The Injury Atlas See it on the nephronRepresentative per-agent electrolyte disturbance incidence where a published figure is citable — open an agent's name for its profile and cited source, or hover its dot for the source inline. Agents without a citable figure are omitted; a tier without a number is not the same as a low number.
LYTE
Electrolyte Disturbance
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).
28signature agents
Deep diveCisplatin ATN & hypomagnesemiaDeep diveEGFR-inhibitor hypomagnesemiaDeep diveIfosfamide FanconiDeep divePemetrexed tubulopathyDeep diveTumor lysisDeep diveBRAF/MEK tubularDeep diveBisphosphonate injuryDeep diveCAR-T AKI
Where it strikes
Distal Tubule / Collecting Duct
Fine-tuning of Na, K, Mg, acid & water
Agents’ overall severity
Each agent’s whole-drug severity grade, not the severity of this lesion specifically — an agent whose signature injury is elsewhere can still be graded severe here.
Moderate· 15Mild· 13
Agents’ onset window
How soon each agent’s kidney toxicity typically appears — a whole-drug tempo, not specific to this lesion.
Hyperacute (<24 h)· 1Acute (days)· 5Subacute (weeks)· 15Delayed (weeks–months)· 2Variable· 5
Real-world reporting for this lesion
FAERS across all lesions →Agents with a disproportionate FAERS reporting signal for electrolyte disturbance (reporting odds ratio with a 95% CI lower bound above 1) — a spontaneous-reporting signal, not incidence or proven causation. FAERS carries reporting and indication biases and has no denominator.
71Corroborated
Documented in the atlas profile and carrying a FAERS signal — the strongest claim the atlas makes.
42Documented, FAERS-silent
Documented in a profile with no reporting signal. Mostly expected: naming this lesion on a report can require a biopsy, and silence is not evidence against the literature.
33Not attributable
A real reporting signal that is not evidence for this drug-lesion pair: no MedDRA term names it, the naming subset asked alone came back flat, or the 2026-08 review attributed the reporting to the population, co-therapy, or class-level literature.
38Reported by name
The terms that name this lesion are disproportionate, but no profile documents it for that agent. Most are echoed by a sibling agent in the same class. Leads for review, never lesions the atlas claims.
5-FluorouracilAbemaciclibAbirateroneAcalabrutinibAdagrasibAfatinibAmivantamabArsenic trioxideAtezolizumabAxitinibAzacitidineBelantamab mafodotinBelzutifanBendamustineBevacizumabBicalutamideBinimetinibBleomycinBlinatumomabBortezomibBrentuximab vedotinCabazitaxelCabozantinibCapecitabineCapmatinibCarboplatinCarfilzomibCeritinibCetuximabCisplatinClofarabineCobimetinibCrizotinibCyclophosphamideCytarabineDabrafenibDacarbazineDasatinibDecitabineDenosumabDinutuximabDocetaxelDoxorubicinDurvalumabElotuzumabEncorafenibEnfortumab vedotinEpcoritamabErdafitinibEribulinErlotinibEtoposideEverolimusFludarabineFutibatinibGefitinibGemcitabineGemtuzumab ozogamicinGlasdegibGlofitamabHydroxyureaIbandronateIbritumomab tiuxetanIbrutinibIdarubicinIfosfamideImatinibImlunestrantInotuzumab ozogamicinInterleukin-2 (high-dose)IpilimumabIrinotecanIsatuximabIvosidenibIxazomibLanreotideLenvatinibLifileucelMelphalanMitotaneMitoxantroneNaxitamabNelarabineNeratinibNiraparibNirogacestatNivolumabObinutuzumabOctreotideOxaliplatinPaclitaxelPamidronatePanitumumabPazopanibPegaspargasePembrolizumabPemetrexedPemigatinibPenpulimabPentostatinPirtobrutinibPolatuzumab vedotinPralatrexatePralsetinibRadium-223 dichlorideRamucirumabRegorafenibRelacorilantRibociclibRituximabSacituzumab govitecanSelinexorSirolimusSonidegibSorafenibSotorasibSunitinibTalazoparibTalquetamabTamoxifenTemozolomideTemsirolimusThalidomideTislelizumabTisotumab vedotinTopotecanTovorafenibTrabectedinTrametinibTrastuzumab deruxtecanTrastuzumab emtansine (T-DM1)Trifluridine/tipiracilTucatinibVandetanibVemurafenibVenetoclaxVinblastineVincristineVinorelbineVismodegibZolbetuximabZoledronic acid
142 agents with a significant LYTE reporting signal.
