What kind of kidney injury does Atezolizumab cause?

Acute Interstitial Nephritis — Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors. Other reported patterns: Glomerular Injury / Proteinuria, Hemorrhagic Cystitis, SIADH / Hyponatremia.

How should kidney function be monitored during Atezolizumab therapy?

Urinalysis with urine protein and microscopy if creatinine rises; Screen for concurrent immune-related adverse events (LFTs, TSH, glucose).

How can kidney injury from Atezolizumab be prevented?

Review and minimize concomitant AIN-associated medications (especially PPIs)

Who is at higher risk of kidney injury from Atezolizumab?

Concurrent proton-pump inhibitors, NSAIDs, or other AIN-associated drugs; Combination checkpoint-inhibitor or chemoimmunotherapy regimens; Lower baseline kidney function; Other concurrent immune-related adverse events.

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Printable monograph

Anti-PD-L1 antibody

Atezolizumab

Tecentriq · ATEZO

Anti-PD-L1 antibody · approved 2016 · 15 citations · FAERS AKI reporting ROR 2.63 (95% CI 2.45–2.83, 728 AKI reports)

Up to date· through 2025

Deeply sourced7/9 · 7 signals

Met: 15 citations
Met: 12+ references
Not met: Accrued over 10+ years (span: 9y)
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.

An anti-PD-L1 antibody that triggers immune-mediated acute interstitial nephritis, occasionally glomerular disease.

ModerateImmune checkpoint inhibitor (anti-PD-L1)

Non-small cell lung cancerSmall cell lung cancerUrothelial carcinomaHepatocellular carcinoma (with bevacizumab)Melanoma (combination)

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Signature kidney injury

Signature lesion

Acute Interstitial Nephritis

Representative incidence3.6%

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.Source: Lumlertgul et al., Eur J Cancer 2023 (class-level ICI-attributed AKI 3.6%; agent-specific AIN rate not separately quantified)

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Typically weeks to a few months out (median ~3–4 months), later than classic drug AIN.

Distilled from: “Typically 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).”

RechallengeCase-by-case

In the multicenter ICI-AKI cohort ~22% were rechallenged and ~23% of those developed recurrent AKI — feasible but an individualized, co-managed decision. PMID 31896554 (opens PubMed in a new tab)

Long-term outlook & thresholds

Renal recoveryOften partial recovery

Class-level checkpoint-inhibitor AKI recovery: in a 138-patient multicenter ICI-AKI cohort, complete, partial, and no recovery of kidney function occurred in roughly 40%, 45%, and 15% of patients respectively. Two covariates carried a better renal prognosis — treatment with steroids, and the PRESENCE of a concomitant tubulointerstitial-nephritis-causing medication (69% of patients were on one). The second is an observational association, not an intervention: the cohort analysed no effect of stopping that drug, and the likeliest reading is that a competing culprit makes the ICI a less certain cause. Rechallenge is feasible in selected patients but recurrent AKI occurs in about a quarter.PMID 31896554 (opens PubMed in a new tab)

CKD trajectory.: Roughly 15% of patients have no renal recovery, leaving residual chronic kidney disease, and recovery is often incomplete (partial recovery in ~45%) — a class-level pattern across checkpoint inhibitors. A separate single-center cohort of 1,037 ICI-treated patients sharpens the comparison: complete kidney recovery was less common after ICI-attributed AKI than after AKI from other causes (54% versus 79%, p=0.01), and ICI-AKI reached higher AKI stages.PMID 37499561 (opens PubMed in a new tab)
Dialysis / RRT.: Severe checkpoint-inhibitor AKI can require dialysis, though most ICI-attributed AKI is not dialysis-requiring.

Long-term outcome and threshold data distilled from the agent's cited literature — educational, not a substitute for the primary sources.

