What kind of kidney injury does Lanreotide cause?

Electrolyte Disturbance — Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia). Other reported patterns: Prerenal / Hemodynamic AKI.

How should kidney function be monitored during Lanreotide therapy?

Serum electrolytes and volume status, especially with diarrhea; Blood glucose (altered insulin/glucagon secretion); Gallbladder/biliary status with chronic use; Renal function in advanced CKD to gauge exposure.

How can kidney injury from Lanreotide be prevented?

Recognize kidney-neutral profile; routine renal-specific prophylaxis not required at normal function Account for increased exposure in severe renal impairment Maintain euvolemia and replace losses in patients with diarrhea

Who is at higher risk of kidney injury from Lanreotide?

Severe chronic kidney disease or dialysis (reduced clearance/increased exposure); Volume depletion from secretory diarrhea; Baseline electrolyte derangement from functioning tumors.

Back to explorer

Printable monograph

Somatostatin analog

Lanreotide

Somatuline · LAN

Somatostatin analog · approved 2007 · 6 citations

Dated evidence· through 2018

Fairly sourced6/9 · 5 signals

Met: 6 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 19y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Not met: Current through 2018
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.

Long-acting somatostatin analog for GEP-NETs; generally kidney-neutral with only mild electrolyte effects and reduced clearance in severe renal impairment.

Mildestablished

Unresectable/locally advanced or metastatic well- or moderately-differentiated, nonfunctioning or functioning gastroenteropancreatic neuroendocrine tumors (GEP-NETs)Carcinoid syndrome symptom controlAcromegaly

§01

Signature kidney injury

Signature lesion

Electrolyte Disturbance

No characteristic intrinsic nephrotoxicity; lanreotide is generally kidney-neutral. Renal adverse events are not a defining feature and are not reliably quantified; mild electrolyte effects are uncommon.Source: Caplin et al., NEJM 2014 (CLARINET; diarrhea-dominant, kidney-neutral)

Onset & rechallenge

Time to injuryVariable / unpredictable

No intrinsic renal injury is described; exposure rises gradually in renal impairment without a defined onset.

Distilled from: “Not applicable for intrinsic injury; exposure rises gradually in renal impairment.”

§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.

Electrolyte Disturbance#1 · Signaturequalitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).
Prerenal / Hemodynamic AKISecondaryqualitative — 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

Lanreotide has no established direct nephrotoxic mechanism. Renal relevance is pharmacokinetic: the drug is partly renally eliminated, so systemic exposure increases and clearance falls in moderate-to-severe renal impairment, but this reflects accumulation rather than tubular/glomerular injury. Antisecretory hormonal actions can rarely contribute to mild electrolyte or glycemic shifts. In the CLARINET pivotal trial the dominant adverse event was diarrhea, not kidney injury.

Clinical presentation

Usually no renal findings. When relevant, presentation is mild: occasional electrolyte or glucose disturbance from hormonal effects, or volume-related changes secondary to GI symptoms (diarrhea). Severe renal impairment manifests as increased drug exposure rather than new kidney pathology.

Management

No renal-specific management is generally required. In significant renal impairment, anticipate higher exposure and monitor for dose-related adverse effects. Manage electrolyte/glucose changes supportively; treat underlying tumor.Lesion-level management framework

Risk factors

Severe chronic kidney disease or dialysis (reduced clearance/increased exposure)
Volume depletion from secretory diarrhea
Baseline electrolyte derangement from functioning tumors

Prevention

Recognize kidney-neutral profile; routine renal-specific prophylaxis not required at normal function
Account for increased exposure in severe renal impairment
Maintain euvolemia and replace losses in patients with diarrhea

Anticancer mechanism· how it treats cancer

Cyclic octapeptide somatostatin analog with high affinity for SSTR2 (and SSTR5) that suppresses secretion of growth hormone and gut/pancreatic hormones and exerts a direct antiproliferative effect on well-differentiated neuroendocrine tumors, prolonging progression-free survival in enteropancreatic NETs.

Note · Reported use of lanreotide (with everolimus) in a hemodialysis patient with metastatic carcinoid supports feasibility in advanced renal failure with appropriate caution.

§04

Clinical depth

Renal dose adjustment

Exposure increases with the degree of renal impairment; some labeling recommends a reduced starting dose in moderate-to-severe renal impairment for certain indications. Consult product information for the specific formulation and indication.

Dialyzability & ESKD dosing

Not established as meaningfully dialyzable for supplemental dosing; depot peptide pharmacology and case experience suggest cautious use in hemodialysis without routine post-dialysis supplementation.

Differential diagnosis

Electrolyte or volume disturbance in a NET patient on lanreotide more likely reflects secretory diarrhea or paraneoplastic hormone effects than a primary tubular lesion; consider concomitant nephrotoxins (e.g., everolimus, contrast) before attributing AKI to lanreotide.

