Trastuzumab deruxtecan
Enhertu · Antibody-drug conjugate (HER2/DXd)
Emerging AKI/proteinuria reports — under-published.
ATNFANCLYTE
Moderate#1 · 73% phenotype match
Zoledronic acid
Zometa · Zol
Bisphosphonate · approved 2001 · 11 citations · FAERS AKI reporting ROR 2.90 (95% CI 2.70–3.10, 825 AKI reports)
Up to date· through 2026
Deeply sourced8/9 · 7 signals
- Met: 11 citations
- Not met: 12+ references
- Met: Accrued over 10+ years (span: 23y)
- Met: Beyond single case reports
- Met: High-impact journal
- Met: Landmark reference
- Met: Current through 2026
- 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 tubule-toxic bisphosphonate — ATN driven by dose and infusion speed.
ModerateBisphosphonate
Hypercalcemia of malignancyBone metastasesMyeloma
§01
Signature kidney injury
Signature lesion
Representative incidence17%
Nephrotoxicity is the dose-limiting toxicity but largely avoidable; no precise population rate. Reported rate: renal toxicity in 17% — 852 patients with symptomatic newly diagnosed multiple myeloma and at least one lytic bone lesion who received at least… (Raje 2018, PMID 29429912).Source: Raje et al., Lancet Oncol 2018
Onset & rechallenge
Time to injuryAcute (~1–7 days)
AKI days to weeks after an infusion.
Distilled from: “Acute — days to weeks after infusion(s).”
Long-term outlook & thresholds
Renal recoveryOften partial recovery
Zoledronate ATN is often partially reversible when doses are held early — creatinine tends to recover partially after withdrawal — but the recovery is incomplete and dose-dependent.PMID 12787420 (opens PubMed in a new tab)
- CKD trajectory.
- Repeated dosing through a rising creatinine can leave persistent CKD.
- Dialysis / RRT.
- Dialysis-requiring AKI has followed even a single standard-dose infusion in patients with no prior nephrotoxic exposure (Marina et al.), so RRT is an uncommon but documented outcome.PMID 39529985 (opens PubMed in a new tab)
Cumulative-dose threshold
4 mg per dose, infused over no less than 15 minutes
Exceeding the 4 mg dose (e.g. the 8 mg arm) or shortening the infusion below 15 minutes sharply raises renal events — the basis for the fixed 4 mg over >=15 minutes standard.PMID 18685574 (opens PubMed in a new tab)
Early-detection biomarkers
- Urinary tubular-injury markers (KIM-1, NGAL) — Early proximal tubular epithelial injury (ATN) — zoledronate's dose- and infusion-rate-dependent signature. Filtered zoledronate concentrates in and directly injures the proximal tubule; in a Wistar-rat comparison it produced significant, sometimes persistent markers of tubular toxicity — most severe and delayed under impaired renal function — flagging tubular necrosis that the serum creatinine can lag. KIM-1 and NGAL are the validated urinary readouts of that proximal-tubular injury.PMID 25976681 (opens PubMed in a new tab)
- Serum creatinine before every infusion — Functional GFR — the label-mandated go/no-go: hold the next oncology dose until creatinine returns to within ~10% of baseline. The series behind this row is why creatinine is worth checking before every dose, but it did not propose the rule: six patients on the labelled 4 mg monthly developed biopsy-proven toxic ATN after a mean 4.7 months of therapy (range 3-9), creatinine rising from a mean 1.4 to 3.4 mg/dL and recovering only to 2.3 mg/dL after withdrawal — late-declaring and incompletely reversible. The pre-dose check and the hold-until-within-10%-of-baseline threshold are the label's; the guideline framing, that severe bisphosphonate nephrotoxicity is largely avoided by measuring serum creatinine before each treatment and temporarily withholding for renal insufficiency, is Perazella's review (PMID 18685574).PMID 12787420 (opens PubMed in a new tab)
Long-term outcome and threshold data distilled from the agent's cited literature — educational, not a substitute for the primary sources.