Recovery across agents

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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 Interstitial Nephritis#1 · Signatureno population incidence denominator
Acute tubulointerstitial nephritis is the dominant renal lesion in immune checkpoint inhibitor-associated AKI, seen in 82.7% (125/151) of biopsied cases in the largest multicenter cohort; anti-PD-L1 agents such as atezolizumab carry a lower AKI risk than anti-PD-1 agents PMID 34625513 (opens PubMed in a new tab)
Glomerular Injury / ProteinuriaRareno population incidence denominator
Checkpoint inhibitor-associated glomerular disease (FSGS, minimal-change/podocytopathy, membranous, pauci-immune GN) is case-level and far less common than AIN PMID 37973491 (opens PubMed in a new tab)
Hemorrhagic CystitisRarequalitative — no citable incidence
Case-level immune-related (irAE) cystitis - immune-mediated, not acrolein toxicity.
SIADH / HyponatremiaRarequalitative — no citable incidence
A monotherapy case with endocrinopathies excluded; the SCLC indication drives much of the reporting.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

3.6%incidence

SeverityModerate

ReversibilityPartially reversible

Evidence15 citations

Nephron map

Glomerulus

Distal Tubule / Collecting Duct

InterstitiumSupporting tissue around the tubules

Bladder / Urothelium

Acute Interstitial Nephritis

Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.

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Kidney injury

Deep diveCheckpoint-inhibitor acute interstitial nephritisRelease the brakes on the immune system to fight the cancer and, weeks to months later, the same unleashed T cells can turn on the kidney's interstitium — a delayed, often steroid-responsive nephritis that hides behind a bland urine and a slowly rising creatinine.

Mechanism of kidney injury

Loss of peripheral immune tolerance from PD-L1 blockade permits activated CD4+/CD8+ T-cell infiltration of the tubulointerstitium, producing acute (often granulomatous) tubulointerstitial nephritis; reactivation of T cells primed against tubulointerstitial self-antigens or haptenizing drugs (PPIs, NSAIDs) is implicated, with a relative paucity of eosinophils compared with classic drug AIN. Glomerular lesions—pauci-immune/crescentic glomerulonephritis, fibrillary GN, and podocytopathies (minimal-change/FSGS)—occur less commonly.

Clinical presentation

Subacute rise in creatinine, sterile pyuria, white-cell casts, and low-grade (sub-nephrotic) proteinuria; eosinophilia/eosinophiluria are variable and often absent. AKI with hematuria and heavier proteinuria suggests a glomerular variant. Frequently accompanied by other immune-related adverse events (rash, colitis, thyroiditis).

Management

Hold the checkpoint inhibitor and exclude prerenal, obstructive, and other causes; pursue kidney biopsy when feasible to confirm AIN versus a glomerular lesion. Corticosteroids (e.g., prednisone ~0.5-1 mg/kg/day with taper) are first-line for immune-related AIN, with most patients recovering at least partial function; steroid-refractory cases may need additional immunosuppression. Rechallenge is individualized after recovery, recognizing a meaningful AKI recurrence rate.Lesion-level management framework

Risk factors

Concurrent proton-pump inhibitors, NSAIDs, or other AIN-associated drugs
Combination checkpoint-inhibitor or chemoimmunotherapy regimens
Lower baseline kidney function
Other concurrent immune-related adverse events

Prevention

Review and minimize concomitant AIN-associated medications (especially PPIs)

Anticancer mechanism· how it treats cancer

Humanized IgG1 monoclonal antibody blocking programmed death-ligand 1 (PD-L1), interrupting PD-1/PD-L1 (and PD-L1/B7.1) inhibitory signaling to restore antitumor T-cell activity. Used across lung, urothelial, hepatocellular, and other cancers, often with bevacizumab or chemotherapy.

Note · Renal immune-related toxicity is a class effect of PD-1/PD-L1 inhibitors; biopsy-based series predominantly show acute interstitial nephritis. Cited incidence figures are class-level rather than atezolizumab-specific, but biopsy-proven atezolizumab AIN and glomerular cases are documented.

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Clinical depth

Renal dose adjustment

No baseline renal dose adjustment (fixed-dose antibody not renally cleared). The relevant 'adjustment' is immune-toxicity grading: per consensus guidance, withhold for grade 2 (creatinine 2-3x baseline) and treat with steroids, and permanently discontinue for grade 3-4 or recurrent severe nephritis.

Dialyzability & ESKD dosing

Not dialyzable—an IgG1 monoclonal antibody cleared by reticuloendothelial catabolism; not removed by hemodialysis and no dose supplementation needed. ESKD patients can receive standard dosing.

Differential diagnosis

Distinguish ICI-AIN from prerenal azotemia (volume/contrast/HCC-related), obstruction, and other drug AIN; the late onset, sterile pyuria with WBC casts, frequent absence of eosinophilia, and concurrent irAEs favor ICI-AIN. Cystatin-C-based eGFR and urine biomarkers (TNF-alpha, IL-9, CXCL9) help separate true AIN from pseudo-AKI and other causes; hematuria with heavier proteinuria points to a glomerular variant requiring biopsy.

