What kind of kidney injury does Cisplatin cause?

Acute Tubular Necrosis — Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate. Other reported patterns: Electrolyte Disturbance, Prerenal / Hemodynamic AKI, Hemorrhagic Cystitis, Fanconi Syndrome, SIADH / Hyponatremia.

Is kidney injury from Cisplatin reversible?

Partially reversible. Typical onset: Acute — creatinine peaks ~day 4–7; magnesium wasting can persist for months..

How should kidney function be monitored during Cisplatin therapy?

Serum creatinine/eGFR at baseline and before each cycle; consider measured or estimated CrCl since injury can lag the dose by days; Serum magnesium (and potassium/calcium) each cycle and between cycles — renal Mg wasting is near-universal and often persists for months; Volume status and urine output during and after the mandatory pre/post-hydration window; Track cumulative platinum dose over the treatment course to anticipate chronic GFR decline; Urinalysis for tubular proteinuria/glycosuria and consider tubular injury markers (e.g., urinary NGAL/KIM-1) when AKI is suspected (research-grade).

How can kidney injury from Cisplatin be prevented?

Vigorous IV saline hydration Magnesium supplementation Dose capping / splitting Substitute carboplatin when feasible Amifostine (selected protocols)

Who is at higher risk of kidney injury from Cisplatin?

High / cumulative dose; Volume depletion; Concurrent nephrotoxins; Older age; Pre-existing CKD.

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Printable monograph

Platinum agent

Cisplatin

Platinol · Cis

Platinum agent · approved 1978 · 20 citations · FAERS AKI reporting ROR 3.39 (95% CI 3.24–3.55, 1,863 AKI reports)

Up to date· through 2025

Deeply sourced9/9 · 8 signals

Met: 20 citations
Met: 12+ references
Met: Accrued over 10+ years (span: 27y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2025
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 archetypal nephrotoxin — concentrated in the proximal tubule by its own transporters.

SevereFirst-generation platinum

TesticularOvarianBladderLungHead & neck

§01

Signature kidney injury

Signature lesion

Acute Tubular Necrosis

Representative incidence30%

20–35% range across studies

AKI in ~20–35% per cycle (classic teaching: ~1 in 3). Hypomagnesemia in 40–100%.Source: Tang et al., Nat Rev Nephrol 2022; Manohar et al., J Nephrol 2017

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Creatinine peaks around day 4–7 after a dose; magnesium wasting can persist for months.

Distilled from: “Acute — creatinine peaks ~day 4–7; magnesium wasting can persist for months.”

Long-term outlook & thresholds

Renal recoveryOften partial recovery

Partly reversible but cumulative: repeated cycles cause stepwise, often incomplete GFR recovery, so baseline CrCl and lifetime platinum exposure guide whether to continue, dose-reduce, or switch to carboplatin. Renal magnesium wasting is the most durable lesion and can persist long after creatinine recovers.PMID 36229672 (opens PubMed in a new tab)

CKD trajectory.: Cumulative platinum dose drives chronic injury; repeated cycles produce stepwise incomplete GFR recovery and progression toward CKD.
Dialysis / RRT.: In cohort work, severe cisplatin-associated AKI is defined as a twofold creatinine rise or kidney replacement therapy within 14 days of the dose.PMID 38538012 (opens PubMed in a new tab)
Outcome marker.: Prophylactic first-day IV magnesium was associated with lower risk of the composite of cisplatin-associated AKI or death (2.7% vs 5.3%; adjusted OR 0.80) in a 13,719-patient multicenter cohort.PMID 40272825 (opens PubMed in a new tab)

Cumulative-dose threshold

High single doses ≥100 mg/m² per cycle (with short cycle intervals); cumulative lifetime platinum exposure

High single doses ≥100 mg/m² per cycle and short cycle intervals raise acute nephrotoxicity risk, and rising cumulative platinum dose drives chronic, stepwise GFR decline — so a defined cumulative ceiling is respected and renal function reassessed before each cycle.

Early-detection biomarkers

Urinary KIM-1 and NGAL — Proximal tubular (S3 segment) injury — early ATN. Urinary proximal-tubular biomarkers rise hours before serum creatinine, flagging cisplatin ATN ahead of the characteristic day 4–7 creatinine peak; monitoring lists urinary NGAL/KIM-1 as research-grade markers when AKI is suspected.PMID 28979774 (opens PubMed in a new tab)
Serum magnesium (with FE-Mg) — Distal magnesium-wasting tubulopathy. Renal Mg wasting is the hallmark lesion — the cited review puts hypomagnesemia at up to 90% of cisplatin-treated patients when no corrective measures are taken — and can persist for months after creatinine recovers, sometimes requiring chronic repletion.PMID 10212589 (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 agents

Host risk modifiers

Germline / pharmacogenomic variants that shift an individual's risk of this agent's kidney injury. Research-grade — not routine clinical testing.

