What kind of kidney injury does Ibandronate cause?

Acute Tubular Necrosis — Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate. Other reported patterns: Electrolyte Disturbance, Glomerular Injury / Proteinuria.

How should kidney function be monitored during Ibandronate therapy?

Serum calcium, phosphate and magnesium periodically; Volume/hydration status around infusion; 25-OH vitamin D (replete before starting to avoid hypocalcemia).

How can kidney injury from Ibandronate be prevented?

Adhere to recommended infusion times Dose-reduce or withhold in renal impairment per label

Who is at higher risk of kidney injury from Ibandronate?

High or rapidly infused IV dose; Pre-existing CKD; Volume depletion; Concurrent nephrotoxins (NSAIDs, aminoglycosides, contrast).

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Printable monograph

Bisphosphonate

Ibandronate

Boniva · Iband

Bisphosphonate · approved 2003 · 9 citations

Recent· through 2024

Deeply sourced7/9 · 6 signals

Met: 9 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 21y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2024
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.

The kidney-gentlest nitrogen bisphosphonate — renal events near placebo at standard doses.

MildNitrogen bisphosphonate

Metastatic bone disease (breast)Hypercalcemia of malignancyPost-menopausal osteoporosis

§01

Signature kidney injury

Signature lesion

Acute Tubular Necrosis

Representative incidence2%

Lower renal risk than zoledronate or pamidronate. In a 2-year phase III breast-cancer trial, adverse renal events with IV ibandronate were ~4% versus ~4.5% with placebo — essentially at background. Bisphosphonates as a class can cause toxic ATN (zoledronate) or collapsing FSGS (pamidronate), but ibandronate is the renal-safety outlier within the class. Reported rate: serum creatinine increase >=44.2 micromol/l in 2% — Women with breast cancer and bone metastases receiving intravenous ibandronate 6 mg every 3-4 weeks for up to 6 months,… (von 2008, PMID 18334511).Source: von Moos et al., Ann Oncol 2008 (serum creatinine rise >=44.2 micromol/l in 2/101; Jackson, Oncologist 2005 for the 4% vs 4.5% placebo comparison)

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Acute when it occurs (days), related to dose and infusion rate; antiresorptive electrolyte effects within the first days.

Distilled from: “Acute when it occurs (days), related to dose and infusion rate; antiresorptive electrolyte effects within the first days.”

§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.

Acute Tubular Necrosis#1 · Signaturequalitative — no citable incidence
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.
Electrolyte DisturbanceSecondary16%PMID 22627092 (opens PubMed in a new tab)
Hypocalcemia ~16% in pooled long-term IV bisphosphonate cohort (incl. ibandronate); grade 3 renal toxicity 0.7%
Glomerular Injury / ProteinuriaRarequalitative — no citable incidence
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

2%incidence

SeverityMild

ReversibilityReversible

Evidence9 citations

Nephron map

Glomerulus

Proximal TubuleBulk reabsorption + drug uptake (OCT2, OATs)

Distal Tubule / Collecting DuctFine-tuning of Na, K, Mg, acid & water

Acute Tubular Necrosis

Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.

§03

Kidney injury

Deep diveBisphosphonate nephrotoxicityThe intravenous bisphosphonates that protect bone in myeloma and metastatic cancer split the nephron between them — pamidronate poisons the podocyte and produces a collapsing FSGS with nephrotic-range proteinuria, while zoledronate poisons the proximal tubule and produces a toxic ATN — and both are dose- and infusion-rate-dependent, so the same monitoring that catches them also prevents them.

Mechanism of kidney injury

Bisphosphonates are filtered, not metabolized, and concentrate in the renal cortex; ~50–60% of an IV dose is renally excreted while the remainder binds bone. High peak tubular concentrations — driven by dose and infusion rate — produce dose-dependent toxic acute tubular necrosis of the proximal tubule (the zoledronate pattern), whereas slow pamidronate accumulation more often injures podocytes (collapsing FSGS). Ibandronate has high bone-binding avidity (~98% bone uptake even in dialysis patients) and is given at lower molar doses over recommended infusion times, so nephrotoxic tubular peaks are rarely reached and clinically significant injury is uncommon.

Clinical presentation

Usually no significant change in serum creatinine at standard dosing. When injury occurs it is a non-oliguric creatinine rise with bland or granular-cast urine consistent with ATN, sometimes accompanied by hypocalcemia, hypophosphatemia or hypomagnesemia from the antiresorptive effect.

