The Injury AtlasRepresentative per-agent pseudo-aki 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.
PSEUDO
Pseudo-AKI
The great mimic — a rise in creatinine from blocked tubular secretion (OCT2/MATE), NOT true injury. The GFR is intact; confirm with cystatin C before stopping effective therapy.
23signature agents
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.
Mild· 23
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)· 2Subacute (weeks)· 15Delayed (weeks–months)· 1Variable· 3
Management approach
Full framework →Recognize it — do NOT stop effective therapy for a transporter-mediated creatinine rise without a true fall in GFR.
Drug-level levers
- Continue therapy; the creatinine rise reflects blocked tubular secretion, not injury.
- Avoid unnecessary dose reduction or discontinuation.
Pharmacologic toolkit
- Confirm with cystatin C — A preserved cystatin C–based eGFR while the creatinine-based eGFR falls confirms pseudo-AKI.
- No specific therapy — None is required for the artifact itself; manage any true coexisting AKI on its own merits.
When to biopsy
Not indicated for an isolated creatinine rise with bland sediment and a preserved cystatin C–based GFR.
Monitoring
- · Cystatin C–based eGFR when creatinine rises
- · Urinalysis to exclude true injury
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.
Cited incidence across agents
Where the literature gives a representative pseudo-aki figure, the agents ranked highest first. Hover a dot for its cited note.
Offending agents
Signature offenders
23Agents for which pseudo-aki is the defining renal lesion.
BosutinibDevelops over months of therapy; time to grade 3b eGFR is shortest with later-line use.Long-term bosutinib is associated with a gradual, generally reversible decline in eGFR. In a long-term analysis, renal adverse events occurred in 9% on first-line and 13% on second-line-or-later bosutinib (the 6% in that analysis is the imatinib comparator arm), and a notable fraction reached grade 3b or worse eGFR (<45 mL/min/1.73 m2), with many recovering on follow-up; the pattern resembles the eGFR decline seen with imatinib.MildAlectinibCreatinine rise within weeks of starting therapy (mean eGFR declines over the first 90 days); reverses after discontinuation.Alectinib is associated with creatinine elevations that are usually benign. In a real-world five-agent ALK-inhibitor cohort (114 patients, 191 treatments; alectinib the most-used at 91), creatinine-based AKI/CKD events were frequent — 10% AKI within 90 days and 14% CKD at 1 year across the cohort, with no alectinib-specific rate reported — but mostly mild and reversible, with few treatment changes attributed to AKI and none requiring dialysis.MildBrigatinibCreatinine changes typically emerge within weeks and tend to reverse on discontinuation.As an ALK inhibitor, brigatinib is associated with creatinine elevations that are generally benign. In a real-world ALK-inhibitor cohort, creatinine-based AKI/CKD events occurred but were mostly mild and reversible across agents including brigatinib; class reviews note elevated creatinine, occasional edema, and rare electrolyte disturbances. A distinct, early-onset pulmonary event (within the first week) is a separate non-renal class concern.MildLorlatinibMetabolic effects and edema appear within weeks of starting therapy.Lorlatinib is characterized by prominent metabolic effects - hypercholesterolemia and hypertriglyceridemia occur in the majority of patients (the leading grade 3/4 toxicity in the CROWN trial) - plus peripheral edema. Direct renal toxicity is limited and, like other ALK inhibitors, creatinine elevations are generally mild and reversible. Renal effects are not well quantified specifically for lorlatinib.MildOlaparibCreatinine rise within weeks of starting therapy; reverses on discontinuation.Olaparib commonly causes a reversible, dose-dependent rise in serum creatinine. In a 66-patient study, median creatinine rose ~14% (and creatinine-based eGFR fell ~13%) on treatment, while cystatin C and cystatin C-based eGFR were unchanged - indicating no true GFR decline. Thrombotic microangiopathy is a rare, case-level event for the PARP-inhibitor class. Reported rate: creatinine-defined acute kidney injury within 12 months of olaparib initiation in 22.1% — Adults with ovarian cancer treated with olaparib at a single major Boston cancer center, 2015-2021 (n=194… (Gupta 2023, PMID 37074956).MildRucaparibWithin the first weeks of treatment.Early reversible serum-creatinine elevation is common and partly drug-specific: rucaparib is a recognized inhibitor of renal cation transporters, and a pooled meta-analysis found markedly higher odds of creatinine rise vs placebo across the class, but grade >=3 renal events were rare (<1%). Reported rate: elevated serum creatinine in 19.7% — Pooled safety population of seven studies of rucaparib monotherapy in patients with recurrent high-grade ovarian… (Adrianto 2024, PMID 