How should kidney function be monitored during Everolimus therapy?

Baseline and periodic urinalysis with quantified proteinuria (UACR or spot protein:creatinine); Serum creatinine / eGFR; Blood pressure; CBC with smear, LDH, and haptoglobin if TMA is suspected (schistocytes, thrombocytopenia); Serum phosphate, potassium, and magnesium; Everolimus trough concentrations in the transplant setting; Fasting glucose and lipids (associated metabolic adverse effects).

How can kidney injury from Everolimus be prevented?

Baseline and ongoing blood-pressure control, favoring ACE inhibitor / ARB in patients who develop proteinuria Avoid unnecessary co-administration with anti-VEGF agents and keep calcineurin-inhibitor levels controlled to limit additive glomerular/endothelial injury

Who is at higher risk of kidney injury from Everolimus?

Pre-existing CKD, baseline proteinuria, or diabetic nephropathy; Concurrent anti-VEGF agent (bevacizumab, VEGF-TKI) — additive proteinuria; Concurrent calcineurin inhibitor (tacrolimus/cyclosporine) — additive TMA risk; Higher drug exposure / elevated troughs (transplant setting); Reduced nephron mass (prior nephrectomy in RCC patients); Poorly controlled hypertension; Conversion from a calcineurin inhibitor to an mTOR inhibitor in transplant recipients.

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Printable monograph

mTOR inhibitor

Everolimus

Afinitor · EVE

mTOR inhibitor · approved 2009 · 12 citations · FAERS AKI reporting ROR 1.93 (95% CI 1.79–2.08, 702 AKI reports)

Up to date· through 2025

Deeply sourced9/9 · 8 signals

Met: 12 citations
Met: 12+ references
Met: Accrued over 10+ years (span: 17y)
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.

The oral rapalog whose podocytes pay in protein — glomerular proteinuria and secondary FSGS, with occasional thrombotic microangiopathy.

ModerateTargeted therapy (mTOR rapalog), late 2000s

Advanced renal cell carcinoma after failure of a VEGF-targeted tyrosine-kinase inhibitor (sunitinib/sorafenib)Progressive pancreatic and GI/lung neuroendocrine tumorsHR-positive, HER2-negative advanced breast cancer (with exemestane) after letrozole/anastrozole failureSubependymal giant-cell astrocytoma (SEGA) and renal angiomyolipoma in tuberous sclerosis complexTSC-associated refractory seizures (Afinitor Disperz)

§01

Signature kidney injury

Signature lesion

Glomerular Injury / Proteinuria

Representative incidence96%

Proteinuria is a class effect of mTOR inhibitors, and with systematic monitoring it is close to universal. A retrospective review of 129 first-line metastatic renal-cell patients found any-grade proteinuria in 81% overall and in 96% of the everolimus arm (44 patients) — the highest of the three regimens compared, against 80% on pazopanib and 64% on bevacizumab. Almost all of it was minor: the study's grade 3-4 proteinuria (24%, 6 patients) occurred entirely in the bevacizumab group, none in the everolimus arm, and 35 of the everolimus patients (80%) simply continued at the same dose under monitoring. So the striking number is detection, not injury — heavy proteinuria and overt podocytopathy remain uncommon, and most nephrotic-range and biopsy-proven FSGS data are still extrapolated from the sirolimus/transplant literature. A phase II trial combining everolimus with bevacizumab reported grade 3-4 proteinuria of 25%, which reflects the added anti-VEGF effect and overstates everolimus alone. Thrombotic microangiopathy is rare and drawn mainly from case reports, typically with concomitant calcineurin-inhibitor or anti-VEGF exposure.Source: Land et al., J Oncol Pharm Pract 2016 (PMID 25505255, everolimus arm 44 patients, any-grade proteinuria 96%); Hainsworth JD et al., J Clin Oncol 2010 (PMID 20368560, everolimus + bevacizumab combination figure)

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Proteinuria emerges over the first weeks to months; thrombotic microangiopathy usually within weeks to months, often with concurrent calcineurin-inhibitor or anti-VEGF exposure.

Distilled from: “Subacute — proteinuria typically emerges over the first weeks to months of therapy; thrombotic microangiopathy usually appears within weeks to months, often in the setting of concurrent calcineurin-inhibitor or anti-VEGF exposure.” · PMID 18631865 (opens PubMed in a new tab)

Long-term outlook & thresholds

Early-detection biomarkers

Quantified proteinuria (urine protein–creatinine ratio) — Glomerular filtration-barrier injury — the mTOR-inhibitor podocytopathy. In first-line metastatic RCC, 96% of the everolimus arm developed proteinuria of some grade (44 patients; the abstract's n counts those with proteinuria, not the arm) — the highest of the three agents compared — which is what makes it worth measuring rather than assuming. Read it as detection, not severity: every grade 3–4 event in that cohort occurred in the bevacizumab arm, and at peak proteinuria 80% of those 44 (n = 35) were managed with continued monitoring at the same dose. Two limits belong with it: the study captured toxicity grade retrospectively and never showed proteinuria preceding a creatinine change, so lead time is assumed rather than demonstrated; and the podocyte/FSGS mechanism that makes the marker compelling comes from the kidney-transplant sirolimus literature and murine work, not from oncology-dose everolimus.PMID 25505255 (opens PubMed in a new tab)

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

§02

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.

