What kind of kidney injury does Asparaginase cause?

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

How should kidney function be monitored during Asparaginase therapy?

Amylase/lipase and abdominal symptoms (pancreatitis); Fibrinogen and antithrombin III; signs of thrombosis; Ammonia if encephalopathy; glucose, triglycerides, LFTs; Creatinine/volume status with any complication; Signs of hypersensitivity reaction.

How can kidney injury from Asparaginase be prevented?

Supportive hydration and prompt management of complications Thrombosis prophylaxis and antithrombin repletion per protocol

Who is at higher risk of kidney injury from Asparaginase?

Asparaginase-induced pancreatitis; Hypersensitivity reactions with hypotension; Thrombotic complications and acquired coagulopathy (low antithrombin III); Hyperammonemia/metabolic stress.

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Printable monograph

Enzyme

Asparaginase

Elspar · ASNase

Enzyme · approved 1978 · 6 citations

Up to date· through 2025

Fairly sourced6/9 · 5 signals

Met: 6 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 43y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Met: Current through 2025
Not 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 enzyme therapy whose rare AKI is downstream of pancreatitis and hemodynamic complications.

MildEnzyme (asparagine depletion)

Acute lymphoblastic leukemiaLymphoblastic lymphoma

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Direct asparaginase nephrotoxicity is uncommon; classic toxicities are hypersensitivity (up to ~30% with E. coli-derived enzyme), pancreatitis, hepatic dysfunction, hyperammonemia, and coagulopathy/thrombosis. When AKI occurs it is typically secondary to pancreatitis, hemodynamic instability, or thrombotic complications rather than a direct tubular toxin, and is not well quantified.Source: Hijiya & van der Sluis, Leuk Lymphoma 2016

Onset & rechallenge

Time to injuryVariable / unpredictable

Renal injury is tied to intercurrent complications arising during induction/intensification therapy, with no defined onset window.

Distilled from: “Linked to intercurrent complications during induction/intensification therapy.”

§02

Renal toxicities, ranked

This agent's defining kidney lesion — its #1 signature. 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.

§03

Kidney injury

Mechanism of kidney injury

No characteristic direct renal toxin effect. Severe asparaginase-induced pancreatitis (third-spacing, SIRS, shock) or thrombotic events (the enzyme depletes antithrombin III, fibrinogen, and plasminogen) can compromise renal perfusion, producing prerenal/ischemic injury; coagulopathy may rarely contribute to renal vascular events.

Clinical presentation

When present, AKI accompanies pancreatitis or hemodynamic compromise: rising creatinine, oliguria, and volume disturbance with an otherwise bland renal picture. Watch for abdominal pain (pancreatitis), thrombosis (including cerebral sinus), and encephalopathy (hyperammonemia).

Management

Treat the underlying complication (pancreatitis, anaphylaxis/shock, thrombosis, hyperammonemia) and support renal perfusion with fluids; prerenal AKI usually reverses with resolution. Discontinue or switch asparaginase formulation for severe toxicity.Lesion-level management framework

Risk factors

Asparaginase-induced pancreatitis
Hypersensitivity reactions with hypotension
Thrombotic complications and acquired coagulopathy (low antithrombin III)
Hyperammonemia/metabolic stress

Prevention

Supportive hydration and prompt management of complications
Thrombosis prophylaxis and antithrombin repletion per protocol

Anticancer mechanism· how it treats cancer

Bacterial enzyme that hydrolyzes circulating asparagine (and some glutamine), starving leukemic lymphoblasts that lack asparagine synthetase and cannot synthesize it. Cornerstone of acute lymphoblastic leukemia (ALL) and lymphoblastic lymphoma regimens.

Note · Rare AKI, predominantly pancreatitis-, thrombosis-, and hemodynamics-mediated; not a direct nephrotoxin and not renally cleared.

