What kind of kidney injury does Talazoparib cause?

Pseudo-AKI — The great mimic — a rise in creatinine from blocked tubular secretion (OCT2/MATE), NOT true injury. The GFR is intact; confirm with cystatin C before stopping effective therapy.

How should kidney function be monitored during Talazoparib therapy?

CBC monthly (and more often after dose changes) — anemia is the most common grade >=3 event; Blood counts more closely in CKD.

How can kidney injury from Talazoparib be prevented?

Renal-function-based starting-dose adjustment

Who is at higher risk of kidney injury from Talazoparib?

Moderate to severe renal impairment (exposure); Concurrent myelosuppressive therapy; Concurrent P-gp/BCRP inhibitors.

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Printable monograph

PARP inhibitor

Talazoparib

Talzenna · Tala

PARP inhibitor · approved 2018 · 6 citations

Up to date· through 2026

Fairly sourced5/9 · 5 signals

Met: 6 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 8y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2026
Not met: Real-world FAERS signal

Describes how this page is sourced, not how dangerous the drug is. Thinly sourced means fewer of the sourcing signals are met — not that the agent is kidney-safe. A rule-based summary, not a formal certainty appraisal.

A potent, renally cleared PARP-trapper — renal impairment raises exposure and dosing must adjust.

MildPARP inhibitor

gBRCA-mutated HER2-negative breast cancerMetastatic castration-resistant prostate cancer (with enzalutamide)

§01

Signature kidney injury

Signature lesion

Pseudo-AKI

Renal clearance is a major elimination route (~two-thirds of dose), so exposure rises with declining renal function: dedicated PK studies show higher AUC and more myelosuppression in moderate-severe impairment, mandating dose reduction. Class-level mild creatinine elevation may occur; severe intrinsic nephrotoxicity is uncommon.Source: Durairaj et al., Clin Pharmacokinet 2021

Onset & rechallenge

Time to injuryHyperacute (<24 h)

The pharmacokinetic effect is present from initiation in patients with reduced renal function, while cytopenias accrue over the first cycles.

Distilled from: “The pharmacokinetic effect is present from initiation in patients with reduced renal function; cytopenias accrue over the first cycles.”

§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.

Pseudo-AKI#1 · Signaturequalitative — no citable incidence
The great mimic — a rise in creatinine from blocked tubular secretion (OCT2/MATE), NOT true injury. The GFR is intact; confirm with cystatin C before stopping effective therapy.

§03

Kidney injury

Mechanism of kidney injury

Talazoparib is substantially renally cleared, so reduced GFR increases drug exposure (and hematologic toxicity) rather than causing direct tubular injury — the dominant renal issue is pharmacokinetic. As with the class, any modest creatinine rise can reflect inhibition of tubular creatinine secretion rather than true filtration loss.

Clinical presentation

Usually no overt nephrotoxicity; the renal concern is pharmacokinetic — higher exposure with anemia, thrombocytopenia, and neutropenia in patients with reduced renal function. Mild reversible creatinine changes are possible.

Management

Reduce the starting dose for moderate (CrCl 30-59: 0.75 mg daily) and severe (CrCl 15-29: 0.5 mg daily) renal impairment per label; manage cytopenias with dose holds/reductions, transfusion, and growth-factor support.Lesion-level management framework

Risk factors

Moderate to severe renal impairment (exposure)
Concurrent myelosuppressive therapy
Concurrent P-gp/BCRP inhibitors

Prevention

Renal-function-based starting-dose adjustment

Anticancer mechanism· how it treats cancer

One of the most potent PARP-trapping inhibitors; exploits homologous-recombination deficiency for synthetic lethality. Used in germline BRCA-mutated HER2-negative breast cancer and, with enzalutamide, in metastatic castration-resistant prostate cancer.

§04

Clinical depth

Renal dose adjustment

Breast-cancer monotherapy: CrCl 60-89 no change; CrCl 30-59 reduce to 0.75 mg once daily; CrCl 15-29 reduce to 0.5 mg once daily. With enzalutamide in mCRPC, label-specific lower doses apply. Not studied on dialysis or in CrCl <15 mL/min.

