Pentostatin
Nipent · Purine analog (ADA inhibitor)
Renally cleared; dose-related acute kidney injury.
ATNLYTESIADH
Moderate#1 · 71% phenotype match
Carboplatin
Paraplatin · Carbo
Platinum agent · approved 1989 · 12 citations · FAERS AKI reporting ROR 2.94 (95% CI 2.82–3.05, 2,626 AKI reports)
Recent· through 2024
Deeply sourced9/9 · 8 signals
- Met: 12 citations
- Met: 12+ references
- Met: Accrued over 10+ years (span: 35y)
- Met: Beyond single case reports
- Met: High-impact journal
- Met: Landmark reference
- Met: Current through 2024
- 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.
Cisplatin's kidney-sparing cousin — dosed by GFR, limited by marrow not kidney.
MildSecond-generation platinum
OvarianLungGerm-cellHead & neck
§01
Signature kidney injury
Signature lesion
Representative incidence5%
Clinically significant nephrotoxicity uncommon at standard doses; emerges mainly at high/myeloablative doses.Source: Gupta et al., Adv Chronic Kidney Dis 2021
Onset & rechallenge
Time to injuryAcute (~1–7 days)
Acute rise when it occurs, essentially confined to high-dose regimens.
Distilled from: “Acute when it occurs (high-dose regimens).”
Long-term outlook & thresholds
Renal recoveryUsually reversible
When carboplatin nephrotoxicity occurs it is typically mild, dose-related ATN with tubular electrolyte (especially magnesium) wasting that is largely reversible - milder and more reversible than the salt-and-magnesium-wasting tubulopathy of its parent cisplatin. Usually manifests as mild or asymptomatic GFR decline rather than dialysis-requiring AKI.PMID 35190107 (opens PubMed in a new tab)
Cumulative-dose threshold
Conventional target AUC 5-6 dosing is the reference safe range; renal risk emerges mainly at high-dose / myeloablative (stem-cell-transplant conditioning) regimens rather than at standard AUC-based dosing.
Renal toxicity, when it occurs, is more likely at high cumulative or high-dose (e.g., transplant-conditioning) regimens than at conventional AUC 5-6 dosing; clinically significant nephrotoxicity is uncommon at standard AUC-based doses and emerges mainly at high/myeloablative doses.PMID 11219485 (opens PubMed in a new tab)
Early-detection biomarkers
- Urinary KIM-1 and NGAL — Early proximal tubular injury. CISPLATIN data, not carboplatin: in 13 patients given a 1-h cisplatin infusion, urinary proximal-tubular markers sampled at baseline, day 3 and day 10 tracked platinum exposure — KIM-1, NGAL, beta-2-microglobulin, clusterin and cystatin C at day 10 against peak urinary platinum, and NGAL, beta-2-microglobulin, clusterin, cystatin C and osteopontin (not KIM-1) at day 3 against unbound plasma platinum — which the authors read as subclinical cisplatin kidney injury. There is no carboplatin arm, and days 3 and 10 are the study's sampling schedule rather than a demonstrated rise window. Carboplatin shares the proximal-tubular uptake and injury pathway at far lower reactivity, so this is a mechanistic rationale for watching tubular markers on platinum therapy, not a validated carboplatin test.PMID 30220072 (opens PubMed in a new tab)
- Serum magnesium — Tubular magnesium wasting. Hypomagnesemia and other tubular electrolyte losses are the most frequent renal finding with carboplatin; a falling serum magnesium is the earliest and most common signal of platinum tubular toxicity and should be checked at baseline and before each cycle.PMID 35190107 (opens PubMed in a new tab)
Long-term outcome and threshold data distilled from the agent's cited literature — educational, not a substitute for the primary sources.
Recovery across agentsHost risk modifiers
Germline / pharmacogenomic variants that shift an individual's risk of this agent's kidney injury. Research-grade — not routine clinical testing.