At the bedside
EGFR hypomagnesemia deep dive →Anti-cancer magnesium wasting — anti-EGFR antibodies and platinums above all — is cumulative and often silent until severe. Grade a level to gauge urgency and route.
Magnesium grade & repletion
CTCAE v5.0Enter a serum magnesium level for its CTCAE grade and a directed-repletion frame. Drug-induced renal magnesium wasting (anti-EGFR antibodies, platinums) is cumulative — grade guides urgency and route.
Enter a level to see the CTCAE grade and repletion frame.
Educational aid only — not medical advice. Grades per NCI CTCAE v5.0, read directly from the column for the unit you enter. CTCAE defers to the reporting lab for the limits of normal; this tool assumes 1.7–2.6 mg/dL. Repletion route and dosing follow local protocol and clinical judgment.
Management approach
Full framework →Replace what is wasted; the drug usually continues.
Drug-level levers
- Therapy is typically continued with ongoing repletion.
- Dose-reduce or hold only for severe, symptomatic, or refractory derangements.
Pharmacologic toolkit
- Magnesium repletion — Oral and IV magnesium for anti-EGFR and cisplatin hypomagnesemia; losses are often substantial and recurrent.
- Potassium / calcium repletion — Correct coexisting hypokalemia and hypocalcemia (often magnesium-dependent).
When to biopsy
Not indicated — this is a functional tubular transport defect, not a structural lesion.
Monitoring
- · Serum magnesium, potassium, and calcium during and after therapy
Educational use only. Educational synthesis of the published literature — not a treatment protocol, dosing guide, or medical advice. Regimens and agents shown are illustrative of what the literature describes; verify against current guidelines (ASON / KDIGO / ASCO / NCCN) and individualize to the patient. Using this site creates no clinician–patient relationship.
What the guidelines say
All guidelines →Society and consensus recommendations that speak to electrolyte disturbance.
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.
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.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.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.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).BCSHGuidelines for the management of tumour lysis syndrome in adults and children with haematological malignancies on behalf of the British Committee for Standards in HaematologyBr J Haematol 2015 · PMID 25876990Risk-adapted prophylaxis and management of TLS in haematological malignancy: hydration with allopurinol for lower-risk and rasburicase for high-risk patients, with monitoring of electrolytes and renal function to prevent and treat AKI.TLS Consensus PanelRecommendations for the evaluation of risk and prophylaxis of tumour lysis syndrome (TLS) in adults and children with malignant diseases: an expert TLS panel consensusBr J Haematol 2010 · PMID 20331465Stratify each patient as low/intermediate/high TLS risk using tumor type, bulk/stage, proliferation rate, baseline laboratory TLS, and renal impairment/involvement, then match prophylaxis intensity (monitoring vs allopurinol vs rasburicase) to the assigned risk level.TLS Expert PanelGuidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based reviewJ Clin Oncol 2008 · PMID 18509186Prevention is the best management: hydration plus prophylactic rasburicase for high-risk patients, hydration plus allopurinol or rasburicase for intermediate-risk, and monitoring for low-risk; for established TLS add aggressive hydration and diuresis plus allopurinol or rasburicase for hyperuricemia. Urinary alkalinization is NOT recommended.Cairo-BishopTumour lysis syndrome: new therapeutic strategies and classificationBr J Haematol 2004 · PMID 15384972Defines the Cairo-Bishop criteria distinguishing laboratory TLS (>=2 metabolic abnormalities: hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia within 3 days before to 7 days after therapy) from clinical TLS (laboratory TLS plus AKI, cardiac arrhythmia, or seizure), with a severity grading scheme adopted by subsequent guidelines.
Cited incidence across agents
Where the literature gives a representative electrolyte disturbance figure, the agents ranked highest first. Hover a dot for its cited note.
Offending agents
Signature offenders
28Agents for which electrolyte disturbance is the defining renal lesion.
