Is kidney injury from Nedaplatin reversible?

Partially reversible. Typical onset: Days after dosing; cumulative with repeated cycles..

How should kidney function be monitored during Nedaplatin therapy?

Serum creatinine and electrolytes (Mg, K) each cycle; Platelet count and CBC (dose-limiting thrombocytopenia); Urinalysis for glycosuria / tubular proteinuria when concerned.

How can kidney injury from Nedaplatin be prevented?

Adequate hydration (>=1000 mL infusion accompanies dosing)

Who is at higher risk of kidney injury from Nedaplatin?

Pre-existing renal impairment; Volume depletion; Prior cisplatin exposure / high cumulative platinum dose; Concomitant nephrotoxins; Ascites or third-spacing (prolonged free-platinum exposure).

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Printable monograph

Platinum agent

Nedaplatin

Aqupla · NDP

Platinum agent · approved 1995 · 11 citations

Recent· through 2023

Fairly sourced6/9 · 5 signals

Met: 11 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 31y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Met: Current through 2023
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 second-generation platinum engineered to spare the kidney that cisplatin punishes.

ModerateSecond-generation platinum

Head and neck squamous cell carcinomaNon-small cell and small cell lung cancerEsophageal carcinomaCervical and ovarian cancerGerm cell tumors

§01

Signature kidney injury

Signature lesion

Acute Tubular Necrosis

Representative incidence9.8%

Lower renal cortical platinum accumulation and less frequent nephrotoxicity than equimolar cisplatin; dose-related proximal tubular injury still occurs, but high-grade AKI is uncommon and not robustly quantified in the renal literature. Myelosuppression (notably thrombocytopenia), not nephrotoxicity, is the dose-limiting toxicity. Reported rate: serum creatinine elevation in 9.8% — Patients with gastrointestinal cancer (esophageal, stomach, colon) in a 16-institution Japanese phase II study of… (Taguchi 1992, PMID 1558398).Source: Taguchi et al., Gan To Kagaku Ryoho 1992

Onset & rechallenge

Time to injuryAcute (~1–7 days)

AKI days after dosing, accumulating with repeated cycles.

Distilled from: “Days after dosing; cumulative with repeated cycles.”

§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.

Acute Tubular Necrosis#1 · Signaturequalitative — no citable incidence
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.
Electrolyte DisturbanceSecondaryqualitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

9.8%incidence

SeverityModerate

ReversibilityPartially reversible

Evidence11 citations

Nephron map

Proximal TubuleBulk reabsorption + drug uptake (OCT2, OATs)

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

Acute Tubular Necrosis

Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.

§03

Kidney injury

Mechanism of kidney injury

Platinum is taken up into S3-segment proximal tubular epithelium (organic cation/OCT2-type and passive transport), where it binds nuclear and mitochondrial DNA and proteins, generating reactive oxygen species and triggering apoptosis/necrosis. Quantitatively, at equitoxic systemic exposure nedaplatin reaches roughly half the renal cortical platinum concentration of cisplatin, so tubular necrosis, urinary NAG, and glycosuria are correspondingly milder. Magnesium and other electrolyte wasting follows tubular damage but is less pronounced than with cisplatin.

Clinical presentation

Rise in serum creatinine, increased urinary N-acetyl-beta-D-glucosaminidase and glucosuria; electrolyte wasting (hypomagnesemia, hypokalemia) can occur but is generally milder than with cisplatin. In renal dysfunction or ascites, free-platinum exposure is prolonged.

Management

Hold or dose-reduce for rising creatinine, correct volume and electrolytes (magnesium, potassium), and provide supportive care. Substituting nedaplatin into platinum regimens has been used to deliver therapy in patients with impaired renal function or prior cisplatin nephrotoxicity.Lesion-level management framework

Risk factors

Pre-existing renal impairment
Volume depletion
Prior cisplatin exposure / high cumulative platinum dose
Concomitant nephrotoxins
Ascites or third-spacing (prolonged free-platinum exposure)

Prevention

Adequate hydration (>=1000 mL infusion accompanies dosing)

Anticancer mechanism· how it treats cancer

Cytotoxic platinum(II) compound (cis-diammine-glycolato-platinum) that, after aquation, forms intrastrand 1,2-d(GpG) DNA cross-links, blocking replication and transcription and triggering apoptosis. Its glycolate leaving group gives more favorable aqueous handling and lower tissue retention than cisplatin. Used mainly in Japan for head and neck, esophageal, lung, cervical, ovarian, and germ cell cancers.

Note · Marketed largely in Japan; the renal-sparing advantage over cisplatin rests on accumulation/pharmacology data and small clinical series rather than large randomized nephrotoxicity trials.

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Clinical depth

Renal dose adjustment

No formally validated CrCl-banded schema in Western labeling; in practice dose is reduced and free-platinum AUC monitored when CrCl is low. Reduce dose / extend interval for baseline renal impairment and avoid stacking with cisplatin-level cumulative platinum.

Dialyzability & ESKD dosing

Free (unbound) platinum is dialyzable like other small-molecule platinums; protein-bound platinum is not. Timing of any platinum agent around hemodialysis should be individualized with pharmacy. Renal clearance is a major elimination route, so ESKD prolongs exposure.