- ABCB1c.1236C>T (rs1128503)
Carboplatin/paclitaxel-treated gynecologic-cancer patients carrying the ABCB1 c.1236C>T variant had higher odds of moderate-to-severe (grade 2-4) nephrotoxicity (adjusted OR 2.40, 95% CI 1.39-4.15), independent of age and diabetes. PMID 32564116 (opens PubMed in a new tab)
- RBMS3rs10663797 (AC deletion)
In a GWAS of platinum-treated cancer patients (including carboplatin), the RBMS3 rs10663797 AC-deletion allele was associated with greater eGFR decline and higher risk of acute kidney injury (OR 5.69, 95% CI 2.54-12.74); a platinum-class renal signal, cisplatin-predominant cohort. PMID 35743677 (opens PubMed in a new tab)
§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.
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.
Hypomagnesemia in 104/144 (72%) ovarian-cancer patients on carboplatin-based chemo (grade 2 in 11%, grade 3/4 in 11%); associated with treatment duration
Case-level hemorrhagic urothelial injury with single-agent carboplatin; most FAERS naming volume rides ifosfamide/cyclophosphamide co-regimens.
Case-level reports, including recurrence after a switch from cisplatin.
Toxicity fingerprint
Tap a signature to trace where it strikes the nephron.
5%incidence
SeverityMild
ReversibilityReversible
Evidence12 citations
Nephron map
Proximal TubuleBulk reabsorption + drug uptake (OCT2, OATs)
Distal Tubule / Collecting DuctFine-tuning of Na, K, Mg, acid & water
Bladder / Urothelium
Acute Tubular Necrosis
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.
§03
Deep diveCisplatin acute tubular necrosis & hypomagnesemiaThe drug that cures testicular cancer poisons its own portal of entry — pumped into the kidney's S3 tubule by OCT2, cisplatin necroses the proximal tubule and, downstream, silences the distal magnesium channel, leaving patients wasting magnesium long after the last dose.Kidney injury
Mechanism of kidney injury
Shares the proximal tubular uptake and injury pathway of cisplatin but with far lower reactivity, so tubular toxicity is modest except in high-dose stem-cell-transplant regimens.
Clinical presentation
Usually mild or asymptomatic GFR decline; electrolyte wasting much less frequent than cisplatin. Thrombocytopenia, not kidney injury, is dose-limiting.
Management
Dose reduction, supportive care.Lesion-level management framework
Risk factors
- High / myeloablative dosing
- Pre-existing CKD
- Prior cisplatin
Prevention
- GFR-based (Calvert) dosing
Anticancer mechanism· how it treats cancer
Same DNA-adduct mechanism as cisplatin but a more stable leaving group slows aquation. Dosed by the Calvert formula, AUC × (GFR + 25).
Note · Preferred over cisplatin when renal sparing matters.
§04
Clinical depth
Renal dose adjustment
Dosed by target AUC using the Calvert formula (dose mg = AUC x [GFR + 25]), so renal function is built directly into the prescription rather than handled by a separate adjustment. Capping the GFR estimate at 125 mL/min guards against overdosing when a creatinine-based estimate runs spuriously high — a consequence of IDMS standardization of creatinine assays, which lowered reported creatinine and so inflated Cockcroft-Gault GFR (McLean et al., Gynecol Oncol 2020, PMID 32220419). The cap is a dosing convention rather than a physiologic ceiling, and it is not unanimous: it is endorsed by the FDA, ASCO and GOG (Fehr et al., ESMO Open 2018, PMID 29531843) and attributed to a 2010 NCI recommendation (Morrow et al., J Oncol Pharm Pract 2019, PMID 30336729), but that same analysis concludes that capping a genuinely high GFR delivers a lower AUC than intended, and ADDIKD 2025 instead treats an eGFR above 125 mL/min/1.73 m2 as the trigger to obtain a directly measured GFR. Lower target AUCs are used as GFR falls; in severe impairment or dialysis-dependent patients, dose individually with pharmacy/onco-nephrology input.
Dialyzability & ESKD dosing
Carboplatin (and its reactive aquated/platinum species) is partially removed by hemodialysis, particularly the unbound platinum fraction; protein-bound platinum that accumulates over days is not efficiently cleared. In dialysis-dependent patients it is dosed to a reduced target AUC with chemotherapy timed relative to HD sessions (commonly drug given a few hours before dialysis), though optimal timing rests on limited pharmacokinetic data.