Monitoring

Urinalysis with urine protein and microscopy if creatinine rises
Screen for concurrent immune-related adverse events (LFTs, TSH, glucose)

Key trials & series

Cortazar Kidney Int 2016 ICI-AKI biopsy series
Cortazar JASN 2020 multicenter ICI-AKI cohort
Gupta J Immunother Cancer 2021 multicenter ICI-AKI cohort

Clinical pearls

ICI-AIN is typically late (months in) and steroid-responsive—unlike classic drug AIN it often lacks eosinophilia.
A concurrent PPI or NSAID is a common co-conspirator; deprescribe it as part of management.
Biopsy when the picture is atypical—atezolizumab also causes glomerular lesions (pauci-immune/crescentic, fibrillary, podocytopathy).
Urinary CXCL9/TNF-alpha/IL-9 and cystatin C help separate true AIN from pseudo-AKI before committing to steroids or rechallenge.
Immune-related non-bacterial cystitis is reported with biopsy support and steroid response — an irAE rather than acrolein-type hemorrhagic cystitis; the bladder-cancer indication adds tumor hematuria to the FAERS term.
A monotherapy case attributes SIADH to atezolizumab with endocrinopathies excluded; the extensive-stage SCLC indication — the archetypal paraneoplastic-SIADH tumor — drives much of the reporting.

irAE atlasImmune-related adverse events of checkpoint blockade, indexed by organ

27 grade-indexed syndromes across 11 organ systems, written for checkpoint blockade as a class rather than per agent — where a rate differs between anti-PD-1, anti-PD-L1, anti-CTLA-4 and combination therapy, the card names the class it was measured in.

Beyond the kidney — non-renal toxicities· 5 organ systems

Class-level context for the major non-renal toxicities of the Anti-PD-L1 antibody class.

Endocrine

Thyroiditis, hypophysitis, diabetes

Thyroiditis, hypophysitis, type-1 diabetes

Gastrointestinal

Diarrhea, colitis, mucositis, perforation

Immune colitis

Hepatic / Liver

Transaminitis, hepatitis, VOD/SOS

Immune hepatitis

Pulmonary

Pneumonitis, ILD, effusions, hypertension

Pneumonitis

Dermatologic

Rash, HFS, SJS/TEN, vitiligo

Rash, vitiligo, rarely SJS/TEN

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References

13 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

13 references · 2016–2025 · 4 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· 2

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 · ModerateOverlap of Thrombotic Microangiopathy and Mesangial Proliferative Glomerulonephritis Caused by Combination Therapy with Atezolizumab and Bevacizumab.Horino T et al. · Intern Med 2023 · PMID 35705272Biopsy-confirmed renal thrombotic microangiopathy overlapping with mesangial proliferative glomerulonephritis and proteinuria from atezolizumab plus bevacizumab in hepatocellular carcinoma.CaseB · ModerateAcute Tubulointerstitial Nephritis and Secondary Renal Amyloidosis: A Rare Complication of Atezolizumab.Ullah N et al. · Cureus 2023 · PMID 38156149Biopsy-proven acute tubulointerstitial nephritis with nephrotic-range proteinuria and secondary (AA) renal amyloidosis during atezolizumab/bevacizumab maintenance for NSCLC.

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.

AbstractRituximab in Atezolizumab-Associated IgA Vasculitis: A Bridge Between Renal Protection and Cancer TreatmentArriola Montenegro JJ, Riaza Ortiz C, Sethi S, Herrmann S · ASN Kidney Week 2025 2025 · Abstract SA-PO0905A 75-year-old man on atezolizumab for metastatic small-cell carcinoma developed IgA vasculitis (skin) plus AKI, with kidney biopsy showing IgA nephropathy with focal necrotizing and crescentic glomerulonephritis and acute tubular injury — a glomerular/vasculitic ICI lesion distinct from the usual interstitial nephritis. Stopping atezolizumab with rituximab and a prednisone taper achieved renal recovery while preserving cancer-treatment options.JournalA case of atezolizumab-associated tubulointerstitial nephritisZakharova E, Makarova T, Vorobyeva O · Journal of Onco-Nephrology 2022Acute tubulointerstitial nephritis attributed to the PD-L1 inhibitor atezolizumab — the classic checkpoint-inhibitor interstitial lesion. Published in the Journal of Onco-Nephrology (not PubMed-indexed).

