How should kidney function be monitored during Olaparib therapy?

Serum creatinine periodically (interpret with the OCT2/MATE artifact in mind); Cystatin C-based eGFR when true GFR matters; CBC for anemia/thrombocytopenia (and to flag possible TMA).

How can kidney injury from Olaparib be prevented?

Recognize the benign, transporter-mediated nature of the creatinine rise Use cystatin C-based eGFR to assess true renal function when needed Avoid unnecessary dose changes for isolated creatinine elevation

Who is at higher risk of kidney injury from Olaparib?

Pre-existing chronic kidney disease (complicates creatinine interpretation); Concurrent drugs affecting tubular creatinine secretion (e.g., trimethoprim, cimetidine).

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Printable monograph

PARP inhibitor

Olaparib

Lynparza · OLAP

PARP inhibitor · approved 2014 · 8 citations

Up to date· through 2026

Deeply sourced7/9 · 6 signals

Met: 8 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 11y)
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 that raises creatinine by blocking tubular transporters, mimicking - but not causing - true GFR loss.

MildPARP inhibitor

Ovarian cancerBreast cancerPancreatic cancerProstate cancer

§01

Signature kidney injury

Signature lesion

Pseudo-AKI

Representative incidence22.1%

Olaparib commonly causes a reversible, dose-dependent rise in serum creatinine. In a 66-patient study, median creatinine rose ~14% (and creatinine-based eGFR fell ~13%) on treatment, while cystatin C and cystatin C-based eGFR were unchanged - indicating no true GFR decline. Thrombotic microangiopathy is a rare, case-level event for the PARP-inhibitor class. Reported rate: creatinine-defined acute kidney injury within 12 months of olaparib initiation in 22.1% — Adults with ovarian cancer treated with olaparib at a single major Boston cancer center, 2015-2021 (n=194… (Gupta 2023, PMID 37074956).Source: Gupta et al., J Natl Cancer Inst 2023

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Creatinine rises within weeks of starting therapy and reverses on discontinuation.

Distilled from: “Creatinine rise within weeks of starting therapy; reverses on discontinuation.”

§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.

Pseudo-AKI#1 · Signature22.1%PMID 37074956 (opens PubMed in a new tab)
AKI (>=1.5x baseline SCr) within 12mo in 22.1% of olaparib-treated; only ~3% drug-attributable, transient eGFR dip that recovers after cessation
Thrombotic MicroangiopathyRarequalitative — no citable incidence
Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

22.1%incidence

SeverityMild

ReversibilityReversible

Evidence8 citations

Nephron map

Glomerulus

Vasculature / Endothelium

Proximal TubuleBulk reabsorption + drug uptake (OCT2, OATs)

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.

§03

Kidney injury

Mechanism of kidney injury

Olaparib inhibits renal tubular transporters (notably OCT2-mediated uptake and MATE1/MATE2-K-mediated efflux) that secrete creatinine, raising serum creatinine and lowering creatinine-based eGFR while measured/cystatin C-based GFR is preserved - a pseudo-AKI. Rare TMA reflects endothelial injury and is mechanistically distinct from this transporter effect.

Clinical presentation

Isolated, reversible creatinine elevation with stable cystatin C-based eGFR and clear discordance between creatinine- and cystatin C-derived eGFR. Rare TMA presents with microangiopathic hemolysis, thrombocytopenia, and AKI. Anemia is the most common overall toxicity and can prompt renal workup.

Management

Most creatinine elevations require no intervention and reverse on discontinuation; confirm preserved true GFR with cystatin C when clinically important (e.g., dosing of co-administered renally cleared drugs). Investigate alternative causes - including rare TMA - if cytopenias or hemolysis accompany the AKI.Lesion-level management framework

Risk factors

Pre-existing chronic kidney disease (complicates creatinine interpretation)
Concurrent drugs affecting tubular creatinine secretion (e.g., trimethoprim, cimetidine)

Prevention

Recognize the benign, transporter-mediated nature of the creatinine rise
Use cystatin C-based eGFR to assess true renal function when needed
Avoid unnecessary dose changes for isolated creatinine elevation

Anticancer mechanism· how it treats cancer

Inhibits poly(ADP-ribose) polymerase (PARP1/2), trapping PARP on DNA single-strand breaks and exploiting synthetic lethality in homologous-recombination-deficient (e.g., BRCA1/2-mutated) tumors. Used in ovarian, breast, pancreatic, and prostate cancers.

