How should kidney function be monitored during Niraparib therapy?

Blood pressure and heart rate at least weekly for the first 2 months, then at least monthly; CBC weekly for the first month (thrombocytopenia/anemia/neutropenia), then monthly; Serum creatinine at baseline and periodically; cystatin C if a true GFR change is in question.

How can kidney injury from Niraparib be prevented?

Optimize/initiate antihypertensives before and during therapy

Who is at higher risk of kidney injury from Niraparib?

Pre-existing hypertension; Cardiovascular disease; Concurrent agents that raise blood pressure.

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Printable monograph

PARP inhibitor

Niraparib

Zejula · Nira

PARP inhibitor · approved 2017 · 8 citations

Up to date· through 2026

Fairly sourced5/9 · 5 signals

Met: 8 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 6y)
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.

The PARP inhibitor with a distinctive hypertension signal — a class outlier on blood pressure.

MildPARP inhibitor

Ovarian cancer (maintenance)Fallopian tube / primary peritoneal cancerBRCA-altered metastatic castration-resistant prostate cancer

§01

Signature kidney injury

Signature lesion

Hypertension

Representative incidence16.9%

Hypertension is a class-distinctive adverse event: a FAERS pharmacovigilance plus RCT meta-analysis estimated ~16.9% any-grade hypertension, disproportionately higher with niraparib than other PARP inhibitors. A small reversible serum-creatinine rise is also seen across the class (pooled OR for creatinine elevation ~5 vs placebo), but grade >=3 nephrotoxicity is <1%.Source: Chen et al., Gynecol Oncol 2024

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Hypertension typically emerges within the first weeks to months of therapy.

Distilled from: “Hypertension typically emerges within the first weeks to months of therapy.”

§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.

Hypertension#1 · Signature22%PMID 31474354 (opens PubMed in a new tab)
Hypertension ~22% (any grade) with single-agent niraparib 300 mg; a recognized class effect requiring BP monitoring
Pseudo-AKIRarequalitative — 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.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

16.9%incidence

SeverityMild

ReversibilityReversible

Evidence8 citations

Nephron map

GlomerulusFiltration barrier (podocytes + endothelium)

Vasculature / EndotheliumGlomerular & peritubular capillaries

Proximal Tubule

Hypertension

Raised blood pressure — archetypally on-target loss of endothelial nitric oxide from VEGF-pathway blockade, studied as a pharmacodynamic marker of drug exposure. Other agents raise it too: vascular effects of BCR-ABL, BTK and RET inhibitors and of copanlisib; abiraterone's mineralocorticoid excess; androgen suppression or blockade.

§03

Kidney injury

Mechanism of kidney injury

Hypertension is thought to be an off-target effect of niraparib — possible inhibition of dopamine/norepinephrine reuptake transporters (DAT/NET) with sympathetic activation and altered vascular tone — distinguishing it from olaparib/rucaparib; intrinsic nephron injury is not characteristic. The mild creatinine elevation shared across the class reflects inhibition of proximal-tubular cation transporters (MATE1/MATE2-K, OCT2) that secrete creatinine, raising serum creatinine without a true fall in GFR ('pseudo-AKI').

Clinical presentation

New or worsened hypertension (occasionally hypertensive crisis), often within the first cycles; modest asymptomatic creatinine rise without proteinuria, active sediment, or other tubular markers. Anemia and thrombocytopenia dominate the non-renal toxicity profile and drive most dose holds.

Management

Manage hypertension with standard antihypertensives (often a calcium-channel blocker or ACE inhibitor/ARB); dose-interrupt then reduce for medically uncontrolled BP, and discontinue for hypertensive crisis. Isolated creatinine rise without other findings usually needs only monitoring; consider cystatin C-based eGFR before attributing a true GFR fall.Lesion-level management framework

Risk factors

Pre-existing hypertension
Cardiovascular disease
Concurrent agents that raise blood pressure

Prevention

Optimize/initiate antihypertensives before and during therapy

Anticancer mechanism· how it treats cancer

Inhibits poly(ADP-ribose) polymerase (PARP1/2) and traps the enzyme on damaged DNA, exploiting homologous-recombination deficiency (synthetic lethality). Used as maintenance in ovarian cancer and, with abiraterone, in BRCA-altered metastatic castration-resistant prostate cancer.