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 38,623 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· 7 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

Glomerular Injury / Proteinuriacorroborated · ROR 15.81 — on the terms that name the lesion (ROR 5)
Acute Interstitial Nephritiscorroborated · ROR 4.92
SIADH / Hyponatremiacorroborated · ROR 3.52 — on the terms that name the lesion (ROR 2.68)
Hemorrhagic Cystitiscorroborated · ROR 1.45 — on the terms that name the lesion (ROR 1.89)

Glomerular Injury / Proteinuria

ROR 15.8195% CI 14.73–16.97· 809 reports

Acute Interstitial Nephritis

ROR 4.9295% CI 4.23–5.73· 168 reports

SIADH / Hyponatremia

ROR 3.5295% CI 3.23–3.84· 515 reports

Electrolyte Disturbance

ROR 3.2095% CI 3.01–3.40· 1,100 reports

Thrombotic Microangiopathy

ROR 2.8595% CI 2.29–3.55· 81 reports

Hypertension

ROR 1.5895% CI 1.49–1.68· 1,111 reports

Hemorrhagic Cystitis

ROR 1.4595% CI 1.26–1.68· 185 reports

FAERS outcomes & reporting trend· 25.4% of reports w/ death · 42.4% w/ hospitalization

25.4%

Reported with a death outcome

9,821 of 38,623 reports

42.4%

Reported with hospitalization

16,375 of 38,623 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 10 systems · 38,623 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 2.6395% CI 2.45–2.83· 728 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 Injury728Proteinuria715

Blood & lymphatic

Anaemia1,351Febrile Neutropenia952Thrombocytopenia842Neutropenia833Platelet Count Decreased745

Gastrointestinal

Diarrhoea1,710Nausea1,062Vomiting811Colitis782

General / constitutional

Pyrexia1,749Fatigue1,500Asthenia947

Respiratory

Dyspnoea1,028Pneumonitis966Interstitial Lung Disease835

Immune / infection

Pneumonia1,134

Metabolic & electrolyte

Decreased Appetite1,110

Endocrine

Hypothyroidism1,079

Vascular

Hypertension996

Skin

Rash958

Guidelines & consensus· 22

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.

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.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.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.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.IC-OSImmune Checkpoint Inhibitor-Associated Cardiovascular Toxic Effects: International Cardio-Oncology Society Position StatementJAMA Oncol 2026 · PMID 41231466Concerns for myocarditis continue to dominate the spectrum of CV toxic effects in patients receiving ICI therapy. Recommendations for management vary according to severity. Multidisciplinary collaborations remain key for managing acute toxic effects and future cancer treatment decisions, including ICI rechallenge.EULAREULAR points to consider for the diagnosis and management of rheumatic immune-related adverse events due to cancer immunotherapy with checkpoint inhibitorsAnn Rheum Dis 2021 · PMID 32327425Oncologists should be encouraged to consult rheumatologists promptly for assessment when rheumatic musculoskeletal and systemic signs or symptoms are suspected due to immunotherapy, and rheumatologists should provide facilitated access for such patients.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.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.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.

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 Atezolizumab 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

Avelumab

Bavencio · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#1 · 76% phenotype match

Cemiplimab

Libtayo · Anti-PD-1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#2 · 76% phenotype match

Dostarlimab

Jemperli · Anti-PD-1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#3 · 76% phenotype match

Durvalumab

Imfinzi · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#4 · 76% phenotype match

Toripalimab

Loqtorzi · PD-1 immune checkpoint inhibitor

Profile

First FDA-approved drug for nasopharyngeal carcinoma; renal risk is class-typical immune-mediated interstitial nephritis.

AINLYTEGLOM

Moderate#5 · 68% phenotype match

Cosibelimab

Unloxcyt · PD-L1 immune checkpoint inhibitor

Profile

PD-L1 blockade for cutaneous SCC — watch for late immune interstitial nephritis

AINGLOMLYTE

Moderate#6 · 68% phenotype match

Compare Atezolizumab 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 Checkpoint inhibitors

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.

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 Atezolizumab’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 Atezolizumab; 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 81 clinical records among all 108 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.