Dialyzability & ESKD dosing

Renally cleared but highly protein-bound; dialyzability not formally established and no validated ESKD dose — avoid or use only with intensive hematologic monitoring.

Differential diagnosis

Cytopenias in a CKD patient on talazoparib usually reflect drug over-exposure (PK), not marrow infiltration or a separate renal lesion. A mild creatinine rise is more likely transporter-mediated than true AKI.

Monitoring

CBC monthly (and more often after dose changes) — anemia is the most common grade >=3 event
Blood counts more closely in CKD

Key trials & series

EMBRACA (gBRCA HER2-negative breast cancer)
TALAPRO-2 (talazoparib + enzalutamide in mCRPC)
Durairaj 2021 dedicated renal-impairment PK study

Clinical pearls

Talazoparib is the renally cleared PARP inhibitor — reduce the dose for CrCl <60 mL/min and watch counts, since exposure (and anemia) climbs as GFR falls.
The principal renal issue is dosing in CKD, not de novo kidney injury.
Confirm an ambiguous creatinine rise with cystatin C before attributing GFR decline.

Where it strikes· nephron segments & injury signatures

Nephron segments

Proximal Tubule

Bulk reabsorption + drug uptake (OCT2, OATs)

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Pseudo-AKI

§05

References

6 primary references — trials, cohorts, mechanism, and reviews. Citation metadata via PubMed / NLM.

Evidence accrual

6 references · 2018–2026 · 2 since 2024

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.

FDA label — boxed warning & renal dosing· renal impairment

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

Renal impairment — from the label

Reduce the dose and monitor for increased adverse reactions for patients with moderate or severe renal impairment. ( 2.6 , 8.7 )

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 1,763 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· 3 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

Pseudo-AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

SIADH / Hyponatremia

ROR 2.6895% CI 1.68–4.26· 18 reports

Hemorrhagic Cystitis

ROR 2.2495% CI 1.30–3.87· 13 reports

Electrolyte Disturbance

ROR 2.1495% CI 1.52–3.00· 34 reports

FAERS outcomes & reporting trend· 18.6% of reports w/ death · 34.8% w/ hospitalization

18.6%

Reported with a death outcome

328 of 1,763 reports

34.8%

Reported with hospitalization

614 of 1,763 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 1,763 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 0.9495% CI 0.53–1.65· 12 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Blood & lymphatic

Anaemia273Thrombocytopenia95Haemoglobin Decreased80Platelet Count Decreased73Febrile Neutropenia68

General / constitutional

Fatigue123Asthenia58Pyrexia34Malaise29

Gastrointestinal

Nausea65Diarrhoea35Vomiting30

Respiratory

Dyspnoea50

Immune / infection

Pneumonia40

Nervous system

Dizziness37

Metabolic & electrolyte

Decreased Appetite33

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 Talazoparib 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

Rucaparib

Rubraca · PARP inhibitor

Profile

Transporter-mediated creatinine rise.

PSEUDO

Mild#1 · 100% phenotype match

Niraparib

Zejula · PARP inhibitor

Profile

Hypertension and creatinine rise.

HTNPSEUDO

Mild#2 · 76% phenotype match

Olaparib

Lynparza · PARP inhibitor

Profile

Benign creatinine rise via OCT2/MATE inhibition.

PSEUDOTMA

Mild#3 · 76% phenotype match

Larotrectinib

Vitrakvi · TRK inhibitor

Profile

Mild creatinine rise; generally well tolerated.

PSEUDO

Mild#4 · 75% phenotype match

Entrectinib

Rozlytrek · TRK/ROS1 TKI

Profile

Creatinine rise via reduced tubular secretion.

PSEUDO

Mild#5 · 75% phenotype match

Tucatinib

Tukysa · HER2 TKI

Profile

Benign creatinine rise via tubular secretion inhibition.

PSEUDO

Mild#6 · 75% phenotype match

Compare Talazoparib 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 Other targeted 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.