Glomerular Injury / Proteinuria#1 · Signaturequalitative — no citable incidence
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.
Thrombotic MicroangiopathySecondaryqualitative — no citable incidence
Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF.
Electrolyte DisturbanceSecondaryqualitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

96%incidence

SeverityModerate

ReversibilityVariable

Evidence12 citations

Nephron map

GlomerulusFiltration barrier (podocytes + endothelium)

Vasculature / Endothelium

Proximal Tubule

Distal Tubule / Collecting Duct

Glomerular Injury / Proteinuria

Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.

§03

Kidney injury

Mechanism of kidney injury

mTORC1 signaling is required for the compensatory podocyte hypertrophy that maintains coverage of the glomerular filtration barrier after podocyte stress or loss; pharmacologic mTOR inhibition impairs this repair program, producing foot-process effacement, podocyte depletion, secondary focal segmental glomerulosclerosis, and proteinuria (Puelles 2019; Letavernier 2008). mTOR blockade also downregulates podocyte VEGF-A and slit-diaphragm proteins (e.g., nephrin) and impairs glomerular endothelial repair, promoting endothelial injury and thrombotic microangiopathy — a risk amplified by concurrent calcineurin inhibitors or anti-VEGF agents. Proximal-tubular effects drive renal phosphate, potassium, and magnesium wasting, producing the electrolyte disturbances seen with this class.

Clinical presentation

Most often new or rising proteinuria detected on dipstick or urine albumin/protein-to-creatinine ratio, usually with preserved or only slowly declining GFR; occasionally nephrotic-range proteinuria with edema and hypoalbuminemia. When biopsied (uncommon in oncology), the lesion is a podocytopathy with foot-process effacement and secondary FSGS. Thrombotic microangiopathy presents as rising creatinine with microangiopathic hemolytic anemia (schistocytes, elevated LDH, low haptoglobin), thrombocytopenia, and sometimes hypertension. Electrolyte manifestations include hypophosphatemia, hypokalemia, and hypomagnesemia.

Management

Quantify proteinuria (UACR or 24-h) and start or optimize RAAS blockade (ACE inhibitor/ARB) with blood-pressure control. Low-grade proteinuria can usually be continued with close monitoring; nephrotic-range or progressively rising proteinuria warrants dose reduction or discontinuation, after which glomerular injury frequently improves. For suspected thrombotic microangiopathy, stop everolimus (and reduce or stop a concomitant calcineurin inhibitor), give supportive care, and involve hematology — drug-associated TMA is generally managed by withdrawal of the offending agent rather than complement blockade. Replace phosphate, potassium, and magnesium as needed. Refer to nephrology for significant or persistent proteinuria, unexplained GFR decline, or consideration of biopsy.Lesion-level management framework

Risk factors

Pre-existing CKD, baseline proteinuria, or diabetic nephropathy
Concurrent anti-VEGF agent (bevacizumab, VEGF-TKI) — additive proteinuria
Concurrent calcineurin inhibitor (tacrolimus/cyclosporine) — additive TMA risk
Higher drug exposure / elevated troughs (transplant setting)
Reduced nephron mass (prior nephrectomy in RCC patients)
Poorly controlled hypertension
Conversion from a calcineurin inhibitor to an mTOR inhibitor in transplant recipients

Prevention

Baseline and ongoing blood-pressure control, favoring ACE inhibitor / ARB in patients who develop proteinuria
Avoid unnecessary co-administration with anti-VEGF agents and keep calcineurin-inhibitor levels controlled to limit additive glomerular/endothelial injury

Anticancer mechanism· how it treats cancer

Oral rapamycin analog (rapalog) that binds FKBP-12 to inhibit mTOR complex 1 (mTORC1), blocking downstream S6K1/4E-BP1 signaling. This arrests G1/S cell-cycle progression, suppresses protein synthesis and proliferation, and reduces HIF-1alpha-driven VEGF production, adding an anti-angiogenic effect.

Note · Everolimus (Afinitor) is the oncology/TSC brand; the same molecule is marketed as Zortress (lower, trough-guided doses) for transplant immunosuppression, where much of the proteinuria/FSGS and TMA literature originates. Because a clean single-agent oncology incidence for glomerular injury is not well established, no single headline incidence is quoted, and quantified figures are attributed to their specific (often combination) trial contexts.

