What kind of kidney injury does Copanlisib cause?

Hypertension — Raised blood pressure — archetypally on-target loss of endothelial nitric oxide from VEGF-pathway blockade, studied as a pharmacodynamic marker of drug exposure. Other agents raise it too: vascular effects of BCR-ABL, BTK and RET inhibitors and of copanlisib; abiraterone's mineralocorticoid excess; androgen suppression or blockade.

Is kidney injury from Copanlisib reversible?

Reversible. Typical onset: Acute and infusion-bound — within hours of each dose, resolving within ~24 h..

How should kidney function be monitored during Copanlisib therapy?

Blood pressure before, during and after each infusion (treatment day); Fasting glucose before each infusion; post-infusion glucose if diabetic; CBC each cycle.

How can kidney injury from Copanlisib be prevented?

Confirm BP <140/90 before each infusion and treat hypertension proactively Optimize fasting glucose before dosing Hold or reduce dose for grade 3+ hypertension or hyperglycemia per label

Who is at higher risk of kidney injury from Copanlisib?

Pre-existing hypertension or diabetes; Inadequate pre-infusion blood-pressure/glucose control; Concurrent agents raising BP or glucose (e.g. steroids); Baseline CKD.

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Printable monograph

Pan-PI3K inhibitor

Copanlisib

Aliqopa · COP

Pan-PI3K inhibitor · approved 2017 · 6 citations

Aging evidence· through 2021

Fairly sourced4/9 · 4 signals

Met: 6 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 7y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Not met: Current through 2021
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.

IV pan-PI3K inhibitor with reproducible transient infusion-related hypertension and hyperglycemia — a vascular/metabolic signature rather than a structural nephropathy.

ModerateIntermittent intravenous PI3K inhibitor

Relapsed follicular lymphoma (>=2 prior systemic therapies)Relapsed indolent B-cell lymphoma (with rituximab; CHRONOS-3)

§01

Signature kidney injury

Signature lesion

Hypertension

Representative incidence29.6%

On monotherapy (CHRONOS-1), transient on-infusion-day hypertension occurs in 29.6% all-grade (grade 3 23.9%), and hyperglycemia in 50.0% all-grade (grade 3 33.1%, grade 4 7.0%); with rituximab (CHRONOS-3) the grade 3-4 rates are higher — hypertension 40% and hyperglycemia 56%. Both peak within hours of the infusion and largely resolve by the next day. Sustained renal injury is uncommon.Source: Dreyling et al., Am J Hematol 2020 (CHRONOS-1; 50.0% all-grade transient hyperglycemia, grade 3 33.1% — an on-target metabolic effect, not renal injury); Matasar et al., Lancet Oncol 2021 (CHRONOS-3; grade 3-4 hyperglycemia 56%, hypertension 40%)

Onset & rechallenge

Time to injuryHyperacute (<24 h)

Infusion-bound — within hours of each dose, resolving within ~24 h.

Distilled from: “Acute and infusion-bound — within hours of each dose, resolving within ~24 h.”

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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.

Hypertension#1 · Signaturequalitative — no citable incidence
Raised blood pressure — archetypally on-target loss of endothelial nitric oxide from VEGF-pathway blockade, studied as a pharmacodynamic marker of drug exposure. Other agents raise it too: vascular effects of BCR-ABL, BTK and RET inhibitors and of copanlisib; abiraterone's mineralocorticoid excess; androgen suppression or blockade.

§03

Kidney injury

Mechanism of kidney injury

PI3K-alpha inhibition transiently impairs endothelial nitric-oxide signaling and insulin-mediated glucose handling, producing a sharp, infusion-day spike in blood pressure and glucose. The hypertension is a hemodynamic/vascular phenomenon; the hyperglycemia is on-target insulin resistance. Both resolve as drug levels fall, so the kidney is exposed to a transient pressure and osmotic load rather than a fixed structural lesion. Severe uncontrolled hypertension or marked hyperglycemia could theoretically contribute to hemodynamic AKI.

Clinical presentation

Predictable blood-pressure rise (often peaking ~2-5 h post-infusion) and hyperglycemia on each treatment day, both typically normalizing by the following morning; symptomatic patients may report headache or flushing. Persistent renal dysfunction is unusual.