NecitumumabDevelops cumulatively over weeks of repeated dosing and worsens with continued therapy; magnesium should be checked before each dose and for at least 8 weeks after completion because deficits can persist.Grade 3-4 hypomagnesemia occurred in about 9% of patients receiving necitumumab plus chemotherapy versus 1% with chemotherapy alone in the pivotal SQUIRE trial; any-grade hypomagnesemia is likely more frequent (as a class, anti-EGFR antibodies are associated with a gradual magnesium fall in many patients over time).ModerateErdafitinibEarly — typically within the first 1-2 cycles, used to guide pharmacodynamic up-titration.Hyperphosphatemia is the most common, on-target class adverse event — reported in ~73-78% of treated patients across studies and used as a pharmacodynamic marker for protocol-driven dose up-titration. Grade >=3 hyperphosphatemia is much less frequent (~2%).ModeratePemigatinibEarly — within the first cycles.Hyperphosphatemia is the most common adverse event in the pivotal FIGHT-202 trial, affecting roughly 60% of patients (any grade), with low rates of severe events; it is on-target and managed with monitoring, diet, and binders.ModerateFutibatinibEarly — within the first cycles.Hyperphosphatemia is the most common adverse event, reported in ~85% of patients (any grade, most low-grade) in the pivotal FOENIX-CCA2 trial; it is on-target, dose-related, and confirmed as a pharmacodynamic effect in first-in-human work.ModerateDenosumabWithin days to a few weeks of dosing (nadir often around 1-2 weeks); can be prolonged given the drug's months-long duration of effect and the absence of a reversal agent.Denosumab is not directly nephrotoxic and is not renally cleared, but the risk of severe hypocalcemia rises sharply as kidney function declines. In a population-based cohort, severe hypocalcemia occurred in 0.2% of all new users but in 14.9% of those with eGFR <15 mL/min/1.73 m2 or on dialysis (mild hypocalcemia 24.1% in that group). Reported rate: hypocalcemia in 17% — 850 patients with symptomatic newly diagnosed multiple myeloma and at least one lytic bone lesion who received at least… (Raje 2018, PMID 29429912).ModerateAbirateroneWithin the first weeks of therapy; recurs if glucocorticoid coverage is inadequate or interrupted.Mineralocorticoid-excess effects are common: in COU-AA-301 fluid retention, hypertension and hypokalemia were all more frequent than with placebo-prednisone. Severe (grade 3–4) hypokalemia, occasionally to 1.7–2.1 mEq/L, is reported even with concomitant prednisone. Meta-analysis confirms an increased relative risk of hypertension. A single-center retrospective cohort of 79 patients reported renal events in 63.3% of abiraterone-treated patients — AKI in 30.4%, half of whom progressed to chronic kidney disease (Pujol-Pujol 2025). Reported rate: grade >=3 hypokalemia in 12% — 597 men with newly diagnosed high-risk metastatic castration-sensitive prostate cancer randomized to abiraterone… (Fizazi 2019, PMID 30987939).ModerateAmivantamabElectrolyte changes during therapy and cumulative; AIN timing not well characterized (subacute, days–weeks after a triggering exposure by analogy to drug AIN).In CHRYSALIS, electrolyte disturbance — notably hypokalemia (grade 3–4 in ~5%) and hypomagnesemia/hypocalcemia — was among the laboratory adverse events, consistent with EGFR-pathway inhibition. Acute interstitial nephritis is an emerging, clinician-flagged signal that is not yet quantified in the published renal literature. Reported rate: grade >=3 hypokalemia in 5% — CHRYSALIS phase I safety population, n = 114 patients with EGFR exon 20 insertion-mutated NSCLC receiving amivantamab… (Park 2021, PMID 34339292).ModerateInfigratinibEarly (first cycle); reversible and dose-dependent, normalizing during the 7-day off-drug interval of the 21-on/7-off cycle.Hyperphosphatemia is the most common adverse event and the defining FGFR class effect — it occurred in 83 of 108 patients (~77%, any grade) in the pivotal trial. Infigratinib-specific nephrocalcinosis/calciphylaxis rates are not quantified (case reports/series only).ModerateDactinomycin (actinomycin D)TLS within hours to days of initiating effective chemotherapy; VOD typically within the first weeks of treatment.Direct nephrotoxicity is not an established feature of dactinomycin. The clinically relevant renal risk is tumor lysis syndrome (TLS) when used against bulky, chemosensitive pediatric tumors; precise incidence attributable to dactinomycin alone is not quantified, as it is given in multi-agent regimens.ModerateMechlorethamineTLS within hours to