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Clinical depth

Renal dose adjustment

No renal-function-based dose adjustment is defined — everolimus is hepatically metabolized (CYP3A4/P-glycoprotein) and its pharmacokinetics are not meaningfully altered by renal impairment, so dosing is instead adjusted for hepatic impairment, CYP3A drug interactions, and toxicity. When nephrotoxicity (heavy proteinuria or TMA) develops, dose interruption/reduction or discontinuation is the lever, not a renal-clearance-based reduction.

Dialyzability & ESKD dosing

Not meaningfully dialyzable and no supplemental post-dialysis dosing is defined: everolimus has a large apparent volume of distribution, is substantially protein-bound (~74%), and is extensively metabolized, so hemodialysis is not expected to remove significant drug. Data in dialysis patients are limited.

Differential diagnosis

Separate mTOR-inhibitor podocytopathy/proteinuria from: anti-VEGF-agent proteinuria and TMA when everolimus is combined with bevacizumab or a VEGF-TKI; calcineurin-inhibitor nephrotoxicity and CNI-associated TMA in transplant recipients; diabetic nephropathy and hypertensive glomerulosclerosis; underlying malignancy-associated glomerulopathy; and other causes of AKI (prerenal, contrast, obstruction). For a TMA picture, consider complement-mediated atypical HUS, TTP, malignancy-associated TMA, and calcineurin-inhibitor TMA as competing/contributing causes.

Monitoring

Baseline and periodic urinalysis with quantified proteinuria (UACR or spot protein:creatinine)
Serum creatinine / eGFR
Blood pressure
CBC with smear, LDH, and haptoglobin if TMA is suspected (schistocytes, thrombocytopenia)
Serum phosphate, potassium, and magnesium
Everolimus trough concentrations in the transplant setting
Fasting glucose and lipids (associated metabolic adverse effects)

Key trials & series

RECORD-1 — registrational phase III of everolimus in advanced clear-cell RCC after VEGF-TKI failure, establishing efficacy and the tolerability/safety profile that underpins AE management guidance
RECORD-4 (Motzer 2015, PMID 26681676) — prospective second-line everolimus in metastatic RCC confirming PFS benefit with a safety profile consistent with prior experience
BOLERO-2 — phase III of everolimus plus exemestane in HR-positive advanced breast cancer (source of much real-world AE-management experience)
Everolimus + bevacizumab phase II in advanced RCC (Hainsworth 2010, PMID 20368560) — 25% grade 3-4 proteinuria, illustrating additive glomerular toxicity when combined with an anti-VEGF agent

Clinical pearls

The signature renal lesion is glomerular, not tubular: think podocyte injury with proteinuria and secondary FSGS — check a urine protein ratio before and during therapy, don't just track creatinine.
mTOR is protective for stressed podocytes; inhibiting it blocks the compensatory hypertrophy that maintains the filtration barrier, which is why proteinuria is a mechanism-based class effect (Puelles 2019; Letavernier 2008).
Proteinuria usually responds to RAAS blockade, dose reduction, or drug withdrawal — most low-grade proteinuria does not require stopping the drug, but nephrotic-range proteinuria should.
Watch for additive glomerular toxicity when everolimus is combined with anti-VEGF agents (bevacizumab, VEGF-TKIs) — the 25% grade 3-4 proteinuria figure comes from a bevacizumab combination and overstates everolimus alone.
Thrombotic microangiopathy is rare and usually appears alongside a calcineurin inhibitor or anti-VEGF drug; screen with LDH, haptoglobin, platelets, and a smear when creatinine rises unexpectedly, and manage primarily by stopping the culprit(s).
Don't forget the electrolytes: proximal-tubular wasting can produce hypophosphatemia, hypokalemia, and hypomagnesemia.

Beyond the kidney — non-renal toxicities· 4 organ systems

Class-level context for the major non-renal toxicities of the mTOR inhibitor class.