Recovery across agents§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.
Notable serum-creatinine rise (dose-defined) in ~9% of patients on IV zoledronic acid for bone metastases (range ~9-12% across retrospective renal-safety series); mechanism is toxic acute tubular necrosis
Acquired Fanconi syndrome in an AJKD case series and single-agent reports, resolving on withdrawal.
Toxicity fingerprint
Tap a signature to trace where it strikes the nephron.
17%incidence
SeverityModerate
ReversibilityPartially reversible
Evidence11 citations
Nephron map
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
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.Kidney injury
Mechanism of kidney injury
Filtered zoledronic acid concentrates in and directly injures the proximal tubular epithelium, producing dose- and infusion-rate-dependent acute tubular necrosis: creatinine rises days to weeks after infusion, often with granular casts and modest proteinuria. Shortening the infusion below 15 minutes or exceeding the 4 mg dose sharply raises renal events — the basis for the fixed 4 mg over ≥15 minutes standard. Injury is often partially reversible when doses are held early, but repeated dosing through a rising creatinine can leave persistent CKD.
Clinical presentation
AKI with a rising creatinine, often with partial recovery after withdrawal.
Management
Hold drug, hydration, supportive care.Lesion-level management framework
Risk factors
- Rapid infusion
- High / frequent dosing
- Pre-existing CKD
- Volume depletion
Prevention
- Slow infusion (≥15 min)
- Dose-adjust for CrCl
- Avoid if CrCl < 30–35
Anticancer mechanism· how it treats cancer
Nitrogen-containing bisphosphonate inhibiting osteoclast-mediated bone resorption. Hypercalcemia of malignancy, bone metastases and myeloma.
Note · The ATN pattern distinguishes it from pamidronate's collapsing FSGS.
§04
Clinical depth
Renal dose adjustment
For multiple myeloma/bone metastases, the label gives a CrCl-banded reduction of the standard 4 mg dose: CrCl 50-60 mL/min → 3.5 mg, 40-49 → 3.3 mg, 30-39 → 3.0 mg; not recommended if CrCl <30 mL/min or in severe renal impairment. Always infuse over no less than 15 minutes (never bolus) and hydrate adequately. For hypercalcemia of malignancy, the risk-benefit must be weighed individually in severe renal impairment, with the 4 mg dose unmodified but careful hydration; withhold subsequent oncology doses until creatinine returns to within ~10% of baseline.
Dialyzability & ESKD dosing
Zoledronic acid is cleared almost entirely by the kidney with minimal hepatic metabolism, so accumulation is expected in advanced CKD/ESKD; pharmacokinetic data in dialysis are limited. It is poorly protein-bound and small, making it theoretically removable, but timing relative to hemodialysis is not well characterized and the drug is generally avoided rather than dose-timed around dialysis. The osteoporosis formulation (Reclast/Aclasta 5 mg) is contraindicated at CrCl <35 mL/min.
Differential diagnosis
Zoledronic acid classically causes dose- and infusion-rate-dependent acute tubular necrosis/toxicity (granular casts, rising creatinine days to weeks after infusion), whereas pamidronate—the other IV aminobisphosphonate—characteristically produces collapsing FSGS with nephrotic-range proteinuria; heavy proteinuria should prompt reconsideration of the agent and a biopsy. Distinguish from prerenal azotemia of malignancy/hypercalcemia (responds to volume, low FeNa), light-chain cast nephropathy in myeloma (free light chains, bland-to-granular sediment), and contrast or NSAID injury by infusion timing and exposure history.
