The Injury Atlas Does the kidney recover? Cross-drug outcomes
AIN
Acute Interstitial Nephritis
Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.
18signature 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.
Severe· 1Moderate· 15Mild· 2
Agents’ overall reversibility
Partially reversible· 15Reversible· 3
Agents’ onset window
How soon each agent’s kidney toxicity typically appears — a whole-drug tempo, not specific to this lesion.
Subacute (weeks)· 1Delayed (weeks–months)· 15Variable· 2
Real-world reporting for this lesion
FAERS across all lesions →Agents with a disproportionate FAERS reporting signal for acute interstitial nephritis (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.
13Corroborated
Documented in the atlas profile and carrying a FAERS signal — the strongest claim the atlas makes.
9Documented, 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.
0Not 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.
31Reported 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.
AIN is systematically undercounted in FAERS — most true cases are filed under the generic “acute kidney injury” term rather than a distinct acute interstitial nephritis code, so the literature-only column is expected to run large here.
AmivantamabArsenic trioxideAtezolizumabAxitinibBendamustineBevacizumabBinimetinibBlinatumomabBrentuximab vedotinBusulfanCarboplatinCarmustine (BCNU)CemiplimabChlorambucilCisplatinCobimetinibCyclophosphamideCytarabineDabrafenibDactinomycin (actinomycin D)DostarlimabDoxorubicinDurvalumabEncorafenibEnfortumab vedotinEtoposideEverolimusFludarabineGemcitabineIfosfamideIpilimumabLoncastuximab tesirineMelphalanNivolumabOxaliplatinPaclitaxelPembrolizumabPemetrexedRelatlimabSirolimusTemozolomideTrametinibVinorelbineZoledronic acid
44 agents with a significant AIN reporting signal.
Management approach
Full framework →Per the ASON position statement: hold the drug, remove AIN cofactors, and treat with corticosteroids; biopsy when feasible to confirm and guide duration.
Drug-level levers
- Withhold the checkpoint inhibitor for grade ≥2 AKI.
- Discontinue concurrent AIN-culprit drugs (PPIs, NSAIDs, antibiotics).
- Permanently discontinue for grade 3–4 or recurrent immune-mediated nephritis.
- Rechallenge can be considered after recovery for lower-grade events — individualized, with close monitoring, given the recurrence risk.
Pharmacologic toolkit
- Corticosteroids — First line for grade ≥2: illustratively prednisone ~0.5–1 mg/kg/day (IV methylprednisolone for severe disease) with a slow taper over 4–6+ weeks.
- Steroid-refractory immunosuppression — For steroid-dependent or refractory AIN, agents such as mycophenolate mofetil or infliximab have been used.
When to biopsy
Favored when feasible to confirm AIN, exclude mimics, and guide steroid duration and rechallenge — but frequently deferred in cancer patients (thrombocytopenia, anticoagulation, single functioning kidney), so empiric corticosteroid treatment is common.
Monitoring
- · Creatinine before each cycle
- · Urinalysis (sterile pyuria, proteinuria)
- · Watch for concurrent immune-related adverse events
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 acute interstitial nephritis.
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.