Differential diagnosis
Carboplatin nephrotoxicity is typically mild, dose-related ATN with electrolyte (especially magnesium) wasting, distinguishing it from the more frequent, severe salt-and-magnesium-wasting tubulopathy of its parent compound cisplatin. Unlike immune checkpoint inhibitor AKI (acute interstitial nephritis, often with sterile pyuria and a steroid response) or bevacizumab/VEGF-pathway injury (proteinuria, hypertension, TMA), carboplatin injury is tubular and largely reversible; rule out volume depletion, contrast, and concomitant nephrotoxins before attributing rises to the drug.
Monitoring
- Estimate GFR (measured or validated equation) before every cycle and recompute the Calvert dose; do not carry forward an old GFR.
- Check serum creatinine, magnesium, potassium, and phosphate at baseline and before each cycle; repeat electrolytes if cytopenias prompt dose delays.
- Replete magnesium proactively and recheck after repletion, since hypomagnesemia is the most common renal-tubular abnormality.
- Track the CBC closely (especially platelets) because myelosuppression is dose-limiting and worsens with reduced renal clearance.
- Watch for spuriously low creatinine (low muscle mass, cachexia) that inflates estimated GFR and risks overdosing.
Key trials & series
- Calvert formula (Calvert et al., J Clin Oncol 1989) — derived carboplatin dosing from target AUC and GFR, the basis for renal-function-adjusted dosing still used today.
- ICON3 (Lancet 2002) — established single-agent carboplatin as having efficacy comparable to platinum combinations in ovarian cancer with a more favorable non-hematologic (including renal) toxicity profile than cisplatin.
- GOG-158 (Ozols et al., J Clin Oncol 2003) — carboplatin/paclitaxel was non-inferior to cisplatin/paclitaxel in ovarian cancer with significantly less nephrotoxicity and electrolyte disturbance.
Clinical pearls
- Carboplatin is substantially less nephrotoxic than cisplatin — its slower-aquating, more stable leaving group means clinically significant AKI is uncommon at standard AUC-based doses.
- Because dose is set by the Calvert formula, accurate GFR is the single most important renal safety step; a falsely high GFR estimate causes overdose, and a falsely low one causes underdosing.
- It does not require the aggressive saline pre/post-hydration and forced diuresis mandated for cisplatin, simplifying outpatient delivery.
- Renal toxicity, when it occurs, is more likely at high cumulative or high-dose (e.g., transplant-conditioning) regimens than at conventional AUC 5-6 dosing.
- Hypomagnesemia and other tubular electrolyte losses are the most frequent renal finding and are usually milder and more reversible than with cisplatin.
- Hemorrhagic urothelial injury (gross hematuria, bladder clots) is reported with single-agent carboplatin — rare, and most FAERS hemorrhagic-cystitis volume still rides on ifosfamide/cyclophosphamide co-regimens.
- SIADH is attributed to carboplatin in case reports (including recurrence after a switch from cisplatin); much of the reporting comes from the SCLC carboplatin-etoposide population.
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
§05
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 · 1989–2024 · 1 since 2022Primary (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.
- 1.LandmarkCarboplatin dosage: prospective evaluation of a simple formula based on renal function.Calvert AH et al. · J Clin Oncol · 1989 · PMID 2681557The landmark Calvert formula deriving dose from GFR to limit toxicity.
- 2.Carboplatin pharmacokinetics in children: the development of a pediatric dosing formula. The United Kingdom Children's Cancer Study Group.Newell DR et al. · J Clin Oncol · 1993 · PMID 8246021Pediatric GFR-based dosing formula.
- 3.Comparative study of cisplatin and carboplatin on pharmacokinetics, nephrotoxicity and effect on renal nuclear DNA synthesis in rats.Yasumasu T et al. · Pharmacol Toxicol · 1992 · PMID 1508841Explains carboplatin's lower nephrotoxicity via less renal platinum accumulation.
- 4.Conventional Chemotherapy Nephrotoxicity.Gupta S et al. · Adv Chronic Kidney Dis · 2021 · PMID 35190107Authoritative onconephrology review of platinum incidence and dose modification.
- 5.Anticancer drug-induced kidney disorders.Kintzel PE et al. · Drug Saf · 2001 · PMID 11219485Review of dose-related platinum renal dysfunction and protective agents.
- 6.Carboplatin-induced hematuria in a patient with stage I seminoma: a case report.Capdevila P et al. · J Med Case Rep · 2024 · PMID 39550593Single-agent adjuvant carboplatin (stage I seminoma) causing frank hematuria with bladder clot.
