What kind of kidney injury does Rucaparib 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.

Is kidney injury from Rucaparib reversible?

Reversible. Typical onset: Within the first weeks of treatment..

How should kidney function be monitored during Rucaparib therapy?

Serum creatinine at baseline and each cycle; cystatin C-based eGFR if true GFR is in doubt; CBC for anemia/thrombocytopenia/neutropenia; Liver enzymes (early transaminase rise is common).

How can kidney injury from Rucaparib be prevented?

Recognize transporter-mediated pseudo-AKI before acting on the number Use cystatin C-based eGFR when true GFR is uncertain

Who is at higher risk of kidney injury from Rucaparib?

Pre-existing CKD (lower reserve); Concurrent transporter-inhibiting drugs (e.g. cimetidine, trimethoprim).

Back to explorer

Printable monograph

PARP inhibitor

Rucaparib

Rubraca · Ruca

PARP inhibitor · approved 2016 · 7 citations

Up to date· through 2026

Fairly sourced5/9 · 5 signals

Met: 7 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 9y)
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 PARP inhibitor whose creatinine bump is mostly a transporter artifact, not true kidney injury.

MildPARP inhibitor

Ovarian cancer (maintenance / treatment)BRCA-mutated metastatic castration-resistant prostate cancer

§01

Signature kidney injury

Signature lesion

Pseudo-AKI

Representative incidence19.7%

Early reversible serum-creatinine elevation is common and partly drug-specific: rucaparib is a recognized inhibitor of renal cation transporters, and a pooled meta-analysis found markedly higher odds of creatinine rise vs placebo across the class, but grade >=3 renal events were rare (<1%). Reported rate: elevated serum creatinine in 19.7% — Pooled safety population of seven studies of rucaparib monotherapy in patients with recurrent high-grade ovarian… (Adrianto 2024, PMID 39266137).Source: Adrianto et al., Taiwan J Obstet Gynecol 2024

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Onset within the first weeks of treatment.

Distilled from: “Within the first weeks of treatment.”

§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 · Signatureno population incidence denominator
PARP-inhibitor class (incl. rucaparib): significantly increased serum-creatinine elevation vs placebo (pooled OR 5.04); >=grade 3 renal events <1% — reflects inhibition of tubular creatinine transport, not GFR loss PMID 42073552 (opens PubMed in a new tab)

§03

Kidney injury

Mechanism of kidney injury

Rucaparib inhibits the proximal-tubular cation transporters MATE1, MATE2-K, and OCT2 that secrete creatinine (and also OCT1 and BCRP), raising serum creatinine without a true reduction in glomerular filtration — a transporter-mediated 'pseudo-AKI' rather than tubular injury. True intrinsic nephrotoxicity is uncommon.

Clinical presentation

Asymptomatic mild creatinine increase early in therapy, typically plateauing and reversible; no proteinuria or active sediment. Cystatin C-based eGFR remains at baseline, confirming the transporter mechanism. Transaminase elevation is a separate, common early laboratory effect.

Management

Usually observation; confirm a stable cystatin C before attributing the rise to true AKI or changing dose. Persistent or progressive elevation, proteinuria, or active sediment warrants standard AKI workup and consideration of alternative causes.Lesion-level management framework

Risk factors

Pre-existing CKD (lower reserve)
Concurrent transporter-inhibiting drugs (e.g. cimetidine, trimethoprim)

Prevention

Recognize transporter-mediated pseudo-AKI before acting on the number
Use cystatin C-based eGFR when true GFR is uncertain

Anticancer mechanism· how it treats cancer

Inhibits and traps PARP1/2/3 on DNA, producing synthetic lethality in homologous-recombination-deficient (BRCA-mutant) tumors. Used in ovarian cancer and BRCA-mutated metastatic castration-resistant prostate cancer.

§04

Clinical depth

Renal dose adjustment

No starting-dose adjustment for mild-moderate renal impairment (CrCl >=30 mL/min); not studied in CrCl <30 mL/min or dialysis — use with caution. Modest exposure increases occur with moderate impairment but rarely require dose change.

Dialyzability & ESKD dosing

Highly protein-bound small molecule; not expected to be appreciably dialyzed. No established ESKD dosing.

Differential diagnosis

Transporter-mediated pseudo-AKI (stable cystatin C, bland urinalysis, no oliguria) vs true AKI from prerenal causes, ATN, or AIN. A flat cystatin C with a rising creatinine is essentially diagnostic of the transporter effect.

Monitoring

Serum creatinine at baseline and each cycle; cystatin C-based eGFR if true GFR is in doubt
CBC for anemia/thrombocytopenia/neutropenia
Liver enzymes (early transaminase rise is common)

Key trials & series

ARIEL3 (recurrent ovarian maintenance)
TRITON2 / TRITON3 (BRCA-mutated mCRPC)
Gasowska-Bodnar 2026 class creatinine meta-analysis

Clinical pearls

Rucaparib raises creatinine by blocking MATE/OCT2 secretion — check cystatin C before calling it AKI or stopping the drug.
The creatinine rise appears within weeks, then plateaus and reverses on discontinuation.
An early transaminase bump is also expected and usually self-limited — do not conflate it with progressive organ injury.

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

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

Evidence accrual

7 references · 2017–2026 · 3 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 (Dec 2025) — not paraphrased or interpreted. Full label on DailyMed .

Renal impairment — from the label

No dosage modification is recommended for patients with mild to moderate renal impairment (creatinine clearance [CLcr] between 30 and 89 mL/min, as estimated by the Cockcroft-Gault method) [see Clinical Pharmacology ( 12.3 )]. Rubraca has not been studied in patients with CLcr < 30 mL/min or patients on dialysis.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 8,779 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.
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 outcomes & reporting trend· 5.8% of reports w/ death · 16.7% w/ hospitalization

5.8%

Reported with a death outcome

505 of 8,779 reports

16.7%

Reported with hospitalization

1,469 of 8,779 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 6 systems · 8,779 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 0.8595% CI 0.65–1.10· 54 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Gastrointestinal

Nausea2,261Diarrhoea790Constipation785Vomiting782Abdominal Pain388

General / constitutional

Fatigue2,551Asthenia680Malaise411Weight Decreased296Pain295

Blood & lymphatic

Anaemia557Platelet Count Decreased539Haemoglobin Decreased359White Blood Cell Count Decreased315

Nervous system

Dysgeusia567Headache439Dizziness408

Metabolic & electrolyte

Decreased Appetite802

Respiratory

Dyspnoea398

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 Rucaparib 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

Talazoparib

Talzenna · PARP inhibitor

Profile

Renally cleared; 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 Rucaparib 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.

Who studies this

The leading contributors to Rucaparib’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 Rucaparib; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.

Pignata, Sandro — their work on Rucaparib, on PubMed (opens in a new tab)2 papers · 36 citesPMID 37668154 (opens PubMed in a new tab)PMID 33099187 (opens PubMed in a new tab)

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 7 clinical records among all 8 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.