§04

Clinical depth

Renal dose adjustment

Large protein cleared by reticuloendothelial proteolysis, not renal filtration - no renal dose adjustment. Management is toxicity-driven (hold/switch for pancreatitis, severe hypersensitivity, or thrombosis).

Dialyzability & ESKD dosing

Large enzyme; not dialyzable. Dialysis/CRRT is used to support AKI or refractory hyperammonemia, not to clear the drug.

Differential diagnosis

Pancreatitis- or sepsis-driven prerenal/ischemic AKI vs thrombotic vascular events vs tumor lysis at induction. The accompanying pancreatitis, coagulopathy, or thrombosis points away from a primary renal lesion.

Monitoring

Amylase/lipase and abdominal symptoms (pancreatitis)
Fibrinogen and antithrombin III; signs of thrombosis
Ammonia if encephalopathy; glucose, triglycerides, LFTs
Creatinine/volume status with any complication
Signs of hypersensitivity reaction

Key trials & series

Pediatric ALL backbone regimens (e.g. COG/Berlin-Frankfurt-Munster protocols) defining the asparaginase toxicity profile

Clinical pearls

Asparaginase rarely touches the kidney directly - look for pancreatitis, thrombosis, or shock as the cause of AKI.
It depletes antithrombin III and fibrinogen, so its renal/vascular risk is thrombotic as much as hemodynamic.
Because clearance is proteolytic, no renal dose adjustment is needed.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Prerenal / Hemodynamic AKI

§05

References

6 primary references — trials, cohorts, mechanism, and reviews. Citation metadata via PubMed / NLM.

Evidence accrual

6 references · 1982–2025 · 3 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.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 309 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.
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 outcomes & reporting trend· 6.1% of reports w/ death · 31.7% w/ hospitalization

6.1%

Reported with a death outcome

19 of 309 reports

31.7%

Reported with hospitalization

98 of 309 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 309 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 0.8995% CI 0.22–3.58· 2 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Gastrointestinal

Nausea24Pancreatitis18Vomiting17

Immune / infection

Hypersensitivity21Anaphylactic Reaction12Stomatococcal Infection9Drug Hypersensitivity7Sepsis6

Blood & lymphatic

Febrile Neutropenia25Neutropenia15Thrombocytopenia6

Skin

Urticaria17Rash16Skin Candida10

General / constitutional

Pyrexia9Fatigue5

Vascular

Haemorrhage6

Metabolic & electrolyte

Decreased Appetite5

Nervous system

Headache5

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 Asparaginase 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

Belzutifan

Welireg · HIF-2α inhibitor

Profile

Anemia/hypoxia; emerging renal profile in VHL/RCC.

PRE

Mild#1 · 89% phenotype match

Dacarbazine

DTIC · Alkylator

Profile

Rare hepatic veno-occlusive disease; minimal direct renal injury.

PRE

Mild#2 · 89% phenotype match

Eribulin

Halaven · Microtubule inhibitor

Profile

Reduced clearance in renal impairment.

PRE

Mild#3 · 89% phenotype match

Irinotecan

Camptosar · Topoisomerase I inhibitor

Profile

Diarrhea-driven prerenal AKI.

PRE

Mild#4 · 89% phenotype match

Mirvetuximab soravtansine

Elahere · Antibody-drug conjugate (FRα/DM4)

Profile

Ocular toxicity dominates; renal involvement indirect/case-level (GI volume loss).

PRE

Mild#5 · 89% phenotype match

Nilotinib

Tasigna · BCR-ABL TKI

Profile

eGFR decline over time.

PRE

Mild#6 · 89% phenotype match

Compare Asparaginase 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.

1Asparaginase· this agentPRE — Prerenal / Hemodynamic AKIMild
2PegaspargasePRE — Prerenal / Hemodynamic AKIFAERS AKIMild
3TasonerminPRE — Prerenal / Hemodynamic AKIModerate
4Interleukin-2 (high-dose)PRE — 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 Asparaginase’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 Asparaginase; 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 12 clinical records among all 20 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.