Management

Manage the acute hypertensive episode with antihypertensives and the hyperglycemia with short-acting agents/insulin as needed; both usually self-resolve before the next cycle. Optimize baseline BP and glucose between cycles. Dose-interrupt or reduce for recurrent grade 3+ events. Sustained AKI is rare and managed supportively.Lesion-level management framework

Risk factors

Pre-existing hypertension or diabetes
Inadequate pre-infusion blood-pressure/glucose control
Concurrent agents raising BP or glucose (e.g. steroids)
Baseline CKD

Prevention

Confirm BP <140/90 before each infusion and treat hypertension proactively
Optimize fasting glucose before dosing
Hold or reduce dose for grade 3+ hypertension or hyperglycemia per label

Anticancer mechanism· how it treats cancer

Intravenous pan-class-I PI3K inhibitor with predominant activity against the alpha and delta isoforms. Intermittent IV dosing blocks PI3K/AKT signaling in follicular and other indolent B-cell lymphomas.

Note · The renal-relevant toxicities (hypertension, hyperglycemia) are transient and infusion-bound rather than a direct structural kidney lesion; the cited incidence figures are real and quantified.

§04

Clinical depth

Renal dose adjustment

No specific dose adjustment for renal impairment in labeling; hepatic metabolism predominates. Dose modification is driven by hypertension, hyperglycemia and cytopenias rather than GFR.

Dialyzability & ESKD dosing

Protein-bound IV agent given intermittently; not expected to be dialyzable, and ESKD dosing is not established.

Differential diagnosis

Distinguish the transient, predictable infusion-day BP/glucose spikes from sustained essential hypertension, from other VEGF-pathway hypertension, and from genuine structural AKI (which would persist between cycles).

Monitoring

Blood pressure before, during and after each infusion (treatment day)
Fasting glucose before each infusion; post-infusion glucose if diabetic
CBC each cycle

Key trials & series

CHRONOS-3 (Matasar, Lancet Oncol 2021) — copanlisib + rituximab, the registrational combination dataset
CHRONOS-1 (Dreyling, Am J Hematol 2020) — monotherapy safety quantifying the hyperglycemia/hypertension signal

Clinical pearls

Hyperglycemia and hypertension here are time-locked to the infusion and transient — a vascular/metabolic signature, not a fixed nephropathy.
Get BP under control before each dose; the infusion-day spike is anticipated and dose-limiting.
Persistent (between-cycle) renal dysfunction should prompt a search for an alternative cause.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Hypertension

§05

References

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

Evidence accrual

6 references · 2014–2021 · 3 since 2019

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.

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 Copanlisib 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

Ripretinib

Qinlock · KIT switch-control inhibitor

Profile

Hypertension and alopecia in GIST.

HTN

Mild#1 · 83% phenotype match

Leuprolide

Lupron · GnRH agonist

Profile

Metabolic syndrome; indirect renal risk.

HTN

Mild#2 · 81% phenotype match

Asciminib

Scemblix · BCR-ABL STAMP inhibitor

Profile

Hypertension and pancreatitis; allosteric BCR-ABL inhibitor.

HTNPRE

Mild#3 · 59% phenotype match

Enzalutamide

Xtandi · Androgen-receptor inhibitor

Profile

Hypertension; rare electrolyte effects.

HTNLYTE

Mild#4 · 57% phenotype match

Dinutuximab

Unituxin · Anti-GD2 antibody

Profile

Capillary-leak syndrome, hypertension and severe pain in neuroblastoma.

PREHTNTMA

Moderate#5 · 57% phenotype match

Ponatinib

Iclusig · BCR-ABL TKI

Profile

Vascular toxicity and hypertension.

HTNPRETMA

Moderate#6 · 54% phenotype match

Compare Copanlisib 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 PI3K / AKT 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.

1DuvelisibPRE — Prerenal / Hemodynamic AKIMild
2GedatolisibLYTE — Electrolyte DisturbanceMild
3IdelalisibPRE — Prerenal / Hemodynamic AKIMild
4Copanlisib· this agentHTN — HypertensionModerate
5CapivasertibPRE — Prerenal / Hemodynamic AKIModerate
6AlpelisibPRE — Prerenal / Hemodynamic AKIModerate
7InavolisibLYTE — Electrolyte DisturbanceFAERS 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.