Monitoring
- Check serum creatinine before EVERY dose; withhold the next oncology dose until creatinine returns to within 10% of baseline (label-mandated)
- For myeloma/bone-metastasis dosing, document CrCl at baseline and select the renal-banded dose (4 mg only if CrCl >60 mL/min; 3.5/3.3/3.0 mg for CrCl 50-60/40-49/30-39); the hypercalcemia-of-malignancy dose is 4 mg unmodified
- Verify infusion time is at least 15 minutes and that the patient is volume-replete before each infusion
- Correct and monitor calcium, magnesium, phosphate and 25-OH vitamin D, repleting vitamin D/calcium to avoid hypocalcemia
- Screen urinalysis/spot protein for tubular proteinuria if creatinine rises, and review the med list for concurrent nephrotoxins (NSAIDs, contrast, aminoglycosides, loop diuretic-driven volume depletion)
Key trials & series
- Major et al. pooled phase III analysis (J Clin Oncol 2001) — zoledronic acid 4-8 mg superior to pamidronate for hypercalcemia of malignancy; the 8 mg arm's excess renal deterioration drove adoption of the 4 mg/15-minute standard
- Rosen et al. myeloma/breast-cancer bone-metastasis trial (Cancer J 2001) — established 4 mg over 15 min q3-4wk and showed renal toxicity rises with higher dose and shorter infusion time
- HORIZON-PFT (Black et al., NEJM 2007) — once-yearly 5 mg in osteoporosis; transient post-dose creatinine rises mostly resolved, but informed the CrCl <35 mL/min contraindication for the osteoporosis dose
- Zometa Renal Safety / Saad et al. CRPC bone-metastasis trial (JNCI 2002) — confirmed creatinine-monitoring and dose-by-renal-function protocol after early grade renal events
Clinical pearls
- Nephrotoxicity is strongly driven by dose AND infusion rate—shortening below 15 minutes or giving 8 mg sharply raised renal events, which is why 4 mg over >=15 min is fixed
- Treat hypocalcemia and hypovitaminosis D proactively: pre-existing low calcium/vitamin D worsens post-infusion hypocalcemia and the metabolic picture
- Injury is often partially reversible if caught early by holding doses, but repeated dosing through a rising creatinine can produce persistent CKD
- In myeloma, weigh the bone benefit against the kidney: distinguishing drug ATN from cast nephropathy matters, and consider denosumab (no renal dosing, not renally cleared) when CrCl is low
- Zoledronate can cause acquired Fanconi syndrome / proximal tubular dysfunction (hypophosphatemia, glycosuria, aminoaciduria, acidosis) that resolves on withdrawal — a distinct lesion from its tubular necrosis.
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
8 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
8 references · 2003–2026 · 4 since 2024Primary (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.
- 1.Denosumab versus zoledronic acid in bone disease treatment of newly diagnosed multiple myeloma: an international, double-blind, double-dummy, randomised, controlled, phase 3 study.Raje N et al. · Lancet Oncol · 2018 · PMID 29429912Source of the stored incidence: Renal toxicity was reported in 85 (10%) patients in the denosumab group versus 146 (17%) in the zoledronic acid group
- 2.Acute renal failure during treatment with Zoledronate in cancer patients.Ben Kridis W et al · J Oncol Pharm Pract · 2026 · PMID 39648704Small single-center retrospective study (n=48 cancer patients on zoledronate, Sfax, Tunisia) found KDIGO-defined AKI in 9 patients (18.8%), requiring dose reduction. On multivariate analysis, AKI was independently associated with baseline creatinine clearance <60 mL/min and low body weight (~53 kg).
- 3.Single zoledronic acid infusion as a cause of acute kidney impairment requiring dialysis in two patients with osteoporosis.Marina D et al · Arch Endocrinol Metab · 2024 · PMID 39529985Case report of two osteoporosis patients (non-cancer, no prior nephrotoxic exposure, one with normal baseline renal function) who developed dialysis-requiring acute kidney injury after a SINGLE standard osteoporosis-dose IV zoledronic acid infusion—extending the nephrotoxicity signal beyond the classic high-cumulative-dose oncology / preexisting-CKD setting and reinforcing the need to monitor renal function in all recipients.