days of effective cytoreduction in bulky lymphoma.Direct nephrotoxicity is not a defining feature. The principal renal hazard is tumor lysis syndrome when treating bulky, rapidly proliferating lymphoma; incidence specifically attributable to mechlorethamine is not quantified because it is used within multi-agent regimens. The 0.016%/0.02% topical gel shows no detectable systemic absorption.ModerateAmsacrineTLS within hours to days of effective cytoreduction.Direct nephrotoxicity is not a prominent feature. The main renal hazard is tumor lysis syndrome during leukemia induction/salvage; incidence specific to amsacrine is not quantified. Pharmacokinetic studies show renal elimination plays only a minor role, with clearance dominated by hepatic metabolism and biliary excretion.ModerateMitotaneAdrenal insufficiency and its electrolyte/volume consequences develop over weeks of therapy as adrenolytic effect accrues; cisplatin-associated AKI in EDP-M is acute, within days of chemotherapy cycles.Intrinsic mitotane nephrotoxicity is not characteristically quantified. Clinically important renal events are indirect (adrenal insufficiency-related electrolyte/volume disturbance) or attributable to co-administered cisplatin in EDP-M; incidence not reliably enumerated for mitotane alone.ModerateStrontium-89 chlorideHematologic nadir typically develops over several weeks (e.g., weeks 4-8) given the long physical half-life; any renal/excretion-related concern relates to the early post-injection days when urinary excretion is highest.Intrinsic nephrotoxicity is not a defining or well-quantified effect; the prominent toxicity is transient myelosuppression (e.g., reversible hematologic toxicity reported in roughly half of treated patients in small series). Renal events are uncommon and not reliably enumerated.ModerateInavolisibHyperglycemia from PI3Kalpha inhibition is an on-target effect that can appear soon after dosing, sometimes with peak glucose elevations in the hours following ingestion, and typically reverses within days of holding the drug.Direct nephrotoxicity from inavolisib is not prominent and renal-specific data are limited; the headline metabolic toxicity is on-target hyperglycemia. In the INAVO120 phase 3 trial, grade 3 or 4 hyperglycemia occurred in 5.6 percent of the inavolisib group versus 0 percent with placebo, alongside higher rates of stomatitis and diarrhea (which can secondarily cause volume and electrolyte loss). A defined inavolisib-specific kidney lesion with an established electrolyte-event incidence rate is not characterized, so no headline signature rate is charted (the 5.6% grade 3/4 hyperglycemia figure is a metabolic, not electrolyte, signal).ModerateAvutometinibEarly. CPK elevation and diarrhea typically emerge within the first one to two cycles (first weeks) of therapy; in a BRAF/MEK-inhibitor cohort, treatment-associated AKI clustered within the first three months. Peripheral edema/fluid retention accrues over weeks to months. Rhabdomyolysis-associated AKI, when it occurs, parallels the peak CPK.No discrete acute-kidney-injury incidence has been reported for avutometinib. The best-quantified kidney-relevant signal is marked creatine phosphokinase (CPK) elevation: in the registrational RAMP 201 combination cohort (avutometinib + defactinib, n=115), grade >=3 CPK elevation occurred in 24% of patients — the single most common grade >=3 treatment-related adverse event — with grade >=3 diarrhea in 8% and anemia in 5%. A CPK rise of this magnitude is a recognized rhabdomyolysis-risk surrogate, not a measured AKI rate: most CPK elevations are asymptomatic skeletal-muscle elevations that do not injure the kidney, but sustained rhabdomyolysis-range values can precipitate pigment (myoglobin-cast) tubular injury, and high-grade diarrhea can drive prerenal azotemia and electrolyte loss. Across the MEK-inhibitor class the FAERS acute-kidney-injury signal is heterogeneous rather than uniformly low: reporting-odds-ratio approximately 1.3 for trametinib but approximately 4.4 for cobimetinib, the latter exceeding vemurafenib's approximately 3.3 in the same analysis (Sanagawa 2021) — though cobimetinib is given only with vemurafenib, so its pharmacovigilance signal cannot be read as a pure MEK effect. All figures derive from a small phase II dataset and are hedged accordingly.ModerateImatinibEdema early; tubular dysfunction and eGFR decline develop over months to years.Periorbital/peripheral edema and fluid retention are common. Clinically meaningful renal injury is uncommon: long-term front-line imatinib is associated with a