ADQIImmune Checkpoint Inhibitor-Associated Acute Kidney Injury: A Report from the 34th Acute Disease Quality Initiative (ADQI) Consensus ConferenceJ Am Soc Nephrol 2026 · PMID 42536415AKI occurs in up to 20% of ICI-treated patients with ICI-AKI accounting for roughly 2-5% of cases, and acute tubulointerstitial nephritis dominates (80-90% of biopsies); no clinical feature reliably separates ICI-AKI from other causes, so kidney biopsy remains the diagnostic gold standard and emerging biomarkers are not yet ready for routine use. Early glucocorticoid initiation (within 3 days of diagnosis) is associated with higher rates of kidney recovery, and recurrent ICI-AKI occurs in fewer than 20% of rechallenged patients, supporting cautious rechallenge in selected patients with individualized multidisciplinary decisions for transplant recipients and other high-risk groups.ASONDiagnosis and management of immune checkpoint inhibitor-associated nephrotoxicity: a position statement from the American Society of Onco-nephrologyKidney Int 2025 · PMID 39455026ICI-AKI most commonly presents as acute interstitial nephritis; nephrology consultation and kidney biopsy should be considered for stage 2 or higher AKI or suspected glomerular disease, but where biopsy is not feasible, prompt empiric corticosteroids (prednisone ~1 mg/kg/day) should be started for clinically suspected ICI-AKI since early steroids improve renal recovery, with cautious individualized consideration of ICI rechallenge after recovery.ESMOManagement of toxicities from immunotherapy: ESMO Clinical Practice Guideline for diagnosis, treatment and follow-upAnn Oncol 2022 · PMID 36270461For ICI-related AKI, exclude alternative etiologies and stop concomitant nephrotoxins (PPIs, NSAIDs); ESMO permits continuing the ICI for stage 1 AKI with monitoring, but recommends withholding the ICI and starting corticosteroids for stage 2 or higher nephritis, escalating immunosuppression for steroid-refractory disease.ASCOManagement of Immune-Related Adverse Events in Patients Treated With Immune Checkpoint Inhibitor Therapy: ASCO Guideline UpdateJ Clin Oncol 2021 · PMID 34724392For grade 2 or higher ICI-related nephritis/AKI, hold the ICI, exclude alternative causes, and initiate corticosteroids (prednisone 0.5-1 mg/kg/day for grade 2, 1-2 mg/kg/day for grade 3-4) tapered over 4-6 weeks once creatinine improves; permanently discontinue for grade 4 toxicity.SITCSociety for Immunotherapy of Cancer (SITC) clinical practice guideline on immune checkpoint inhibitor-related adverse eventsJ Immunother Cancer 2021 · PMID 34172516Grade ICI-related AKI by CTCAE; for persistent grade 2 or higher renal toxicity, discontinue the ICI, exclude other causes, and treat with corticosteroids with a taper begun once creatinine improves toward grade 1, considering kidney biopsy and additional immunosuppression for refractory cases.PUMCH Expert PanelClinical recommendations on diagnosis and treatment of immune checkpoint inhibitor-induced renal immune-related adverse eventsThorac Cancer 2020 · PMID 32232975Screen and monitor with serum creatinine, urinalysis/sediment, and 24-hour urine protein; strongly recommend kidney biopsy to confirm ICI-related ATIN and exclude other AKI causes, withdraw nephrotoxins (PPIs, NSAIDs), and initiate corticosteroids when a grade 2 or higher renal irAE is highly suspected, with multidisciplinary decisions on ICI withdrawal and rechallenge.ASCOManagement of Immune-Related Adverse Events in Patients Treated With Immune Checkpoint Inhibitor Therapy: American Society of Clinical Oncology Clinical Practice GuidelineJ Clin Oncol 2018 · PMID 29442540Withhold the checkpoint inhibitor and start corticosteroids for grade 2 or higher immune-related renal toxicity after excluding other causes of AKI, with steroid taper as renal function recovers and permanent discontinuation for severe (grade 4) events.
Offending agents
Signature offenders
18Agents for which acute interstitial nephritis is the defining renal lesion.