SLC22A2 (OCT2)rs316019 c.808G>T (Ala270Ser)
OCT2 mediates uptake of cisplatin into renal proximal tubule cells; the variant T (270Ser) allele reduces tubular uptake, so carriers show blunted serum-creatinine rise after cisplatin — the reference GG genotype is at HIGHER nephrotoxicity risk, the T allele is protective. Most consistently replicated cisplatin renal PGx signal. PMID 19625999 (opens PubMed in a new tab)
GSTP1rs1695 (Ile105Val, A>G)
Glutathione S-transferase P1 detoxifies platinum in the kidney. Patients homozygous for the variant GG (105Val) genotype showed ~2-fold or greater increases in urinary AKI biomarkers (KIM-1, calbindin, NGAL at day 3; IL-18 at day 10) after cisplatin, indicating greater proximal-tubule injury. PMID 28640195 (opens PubMed in a new tab)
ERCC18092C>A (rs3212986) / Asn118Asn (rs11615)
Nucleotide-excision-repair gene; the two polymorphisms are highly linked and together accounted for an additional 13% of interindividual variability in eGFR change (n=79). Homozygous 8092A carriers showed NO reduction in eGFR versus an 11.5% mean decrease in C-allele carriers (p=0.004); homozygous carriers of the Asn118Asn C allele showed no reduction versus a 12.8% decrease in T-allele carriers (p=0.047). The protective genotypes are therefore 8092 AA and Asn118Asn CC — the C allele at 8092 and the T allele at Asn118Asn mark the higher-risk group. PMID 21902499 (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.

Acute Tubular Necrosis#1 · Signature5%PMID 38538012 (opens PubMed in a new tab)
Severe CP-AKI (>=2x rise in serum creatinine or dialysis within 14 days) occurred in 3.3-5.2% across a 24,717-patient multicenter cohort; any-grade AKI is far more common (up to ~69% with high-dose concurrent chemoradiation).
Electrolyte DisturbanceSecondary56%PMID 28049899 (opens PubMed in a new tab)
Hypomagnesemia in 56.3% of patients receiving single-agent cisplatin (RIFLE-based retrospective cohort); reflects distal tubular Mg2+ (and K+/Ca2+) wasting.
Prerenal / Hemodynamic AKIRarequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Hemorrhagic CystitisRarequalitative — no citable incidence
A single other-causes-excluded case report; FAERS reporting mostly reflects ifosfamide/cyclophosphamide co-therapy.
Fanconi SyndromeRarequalitative — no citable incidence
Case-level acute Fanconi syndrome and renal salt wasting, including in ifosfamide-free regimens.
SIADH / HyponatremiaRarequalitative — no citable incidence
Case reports with positive dechallenge; renal salt wasting is the better-characterized cisplatin dysnatremia and is often miscoded as SIADH.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

30%incidence

SeveritySevere

ReversibilityPartially reversible

Evidence20 citations

Nephron map

Vasculature / Endothelium

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

Kidney injury

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.Appears in 4 documented synergy combinations

Mechanism of kidney injury

Actively imported into proximal tubular cells via the OCT2 and Ctr1 transporters, then concentrated in the S3 segment, where it triggers mitochondrial injury, oxidative stress, DNA damage and a pro-inflammatory (TNF-α) cascade. Also vasoconstricts the afferent arteriole and induces a distal magnesium-wasting tubulopathy.

Clinical presentation

Non-oliguric AKI with creatinine peaking day 4–7, hypomagnesemia (with secondary hypocalcemia/hypokalemia, tetany), polyuria and granular casts.

Management

Hold or discontinue, IV fluids, aggressive Mg/K repletion, supportive AKI care, dialysis if severe.Lesion-level management framework

Risk factors

High / cumulative dose
Volume depletion
Concurrent nephrotoxins
Older age
Pre-existing CKD

Prevention

Vigorous IV saline hydration
Magnesium supplementation
Dose capping / splitting
Substitute carboplatin when feasible
Amifostine (selected protocols)

Anticancer mechanism· how it treats cancer

Forms intra- and inter-strand DNA cross-links that block replication and transcription, driving apoptosis. Backbone of testicular, ovarian, bladder, lung and head & neck regimens.