39266137).MildTalazoparibThe pharmacokinetic effect is present from initiation in patients with reduced renal function; cytopenias accrue over the first cycles.Renal clearance is a major elimination route (~two-thirds of dose), so exposure rises with declining renal function: dedicated PK studies show higher AUC and more myelosuppression in moderate-severe impairment, mandating dose reduction. Class-level mild creatinine elevation may occur; severe intrinsic nephrotoxicity is uncommon.MildCapmatinibEarly — within the first cycles.Increased blood creatinine is a common treatment-related adverse event (~21% in GEOMETRY mono-1; higher in some Asian subsets), and peripheral edema is the single most common adverse event (~47%); most events are grade 1-2 and reversible.MildTepotinibEarly — within the first cycles.Blood creatinine increase and peripheral edema are the main treatment-related adverse events in the VISION program: in the 255-patient METex14 safety analysis, all-cause creatinine increase occurred in 25.9% and edema — the most common adverse event of clinical interest — in 69.8%. Both are generally mild to moderate and manageable, rarely leading to discontinuation.MildAbemaciclibEarly — within the first weeks (median onset ~3 weeks), stable thereafter, reversible on discontinuation.A benign serum-creatinine rise occurs in roughly one-fifth of patients (~20% in a single-center series; a class effect across CDK4/6 inhibitors), almost always grade 1–2 and without true GFR loss. In a dedicated CDK4/6-inhibitor cohort, ~73% of creatinine rises were confirmed pseudo-AKI by cystatin C–based eGFR.MildPalbociclibOften within the first 1-2 cycles (median onset roughly 30-35 days); creatinine plateaus and reverses after dose hold or discontinuation.A reversible rise in serum creatinine is common, but true structural kidney injury is uncommon. CDK4/6 inhibitors block the proximal-tubule transporters that secrete creatinine, producing a 'pseudo-AKI' picture. In a single-center palbociclib cohort 16% (8 of 50) met creatinine-based AKI criteria (Ly, PMID 39648753); the 17.5% often quoted is the whole mixed CDK4/6-inhibitor cohort of 234 patients, not the palbociclib arm. Where cystatin C was available, 73% of those events proved to be pseudo-AKI rather than a true GFR decline.MildRibociclibFirst cycles (median onset roughly 6 weeks for the creatinine signal); reversible on hold or discontinuation. QTc effects are dose- and concentration-dependent and seen early.Like other CDK4/6 inhibitors, ribociclib produces a frequent, reversible creatinine rise via inhibition of tubular creatinine secretion (pseudo-AKI ~14% in a class-effect analysis); clinically meaningful structural AKI is uncommon. A retrospective cohort of palbociclib/ribociclib patients found a >=20% creatinine-clearance decline in about 23%.MildRepotrectinibEarly after initiation; stable thereafter (a step change, not a progressive decline).An apparent rise in serum creatinine is described that often reflects inhibition of tubular creatinine secretion rather than a true fall in GFR (pseudo-AKI). Genuine intrinsic nephrotoxicity is not a characteristic feature and is not well quantified. This pattern is increasingly recognized across kinase inhibitors (e.g., ALK TKIs, where most creatinine-based eGFR changes do not require treatment change).MildTucatinibWithin the first weeks of therapy; plateaus and is fully reversible within days of discontinuation.A mild creatinine increase is common and expected, but it reflects inhibition of tubular creatinine secretion (a 'pseudo-AKI' artifact) rather than true GFR loss. Dedicated transporter/PK studies show tucatinib inhibits renal OCT2 and MATE1/MATE2-K without changing iohexol-measured GFR.MildMomelotinibAny tumor-lysis risk is early; otherwise no defined renal onset.Treatment-emergent 'nephropathy' — a predominantly low-grade, isolated serum-creatinine rise — is now a recognized and frequent momelotinib signal, reported in ~17-29% across real-world cohorts (~29% in first-line real-world use; ~17% CTCAE grade 1-2 creatinine increase in a retrospective real-world cohort). Momelotinib pharmacokinetics are unchanged across renal impairment, arguing the creatinine rise reflects altered tubular handling rather than a true GFR fall (a pseudo-AKI). Tumor-lysis at initiation in high-burden disease remains a separate, indirect risk.MildEntrectinibWithin the first weeks of therapy; reversible on discontinuation.A mild blood-creatinine increase is recognized and is attributed to reduced tubular creatinine secretion rather than true GFR decline (a pseudo-AKI pattern). It is typically modest, early and reversible; a meaningful structural-AKI rate is not established.MildZongertinibNot established; any creatinine change would emerge during early therapy by class analogy.Renal data are not established. In Beamion LUNG-1 the toxicity profile was mainly low-grade (diarrhea, rash) with no drug-related interstitial