Management

Withhold for renal-function decline, hydrate, and provide supportive care; injury is typically reversible. Correct co-existing hypocalcemia/hypophosphatemia. No specific antidote.Lesion-level management framework

Risk factors

High or rapidly infused IV dose
Pre-existing CKD
Volume depletion
Concurrent nephrotoxins (NSAIDs, aminoglycosides, contrast)

Prevention

Adhere to recommended infusion times
Dose-reduce or withhold in renal impairment per label

Anticancer mechanism· how it treats cancer

Nitrogen-containing bisphosphonate that inhibits farnesyl pyrophosphate synthase in the mevalonate pathway of osteoclasts, disrupting prenylation of small GTPases (Ras/Rho/Rac), impairing osteoclast cytoskeleton and survival and thereby suppressing bone resorption. Used for malignancy-associated bone disease, hypercalcemia of malignancy and post-menopausal osteoporosis.

§04

Clinical depth

Renal dose adjustment

Oral/IV for osteoporosis: no adjustment for CrCl ≥30 mL/min; not recommended (or use with caution) below 30 mL/min. Oncology IV dosing should be reduced and infused slowly in renal impairment; withhold for acute decline in renal function and reassess.

Dialyzability & ESKD dosing

Negligible plasma drug at steady state due to rapid bone uptake; not meaningfully dialyzed. In hemodialysis patients a reduced IV dose (e.g., 2 mg) given after dialysis achieves equivalent bone binding (Bergner 2005).

Differential diagnosis

Distinguish drug-related ATN from hypercalcemia-of-malignancy pre-renal AKI (which the bisphosphonate is treating) and from contrast or NSAID injury; collapsing FSGS with heavy proteinuria is classically the pamidronate pattern, but biopsy-proven collapsing FSGS/podocytopathy with nephrotic-range proteinuria has been reported rarely with ibandronate itself (PMIDs 26197890, 38383148), so it does not exclude ibandronate as the cause.

Monitoring

Serum calcium, phosphate and magnesium periodically
Volume/hydration status around infusion
25-OH vitamin D (replete before starting to avoid hypocalcemia)

Key trials & series

The Jackson Oncologist 2005 renal-safety pooled analysis (~4% vs ~4.5% placebo)
Markowitz Kidney Int 2003 zoledronate toxic-ATN series (class comparator)

Clinical pearls

Ibandronate is the bisphosphonate to choose when renal safety is paramount — its renal-event rate sits at placebo level.
Tubular peak concentration (dose ÷ infusion time), not cumulative dose, drives bisphosphonate ATN — never shorten the infusion.
In ESKD, exploit high bone avidity: a 2 mg dose binds bone like 4–5 mg in normal kidneys, so dose down.
Replete vitamin D and watch calcium — antiresorptive hypocalcemia is the more common 'electrolyte' event than any tubular injury.

Beyond the kidney — non-renal toxicities· 1 organ systems

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

Musculoskeletal

Myalgia, myositis, rhabdomyolysis, ONJ

Osteonecrosis of the jaw, hypocalcemia, acute-phase reaction

§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 · 2003–2020 · 1 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· 2

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 · ModerateCollapsing focal segmental glomerulosclerosis following long-term treatment with oral ibandronate: case report and review of literature.Jia N et al. · BMC Cancer 2015 · PMID 26197890A breast cancer patient developed heavy proteinuria and nephrotic syndrome with biopsy-proven collapsing FSGS after 29 months of oral ibandronate, partially reversible with drug cessation plus immunosuppression.CaseB · ModeratePodocyte Disease Following Treatment with Intravenous Ibandronate in an Older Patient.Chung YR et al. · Ann Geriatr Med Res 2024 · PMID 38383148An 88-year-old woman developed proteinuria, hypoalbuminemia and elevated creatinine with biopsy-proven podocyte disease (FSGS) after IV ibandronate for osteoporosis, partially reversible after drug discontinuation.

FDA label — boxed warning & renal dosing· renal impairment

Quoted verbatim from this agent's current FDA label (Aug 2026) — not paraphrased or interpreted. Full label on DailyMed .

Renal impairment — from the label

Ibandronate sodium is not recommended for use in patients with severe renal impairment (creatinine clearance less than 30 mL/min).