IpilimumabDelayed and variable: typically weeks to several months after initiation. Median time to AKI in biopsy cohorts was roughly 3 months (about 91 days; ~4 cycles); combination ipilimumab/nivolumab nephritis can appear after only one or two doses, and onset after drug discontinuation has been described.Clinically significant kidney injury from ipilimumab monotherapy is uncommon; renal immune-related adverse events are reported in roughly 1-2% of patients on single-agent checkpoint blockade. The dominant driver of elevated incidence is combination therapy: in real-world ICI cohorts any-cause AKI reaches about 16-17%, but only a minority is true immune-mediated nephritis. The combination of ipilimumab plus nivolumab carries a substantially higher and more severe AKI risk than either single agent. In a pooled analysis of biopsy-proven ICI-related acute tubulointerstitial nephritis, all patients on dual ICI blockade developed stage 3 AKI versus about half on a single agent, and complete renal recovery was less likely with dual blockade.SevereImmune Checkpoint InhibitorsDelayed — median ~14 weeks after starting therapy.ICI-associated AKI ~2–5% (higher with combination therapy); ~93% of biopsies show interstitial nephritis.ModerateAtezolizumabTypically weeks to a few months after initiation (median time to checkpoint-inhibitor AKI is on the order of 3-4 months, characteristically later than classic drug AIN).Across the checkpoint-inhibitor class, any acute kidney injury occurs in roughly 15-17% of treated patients in cohort studies, while clinically significant immune-related AKI (most often acute interstitial nephritis) affects a smaller subset (commonly a few percent). Meta-analysis suggests anti-PD-L1 agents like atezolizumab carry somewhat lower AKI risk than anti-PD-1 agents; PD-L1-specific rates are not precisely separated. A separate real-world cohort of 1,037 ICI-treated patients supplies the drug-attributable denominator this class otherwise lacks: 18.2% developed AKI of any cause, but only 3.6% (37 patients) had AKI attributed to the checkpoint inhibitor itself — a class figure, not an atezolizumab-specific one.ModerateDurvalumabWeeks to several months after starting therapy.As with the PD-1/PD-L1 class, any AKI occurs in roughly 15-17% of treated patients, with immune-related AIN representing a smaller, clinically significant fraction (a few percent). Anti-PD-L1 agents trend toward lower AKI risk than anti-PD-1 agents; durvalumab-specific rates are not separately well quantified. A separate real-world cohort of 1,037 ICI-treated patients supplies the drug-attributable denominator this class otherwise lacks: 18.2% developed AKI of any cause, but only 3.6% (37 patients) had AKI attributed to the checkpoint inhibitor itself — a class figure, not a durvalumab-specific one.ModerateAvelumabWeeks to months after initiation.Immune-related nephritis follows the PD-1/PD-L1 class pattern: any AKI in roughly 15-17% of patients and clinically significant immune-related AIN in a smaller subset. Anti-PD-L1 agents trend toward lower AKI risk than anti-PD-1 agents; avelumab-specific renal incidence is not separately quantified and rests on class-level pharmacovigilance and meta-analysis data. A separate real-world cohort of 1,037 ICI-treated patients supplies the drug-attributable denominator this class otherwise lacks: 18.2% developed AKI of any cause, but only 3.6% (37 patients) had AKI attributed to the checkpoint inhibitor itself — a class figure, not an avelumab-specific one.ModerateCemiplimabWeeks to months after initiation.Follows the PD-1/PD-L1 class profile: any AKI in roughly 15-17% of patients, with immune-related AIN in a smaller clinically significant subset. As an anti-PD-1 agent it may carry somewhat higher AKI risk than anti-PD-L1 agents, and pharmacovigilance data show an immune-nephropathy signal; cemiplimab-specific renal incidence is not separately quantified. A separate real-world cohort of 1,037 ICI-treated patients supplies the drug-attributable denominator this class otherwise lacks: 18.2% developed AKI of any cause, but only 3.6% (37 patients) had AKI attributed to the checkpoint inhibitor itself — a class figure, not a cemiplimab-specific one.ModerateDostarlimabWeeks to months after initiation.Consistent with the PD-1/PD-L1 class: any AKI in roughly 15-17% of treated patients, with immune-related AIN in a smaller clinically significant subset. As a newer anti-PD-1 agent, dostarlimab-specific renal incidence is not separately quantified. A separate real-world cohort of 1,037 ICI-treated patients supplies the drug-attributable denominator this class otherwise lacks: 