lung disease; renal events were not a defining signal. By analogy to other HER2/TKI agents (tucatinib), any creatinine rise is most likely a benign tubular-secretion (pseudo-AKI) effect rather than true injury.MildLarotrectinibEarly (days to weeks), stable/plateauing, and fully reversible on interruption or discontinuation.The larotrectinib-specific creatinine effect is not separately quantified; the mechanism is extrapolated from the TKI class (the tucatinib OCT2/MATE study and crizotinib's ~21% early, reversible, secretion-driven rise). The clinically important real toxicities are hepatic (transaminase elevation) and neurologic, not renal.MildVorasidenibA transporter-mediated creatinine rise, if it occurs, appears early (within the first weeks to first cycles) and plateaus; it is dose-related and stable rather than progressive.Direct nephrotoxicity is minimal. No vorasidenib-specific AKI signal has been reported; in the registrational INDIGO phase 3 trial the predominant grade >=3 toxicity was hepatic (ALT elevation in ~9.6%), not renal. A mild, reversible serum-creatinine increase — a transporter-mediated pseudo-AKI — is the expected renal finding. A precise renal-event incidence is not quantified.MildVimseltinibCPK elevations and edema emerge early, typically within the first 1-2 treatment cycles (28-day cycles); any associated creatinine change tracks with these rather than following a delayed structural pattern.No clinically significant direct nephrotoxicity was identified in the pivotal MOTION phase 3 trial. There is no recognized signature renal lesion (no ATN, AIN, TMA, or glomerular injury attributable to the drug). The kidney-relevant practical issue is interpretive: the dominant laboratory abnormality is treatment-emergent creatine phosphokinase (CPK) elevation — grade 3/4 in 8/83 (10%) of vimseltinib patients in MOTION — together with peripheral/periorbital edema, either of which can perturb serum creatinine or muscle-derived markers without true GFR loss. Renal-specific events were not reported as a notable safety signal.MildTaletrectinibClass-effect transporter inhibition produces a creatinine rise early after initiation that tends to plateau and is dose-dependent. Drug-specific onset timing for taletrectinib is not separately characterized.Drug-specific renal toxicity data for taletrectinib are limited. In the pooled TRUST-I and TRUST-II registrational safety population (352 patients at 600 mg once daily), the dominant treatment-emergent events were gastrointestinal and hepatic (elevated AST/ALT), with no defined intrinsic kidney lesion; renal-specific incidence figures are not separately reported. The expected renal signal, extrapolated from the ROS1/TRK-TKI class, is a mild, benign rise in serum creatinine from inhibition of tubular creatinine secretion rather than true GFR loss (pseudo-AKI). A precise incidence for taletrectinib-attributable creatinine elevation is not established.MildEnsartinibA benign creatinine rise tends to appear early and stabilize; cyst development in the ALK-TKI class is generally a later, cumulative imaging finding over months of therapy.Renal-specific incidence for ensartinib is not separately quantified; in the eXalt3 phase 3 trial serious adverse events, dose reductions, and discontinuations were similar to crizotinib with no new safety signals, and edema and a creatinine rise are described for ensartinib. The renal signature is therefore class-extrapolated from the ALK TKIs, where crizotinib is the index agent for both a benign reduced-tubular-secretion creatinine rise and the development/progression of renal cysts. No defined ensartinib-attributable kidney lesion or incidence rate is established. Reported rate: creatinine elevation in 35.4% — 48 patients with advanced ALK- or ROS1-positive NSCLC enrolled at 2 centers in China and treated with single-agent oral… (Ma 2022, PMID 36647478).MildImlunestrantNo renal onset for imlunestrant itself. When present, the abemaciclib-related creatinine rise appears within the first weeks of the combination and then remains stable.There is no meaningful renal signal for imlunestrant, and no discrete drug-specific incidence of acute kidney injury. In the phase 3 EMBER-3 trial (Jhaveri, N Engl J Med 2024; n=874) grade 3 or higher adverse events occurred in only 17.1% with imlunestrant monotherapy — comparable to standard endocrine therapy (20.7%) — with the toxicity profile of an oral SERD (low-grade fatigue, diarrhea, nausea) rather than a nephrotoxic one. The one renal-relevant nuance is not imlunestrant itself but its combination partner: abemaciclib inhibits the renal tubular transporters (OCT2/MATE) that secrete creatinine, producing an early, benign, non-progressive rise in serum creatinine without a true fall in glomerular filtration — so the imlunestrant-abemaciclib combination (grade 3+ adverse events 48.6%) can show a creatinine bump that must not be mistaken for kidney injury.Mild