- 4.Safety of low dose inpatient zoledronic acid in acute hip fracture patients with advanced chronic kidney disease.Sun X et al · J Bone Miner Res · 2026 · PMID 41493104Real-world propensity-matched cohort (46 reduced-dose inpatient ZA patients, avg 2.7 mg and <=3 mg, vs 98 untreated controls; mean age ~90, mean CrCl ~31 mL/min) in acute hip-fracture patients with advanced CKD (CrCl <35 mL/min).
- 5.LandmarkToxic acute tubular necrosis following treatment with zoledronate (Zometa).Markowitz GS et al. · Kidney Int · 2003 · PMID 12787420Landmark series establishing zoledronate as a cause of toxic ATN.
- 6.Bisphosphonate nephrotoxicity.Perazella MA et al. · Kidney Int · 2008 · PMID 18685574Contrasts zoledronate ATN with pamidronate collapsing FSGS.
- 7.Fanconi syndrome induced by zoledronic acid: Two case reports.Chen Y et al. · Medicine (Baltimore) · 2026 · PMID 41894284Two prostate-cancer cases of zoledronate-induced Fanconi syndrome resolving over 1-3 months after withdrawal.
- 8.A case of acquired Fanconi syndrome induced by zoledronic acid.Yoshinami T et al. · Intern Med · 2011 · PMID 21532237Case of acquired Fanconi syndrome induced by zoledronic acid.
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.
CaseB · ModerateZoledronic Acid-Associated Fanconi Syndrome in Patients With Cancer.Portales-Castillo I et al. · Am J Kidney Dis 2022 · PMID 35219759Series of four cancer patients who developed AKI with generalized proximal tubular dysfunction (Fanconi syndrome) about one week after zoledronic acid infusion.CaseB · ModerateSevere Hypophosphatemia as the Initial Presentation of Renal Fanconi's Syndrome and Distal Renal Tubular Acidosis Related to Zoledronic Acid: A Case Report and Literature Review.Wu Y et al. · Kidney Blood Press Res 2023 · PMID 3641260764-year-old with lung adenocarcinoma bone metastases on 5 years of zoledronic acid developed Fanconi syndrome and distal RTA; renal biopsy showed toxic tubular necrosis. Biopsy-proven; partially mitigated by extending the dosing interval.CaseB · ModerateEarly onset acute tubular necrosis following single infusion of zoledronate.Yachoui R · Clin Cases Miner Bone Metab 2016 · PMID 27920815Osteoporosis patient developed biopsy-proven toxic acute tubular necrosis with creatinine rising from 1.1 to 5.5 mg/dL twelve days after a single zoledronate infusion.
What gets reported — FAERS
Everything below is FAERS — adverse events someone chose to report, about 39,907 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· 9 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
- Fanconi Syndromecorroborated · ROR 14.24 — on the terms that name the lesion (ROR 21.58)
- Acute Tubular Necrosiscorroborated · ROR 10.1
Fanconi Syndrome
ROR 14.2495% CI 12.00–16.90· 135 reports
Acute Tubular Necrosis
ROR 10.1095% CI 8.73–11.69· 185 reports
Electrolyte Disturbance
ROR 4.1795% CI 3.96–4.39· 1,465 reports
Acute Interstitial Nephritis
ROR 2.9995% CI 2.47–3.62· 106 reports
Hemorrhagic Cystitis
ROR 2.8695% CI 2.58–3.16· 373 reports
SIADH / Hyponatremia
ROR 2.0795% CI 1.86–2.32· 316 reports
Hypertension
ROR 1.8595% CI 1.76–1.96· 1,337 reports
Crystal / Obstructive Nephropathy
ROR 1.8195% CI 1.57–2.08· 191 reports
Glomerular Injury / Proteinuria
ROR 1.8195% CI 1.49–2.20· 100 reports
FAERS outcomes & reporting trend· 12.9% of reports w/ death · 28.8% w/ hospitalization
12.9%
Reported with a death outcome
5,133 of 39,907 reports
28.8%
Reported with hospitalization
11,501 of 39,907 reports
Reports per year
- 2015: 1,331 reports
- 2016: 1,465 reports
- 2017: 1,673 reports
- 2018: 2,317 reports
- 2019: 2,673 reports
- 2020: 2,707 reports
- 2021: 2,705 reports
- 2022: 2,796 reports
- 2023: 3,043 reports
- 2024: 3,315 reports
- 2025: 3,546 reports
- 2026: 1,627 reports
Yearly FAERS report volume · most recent year is partial.