Note · Both the AKI and hypomagnesemia ranges are definition-, dose- and hydration-dependent.

§04

Clinical depth

Renal dose adjustment

No fixed CrCl-banded schedule in the FDA label, and two different conventions circulate that must not be blended. Many centers treat CrCl as an eligibility floor: avoid or withhold cisplatin when baseline CrCl is below ~50-60 mL/min and substitute carboplatin (AUC-dosed by GFR). Renal-dosing tables instead continue treatment into that range at a reduced dose (~25% reduction for CrCl 46-60, ~50% for CrCl 30-45) with intensified hydration and CrCl reassessment every cycle. Because the reduction bands sit entirely inside the range the eligibility floor excludes, confirm which rule the treating protocol uses before dosing below ~60 mL/min. High single doses (e.g., >=100 mg/m2) per cycle and short cycle intervals raise nephrotoxicity risk; cumulative platinum dose drives chronic injury, so respect a defined cumulative ceiling and reassess renal function before each cycle.

Dialyzability & ESKD dosing

Free (unbound, ultrafilterable) platinum is small and dialyzable, but cisplatin binds plasma proteins irreversibly within hours and that bound fraction is not removed by hemodialysis, so dialysis does not reliably rescue overdose once binding has occurred. In ESKD/HD, free platinum accumulates because renal elimination is lost; if cisplatin is used, give reduced doses and time HD relative to infusion in coordination with pharmacy (limited data).

Differential diagnosis

Cisplatin injury is a proximal-tubule ATN that classically appears days after dosing with a bland-to-muddy-brown granular sediment, non-oliguric AKI, and out-of-proportion renal magnesium wasting (low Mg with inappropriately high FE-Mg). Disproportionate, persistent hypomagnesemia with hypokalemia/hypocalcemia distinguishes platinum tubulopathy from prerenal azotemia (low FeNa, volume-responsive) and from contrast or other concurrent nephrotoxin injury.

Monitoring

Serum creatinine/eGFR at baseline and before each cycle; consider measured or estimated CrCl since injury can lag the dose by days
Serum magnesium (and potassium/calcium) each cycle and between cycles — renal Mg wasting is near-universal and often persists for months
Volume status and urine output during and after the mandatory pre/post-hydration window
Track cumulative platinum dose over the treatment course to anticipate chronic GFR decline
Urinalysis for tubular proteinuria/glycosuria and consider tubular injury markers (e.g., urinary NGAL/KIM-1) when AKI is suspected (research-grade)

Key trials & series

Kemp/Capizzi amifostine RCT in advanced ovarian cancer (J Clin Oncol 1996; WR-2721/amifostine cytoprotection) — amifostine reduced cisplatin-induced renal toxicity and Mg wasting without compromising efficacy
Cornelison & Reed review and the classic Stanford/NCI hydration-and-mannitol regimens establishing forced saline diuresis as the standard that lowered cisplatin nephrotoxicity from a dose-limiting problem to a manageable one

Clinical pearls

Vigorous isotonic saline hydration (pre- and post-infusion) with adequate urine flow is the single most effective nephroprotective measure; never give cisplatin to a volume-depleted patient.
Hypomagnesemia from renal Mg wasting is the hallmark and most durable electrolyte lesion — it can persist long after creatinine recovers and may require chronic oral/IV repletion.
Injury is partly reversible but cumulative: repeated cycles cause stepwise, often incomplete GFR recovery, so baseline CrCl and lifetime platinum exposure guide whether to continue, dose-reduce, or switch to carboplatin.
Routine mannitol and high-volume saline are standard, but amifostine is the only agent with randomized evidence for renal protection and is not used universally because of toxicity and cost; magnesium supplementation is widely practiced though hard outcome data are limited.
When renal function precludes cisplatin, carboplatin (AUC-dosed by GFR) is the usual substitute — far less nephrotoxic but myelosuppressive and not always therapeutically equivalent.
Hemorrhagic cystitis is attributed to cisplatin in a single other-causes-excluded pediatric case; the FAERS signal is far larger than that supports and mostly reflects ifosfamide/cyclophosphamide co-therapy.
Acute Fanconi syndrome and renal salt wasting are documented cisplatin proximal-tubule lesions, including in ifosfamide-free regimens.
Cisplatin causes both SIADH (case reports with dechallenge) and — more characteristically — renal salt wasting; the two are routinely confused, so assess volume status before fluid-restricting a hyponatremic patient.