18.2% developed AKI of any cause, but only 3.6% (37 patients) had AKI attributed to the checkpoint inhibitor itself — a class figure, not a dostarlimab-specific one.ModerateRelatlimabDelayed — typically weeks to months after initiation (long latency is characteristic of ICI-AIN).LAG-3-specific renal literature is thin: dedicated searches return no relatlimab AKI cohort or case series, and the pivotal RELATIVITY-047 trial reported aggregate grade 3/4 treatment-related adverse events (about 18.9% with the combination vs 9.7% with nivolumab alone) without an isolated nephritis rate. The renal signal is therefore class-based — immune checkpoint inhibitors cause acute interstitial nephritis, the dominant lesion in 80–90%+ of biopsied ICI-AKI cases, with combination immunotherapy a recognized risk factor.ModerateTislelizumabDelayed: commonly weeks to several months after initiation (often 8-12+ weeks); can occur after multiple cycles or after a single dose, and rarely after drug discontinuation.Drug-specific renal data are sparse: the registrational ESCC trials (RATIONALE-302, RATIONALE-306) did not report nephritis as a notable adverse event, and no tislelizumab-specific biopsy series exists. Reasoning from the PD-1 class, immune-mediated acute interstitial nephritis (the class signature) is uncommon at roughly 1-3% of treated patients, while any-cause AKI in real-world ICI cohorts is far higher (16-17%) but mostly prerenal/non-immune rather than true ICI-nephritis.ModerateToripalimabDelayed; PD-1-related AIN characteristically appears 3-10 months after initiation (later than CTLA-4 agents), though it can occur at any point during or after treatment.Drug-specific renal data are limited; reasoning from the PD-1 class is required. Across PD-1/PD-L1 agents, clinically significant immune-related AKI (predominantly AIN) occurs in roughly 1-5% of patients, with attributable PD-L1-related AKI under 1% in one large cohort but pooled estimates as high as ~3-5% with platinum co-therapy. In the JUPITER-02 registrational trial, immune-related adverse events were more frequent with toripalimab (54.1% vs 21.7%) and grade ≥3 irAEs occurred in 9.6%, but kidney-specific irAEs were not individually quantified.ModerateRetifanlimabUsually delayed — weeks to several months after initiation (median ~3 months for ICI-AIN), but can occur at any point including after discontinuation.Renal immune-related adverse events are uncommon with PD-1 monotherapy. Across the checkpoint-inhibitor class, checkpoint-attributed AKI occurs in roughly 2-5% of treated patients (a 2023 meta-analysis of 24,048 patients pooled it at 5.7%) and biopsy-confirmed immune-related AIN in approximately 1-3%, with higher rates when combined with CTLA-4 blockade or nephritogenic co-medications (PPIs, NSAIDs). Any-cause AKI in real-world ICI cohorts runs far higher (~16-17%) but is mostly prerenal or non-immune rather than true ICI-nephritis. Retifanlimab's registrational program did not flag nephritis as a prominent signal; in the phase III POD1UM-303 anal-cancer trial the dominant grade ≥3 events were chemotherapy-driven cytopenias (neutropenia 35%, anemia 20%), not renal events.ModerateCosibelimabDelayed and variable — typically weeks to months after initiation. Pooled ICI data place median time to AKI at roughly 3-4 months (~108 days), though onset ranges from a few weeks to after treatment discontinuation.Drug-specific renal data are limited. In the pivotal phase 1 metastatic CSCC cohort (n=78), immune-related adverse events occurred in 23.1% of patients (grade 3 in 2.6%; no grade 4/5), with no nephritis-specific signal reported and a favorable overall safety profile. By class, immune-mediated nephritis/AKI with checkpoint inhibitors is uncommon: a 2023 systematic review and meta-analysis of 27 studies (24,048 patients) found a pooled all-cause AKI incidence of ~5.7%, with clinically significant immune-mediated nephritis substantially lower (roughly 1-3%), and anti-PD-L1 agents tending toward the lower end of that range versus CTLA-4 or combination regimens.ModeratePenpulimabVariable and often delayed: ICI-associated AIN commonly emerges weeks to several months after initiation (median around 3-4 months), and can appear after multiple cycles or even after discontinuation. Chemotherapy-related ATN in the combination regimen tends to occur earlier, peri-infusion.Penpulimab-specific renal data are limited. In the pivotal first-line phase 3 trial (penpulimab plus chemotherapy), grade >=3 immune-related adverse events occurred in only 4.1% of patients, and renal events were not separately prominent; the most common toxicities were hematologic. By