Cisplatin

Acute Tubular Necrosis — representative incidence ~30% (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

Reported injury signatures: Acute Tubular Necrosis, Electrolyte Disturbance, Prerenal / Hemodynamic AKI, Hemorrhagic Cystitis, Fanconi Syndrome, SIADH / Hyponatremia.

1. Acute Tubular NecrosisPrimary~5%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).
2. Electrolyte DisturbanceSecondary~56%Hypomagnesemia in 56.3% of patients receiving single-agent cisplatin (RIFLE-based retrospective cohort); reflects distal tubular Mg2+ (and K+/Ca2+) wasting.
3. Prerenal / Hemodynamic AKIRare
4. Hemorrhagic CystitisRareA single other-causes-excluded case report; FAERS reporting mostly reflects ifosfamide/cyclophosphamide co-therapy.
5. Fanconi SyndromeRareCase-level acute Fanconi syndrome and renal salt wasting, including in ifosfamide-free regimens.
6. SIADH / HyponatremiaRareCase reports with positive dechallenge; renal salt wasting is the better-characterized cisplatin dysnatremia and is often miscoded as SIADH.

Acute (~1–7 days) — Creatinine peaks around day 4–7 after a dose; magnesium wasting can persist for months.

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

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

• 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)

• 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

• 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.

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.

• ADQI (2026) — Conventional cytotoxic chemotherapy-associated nephrotoxicity: consensus report of the 34th Acute Disease Quality Initiative (ADQI) WorkgroupCisplatin 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.Kidney Int · PMID 41881107
• Expert Consensus (2022) — The 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 PatientsConsensus 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).Int J Prev Med · PMID 35392316
• ADQI (2026) — The nephrotoxic effects of anti-cancer therapies: consensus report of the 34th Acute Disease Quality Initiative workgroupProvides 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.Nat Rev Nephrol · PMID 41361704
• SIRM (2022) — SIRM-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)Recommends 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.Radiol Med · PMID 35303246
• KDIGO (2020) — KDIGO Controversies Conference on onco-nephrology: understanding kidney impairment and solid-organ malignancies, and managing kidney cancerIdentifies 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.Kidney Int · PMID 33126977
• KDIGO (2020) — KDIGO Controversies Conference on onco-nephrology: kidney disease in hematological malignancies and the burden of cancer after kidney transplantationAddresses 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.Kidney Int · PMID 33276867
• ADDIKD (2025) — Integrating International Consensus Guidelines for Anticancer Drug Dosing in Kidney Dysfunction (ADDIKD) into everyday practiceProvides 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.EClinicalMedicine · PMID 40290844
• ADDIKD (2025) — Aligning kidney function assessment in patients with cancer to global practices in internal medicineThree 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.EClinicalMedicine · PMID 40290845
• ADDIKD (2025) — A methodology for determining dosing recommendations for anticancer drugs in patients with reduced kidney functionEstablishes 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.EClinicalMedicine · PMID 40290846
• KDIGO (2013) — Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1)Defines/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.Crit Care · PMID 23394211
• KDIGO (2024) — Executive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknownsEvaluate 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.Kidney Int · PMID 38519239
• KDIGO (2021) — Executive summary of the KDIGO 2021 Guideline for the Management of Glomerular DiseasesProvides 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.Kidney Int · PMID 34556300
• KDIGO (2024) — Executive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of ANCA-Associated VasculitisUpdates 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.Kidney Int · PMID 38388147
• KDIGO (2024) — Executive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of Lupus NephritisUpdates 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.Kidney Int · PMID 38182299
• KDIGO (2025) — Executive summary of the KDIGO 2025 Clinical Practice Guideline for the Management of Immunoglobulin A Nephropathy (IgAN) and Immunoglobulin A Vasculitis (IgAV)Encourages 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.Kidney Int · PMID 40975525