modest, measurable decline in eGFR over years, while proximal tubular dysfunction (hypophosphatemia, aminoaciduria, rare Fanconi syndrome) and AKI (including rare urate nephropathy from disease cytoreduction) are described at the case level.MildNirogacestatDuring therapy; not well characterized.Hypophosphatemia occurred in 42% of nirogacestat-treated patients in the DeFi trial, alongside other electrolyte disturbances; the characteristic DeFi-trial toxicities were diarrhea, rash, nausea, fatigue and ovarian dysfunction. Beyond the phosphate signal, renal-specific incidence is not well quantified.MildSunvozertinibElectrolyte changes can appear within the first weeks to months of therapy; hypomagnesemia risk rises with treatment duration.No established AKI rate. As with the EGFR-inhibitor class, the renal-relevant signal is electrolyte disturbance — particularly hypomagnesemia (renal Mg wasting) and diarrhea-driven losses, with a hyponatremia/SIADH-like pattern possible — rather than structural nephron injury. WU-KONG6 reported diarrhea and skin/EGFR-pathway toxicities as dominant; renal-specific events are not quantified.MildVinflunineElectrolyte/prerenal effects can appear within days of a cycle; PK accumulation in renal impairment is immediate but mitigated by protocol dose reduction.No strong direct nephrotoxic signal. Vinflunine is given to renally impaired, cisplatin-unfit patients with a defined dose-reduction schema, and tolerability in renal impairment mirrors that of patients with normal renal function once dose-banded. SIADH/hyponatremia is a class-level vinca-alkaloid effect rather than a quantified vinflunine-specific rate. Reported rate: grade >=3 hyponatremia in 12% — 51 patients with relapse-sensitive or relapse-refractory small cell lung cancer treated with single-agent vinflunine… (Spigel 2010, PMID 20521355).MildTeniposideNo characteristic renal onset; pharmacokinetic exposure effects are immediate but clinically modest.Minimal direct nephrotoxicity. Teniposide is highly protein-bound with low renal clearance (only ~5-20% of a dose is recovered in urine versus a larger fraction for etoposide), so the kidney is a minor elimination route and direct renal injury is not a characteristic toxicity. Renal relevance is pharmacokinetic/exposure-related and not quantified as a discrete nephrotoxicity rate.MildOctreotideNot applicable for intrinsic injury; pharmacokinetic accumulation in renal failure is gradual.No characteristic intrinsic nephrotoxicity; octreotide is generally considered kidney-neutral. Renal events are rare, indirect, and not reliably quantified. Mild electrolyte disturbances are uncommon.MildLanreotideNot applicable for intrinsic injury; exposure rises gradually in renal impairment.No characteristic intrinsic nephrotoxicity; lanreotide is generally kidney-neutral. Renal adverse events are not a defining feature and are not reliably quantified; mild electrolyte effects are uncommon.MildDarolutamideNot applicable for intrinsic injury; exposure differences in renal impairment are present from initiation and steady state (reached in ~2 days).No characteristic intrinsic nephrotoxicity. In ARAMIS, rates of adverse events including hypertension were similar to placebo. Renal-relevant findings are pharmacokinetic (increased exposure in severe renal impairment); intrinsic renal injury incidence not meaningfully quantified.MildCetuximabDevelops insidiously over weeks to months of therapy and is cumulative — the nadir deepens the longer treatment continues, so the largest deficits typically appear after several months. Reversible: renal magnesium handling recovers over weeks (usually within about 4-8 weeks) after cetuximab is stopped.Hypomagnesemia is an on-target class effect. In the defining prospective cohort (Tejpar, Lancet Oncol 2007), 95/98 patients (97%) developed a declining serum magnesium slope on EGFR-antibody therapy. Cetuximab-specific pooled data give an any-grade incidence of ~36% (Cao, Chemotherapy 2010; 19 trials, 95% CI 22-54%), with grade 3-4 hypomagnesemia — a CTCAE serum-magnesium threshold, not a symptom rate — in roughly 5-6%; a pooled analysis of randomized anti-EGFR antibody trials (cetuximab and panitumumab together) reports an overall any-grade incidence of 17% across the class (Petrelli, Expert Opin Drug Saf 2011). Versus control, the relative risk is ~3.9 for cetuximab specifically and ~5.83 across anti-EGFR antibodies (Petrelli, Expert Opin Drug Saf 2011). Magnesium falls cumulatively, deepening with treatment duration.MildPanitumumabDevelops over weeks of therapy and is cumulative, deepening