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

17 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

17 references · 1998–2025 · 5 since 2023

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· 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 · ModerateReversible renal-limited thrombotic microangiopathy due to gemcitabine-dexamethasone-cisplatin therapy: a case report.Nishikubo M et al. · BMC Nephrol 2021 · PMID 33980166Biopsy-proven renal-limited thrombotic microangiopathy with AKI and proteinuria after cisplatin-containing chemotherapy, a rare glomerular endothelial injury.CaseC · LimitedRenal Salt Wasting Following Cisplatin.Latcha S et al. · Kidney360 2024 · PMID 38353669Case of cisplatin-induced renal salt wasting with hyponatremia, an uncommon tubular sodium-handling complication beyond classic ATN.CaseC · LimitedProfound hyponatremia and dehydration: A case of cisplatin induced renal salt wasting syndrome.George TB et al. · Physiol Rep 2023 · PMID 36868561Elderly man with recurrent profound hyponatremia and urinary sodium loss diagnosed as cisplatin-induced renal salt wasting syndrome.

Conference abstracts & journal reports· 2 non-PubMed

Non-PubMed sources — conference abstracts (e.g. ASN Kidney Week, badged Abstract) and case reports from non-indexed field journals (e.g. Journal of Onco-Nephrology, badged Journal). Included for completeness; weigh below peer-reviewed PubMed citations.

AbstractPlatinum Based Chemotherapy Related Hypomagnesemia Treated With Sodium Glucose Cotransporter 2 (SGLT2) Inhibitors in Non-Diabetic Cancer PatientsHammad N, Rashidi A · ASN Kidney Week 2022 2022 · Abstract SA-PO518Refractory renal magnesium wasting from platinum chemotherapy (cisplatin/carboplatin) that resisted conventional magnesium and amiloride repletion responded to an SGLT2 inhibitor (dapagliflozin) in non-diabetic cancer patients — an off-label management angle for the classic cisplatin distal-tubular magnesium leak.AbstractRenal-Limited Thrombotic Microangiopathy from Bleomycin-Etoposide-Cisplatin Chemotherapy in a Young Male with Testicular CancerRizvi AW, Brodsky SV, Gutkoski T, Yau A · ASN Kidney Week 2023 2023 · Abstract SA-PO218A young man with testicular cancer on bleomycin-etoposide-cisplatin developed biopsy-confirmed renal-limited thrombotic microangiopathy with rising creatinine and proteinuria — a reminder that cisplatin-containing regimens cause endothelial/TMA injury beyond the better-known acute tubular necrosis and electrolyte wasting.

FDA label — boxed warning & renal dosing· boxed warning · renal impairment

Quoted verbatim from this agent's current FDA label (Jun 2026) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: NEPHROTOXICITY, PERIPHERAL NEUROPATHY, NAUSEA AND VOMITING and MYELOSUPPRESSION. • Nephrotoxicity: cisplatin for injection can cause severe renal toxicity, including acute renal failure. Severe renal toxicities are dose-related and cumulative. Ensure adequate hydration and monitor renal function and electrolytes. Consider dose reductions or alternative treatments in patients with renal impairment [see Dosage and Administration ( 2.1 ) and Warnings and Precautions ( 5.1 )]. • Peripheral Neuropathy: cisplatin for injection can cause dose-related peripheral neuropathy that becomes more severe with repeated courses of the drug [see Warnings and Precautions ( 5.2 )]. • Nausea and Vomiting: cisplatin for injection can cause severe nausea and vomiting. Use highly effective antiemetic premedication [see Dosage and Administration ( 2.1 ) and Warnings and Precautions ( 5.3 )]. • Myelosuppression: cisplatin for injection can cause severe myelosuppression with fatalities due to infections. Monitor blood counts accordingly. Interruption of therapy may be required [see Warnings and Precautions ( 5.4 )]. WARNING: NEPHROTOXICITY, PERIPHERAL NEUROPATHY, NAUSEA AND VOMITING, and MYELOSUPPRESSION See full prescribing information for complete boxed warning. • Nephrotoxicity: cisplatin for injection can cause severe renal toxicity, including acute renal failure. Ensure adequate hydration.…

Renal impairment — from the label

Patients with baseline renal impairment may be more susceptible to nephrotoxicity [see Warnings and Precautions ( 5.1 )] . Ensure adequate hydration before, during, and after cisplatin for injection administration [see Dosage and Administration ( 2.1 )]. Measure serum creatinine, blood urea nitrogen, creatinine clearance, and serum electrolytes prior to initiating therapy, and as clinically indicated. Consider alternative treatments or reduce the dose of cisplatin for injection for patients with baseline renal impairment or who develop significant reductions in creatinine clearance during treatment with cisplatin for injection according to clinical treatment guidelines [see Dosage and Administration ( 2.5 )].

