomitant nephrotoxins, and incorporates evidence that IV magnesium supplementation may reduce cisplatin-associated AKI; emphasizes risk stratification and standardized AKI definitions.SIRMSIRM-SIN-AIOM: appropriateness criteria for evaluation and prevention of renal damage in the patient undergoing contrast medium examinations-consensus statements from Italian College of Radiology (SIRM), Italian College of Nephrology (SIN) and Italian Association of Medical Oncology (AIOM)Radiol Med 2022 · PMID 35303246Recommends eGFR-based renal risk assessment and pre/post-contrast isotonic saline or sodium bicarbonate hydration; advises maintaining a 5-7 day interval between iodinated contrast administration and cisplatin in cancer patients to reduce additive nephrotoxicity.KDIGOKDIGO Controversies Conference on onco-nephrology: understanding kidney impairment and solid-organ malignancies, and managing kidney cancerKidney Int 2020 · PMID 33126977Identifies platinum compounds (especially cisplatin) as leading cytotoxic causes of acute tubular injury, AKI, and electrolyte/magnesium wasting; calls for interdisciplinary onco-nephrology care, accurate GFR estimation, and individualized drug dosing in patients with reduced kidney function.KDIGOKDIGO Controversies Conference on onco-nephrology: kidney disease in hematological malignancies and the burden of cancer after kidney transplantationKidney Int 2020 · PMID 33276867Addresses chemotherapy-associated AKI/CKD in hematologic cancer, GFR estimation and chemotherapy dosing in patients with reduced kidney function, and management priorities and research gaps for onco-nephrology care.ADDIKDIntegrating International Consensus Guidelines for Anticancer Drug Dosing in Kidney Dysfunction (ADDIKD) into everyday practiceEClinicalMedicine 2025 · PMID 40290844Provides GRADE-based, drug-specific dose-adjustment recommendations for anticancer agents in kidney dysfunction (illustrated for methotrexate, cisplatin, carboplatin and nivolumab); the recommendations build on Part 1's standardised CKD-EPI eGFR assessment rather than Cockcroft-Gault creatinine clearance.ADDIKDAligning kidney function assessment in patients with cancer to global practices in internal medicineEClinicalMedicine 2025 · PMID 40290845Three consensus recommendations: assess kidney function by GFR (measured GFR or CKD-EPI eGFR), classify it using KDIGO categories, and use this uniform approach to dose anticancer drugs — moving cancer medicine away from Cockcroft-Gault estimated creatinine clearance.ADDIKDA methodology for determining dosing recommendations for anticancer drugs in patients with reduced kidney functionEClinicalMedicine 2025 · PMID 40290846Establishes that, where RCT evidence is lacking, anticancer drug dosing recommendations in kidney dysfunction should be derived by critically appraising observational literature via GRADE combined with structured international multidisciplinary consensus voting.KDIGODiagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1)Crit Care 2013 · PMID 23394211Defines/stages AKI by serum creatinine and urine output; emphasizes avoiding nephrotoxins, maintaining euvolemia/perfusion, dose-adjusting drugs to kidney function, and monitoring high-risk patients — the framework applied to nephrotoxic anti-cancer agents.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknownsKidney Int 2024 · PMID 38519239Evaluate and risk-stratify CKD, manage to delay progression and its complications, and practise explicit medication management and drug stewardship — the framework the atlas's G1–G5 eGFR banding and every renal dose-adjustment recommendation sit inside. Because the guideline excludes dialysis and transplant recipients by its own statement of scope, its recommendations do not carry to those settings, where this atlas's dialyzability and post-transplant guidance rests on other sources.KDIGOExecutive summary of the KDIGO 2021 Guideline for the Management of Glomerular DiseasesKidney Int 2021 · PMID 34556300Provides the staging/treatment framework for drug-associated glomerular lesions (e.g., bisphosphonate- and interferon-related collapsing FSGS, VEGF-inhibitor podocytopathy/proteinuria), including immunosuppression and supportive RAAS-blockade strategies.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of ANCA-Associated VasculitisKidney Int 2024 · PMID 38388147Updates immunosuppressive induction (rituximab/cyclophosphamide), incorporates avacopan and lower-dose or glucocorticoid-sparing regimens — the management framework for drug- and checkpoint-inhibitor-associated ANCA/pauci-immune glomerulonephritis.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of Lupus NephritisKidney Int 2024 · PMID 38182299Updates first-line lupus nephritis therapy to combination immunosuppression with the addition of belimumab or a calcineurin inhibitor (voclosporin) — informs management of immune-complex/lupus-like glomerulonephritis encountered with immunotherapy.KDIGOExecutive summary of the KDIGO 2025 Clinical Practice Guideline for the Management of Immunoglobulin A Nephropathy (IgAN) and Immunoglobulin A Vasculitis (IgAV)Kidney Int 2025 · PMID 40975525Encourages liberal kidney biopsy and stricter proteinuria control (<0.5 g/d, ideally <0.3 g/d) with RAAS blockers, SGLT2 inhibitors, and targeted-release budesonide — the framework for IgA-dominant glomerular lesions, including those triggered by immune-modulating cancer therapy.

Where Bicalutamide 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

Relatlimab

Opdualag · Immune checkpoint inhibitor (anti-LAG-3)

Profile

2022 LAG-3 inhibitor (with nivolumab); class immune-mediated AIN, amplified by combination ICI.

AIN

Moderate#1 · 81% phenotype match

Cobimetinib

Cotellic · MEK inhibitor

Profile

Real-world AKI signal with BRAF partners.

ATNAIN

Mild#2 · 53% phenotype match

Encorafenib

Braftovi · BRAF inhibitor

Profile

Class tubular signal; usually mild.

ATNAIN

Mild#3 · 53% phenotype match

Idelalisib

Zydelig · PI3Kδ inhibitor

Profile

Immune-mediated colitis → volume-depletion prerenal AKI; transaminitis.

PREAIN

Mild#4 · 52% phenotype match

Duvelisib

Copiktra · PI3Kδ/γ inhibitor

Profile

Colitis and diarrhea → prerenal AKI.

PREAIN

Mild#5 · 51% phenotype match

Checkpoint inhibitors (pembrolizumab · nivolumab · ipilimumab)

Immune checkpoint inhibitor

Profile

Acute interstitial nephritis with long latency.

AINGLOMLYTE

Moderate#6 · 51% phenotype match

Compare Bicalutamide 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 Hormonal / endocrine

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 Bicalutamide’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 Bicalutamide; 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 9 clinical records among all 12 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.