Monitoring

Serum electrolytes and volume status, especially with diarrhea
Blood glucose (altered insulin/glucagon secretion)
Gallbladder/biliary status with chronic use
Renal function in advanced CKD to gauge exposure

Key trials & series

CLARINET (Caplin et al., NEJM 2014): lanreotide Autogel 120 mg prolonged PFS vs placebo in metastatic enteropancreatic NETs; most common adverse event diarrhea, not nephrotoxicity
Hemodialysis case of everolimus + lanreotide for metastatic atypical bronchial carcinoid (Brizzi et al., BMC Cancer 2018)

Clinical pearls

Mild electrolyte/glucose effects derive from broad antisecretory hormonal action.
Feasible in hemodialysis with caution per case reports.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Distal Tubule / Collecting Duct

Fine-tuning of Na, K, Mg, acid & water

Injury signatures

Electrolyte Disturbance Prerenal / Hemodynamic AKI

§05

References

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

Evidence accrual

6 references · 1999–2018 · 3 since 2016

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.

FDA label — boxed warning & renal dosing· renal impairment

Quoted verbatim from this agent's current FDA label (Feb 2025) — not paraphrased or interpreted. Full label on DailyMed .

Renal impairment — from the label

Acromegaly Lanreotide has been studied in patients with end-stage renal function on dialysis, but has not been studied in patients with mild, moderate, or severe renal impairment. It is recommended that patients with moderate or severe renal impairment receive a starting dose of lanreotide of 60 mg. Caution should be exercised when considering patients with moderate or severe renal impairment for an extended dosing interval of Lanreotide Injection 120 mg every 6 or 8 weeks [see Dosage and Administration ( 2.1 ) and Clinical Pharmacology ( 12.3 )] . Neuroendocrine Tumors (NET) – Gastroenteropancreatic Neuroendocrine Tumors No effect was observed in total clearance of lanreotide in patients with mild to moderate renal impairment receiving Lanreotide Injection 120 mg. Patients with severe renal impairment were not studied [see Clinical Pharmacology ( 12.3 )] .

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 7,795 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· 4 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 1.5 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Crystal / Obstructive Nephropathy

ROR 3.8595% CI 3.08–4.80· 79 reports

Hypertension

ROR 2.8595% CI 2.58–3.16· 395 reports

SIADH / Hyponatremia

ROR 1.5195% CI 1.12–2.02· 45 reports

Electrolyte Disturbance

ROR 1.5095% CI 1.24–1.82· 106 reports

FAERS outcomes & reporting trend· 18.2% of reports w/ death · 20.3% w/ hospitalization

18.2%

Reported with a death outcome

1,422 of 7,795 reports

20.3%

Reported with hospitalization

1,586 of 7,795 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 7,795 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 0.5195% CI 0.35–0.73· 29 AKI reports ·AKI is reported less often than for other drugs (CI entirely below 1) — no disproportionate signal.

Gastrointestinal

Diarrhoea1,415Nausea725Abdominal Pain568Vomiting364Abdominal Pain Upper311

General / constitutional

Fatigue972Injection Site Pain596Malaise435Asthenia413Weight Decreased398

Nervous system

Headache502Dizziness414

Metabolic & electrolyte

Decreased Appetite277

Musculoskeletal

Arthralgia272

Respiratory

Dyspnoea246

Vascular

Hypertension229

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 Lanreotide 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

Darolutamide

Nubeqa · Androgen receptor inhibitor (ARSI)

Profile

Not nephrotoxic; exposure rises in severe renal impairment, so consider dose adaptation.

LYTEPRE

Mild#1 · 99% phenotype match

Octreotide

Sandostatin · Somatostatin analog

Profile

Kidney-neutral/possibly renoprotective; renally cleared, caution in severe CKD/dialysis.

LYTEPRE

Mild#2 · 98% phenotype match

Mitotane

Lysodren · Adrenolytic

Profile

Indirect: hypoadrenalism drives hyponatremia/prerenal; cisplatin nephrotoxicity in EDP-M.

LYTEPRE

Moderate#3 · 91% phenotype match

Glasdegib

Daurismo · Hedgehog (SMO) inhibitor

Profile

QT prolongation and muscle spasms; AML.

PRELYTE

Mild#4 · 88% phenotype match

Sevabertinib

Hyrnuo · HER2/EGFR TKI

Profile

2025 reversible HER2/EGFR TKI; profuse diarrhea (84-91%) → prerenal AKI, plus EGFR-pathway renal magnesium wasting.

PRELYTE

Mild#5 · 87% phenotype match

Gedatolisib

Revtorpyk · Pan-PI3K inhibitor

Profile

2026 IV pan-PI3K + mTORC1/2 (breast); on-target hyperglycemia and low-grade Na/K/Mg drift — creatinine up 14% vs 8% control, grade 3-4 rare.

LYTEPRE

Mild#6 · 87% phenotype match

Compare Lanreotide 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 Hormonal / endocrine

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 Lanreotide’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 Lanreotide; 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 18 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.