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 77,664 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

SIADH / Hyponatremiacorroborated · ROR 6.04 — on the terms that name the lesion (ROR 7.44)
Electrolyte Disturbancecorroborated · ROR 5.41 — on the terms that name the lesion (ROR 14.23)
Acute Tubular Necrosiscorroborated · ROR 5.17
Fanconi Syndromecorroborated · ROR 4.54 — on the terms that name the lesion (ROR 7.11)
Hemorrhagic Cystitiscorroborated · ROR 1.52 — on the terms that name the lesion (ROR 8.51)
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

SIADH / Hyponatremia

ROR 6.0495% CI 5.76–6.34· 1,736 reports

Thrombotic Microangiopathy

ROR 5.5995% CI 5.00–6.25· 314 reports

Electrolyte Disturbance

ROR 5.4195% CI 5.23–5.59· 3,623 reports

Acute Tubular Necrosis

ROR 5.1795% CI 4.47–5.98· 185 reports

Fanconi Syndrome

ROR 4.5495% CI 3.66–5.63· 85 reports

Acute Interstitial Nephritis

ROR 2.4495% CI 2.09–2.84· 168 reports

Glomerular Injury / Proteinuria

ROR 2.0195% CI 1.76–2.30· 216 reports

Hemorrhagic Cystitis

ROR 1.5295% CI 1.37–1.68· 388 reports

Crystal / Obstructive Nephropathy

ROR 1.4595% CI 1.30–1.63· 299 reports

FAERS outcomes & reporting trend· 19.2% of reports w/ death · 41.7% w/ hospitalization

19.2%

Reported with a death outcome

14,918 of 77,664 reports

41.7%

Reported with hospitalization

32,402 of 77,664 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 77,664 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 3.3995% CI 3.24–3.55· 1,863 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 Injury1,863

Blood & lymphatic

Neutropenia4,877Febrile Neutropenia4,606Anaemia4,051Thrombocytopenia3,787Myelosuppression2,662

Gastrointestinal

Nausea5,437Vomiting4,564Diarrhoea3,760Mucosal Inflammation1,927

General / constitutional

Pyrexia3,398Fatigue2,505Asthenia2,057

Immune / infection

Pneumonia2,361Sepsis2,096

Metabolic & electrolyte

Dehydration2,460Decreased Appetite1,884

Respiratory

Dyspnoea1,942Pulmonary Embolism1,582

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 Cisplatin 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

Ifosfamide

Ifex · Oxazaphosphorine alkylator

Profile

Chloroacetaldehyde → Fanconi syndrome.

FANCATNLYTE

Severe#1 · 62% phenotype match

Carboplatin

Paraplatin · Platinum agent

Profile

Kidney-sparing; GFR-dosed by the Calvert formula.

ATNLYTECYST

Mild#2 · 58% phenotype match

Arsenic trioxide

Trisenox · Differentiating agent

Profile

Differentiation syndrome; QT prolongation.

PREATNLYTE

Moderate#3 · 52% phenotype match

Enasidenib

Idhifa · IDH2 inhibitor

Profile

Differentiation syndrome and tumor lysis.

PREATNLYTE

Moderate#4 · 52% phenotype match

Ivosidenib

Tibsovo · IDH1 inhibitor

Profile

Differentiation syndrome → AKI; tumor lysis.

PRELYTEATN

Moderate#5 · 52% phenotype match

Avutometinib

Avmapki (co-packaged with defactinib as Avmapki Fakzynja) · RAF/MEK inhibitor

Profile

RAF/MEK clamp; CK elevation/rhabdomyolysis and tubular electrolyte wasting.

LYTEATNPRE

Moderate#6 · 50% phenotype match

Compare Cisplatin 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
3NedaplatinATN — Acute Tubular NecrosisModerate
4Cisplatin· this agentATN — 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 Cisplatin’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 Cisplatin; 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 142 clinical records among the 300 most-relevant of 6,782 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.