Pulmonary

Pneumonitis, ILD, effusions, hypertension

Non-infectious pneumonitis

Endocrine

Thyroiditis, hypophysitis, diabetes

Hyperglycemia, hyperlipidemia

Gastrointestinal

Diarrhea, colitis, mucositis, perforation

Stomatitis

Immune / Infusion

CRS, infusion reactions, irAEs, anaphylaxis

Immunosuppression / infection

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References

9 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

9 references · 2008–2020 · 3 since 2018

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· 3

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 · ModerateEverolimus-induced nephrotic syndrome precipitated by interaction with voriconazole in a patient with Hodgkin's lymphoma.Tran PN et al. · J Clin Pharm Ther 2017 · PMID 28661568A Hodgkin's lymphoma patient on everolimus developed biopsy-proven nephrotic syndrome (thrombotic microangiopathic vasculopathy and thin basement membrane nephropathy) that resolved on everolimus discontinuation.CaseB · ModerateAcute Tubular Necrosis Attributed to High-Dose Everolimus with High-Potency Bisphosphonates for Advanced Breast Cancer: A Case Report.Loewenstein I et al. · Nephron 2025 · PMID 39900014A 69-year-old woman with advanced breast cancer developed biopsy-confirmed acute tubular necrosis requiring dialysis shortly after starting everolimus (with concurrent bisphosphonate), reversing after everolimus withdrawal.CaseC · LimitedEverolimus-associated focal segmental glomerulosclerosis in a liver transplant recipient.Manabe S et al. · Nephrology (Carlton) 2021 · PMID 33300227A liver transplant recipient on everolimus developed focal segmental glomerulosclerosis, implicating everolimus in this proteinuric glomerular lesion.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 50,589 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· 10 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

Thrombotic Microangiopathycorroborated · ROR 8.13
Glomerular Injury / Proteinuriacorroborated · ROR 5.15 — on the terms that name the lesion (ROR 3.31)
Electrolyte Disturbancecorroborated · ROR 2.19 — on the terms that name the lesion (ROR 2.22)

Thrombotic Microangiopathy

ROR 8.1395% CI 7.25–9.12· 297 reports

Glomerular Injury / Proteinuria

ROR 5.1595% CI 4.64–5.72· 356 reports

Acute Tubular Necrosis

ROR 4.6095% CI 3.81–5.56· 108 reports

Hypertension

ROR 2.4095% CI 2.30–2.50· 2,167 reports

Electrolyte Disturbance

ROR 2.1995% CI 2.05–2.33· 995 reports

Fanconi Syndrome

ROR 2.1995% CI 1.50–3.20· 27 reports

SIADH / Hyponatremia

ROR 1.6695% CI 1.49–1.85· 321 reports

Hemorrhagic Cystitis

ROR 1.5095% CI 1.32–1.70· 250 reports

Acute Interstitial Nephritis

ROR 1.4495% CI 1.13–1.84· 65 reports

Crystal / Obstructive Nephropathy

ROR 1.4495% CI 1.25–1.66· 193 reports

FAERS outcomes & reporting trend· 21.5% of reports w/ death · 30% w/ hospitalization

21.5%

Reported with a death outcome

10,868 of 50,589 reports

30%

Reported with hospitalization

15,177 of 50,589 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 50,589 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 1.9395% CI 1.79–2.08· 702 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Gastrointestinal

Diarrhoea4,073Stomatitis3,189Nausea2,854Vomiting2,139Abdominal Pain1,178

General / constitutional

Fatigue3,811Pyrexia2,142Weight Decreased1,938Asthenia1,901Malaise1,881

Respiratory

Dyspnoea2,637Cough1,895Pneumonitis1,207

Metabolic & electrolyte

Decreased Appetite2,125Dehydration1,089

Skin

Rash1,978

Immune / infection

Pneumonia1,705

Blood & lymphatic

Anaemia1,450

Nervous system

Headache1,366

Guidelines & consensus· 13

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.

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 Everolimus 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

Temsirolimus

Torisel · mTOR inhibitor

Profile

Proteinuria and glomerular effects; less firmly quantified than everolimus.

GLOMLYTE

Mild#1 · 71% phenotype match

Sorafenib

Nexavar · VEGFR TKI

Profile

Anti-angiogenic hypertension and proteinuria; occasional TMA.

HTNGLOMTMA

Moderate#2 · 69% phenotype match

mTOR inhibitors (everolimus · temsirolimus)

mTOR inhibitor

Profile

Podocyte injury → proteinuria and FSGS.

GLOMATNTMA

Mild#3 · 61% phenotype match

Pazopanib

Votrient · VEGFR TKI

Profile

VEGFR-TKI; hypertension, proteinuria, TMA.

GLOMHTNTMA

Moderate#4 · 57% phenotype match

Axitinib

Inlyta · VEGFR TKI

Profile

Potent VEGFR-TKI; hypertension and proteinuria dominate.

HTNGLOMTMA

Moderate#5 · 57% phenotype match

Bortezomib

Velcade · Proteasome inhibitor

Profile

Rare TMA; reverses myeloma cast nephropathy.

TMAGLOM

Moderate#6 · 56% phenotype match

Compare Everolimus 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 mTOR 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.

1TemsirolimusGLOM — Glomerular Injury / ProteinuriaMild
2mTOR inhibitors (everolimus · temsirolimus)GLOM — Glomerular Injury / ProteinuriaMild
3SirolimusGLOM — Glomerular Injury / ProteinuriaFAERS AKIModerate
4Everolimus· this agentGLOM — Glomerular Injury / ProteinuriaFAERS AKIModerate

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 Everolimus’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 Everolimus; 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 201 clinical records among the 300 most-relevant of 620 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.