How should kidney function be monitored during Abiraterone therapy?

Serum potassium every cycle (more often if abnormal); Blood pressure at each visit; Fluid/edema status; Liver function tests per label; Adherence to prednisone.

How can kidney injury from Abiraterone be prevented?

Co-administer prednisone/prednisolone exactly as labeled Pre-emptive potassium repletion Use eplerenone (not spironolactone) for residual mineralocorticoid activity

Who is at higher risk of kidney injury from Abiraterone?

Inadequate or missed glucocorticoid co-therapy; Baseline hypertension or hypokalemia; Concurrent loop/thiazide diuretics; Pre-existing adrenal suppression.

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Printable monograph

CYP17 inhibitor

Abiraterone

Zytiga · Abi

CYP17 inhibitor · approved 2011 · 11 citations · FAERS AKI reporting ROR 1.64 (95% CI 1.50–1.79, 484 AKI reports)

Up to date· through 2025

Deeply sourced8/9 · 7 signals

Met: 11 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 14y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2025
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.

CYP17 blockade drives an ACTH-mediated mineralocorticoid excess — hypokalemia, hypertension, edema.

ModerateAndrogen-biosynthesis inhibitor

Metastatic castration-resistant prostate cancerMetastatic castration-sensitive prostate cancer

§01

Signature kidney injury

Signature lesion

Electrolyte Disturbance

Representative grade ≥3 incidence12%

Mineralocorticoid-excess effects are common: in COU-AA-301 fluid retention, hypertension and hypokalemia were all more frequent than with placebo-prednisone. Severe (grade 3–4) hypokalemia, occasionally to 1.7–2.1 mEq/L, is reported even with concomitant prednisone. Meta-analysis confirms an increased relative risk of hypertension. A single-center retrospective cohort of 79 patients reported renal events in 63.3% of abiraterone-treated patients — AKI in 30.4%, half of whom progressed to chronic kidney disease (Pujol-Pujol 2025). Reported rate: grade >=3 hypokalemia in 12% — 597 men with newly diagnosed high-risk metastatic castration-sensitive prostate cancer randomized to abiraterone… (Fizazi 2019, PMID 30987939).Source: Fizazi et al., Lancet Oncol 2019 (LATITUDE)

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Within the first weeks of therapy; recurs if glucocorticoid coverage is inadequate or interrupted.

Distilled from: “Within the first weeks of therapy; recurs if glucocorticoid coverage is inadequate or interrupted.”

§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.

Electrolyte Disturbance#1 · Signatureno population incidence denominator
Mineralocorticoid excess — hypokalemia significantly more frequent than prednisone/placebo (COU-AA-301) PMID 21612468 (opens PubMed in a new tab)
HypertensionSecondaryno population incidence denominator
Mineralocorticoid-driven hypertension, more frequent vs placebo (COU-AA-301) PMID 21612468 (opens PubMed in a new tab)

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

12%grade ≥3 incidence

SeverityModerate

ReversibilityReversible

Evidence11 citations

Nephron map

Glomerulus

Vasculature / Endothelium

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

Electrolyte Disturbance

Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).

§03

Kidney injury

Mechanism of kidney injury

CYP17 inhibition reduces cortisol synthesis, triggering a compensatory rise in pituitary ACTH that drives accumulation of upstream steroid precursors with intact mineralocorticoid activity — chiefly 11-deoxycorticosterone and corticosterone. These agonize the mineralocorticoid receptor in the aldosterone-sensitive distal nephron (principal cells of the late distal tubule/collecting duct), upregulating ENaC and the Na-K-ATPase: sodium and water are retained while potassium and hydrogen are wasted. The result is hypokalemia, metabolic alkalosis, volume expansion and hypertension. Co-administered prednisone suppresses ACTH and largely prevents this; missed glucocorticoid coverage unmasks it. Intrinsic tubular toxicity is not a feature.

Clinical presentation

Hypokalemia (sometimes severe — weakness, ileus, lethargy, arrhythmia or seizure), hypertension, peripheral edema and a hypokalemic metabolic alkalosis with low urinary potassium-sparing only if MR antagonism is added. Renin and aldosterone are suppressed (an apparent-mineralocorticoid-excess biochemical picture). AKI is not rare — a retrospective cohort reported AKI in ~30% of treated patients, half progressing to CKD — but it is typically hemodynamic/secondary to the mineralocorticoid and volume effects rather than intrinsic tubular toxicity.

Management

Replete potassium and treat hypertension; optimize/intensify glucocorticoid dosing to suppress ACTH drive. For refractory mineralocorticoid excess add a mineralocorticoid-receptor antagonist — eplerenone is preferred (a real-world cohort showed it controls toxicity and can even allow steroid-sparing), or amiloride to block ENaC. Spironolactone is avoided in prostate cancer because of partial androgen-receptor agonism.Lesion-level management framework

Risk factors

Inadequate or missed glucocorticoid co-therapy
Baseline hypertension or hypokalemia
Concurrent loop/thiazide diuretics
Pre-existing adrenal suppression

Prevention

Co-administer prednisone/prednisolone exactly as labeled
Pre-emptive potassium repletion
Use eplerenone (not spironolactone) for residual mineralocorticoid activity

Anticancer mechanism· how it treats cancer

Inhibits CYP17A1 (17α-hydroxylase/C17,20-lyase), the rate-limiting enzyme of androgen biosynthesis, blocking testosterone production in testes, adrenals and tumor. Given with prednisone for metastatic castration-resistant and high-risk castration-sensitive prostate cancer.

Note · The signature is an electrolyte/blood-pressure syndrome from secondary mineralocorticoid excess, not a primary tubular toxin.