Note · The hallmark creatinine rise is a transporter (OCT2/MATE) artifact, not true nephrotoxicity; TMA is rare.

§04

Clinical depth

Renal dose adjustment

No starting-dose change for mild renal impairment (CrCl 51-80). For moderate impairment (CrCl 31-50), reduce the dose (e.g., to 200 mg twice daily) per labeling. Severe impairment/ESKD (CrCl <30) is not recommended due to limited data; if used, monitor closely.

Dialyzability & ESKD dosing

Olaparib is protein-bound and predominantly hepatically metabolized (CYP3A); dialyzability is not well characterized and it is not relied upon for clearance. Avoid in dialysis-dependent ESKD given sparse data.

Differential diagnosis

The defining distinction is pseudo-AKI (creatinine up, cystatin C-based eGFR stable) versus true AKI. If hemolysis and thrombocytopenia accompany the creatinine rise, evaluate for PARP-inhibitor TMA rather than a transporter artifact.

Monitoring

Serum creatinine periodically (interpret with the OCT2/MATE artifact in mind)
Cystatin C-based eGFR when true GFR matters
CBC for anemia/thrombocytopenia (and to flag possible TMA)

Key trials & series

Bruin et al. olaparib creatinine vs cystatin C study (mechanistic, 2021)
SOLO-1 (first-line maintenance in BRCA-mutated ovarian cancer; safety dataset)

Clinical pearls

Olaparib’s creatinine rise is an OCT2/MATE transporter artifact - check cystatin C before assuming true GFR loss.
Use cystatin C-based eGFR when dosing other renally cleared drugs in olaparib-treated patients.
A creatinine rise with new hemolysis/thrombocytopenia is not the artifact - work up for TMA.

§05

References

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

Evidence accrual

8 references · 2015–2026 · 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 (Jul 2025) — not paraphrased or interpreted. Full label on DailyMed .

Renal impairment — from the label

No dosage modification is recommended in patients with mild renal impairment (CLcr 51 to 80 mL/min estimated by Cockcroft-Gault). Reduce Lynparza dosage to 200 mg twice daily in patients with moderate renal impairment (CLcr 31 to 50 mL/min) [see Dosage and Administration (2.5) ]. There are no data in patients with severe renal impairment or end-stage disease (CLcr ≤30 mL/min) [see Clinical Pharmacology (12.3) ].

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 20,798 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· 28.5% of reports w/ death · 18.4% w/ hospitalization

28.5%

Reported with a death outcome

5,936 of 20,798 reports

18.4%

Reported with hospitalization

3,825 of 20,798 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 20,798 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 0.4095% CI 0.31–0.51· 60 AKI reports ·AKI is reported less often than for other drugs (CI entirely below 1) — no disproportionate signal.

Renal & urinary

Renal Impairment371

Gastrointestinal

Nausea1,827Vomiting724Diarrhoea615Constipation438

Blood & lymphatic

Anaemia1,622Haemoglobin Decreased441Myelosuppression432Platelet Count Decreased401Thrombocytopenia368

General / constitutional

Fatigue1,762Asthenia613Pain400Malaise383

Nervous system

Neuropathy Peripheral649Headache404Dizziness357

Respiratory

Dyspnoea398Interstitial Lung Disease384

Metabolic & electrolyte

Decreased Appetite543

Musculoskeletal

Arthralgia370

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 Olaparib 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 · 76% phenotype match

Talazoparib

Talzenna · PARP inhibitor

Profile

Renally cleared; creatinine rise.

PSEUDO

Mild#2 · 76% phenotype match

Niraparib

Zejula · PARP inhibitor

Profile

Hypertension and creatinine rise.

HTNPSEUDO

Mild#3 · 68% phenotype match

Alectinib

Alecensa · ALK TKI

Profile

Creatinine rise via reduced tubular secretion.

PSEUDOPRE

Mild#4 · 57% phenotype match

Bosutinib

Bosulif · BCR-ABL TKI

Profile

Reversible eGFR decline.

PSEUDOPRE

Mild#5 · 57% phenotype match

Ceritinib

Zykadia · ALK TKI

Profile

GI-driven prerenal AKI.

PREPSEUDO

Mild#6 · 57% phenotype match

Compare Olaparib 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 Olaparib’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 Olaparib; 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 Olaparib, 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 13 clinical records among all 15 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.