with treatment duration and repeated every-2-week dosing. Recovery after discontinuation is typically slow — over several weeks to a couple of months — as distal-tubule magnesium handling gradually normalizes; hypomagnesemia can persist or transiently worsen shortly after the last dose.Hypomagnesemia is the signature renal-tubular toxicity and one of panitumumab's most frequent adverse effects. Any-grade rates cluster around 30-40% across RAS/KRAS wild-type mCRC trials, with grade 3-4 hypomagnesemia in roughly 3-7%; it is dose- and duration-related and deepens with cumulative exposure (Van Cutsem, J Clin Oncol 2007, established it as a frequent toxicity of the registration monotherapy trial). Rates are consistently HIGHER than with cetuximab: a pooled analysis put the relative risk of hypomagnesemia at ~12.6 for panitumumab versus ~3.9 for cetuximab (Petrelli, Expert Opin Drug Saf 2011), and in the head-to-head ASPECCT trial grade 3-4 hypomagnesemia was 7% with panitumumab versus 3% with cetuximab (Price, Lancet Oncol 2014).MildFedratinibGI adverse events appear early — typically within the first one to two treatment cycles — and tend to diminish over time with supportive care and dose management; the associated electrolyte and creatinine changes track these early GI events. Reduced clearance in renal impairment is present from the first dose (higher exposure independent of time on drug).There is no established incidence of direct fedratinib-induced kidney injury; the renal story is pharmacokinetic and GI-driven rather than a discrete nephrotoxic lesion. In the pivotal placebo-controlled JAKARTA phase 3 trial, gastrointestinal symptoms were among the most common adverse events and "increased levels of serum creatinine" was reported as a common laboratory abnormality — but neither a rate of clinically significant AKI nor a discrete electrolyte-depletion incidence was separately quantified, so a headline nephrotoxicity percentage cannot be stated without overstating the evidence. The dedicated phase 1 renal-impairment study found systemic exposure (AUC) roughly 1.9-fold higher in severe renal impairment, which is the basis for a mandated dose reduction rather than an injury rate.MildRelacorilantElectrolyte shifts, if they develop, track cumulative cortisol/MR activation over the treatment course rather than a single dose, and are typically detected on routine chemistry monitoring during cycles rather than as an acute event.No discrete drug-specific incidence of relacorilant acute kidney injury is published; in the registrational phase 3 ROSELLA trial (Olawaiye, Lancet 2025; n=381) the adverse-event profile with relacorilant plus nab-paclitaxel was similar to nab-paclitaxel alone after adjusting for exposure, and no new safety signals were reported. The renal-relevant concern is electrolyte, specifically hypokalemia, inferred from the pharmacology of GR antagonism rather than from a large observed AKI signal. The precedent is mifepristone, a non-selective GR/PR antagonist, where blocking cortisol's own receptor allowed cortisol to activate the mineralocorticoid receptor and produce clinically significant, spironolactone-responsive hypokalemia (Chu, J Clin Endocrinol Metab 2001). Relacorilant is a selective GR antagonist designed to reduce this and other off-target effects, so the hypokalemia risk is expected to be milder — a monitoring point, not a dominant toxicity.MildGedatolisibHyperglycemia is an early, exposure-linked effect — fasting glucose moves within the first infusions and tracks the weekly dosing cycle; electrolyte drift appears on routine monitoring across early cycles rather than as an acute event.No discrete drug-specific incidence of gedatolisib acute kidney injury is published; the renal-relevant signal is laboratory-level. In the VIKTORIA-1 triplet arm the FDA label's laboratory table reports increased creatinine in 14% (grade 3-4 0.8%) versus 8% (0.8%) on fulvestrant alone, decreased sodium in 21% (grade 3-4 1.6%), decreased potassium in 19% (1.6%) and decreased magnesium in 19% (0%) — all-grade drift, with severe events rare. The dominant metabolic effect is on-target hyperglycemia: increased fasting glucose in 46% of triplet-arm and 57% of doublet-arm patients on the label's laboratory table, while grade >=3 treatment-related hyperglycemia in the VIKTORIA-1 publication was 2.3% in both gedatolisib arms (Hurvitz, J Clin Oncol 2026) — markedly gentler than daily oral PI3K-alpha inhibition. In a phase II HER2-positive combination, any-grade hyperglycemia was 25.0% with grade 3 in 2.3% (Kim, ESMO Open 2026).Mild