- 7.Carboplatin-induced hematuria in a patient of breast carcinoma. A case report.Taj A et al. · Am J Ther · 2011 · PMID 20838327Carboplatin-attributed gross hematuria in breast cancer.
- 8.Syndrome of inappropriate anti-diuretic hormone secretion secondary to carboplatin after docetaxel-carboplatin-trastuzumab combination for early stage HER-2 positive breast cancer.Turner N et al. · Asia Pac J Clin Oncol · 2012 · PMID 22897880SIADH after docetaxel-carboplatin-trastuzumab with carboplatin identified as the causative agent; no recurrence on resuming the other two drugs.
- 9.Syndrome of Inappropriate Secretion of Antidiuretic Hormone Caused by Carboplatin After Switching from Cisplatin in a Metastatic Urethral Cancer Patient.Sugiyama Y et al. · Urol Case Rep · 2017 · PMID 28271051SIADH recurring under carboplatin itself after a switch from cisplatin — the dysnatremia followed the substituted agent.
Case reports — ranked by strength· 3
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.
CaseB · ModerateCarboplatin-related acute interstitial nephritis in a patient with pancreatic neuroendocrine tumor.Asai A et al. · CEN Case Rep 2020 · PMID 31834568Biopsy-proven acute interstitial nephritis after carboplatin causing AKI (creatinine to 6.81 mg/dL), the second reported case of carboplatin-related AIN beyond the usual acute tubular necrosis.CaseC · LimitedCarboplatin-related hematuria and acute renal failure.Agraharkar M et al. · Am J Kidney Dis 1998 · PMID 10074593Carboplatin damage to urothelial/transitional epithelium producing gross hematuria, blood-clot ureteral obstruction with bilateral hydronephrosis and acute renal failure.CaseC · LimitedEnd-stage renal disease following carboplatin chemotherapy for a nasopharyngeal carcinoma.Tarrass F et al. · Ren Fail 2007 · PMID 18067055Carboplatin-induced acute tubular necrosis that progressed irreversibly to dialysis-dependent end-stage renal disease, an exceedingly rare outcome of carboplatin nephrotoxicity.
FDA label — boxed warning & renal dosing· boxed warning · renal impairment
Quoted verbatim from this agent's current FDA label (Sep 2025) — not paraphrased or interpreted. Full label on DailyMed .
Boxed warning
WARNING: HYPERSENSITIVITY REACTIONS, INCLUDING ANAPHYLAXIS Serious and life-threatening hypersensitivity reactions, including anaphylaxis, can occur with KYXATA within minutes of administration during any cycle. Immediately discontinue KYXATA for severe hypersensitivity reactions and administer appropriate treatment for management of the hypersensitivity reaction [see Warnings and Precautions (5.1) ]. WARNING: HYPERSENSITIVITY REACTIONS, INCLUDING ANAPHYLAXIS Serious and life-threatening hypersensitivity reactions, including anaphylaxis, can occur with KYXATA within minutes of administration during any cycle. ( 5.1 ) Immediately withhold KYXATA for severe hypersensitivity reactions and administer appropriate treatment for management of the hypersensitivity reaction. ( 5.1 )
Renal impairment — from the label
Reduce the dose for patients with creatinine clearance of 16 to 59 mL/min who will be administered a dose based on body surface area. ( 8.6 , 2.4 )
What gets reported — FAERS
Everything below is FAERS — adverse events someone chose to report, about 126,274 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· 9 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
- Acute Tubular Necrosiscorroborated · ROR 4.88
- Electrolyte Disturbancecorroborated · ROR 3.69 — on the terms that name the lesion (ROR 10.21)
- SIADH / Hyponatremiacorroborated · ROR 3.61 — on the terms that name the lesion (ROR 5.65)
- Hemorrhagic Cystitiscorroborated · ROR 1.64 — on the terms that name the lesion (ROR 6.05)
Acute Interstitial Nephritis
ROR 5.6495% CI 5.20–6.11· 616 reports
Thrombotic Microangiopathy
ROR 5.4895% CI 5.01–6.00· 496 reports
Acute Tubular Necrosis
ROR 4.8895% CI 4.34–5.50· 282 reports
Glomerular Injury / Proteinuria
ROR 4.1695% CI 3.87–4.49· 713 reports
Electrolyte Disturbance
ROR 3.6995% CI 3.58–3.81· 4,085 reports
Fanconi Syndrome
ROR 3.6995% CI 3.06–4.45· 112 reports
SIADH / Hyponatremia
ROR 3.6195% CI 3.44–3.79· 1,707 reports
Hemorrhagic Cystitis
ROR 1.6495% CI 1.52–1.77· 681 reports
Crystal / Obstructive Nephropathy
ROR 1.1195% CI 1.00–1.23· 372 reports
FAERS outcomes & reporting trend· 15.9% of reports w/ death · 42.8% w/ hospitalization
15.9%
Reported with a death outcome
20,030 of 126,274 reports
42.8%
Reported with hospitalization
54,090 of 126,274 reports
Reports per year
- 2015: 3,759 reports
- 2016: 4,289 reports
- 2017: 5,628 reports
- 2018: 7,631 reports
- 2019: 7,570 reports
- 2020: 7,830 reports
- 2021: 9,234 reports
- 2022: 11,524 reports
- 2023: 12,551 reports
- 2024: 13,570 reports
- 2025: 14,117 reports
- 2026: 6,805 reports
Yearly FAERS report volume · most recent year is partial.
