Is kidney injury from Interleukin-2 (high-dose) reversible?

Reversible. Typical onset: Acute — during the treatment cycle..

How should kidney function be monitored during Interleukin-2 (high-dose) therapy?

Daily (often twice-daily) serum creatinine and BUN during each inpatient high-dose IL-2 cycle, with dose-hold thresholds defined in advance (e.g., creatinine >4-4.5 mg/dL or progressive oliguria); Strict hourly intake/output and daily weights to track capillary-leak-driven intravascular volume depletion, third-spacing, and oliguria; Continuous blood pressure/hemodynamic monitoring (frequently ICU/step-down level) to detect the hypotension that drives prerenal azotemia; Electrolytes including potassium, bicarbonate, magnesium, and phosphate, plus acid-base status, given fluid shifts and pressor/fluid management; Confirm recovery of creatinine toward baseline before initiating the next cycle, and reassess cumulative renal reserve before re-treatment.

How can kidney injury from Interleukin-2 (high-dose) be prevented?

Careful fluid / hemodynamic management

Who is at higher risk of kidney injury from Interleukin-2 (high-dose)?

Pre-existing CKD; Hypotension; Concurrent nephrotoxins.

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Printable monograph

Cytokine

Interleukin-2 (high-dose)

Proleukin · IL-2

Cytokine · approved 1992 · 10 citations · FAERS AKI reporting ROR 4.95 (95% CI 3.65–6.71, 43 AKI reports)

Dated evidence· through 2011Teaching classic· capillary-leak prerenal AKI

The archetype of hemodynamic, capillary-leak acute kidney injury: high-dose interleukin-2 drives a systemic vascular-leak syndrome with hypotension and prerenal azotemia. Largely displaced by checkpoint inhibitors, it remains the canonical teaching case for cytokine-driven prerenal injury — a conceptual forerunner of CAR-T cytokine-release-associated AKI.

Deeply sourced7/9 · 6 signals

Met: 10 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 24y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Not met: Current through 2011
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.

Capillary leak drains the circulation — the kidney starves, then recovers.

ModerateCytokine immunotherapy

Metastatic melanomaRenal cell

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Oliguria / prerenal AKI is very common during therapy at high dose — but reversible.Source: Belldegrun et al., Ann Intern Med 1987

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Acute AKI during the treatment cycle.

Distilled from: “Acute — during the treatment cycle.”

§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.

Prerenal / Hemodynamic AKI#1 · Signaturequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Electrolyte DisturbanceRarequalitative — no citable incidence
Hypomagnesemia and hypophosphatemia reported across high-dose IL-2 trials.
SIADH / HyponatremiaRarequalitative — no citable incidence
A case report with high-dose bolus IL-2 monotherapy.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityModerate

ReversibilityReversible

Evidence10 citations

Nephron map

Vasculature / Endothelium

Distal Tubule / Collecting Duct

Prerenal / Hemodynamic AKI

Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

§03

Kidney injury

Mechanism of kidney injury

Vascular (capillary) leak syndrome depletes the intravascular volume and drops blood pressure, starving renal perfusion (prerenal); secondary cytokines add an intrinsic component with a reduced filtration fraction.

Clinical presentation

Oliguria, hypotension, weight gain and edema with a rising BUN/creatinine and a very low fractional excretion of sodium during treatment.

Management

Dose-hold, hemodynamic support (judicious fluids/pressors), supportive care.Lesion-level management framework

Risk factors

Pre-existing CKD
Hypotension
Concurrent nephrotoxins

Prevention

Careful fluid / hemodynamic management

Anticancer mechanism· how it treats cancer

Recombinant aldesleukin stimulates T-cell and NK proliferation for anti-tumor immunity. Metastatic melanoma and renal cell carcinoma.

Note · Reversibility is the key teaching point — typically resolves within a dose-hold.

§04

Clinical depth

Renal dose adjustment

No formal CrCl-based dose reduction is defined; high-dose aldesleukin (600,000 IU/kg IV q8h x up to 14 doses per cycle) is dosed by weight, but the label mandates withholding doses for nephrotoxicity. Treatment is contraindicated/should not be initiated with significant baseline renal impairment, and a held dose is generally not made up. In practice individual doses are skipped (not reduced) when serum creatinine rises (commonly >4-4.5 mg/dL) or oliguria/hypotension develops, with the next cycle deferred until renal function recovers.

Dialyzability & ESKD dosing

Not applicable in the usual sense — high-dose IL-2 nephrotoxicity is a transient prerenal/hemodynamic AKI that resolves with drug discontinuation and volume resupport, so renal replacement therapy is rarely required. Dialyzability of aldesleukin itself is not clinically relevant given its short half-life and the reversible nature of the injury; data in established ESKD/hemodialysis patients are essentially absent and high-dose IL-2 is generally avoided in dialysis-dependent patients.