Differential diagnosis

Distinguish platinum ATN (bland-to-granular sediment, tubular proteinuria, Mg wasting, days after dosing) from prerenal azotemia (low FeNa, responds to volume) and from cisplatin carryover injury. Persistent isolated hypomagnesemia favors platinum tubulopathy over prerenal physiology.

Monitoring

Serum creatinine and electrolytes (Mg, K) each cycle
Platelet count and CBC (dose-limiting thrombocytopenia)
Urinalysis for glycosuria / tubular proteinuria when concerned

Key trials & series

Japanese phase II program (Ota, Gan To Kagaku Ryoho 1996) establishing 80-100 mg/m2 dosing and the reduced GI/renal toxicity signal
Nedaplatin-vindesine vs cisplatin-vindesine randomized NSCLC comparison showing significantly less nephro/GI toxicity

Clinical pearls

Thrombocytopenia, not AKI, is the dose-limiting toxicity - watch platelets as closely as creatinine.
Useful as a platinum substitute when cisplatin nephrotoxicity precludes further cisplatin, but it is not nephrotoxicity-free.

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

Class-level context for the major non-renal toxicities of the Platinum agent class.

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

Peripheral neuropathy (esp. oxaliplatin) and ototoxicity (cisplatin)

Hematologic

Cytopenias, thrombosis, TMA

Myelosuppression — thrombocytopenia prominent with carboplatin

Gastrointestinal

Diarrhea, colitis, mucositis, perforation

Severe nausea and vomiting

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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 · 1992–2019 · 1 since 2017

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 · LimitedCase Report: Etoposide-nedaplatin induced rhabdomyolysis in a small cell lung cancer patient.Xu X et al. · Front Pharmacol 2023 · PMID 37675043Case report of etoposide-nedaplatin chemotherapy-induced rhabdomyolysis, a complication that can precipitate acute renal failure/tubular injury.CaseC · LimitedHypomagnesemia because of nedaplatin for cervical cancer: A case report.Komoda J et al. · J Gen Fam Med 2023 · PMID 37484120Case report of nedaplatin-induced renal tubular electrolyte wasting (hypomagnesemia and hypocalcemia) in a woman treated for cervical cancer, reflecting platinum tubular injury.

Guidelines & consensus· 15

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.

ADQIConventional cytotoxic chemotherapy-associated nephrotoxicity: consensus report of the 34th Acute Disease Quality Initiative (ADQI) WorkgroupKidney Int 2026 · PMID 41881107Cisplatin is identified as a leading cytotoxic nephrotoxin; the workgroup details preventive measures (adequate isotonic hydration, correction of volume depletion, avoidance of concurrent nephrotoxins, attention to electrolyte/magnesium wasting) and management of cisplatin-associated AKI, with a research agenda for knowledge gaps.Expert ConsensusThe Prevention of Cisplatin-Induced Nephrotoxicity: A General Consensus Statement of a Group of Oncologist-Hematologists, Adult and Pediatric Nephrologists, Radiation Oncologists, Clinical Pathologists, Clinical Pharmacologists, and Renal Physiologists on Cisplatin Therapy in Cancer PatientsInt J Prev Med 2022 · PMID 35392316Consensus on modifiable factors for cisplatin nephrotoxicity prevention, addressing hydration methods, magnesium supplementation, dextrose, avoidance of NSAIDs and renin-angiotensin system inhibitors and contrast agents around cisplatin, GFR assessment, antioxidants, and patient factors (age, sex, female hormones).

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 Nedaplatin 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

Melphalan flufenamide (melflufen)

Pepaxto · Peptide-conjugated alkylator

Profile

Delivers melphalan intracellularly; BRIDGE supports a reduced 30 mg dose in moderate renal impairment.

ATNLYTE

Moderate#1 · 86% phenotype match

Telisotuzumab vedotin (Teliso-V)

Emrelis · c-Met ADC (MMAE)

Profile

c-Met MMAE antibody-drug conjugate; proximal tubular ATN risk extrapolated from the ADC/MMAE class.

ATNLYTE

Moderate#2 · 86% phenotype match

Plicamycin (mithramycin)

Mithracin · Antitumor antibiotic

Profile

Cumulative tubular ATN; hypocalcemia is an on-target antiresorptive effect.

ATNLYTE

Moderate#3 · 78% phenotype match

Trabectedin

Yondelis · Marine alkylating agent

Profile

Rhabdomyolysis → pigment nephropathy; hepatotoxicity.

ATNLYTE

Moderate#4 · 75% phenotype match

Enfortumab vedotin

Padcev · Antibody-drug conjugate (Nectin-4/MMAE)

Profile

Emerging AKI and electrolyte signals in urothelial cancer.

ATNLYTEPRE

Moderate#5 · 73% phenotype match

Trastuzumab deruxtecan

Enhertu · Antibody-drug conjugate (HER2/DXd)

Profile

Emerging AKI/proteinuria reports — under-published.

ATNFANCLYTE

Moderate#6 · 73% phenotype match

Compare Nedaplatin 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 Platinum 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.

1OxaliplatinTMA — Thrombotic MicroangiopathyFAERS AKIMild
2CarboplatinATN — Acute Tubular NecrosisFAERS AKIMild
3Nedaplatin· this agentATN — Acute Tubular NecrosisModerate
4CisplatinATN — Acute Tubular NecrosisFAERS AKISevere

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 Nedaplatin’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 Nedaplatin; 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 36 clinical records among all 77 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.