FAERS adverse-event signal — all organ systems· 8 systems · 39,907 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 2.9095% CI 2.70–3.10· 825 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.
General / constitutional
Pain3,151Pyrexia2,811Fatigue2,797Asthenia1,970Malaise1,579
Musculoskeletal
Arthralgia3,218Osteonecrosis Of Jaw2,708Myalgia1,866Pain In Extremity1,676Bone Pain1,586
Gastrointestinal
Nausea2,819Diarrhoea2,278Vomiting2,061
Nervous system
Headache2,367Dizziness1,435
Blood & lymphatic
Neutropenia1,391Anaemia1,178
Respiratory
Dyspnoea1,652
Metabolic & electrolyte
Decreased Appetite1,322
Immune / infection
Pneumonia1,049
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.
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 Zoledronic acid 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.
Phenotype-similar agents· the numbered markers on the map above
Profile
Imatinib
Gleevec · BCR-ABL TKI
Fluid retention; rare Fanconi and AKI.
LYTEFANCATN
Mild#2 · 68% phenotype match
Streptozocin
Zanosar · Nitrosourea alkylator
Classic proximal tubular toxin → Fanconi and dose-limiting AKI.
FANCATNLYTE
Severe#3 · 68% phenotype match
Azacitidine
Vidaza · Hypomethylating agent
Proximal (type 2) RTA / Fanconi-like tubulopathy; overt AKI uncommon.
FANCATNLYTE
Moderate#4 · 65% phenotype match
Lenalidomide
Revlimid · Immunomodulatory drug (IMiD)
Renally cleared; AKI and rare Fanconi/TMA.
ATNFANCTMA
Moderate#5 · 62% phenotype match
Ibandronate
Boniva · Bisphosphonate
Lower renal risk than zoledronate.
ATNLYTEGLOM
Mild#6 · 59% phenotype match
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.
- 1IbandronateATN — Acute Tubular NecrosisMild
- 2DenosumabLYTE — Electrolyte DisturbanceModerate
- 3Zoledronic acid· this agentATN — 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 Zoledronic acid’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 Zoledronic acid; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.
- Raje, Noopur — their work on Zoledronic acid, on PubMed (opens in a new tab)6 papers · 766 citesPMID 29480139 (opens PubMed in a new tab)PMID 29429912 (opens PubMed in a new tab)PMID 29341831 (opens PubMed in a new tab)
- Terpos, Evangelos — their work on Zoledronic acid, on PubMed (opens in a new tab)5 papers · 647 citesPMID 33249579 (opens PubMed in a new tab)PMID 30285492 (opens PubMed in a new tab)PMID 29480139 (opens PubMed in a new tab)
- Morgan, Gareth J — their work on Zoledronic acid, on PubMed (opens in a new tab)4 papers · 720 citesPMID 24673708 (opens PubMed in a new tab)PMID 23690408 (opens PubMed in a new tab)PMID 23233603 (opens PubMed in a new tab)
- Camacho, Pauline M — their work on Zoledronic acid, on PubMed (opens in a new tab)2 papers · 489 citesPMID 27662240 (opens PubMed in a new tab)PMID 27643923 (opens PubMed in a new tab)
- Watts, Nelson B — their work on Zoledronic acid, on PubMed (opens in a new tab)2 papers · 489 citesPMID 27662240 (opens PubMed in a new tab)PMID 27643923 (opens PubMed in a new tab)
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 125 clinical records among all 153 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.