FAERS adverse-event signal — all organ systems· 9 systems · 126,274 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 2.9495% CI 2.82–3.05· 2,626 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.
Renal & urinary
Acute Kidney Injury2,626
Blood & lymphatic
Neutropenia7,435Anaemia7,235Febrile Neutropenia6,609Thrombocytopenia5,938Myelosuppression3,814
Gastrointestinal
Nausea7,052Diarrhoea6,243Vomiting5,151
General / constitutional
Pyrexia4,847Fatigue4,730Asthenia3,896
Immune / infection
Pneumonia3,380Sepsis2,751
Skin
Rash3,190Alopecia2,562
Respiratory
Dyspnoea5,431
Metabolic & electrolyte
Decreased Appetite2,894
Nervous system
Neuropathy Peripheral2,695
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 Carboplatin 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.
Phenotype-similar agents· the numbered markers on the map above
Profile
Nedaplatin
Aqupla · Platinum agent
Second-gen platinum with reduced renal toxicity vs cisplatin.
ATNLYTE
Moderate#2 · 71% phenotype match
Ibandronate
Boniva · Bisphosphonate
Lower renal risk than zoledronate.
ATNLYTEGLOM
Mild#3 · 60% phenotype match
Imatinib
Gleevec · BCR-ABL TKI
Fluid retention; rare Fanconi and AKI.
LYTEFANCATN
Mild#4 · 60% phenotype match
Cisplatin
Platinol · Platinum agent
Proximal tubular ATN + magnesium wasting; the archetype.
ATNLYTEPRE
Severe#5 · 58% phenotype match
Melphalan flufenamide (melflufen)
Pepaxto · Peptide-conjugated alkylator
Delivers melphalan intracellularly; BRIDGE supports a reduced 30 mg dose in moderate renal impairment.
ATNLYTE
Moderate#6 · 56% phenotype match
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
- 2Carboplatin· this agentATN — Acute Tubular NecrosisFAERS AKIMild
- 3NedaplatinATN — 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 Carboplatin’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 Carboplatin; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.
- Pearson, Andrew D J — their work on Carboplatin, on PubMed (opens in a new tab)2 papers · 376 citesPMID 28259608 (opens PubMed in a new tab)PMID 19850470 (opens PubMed in a new tab)
- Gupta, Shruti — their work on Carboplatin, on PubMed (opens in a new tab)2 papers · 68 citesPMID 37074956 (opens PubMed in a new tab)PMID 35190107 (opens PubMed in a new tab)
- Veening, Margreet A — their work on Carboplatin, on PubMed (opens in a new tab)2 papers · 139 citesPMID 30855726 (opens PubMed in a new tab)PMID 24101439 (opens PubMed in a new tab)
- Chitapanarux, Imjai — their work on Carboplatin, on PubMed (opens in a new tab)2 papers · 127 citesPMID 27435245 (opens PubMed in a new tab)PMID 17467265 (opens PubMed in a new tab)
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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 130 clinical records among the 300 most-relevant of 992 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.