§04

Clinical depth

Renal dose adjustment

No formal renal dose adjustment for mild–moderate impairment (not studied in severe CKD/ESKD). Hepatic impairment requires dose reduction. The actionable adjustment is glucocorticoid coverage and potassium/BP management, not renal dosing.

Dialyzability & ESKD dosing

Highly protein-bound (>99%) and hepatically metabolized (CYP3A4/SULT2A1); not meaningfully dialyzable. No specific ESKD dosing established — manage electrolytes clinically.

Differential diagnosis

Differentiate ACTH-driven secondary mineralocorticoid excess (low renin, low aldosterone, hypokalemic alkalosis, responds to eplerenone/steroid) from primary hyperaldosteronism (high aldosterone), diuretic effect, and GI potassium loss. AKI does not argue against abiraterone. Assess volume status, potassium and blood pressure first — the mechanism is usually hemodynamic/mineralocorticoid-mediated rather than intrinsic tubular toxicity — and pursue a separate cause when those are unremarkable.

Monitoring

Serum potassium every cycle (more often if abnormal)
Blood pressure at each visit
Fluid/edema status
Liver function tests per label
Adherence to prednisone

Key trials & series

COU-AA-301 (de Bono NEJM 2011) and COU-AA-302 mCRPC trials
LATITUDE / STAMPEDE castration-sensitive trials
Gill Clin Genitourin Cancer 2017 eplerenone real-world cohort

Clinical pearls

The syndrome is apparent mineralocorticoid excess: low renin AND low aldosterone with hypokalemic alkalosis — the culprit is deoxycorticosterone, not aldosterone.
Use eplerenone, NOT spironolactone — spironolactone's androgen-receptor agonism can blunt the anticancer effect.
Most hypokalemia is preventable by ensuring the patient actually takes the co-prescribed prednisone.
Eplerenone can permit steroid-sparing in selected patients who must avoid prednisone (Gill 2017).

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

Class-level context for the major non-renal toxicities of the CYP17 inhibitor 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

9 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

9 references · 2011–2025 · 4 since 2023

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 · LimitedSevere Late-Onset Abiraterone-Induced Hypokalemia in a Diabetic Patient With Concomitant Adrenal Gland Incidentaloma: A Diagnostic Challenge.Tumminia A et al. · Case Rep Endocrinol 2025 · PMID 40521126Delayed-onset severe refractory hypokalemia from abiraterone-induced mineralocorticoid excess driving renal potassium wasting, resolved by switching to dexamethasone.CaseC · LimitedAscending Flaccid Paralysis Secondary to Hypokalemia in A Cancer Patient using Abiraterone - A Case Report.de Almeida DCB et al. · Curr Drug Saf 2023 · PMID 35469572Severe hypokalemia from abiraterone-induced secondary hyperaldosteronism (renal potassium wasting) presenting as ascending flaccid paralysis despite prednisone.

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

No dosage adjustment is necessary for patients with renal impairment [see Clinical Pharmacology ( 12.3 )].

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 40,959 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· 4 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 3.09 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
Hypertensioncorroborated · ROR 1.65 — on the terms that name the lesion (ROR 1.92)

Electrolyte Disturbance

ROR 3.0995% CI 2.92–3.28· 1,129 reports

Hemorrhagic Cystitis

ROR 2.6295% CI 2.35–2.91· 351 reports

Crystal / Obstructive Nephropathy

ROR 2.3295% CI 2.05–2.63· 251 reports

Hypertension

ROR 1.6595% CI 1.56–1.75· 1,228 reports

FAERS outcomes & reporting trend· 20.5% of reports w/ death · 26.9% w/ hospitalization

20.5%

Reported with a death outcome

8,380 of 40,959 reports

26.9%

Reported with hospitalization

11,036 of 40,959 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 40,959 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 1.6495% CI 1.50–1.79· 484 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

Urinary Tract Infection714

General / constitutional

Fatigue2,680Asthenia1,317Fall950Pain639Weight Decreased622

Gastrointestinal

Nausea1,024Diarrhoea982Vomiting669

Vascular

Hot Flush1,491Hypertension791

Metabolic & electrolyte

Decreased Appetite791Hypokalaemia748

Nervous system

Dizziness842

Respiratory

Dyspnoea784

Immune / infection

Pneumonia749

Blood & lymphatic

Anaemia718

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 Abiraterone 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

Enzalutamide

Xtandi · Androgen-receptor inhibitor

Profile

Hypertension; rare electrolyte effects.

HTNLYTE

Mild#1 · 72% phenotype match

Relacorilant

Lifyorli · Selective glucocorticoid-receptor antagonist

Profile

2026 GR antagonist (ovarian); hypokalemia via cortisol/mineralocorticoid receptor — the mifepristone effect, blunted by GR-selectivity.

LYTEHTN

Mild#2 · 69% phenotype match

Denosumab

Xgeva · Anti-RANKL antibody

Profile

Severe hypocalcemia in low GFR; not directly nephrotoxic.

LYTE

Moderate#3 · 65% phenotype match

Necitumumab

Portrazza · Anti-EGFR antibody

Profile

Severe hypomagnesemia, class effect.

LYTE

Moderate#4 · 65% phenotype match

Inavolisib

Itovebi · PI3Kα inhibitor

Profile

PI3Kα inhibitor whose renal-relevant toxicity is on-target hyperglycemia and electrolyte shifts, not a kidney lesion.

LYTE

Moderate#5 · 62% phenotype match

Tamoxifen

Nolvadex · SERM

Profile

Hypercalcemia flare; rare hyponatremia.

SIADHLYTEPRE

Mild#6 · 59% phenotype match

Compare Abiraterone 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 Abiraterone’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 Abiraterone; 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 17 clinical records among all 21 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.