§04

Clinical depth

Renal dose adjustment

No formal renal dose adjustment for mild-moderate impairment; not studied in CrCl <30 mL/min or on dialysis (use with caution). Individualized starting dose (200 mg) is recommended by weight (<77 kg) and platelet count (<150,000/µL) for hematologic, not renal, safety.

Dialyzability & ESKD dosing

Small molecule but highly protein-bound (~83%) with a large volume of distribution; not expected to be meaningfully removed by hemodialysis. No validated ESKD dosing — extrapolate cautiously and prioritize cytopenia monitoring.

Differential diagnosis

Distinguish drug-induced hypertension from pain-, steroid-, or volume-related BP elevation and from VEGF-pathway hypertension if on combination therapy. For the creatinine bump, distinguish transporter-mediated pseudo-AKI (stable cystatin C, bland sediment, no oliguria) from true AKI (rising cystatin C, proteinuria, active sediment).

Monitoring

Blood pressure and heart rate at least weekly for the first 2 months, then at least monthly
CBC weekly for the first month (thrombocytopenia/anemia/neutropenia), then monthly
Serum creatinine at baseline and periodically; cystatin C if a true GFR change is in question

Key trials & series

PRIMA/ENGOT-OV26 (first-line ovarian maintenance — hypertension signal)
NOVA (recurrent ovarian maintenance)
MAGNITUDE (niraparib + abiraterone in mCRPC — hypertension among most common grade >=3 events)
Chen 2024 FAERS + RCT meta-analysis (class-distinctive hypertension)

Clinical pearls

Among PARP inhibitors, niraparib is the hypertension outlier — check and treat BP proactively rather than reflexively dose-reducing the drug.
A small early creatinine rise is usually a transporter artifact; cystatin C-based eGFR avoids unnecessary biopsies and dose changes.
Thrombocytopenia, not nephrotoxicity, is the dose-limiting toxicity — individualize the starting dose by weight and platelets.

§05

References

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

Evidence accrual

8 references · 2020–2026 · 4 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.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 22,116 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· 5 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

Hypertensioncorroborated · ROR 10.61 — on the terms that name the lesion (ROR 6)
Pseudo-AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Hypertension

ROR 10.6195% CI 10.24–10.99· 3,639 reports

SIADH / Hyponatremia

ROR 2.2495% CI 1.94–2.58· 189 reports

Hemorrhagic Cystitis

ROR 1.7795% CI 1.49–2.11· 129 reports

Crystal / Obstructive Nephropathy

ROR 1.4395% CI 1.16–1.77· 84 reports

Electrolyte Disturbance

ROR 1.3495% CI 1.19–1.52· 270 reports

FAERS outcomes & reporting trend· 6.5% of reports w/ death · 22.9% w/ hospitalization

6.5%

Reported with a death outcome

1,433 of 22,116 reports

22.9%

Reported with hospitalization

5,057 of 22,116 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 22,116 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 0.3395% CI 0.25–0.43· 53 AKI reports ·AKI is reported less often than for other drugs (CI entirely below 1) — no disproportionate signal.

Gastrointestinal

Nausea5,789Constipation4,109Vomiting2,036Diarrhoea1,154

General / constitutional

Fatigue5,237Asthenia1,857Malaise1,082Pain1,066

Blood & lymphatic

Platelet Count Decreased4,132Haemoglobin Decreased1,752Anaemia1,466White Blood Cell Count Decreased1,411

Nervous system

Headache2,370Dizziness1,605Neuropathy Peripheral1,108

Vascular

Blood Pressure Increased2,459Hypertension1,313

Psychiatric

Insomnia2,841

Metabolic & electrolyte

Decreased Appetite1,885

Respiratory

Dyspnoea1,433

Musculoskeletal

Arthralgia1,222

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 Niraparib 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

Brigatinib

Alunbrig · ALK TKI

Profile

Creatinine elevation; usually benign.

PSEUDOPREHTN

Mild#3 · 73% phenotype match

Pralsetinib

Gavreto · RET inhibitor

Profile

Hypertension; rare AKI.

HTNPREPSEUDO

Mild#4 · 73% phenotype match

Olaparib

Lynparza · PARP inhibitor

Profile

Benign creatinine rise via OCT2/MATE inhibition.

PSEUDOTMA

Mild#5 · 68% phenotype match

Alectinib

Alecensa · ALK TKI

Profile

Creatinine rise via reduced tubular secretion.

PSEUDOPRE

Mild#6 · 57% phenotype match

Compare Niraparib 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 Niraparib’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 Niraparib; 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 11 clinical records among all 12 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.