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 3,079 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· 6 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

Glomerular Injury / Proteinuriacorroborated · ROR 3.29 — on the terms that name the lesion (ROR 6.35)
Electrolyte Disturbancecorroborated · ROR 1.47 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
Acute Tubular NecrosisNot measurable in reporting — Reporters cannot reliably name this lesion, so its absence from FAERS is expected and is not evidence against the documented injury.

Fanconi Syndrome

ROR 14.6995% CI 8.12–26.58· 11 reports

Hemorrhagic Cystitis

ROR 6.9295% CI 5.45–8.79· 69 reports

Glomerular Injury / Proteinuria

ROR 3.2995% CI 1.95–5.56· 14 reports

Hypertension

ROR 2.9795% CI 2.53–3.48· 162 reports

Crystal / Obstructive Nephropathy

ROR 2.8395% CI 1.88–4.26· 23 reports

Electrolyte Disturbance

ROR 1.4795% CI 1.08–2.00· 41 reports

FAERS outcomes & reporting trend· 9.6% of reports w/ death · 22.4% w/ hospitalization

9.6%

Reported with a death outcome

295 of 3,079 reports

22.4%

Reported with hospitalization

689 of 3,079 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 3,079 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 0.58–1.39· 20 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

General / constitutional

Fatigue212Fall176Pain167Asthenia161Back Pain140

Musculoskeletal

Arthralgia261Femur Fracture219Myalgia142Pain In Extremity141Osteonecrosis Of Jaw130

Gastrointestinal

Diarrhoea244Nausea238Vomiting143Abdominal Pain Upper131

Nervous system

Headache217Dizziness178

Respiratory

Dyspnoea154Cough124

Psychiatric

Insomnia124

Skin

Pruritus123

Metabolic & electrolyte

Decreased Appetite99

Guidelines & consensus· 14

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.

ASCO / CCORole of Bone-Modifying Agents in Metastatic Breast Cancer: An American Society of Clinical Oncology-Cancer Care Ontario Focused Guideline UpdateJ Clin Oncol 2017 · PMID 29035643Endorses denosumab 120 mg SC q4w, pamidronate 90 mg IV q3-4w, or zoledronic acid 4 mg IV q12w or q3-4w; nitrogen bisphosphonates require renal function monitoring and dose/interval adjustment for impaired clearance, whereas denosumab needs no renal dose adjustment (with hypocalcemia risk in CKD).

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 Ibandronate 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

Nedaplatin

Aqupla · Platinum agent

Profile

Second-gen platinum with reduced renal toxicity vs cisplatin.

ATNLYTE

Moderate#1 · 68% phenotype match

Imatinib

Gleevec · BCR-ABL TKI

Profile

Fluid retention; rare Fanconi and AKI.

LYTEFANCATN

Mild#2 · 65% phenotype match

Melphalan flufenamide (melflufen)

Pepaxto · Peptide-conjugated alkylator

Profile

Delivers melphalan intracellularly; BRIDGE supports a reduced 30 mg dose in moderate renal impairment.

ATNLYTE

Moderate#3 · 65% phenotype match

Datopotamab deruxtecan (Dato-DXd)

Datroway · Antibody-drug conjugate (TROP2/DXd)

Profile

2025 TROP2 ADC; renal signal theoretical, extrapolated from the ADC class.

ATNGLOM

Moderate#4 · 64% phenotype match

Telisotuzumab vedotin (Teliso-V)

Emrelis · c-Met ADC (MMAE)

Profile

c-Met MMAE antibody-drug conjugate; proximal tubular ATN risk extrapolated from the ADC/MMAE class.

ATNLYTE

Moderate#5 · 64% phenotype match

Carboplatin

Paraplatin · Platinum agent

Profile

Kidney-sparing; GFR-dosed by the Calvert formula.

ATNLYTECYST

Mild#6 · 60% phenotype match

Compare Ibandronate 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 Bisphosphonates & bone

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.

1Ibandronate· this agentATN — Acute Tubular NecrosisMild
2DenosumabLYTE — Electrolyte DisturbanceModerate
3Zoledronic acidATN — Acute Tubular NecrosisFAERS AKIModerate
4PamidronateGLOM — 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 Ibandronate’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 Ibandronate; 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 46 clinical records among all 73 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.