Differential diagnosis

High-dose IL-2 AKI is overwhelmingly prerenal/hemodynamic from capillary (vascular) leak syndrome causing intravascular volume depletion and hypotension, so it should show a bland sediment, low FeNa, and rapid reversal with volume/pressor support and drug cessation. Distinguish from true acute tubular necrosis (which would not reverse as quickly and may follow prolonged hypotension), from concurrent nephrotoxins (contrast, NSAIDs, aminoglycosides) given for the febrile/septic-appearing picture, and from sepsis itself, since IL-2 induces a SIRS-like state that can mimic septic shock.

Monitoring

Daily (often twice-daily) serum creatinine and BUN during each inpatient high-dose IL-2 cycle, with dose-hold thresholds defined in advance (e.g., creatinine >4-4.5 mg/dL or progressive oliguria)
Strict hourly intake/output and daily weights to track capillary-leak-driven intravascular volume depletion, third-spacing, and oliguria
Continuous blood pressure/hemodynamic monitoring (frequently ICU/step-down level) to detect the hypotension that drives prerenal azotemia
Electrolytes including potassium, bicarbonate, magnesium, and phosphate, plus acid-base status, given fluid shifts and pressor/fluid management
Confirm recovery of creatinine toward baseline before initiating the next cycle, and reassess cumulative renal reserve before re-treatment

Key trials & series

Fyfe 1995 (J Clin Oncol pooled analysis of 255 metastatic RCC patients): established durable responses to high-dose IL-2 and characterized its severe but largely reversible toxicity profile, including hypotension and reversible renal dysfunction from capillary leak
Atkins 1999 (high-dose IL-2 pooled metastatic melanoma analysis): documented durable complete responses alongside the expected reversible organ toxicities including oliguria/azotemia requiring intensive supportive care
SELECT trial (prospective high-dose IL-2 in metastatic RCC, Clin Cancer Res): contemporary safety/efficacy series reaffirming that renal and hemodynamic toxicities are manageable and reversible with modern supportive protocols

Clinical pearls

Oliguria and a rising creatinine are expected, anticipated, dose-limiting toxicities — they trigger holding doses rather than abandoning therapy, and renal function typically recovers between cycles
Aggressive crystalloid resuscitation is double-edged: fluids support renal perfusion but worsen pulmonary/peripheral edema from capillary leak, so management balances vasopressors (e.g., low-dose pressors) against volume
Avoid stacking nephrotoxins — hold NSAIDs, aminoglycosides, and elective iodinated contrast during high-dose IL-2 cycles, since added insults can convert reversible prerenal azotemia into established ATN
Baseline cardiac, pulmonary, and renal reserve must be adequate before high-dose IL-2; patients with pre-existing CKD or borderline function tolerate the hemodynamic stress poorly and are generally excluded
High-dose IL-2 trials repeatedly report hypomagnesemia and hypophosphatemia — an electrolyte lesion in its own right, beyond the capillary-leak prerenal picture.
SIADH is reported with high-dose bolus IL-2 monotherapy, coherent with its water-retentive capillary-leak physiology.

Beyond the kidney — non-renal toxicities· 2 organ systems

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

Immune / Infusion

CRS, infusion reactions, irAEs, anaphylaxis

Flu-like syndrome, capillary leak (IL-2)

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

Depression, fatigue (interferon)

§05

References

7 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

7 references · 1987–2011 · 2 since 2009

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.

CaseC · LimitedAcute tubular necrosis after interleukin-2 therapy.Nzerue MC · Cent Afr J Med 1993 · PMID 8020090Case of acute renal tubular necrosis complicating IL-2 immunotherapy for metastatic renal cell cancer, reversible with aggressive fluid replacement, dopamine, and cautious diuresis.CaseC · LimitedInterstitial nephritis in a patient receiving adoptive immunotherapy with recombinant interleukin-2 and lymphokine-activated killer cells.Feinfeld DA et al. · Am J Nephrol 1991 · PMID 1819216First reported case of autopsy-confirmed acute interstitial nephritis (T-lymphocyte renal infiltrate with tubulitis) during recombinant IL-2/LAK immunotherapy, with acute renal failure out of proportion to reduced renal perfusion.CaseC · Limited[Acute renal failure associated with immunotherapy for metastatic cancer].Morales J et al. · Rev Med Chil 1994 · PMID 7597341Case report of acute renal failure occurring with IL-2 plus interferon-gamma immunotherapy for metastatic cancer.