class, immune checkpoint inhibitor-associated AKI (predominantly acute tubulointerstitial nephritis) occurs in roughly 2-5% of patients on PD-1 monotherapy, with higher rates when combined with nephrotoxic chemotherapy. Platinum (cisplatin) and gemcitabine in the registrational backbone independently contribute ATN and (rarely) thrombotic microangiopathy risk, so observed kidney injury in this regimen is often multifactorial.ModerateSugemalimabDelayed — typically weeks to months after initiation; in the multicenter ICI-AKI cohort median time from checkpoint-inhibitor start to AKI was about 14 weeks (IQR 6-37), later than most other drug-induced AIN.No sugemalimab-specific renal-injury incidence has been published; the GEMSTONE registrational trials reported no nephritis among the most common grade 3-4 treatment-related adverse events (which were dominated by myelosuppression and immune-mediated pneumonitis). By extrapolation from the PD-1/PD-L1 checkpoint-inhibitor class, immune-related AKI occurs in roughly 2-5% of treated patients (higher with combination checkpoint blockade), with clinically significant/biopsy-confirmed acute interstitial nephritis being the dominant lesion. A separate real-world cohort of 1,037 ICI-treated patients supplies the drug-attributable denominator this class otherwise lacks: 18.2% developed AKI of any cause, but only 3.6% (37 patients) had AKI attributed to the checkpoint inhibitor itself — a class figure, not a sugemalimab-specific one.ModerateNivolumabCharacteristically delayed compared with other drug-induced AIN: median time from ICI initiation to AKI was about 14 weeks (IQR 6-37) in a 138-patient multicenter cohort, and 91 days in the original series; onset ranges from weeks to many months and can follow drug discontinuation.Clinically significant ICI-attributed AKI is uncommon but not rare. A 2023 systematic review/meta-analysis of real-world data (18 studies, ~12,000 ICI-treated patients) found a pooled incidence of all-cause AKI during ICI therapy of about 16%, but AKI specifically attributed to the ICI of roughly 3.5%. Risk is higher with combination ICI regimens (e.g., nivolumab-ipilimumab) than with PD-1 monotherapy. Among biopsied ICI-AKI, acute tubulointerstitial nephritis is the dominant lesion (>90%); glomerular lesions and thrombotic microangiopathy are reported but uncommon.ModeratePembrolizumabDelayed and highly variable, typically weeks to months after initiation; multicenter cohorts reported median onsets around 14-16 weeks. Can occur after a single dose or after many months, and may recur on rechallenge.In real-world cohorts of patients receiving immune checkpoint inhibitors, any AKI is common (roughly 16-18%), but AKI attributable to the checkpoint inhibitor itself (ICPi-AKI) is less frequent. A single-center cohort reported AKI in 16.5% of ICI-treated patients with checkpoint-attributable nephrotoxicity in a minority, while a larger real-world study found ICPi-AKI in about 3.6%. Acute interstitial nephritis is the dominant biopsy lesion (>80% in the largest multicenter series). These figures are pooled across PD-1/PD-L1/CTLA-4 agents rather than pembrolizumab-specific.ModerateBicalutamideIf AIN occurs, typically subacute over weeks of exposure (idiosyncratic).Bicalutamide is largely kidney-neutral. Pharmacokinetics are unaffected by renal impairment and no renal dose adjustment is required. Acute interstitial nephritis is, at most, a rare idiosyncratic case-report-level event; no meaningful incidence rate is established.MildDabrafenibVariable and biphasic. Pyrexia-associated AKI clusters early, in the first weeks to months of therapy and coincides with febrile episodes. Biopsy-proven granulomatous/acute interstitial nephritis has appeared anywhere from a few weeks to as late as ~5 years into treatment.AKI is relatively common on dabrafenib-based therapy but usually mild and reversible. In the largest cohort, 42/199 (21%) of patients on dabrafenib/trametinib developed AKI within 12 months, and roughly 24% of those episodes occurred during the drug-induced febrile (pyrexia) syndrome (Seethapathy 2022). Pharmacovigilance places dabrafenib well below vemurafenib: FAERS acute-kidney-injury reporting-odds-ratio approximately 1.35 (95% CI 1.15–1.60) for dabrafenib versus approximately 3.28 for vemurafenib (Sanagawa 2021). Biopsy-proven granulomatous/acute interstitial nephritis and clinically significant electrolyte disorders (hyponatremia, hypokalemia, hypophosphatemia) are each individually rare — documented mainly in case reports and small FAERS counts. Registrational trials did not flag renal toxicity; the signal emerged post-marketing.Mild