FDA label — boxed warning & renal dosing· boxed warning

Quoted verbatim from this agent's current FDA label (Dec 2024) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: CAPILLARY LEAK SYNDROME (CLS), NEUROLOGIC TOXICITIES and SERIOUS INFECTIONS Capillary leak syndrome (CLS), including life threatening or fatal reactions, has occurred in patients treated with Proleukin. Do not administer Proleukin to patients with significant cardiac, pulmonary, renal, and hepatic impairment. Administer Proleukin in a hospital setting with an intensive care facility. Withhold or discontinue Proleukin as recommended [see Dosage and Administration (2.4) , Contraindications (4) , Warnings and Precautions (5.1) ] . Neurologic toxicities, which may be life-threatening or result in coma or permanent neurological deficits, have occurred in patients treated with Proleukin. Withhold or discontinue Proleukin as recommended [see Dosage and Administration (2.4) , Warnings and Precautions (5.2) ] . Serious Infections including sepsis and bacterial endocarditis have occurred in patients treated with Proleukin. Treat pre-existing bacterial infections prior to initiation of Proleukin therapy and withhold Proleukin as recommended [see Dosage and Administration (2.4) , Warnings and Precautions (5.3) ] . WARNING: CAPILLARY LEAK SYNDROME (CLS), NEUROLOGIC TOXICITY, AND SERIOUS INFECTIONS See full prescribing information for complete boxed warning. Capillary Leak Syndrome (CLS) including life-threatening or fatal reactions, has occurred in patients treated with Proleukin.…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 1,231 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· 5 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

Electrolyte Disturbancecorroborated · ROR 7.76 — on the terms that name the lesion (ROR 11.13)
SIADH / Hyponatremiacorroborated · ROR 6.92 — on the terms that name the lesion (ROR 5.03)
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Thrombotic Microangiopathy

ROR 8.8695% CI 4.42–17.75· 8 reports

Electrolyte Disturbance

ROR 7.7695% CI 6.20–9.71· 82 reports

SIADH / Hyponatremia

ROR 6.9295% CI 4.87–9.84· 32 reports

Fanconi Syndrome

ROR 6.6695% CI 1.66–26.66· 2 reports

Hypertension

ROR 1.9395% CI 1.43–2.62· 43 reports

FAERS outcomes & reporting trend· 16.8% of reports w/ death · 48.9% w/ hospitalization

16.8%

Reported with a death outcome

207 of 1,231 reports

48.9%

Reported with hospitalization

602 of 1,231 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 1,231 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 4.9595% CI 3.65–6.71· 43 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 Injury43

General / constitutional

Pyrexia148Fatigue66Chills62Pain61

Respiratory

Dyspnoea65Hypoxia54Pulmonary Oedema40Pleural Effusion39Respiratory Failure39

Gastrointestinal

Diarrhoea82Vomiting71Nausea69

Blood & lymphatic

Thrombocytopenia83Febrile Neutropenia51Anaemia46Pancytopenia37

Vascular

Hypotension111

Cardiac

Atrial Fibrillation48Tachycardia46

Immune / infection

Sepsis42Pneumonia38

Metabolic & electrolyte

Dehydration38

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 Interleukin-2 (high-dose) 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

Selinexor

Xpovio · XPO1 (nuclear export) inhibitor

Profile

Hyponatremia is common and dose-limiting.

SIADHLYTEPRE

Moderate#1 · 75% phenotype match

Catumaxomab

Removab · Trifunctional bispecific (EpCAM×CD3)

Profile

Intraperitoneal; cytokine-release- and ascites/paracentesis-driven prerenal AKI; withdrawn (EU) 2017.

PRELYTE

Moderate#2 · 71% phenotype match

Vinflunine

Javlor · Vinca alkaloid

Profile

Used because of renal impairment (cisplatin-unfit urothelial); CrCl-based dose bands; watch SIADH/hyponatremia.

LYTEPRESIADH

Mild#3 · 70% phenotype match

Loncastuximab tesirine

Zynlonta · Antibody-drug conjugate (CD19/PBD)

Profile

Capillary-leak-type edema, effusions and AKI.

PRELYTE

Moderate#4 · 70% phenotype match

Capivasertib

Truqap · AKT inhibitor

Profile

2023 breast-cancer AKT inhibitor; AKI with diarrhea/hyperglycemia.

PRELYTE

Moderate#5 · 70% phenotype match

Afamitresgene autoleucel (Afami-cel)

Tecelra · MAGE-A4 TCR-T cell therapy

Profile

First TCR-T cell therapy for a solid tumor; CRS-associated hemodynamic AKI.

PRELYTE

Moderate#6 · 70% phenotype match

Compare Interleukin-2 (high-dose) 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 Cytokines & enzymes

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.

1AsparaginasePRE — Prerenal / Hemodynamic AKIMild
2PegaspargasePRE — Prerenal / Hemodynamic AKIFAERS AKIMild
3TasonerminPRE — Prerenal / Hemodynamic AKIModerate
4Interleukin-2 (high-dose)· this agentPRE — Prerenal / Hemodynamic AKIFAERS AKIModerate
5Interferon-αGLOM — Glomerular Injury / ProteinuriaSevere

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 Interleukin-2 (high-dose)’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 Interleukin-2 (high-dose); 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 103 clinical records among the 300 most-relevant of 510 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.