Dasatinib
Sprycel · BCR-ABL TKI
Nephrotic-range proteinuria — a notable signal.
GLOM
Moderate#1 · 84% phenotype match
Pamidronate
Aredia · Pam
Bisphosphonate · approved 1991 · 6 citations
Dated evidence· through 2011
Fairly sourced6/9 · 5 signals
- Met: 6 citations
- Not met: 12+ references
- Met: Accrued over 10+ years (span: 10y)
- Met: Beyond single case reports
- Met: High-impact journal
- Met: Landmark reference
- Not met: Current through 2011
- 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 first drug ever tied to collapsing FSGS — a podocyte, not tubular, toxin.
SevereBisphosphonate
Hypercalcemia of malignancyMyeloma bone disease
§01
Signature kidney injury
Signature lesion
Representative incidence7.7%
Not well quantified; the histopathologic pattern comes from case series, notably at higher-than-approved doses. Reported rate: renal deterioration in 7.7% — Patients with multiple myeloma or metastatic breast cancer receiving 1-hour intravenous pamidronate infusions, British… (de 2006, PMID 17156591).Source: de Lemos et al., J Oncol Pharm Pract 2006
Onset & rechallenge
Time to injuryDelayed (>6 weeks / cumulative)
Develops over months to years of therapy (15–48 months in the Markowitz 2001 series).
Distilled from: “Subacute to delayed — months to years of therapy (15–48 months in the Markowitz 2001 series).”
Long-term outlook & thresholds
Renal recoveryNot reported
The landmark series characterizes PRESENTATION, not follow-up: seven patients with normal baseline renal function developed collapsing FSGS after 15–48 months of pamidronate and presented with a mean serum creatinine of 3.6 mg/dL and full nephrotic syndrome (mean 24-h protein 12.4 g/d). Five of the seven had been escalated ABOVE the approved 90 mg monthly dose (180 mg in two, 360 mg in three); at the recommended 90 mg monthly, renal toxicity is infrequent. No recovery outcomes are reported, so this atlas does not state one — but because the presenting proteinuria is nephrotic-range, a rising urine protein rather than creatinine is the actionable signal.PMID 11373339 (opens PubMed in a new tab)
- CKD trajectory.
- Patients presented already in renal failure — mean serum creatinine 3.6 mg/dL after 15–48 months of therapy — so the lesion declares itself late, with substantial function already lost.
Two different questions. Quick facts lists this agent's Reversibility as "Often irreversible" — this atlas's reading of the injury across its cited literature. The badge above is narrower: it reports only what the outcome study cited here measured, and that study does not follow renal recovery. The two are not in conflict, and the absence of a measured trajectory is not evidence that the kidney recovers.
Cumulative-dose threshold
Above the approved 90 mg monthly dose — supratherapeutic 180–360 mg monthly
Every patient in the landmark collapsing-FSGS series started at or below the recommended 90 mg monthly, and five of seven were then escalated (180 mg monthly in two, 360 mg in three); at the recommended 90 mg dose renal toxicity is infrequent. The 2–4 hour infusion is label guidance, not a finding of this series.PMID 11373339 (opens PubMed in a new tab)
Early-detection biomarkers
- Urinary protein / albumin — Glomerular podocyte injury (collapsing FSGS). New or rising proteinuria is the earliest actionable signal — the podocytopathy presents with new, often nephrotic-range proteinuria (mean 12.4 g/day in the landmark series) before an overt creatinine rise, unlike a tubular AKI.PMID 11373339 (opens PubMed in a new tab)
- Serum creatinine — Falling GFR / progressive renal failure. Guideline-recommended monitoring of serum creatinine prior to each infusion — with dose reduction or temporary withholding for renal insufficiency — is how severe bisphosphonate nephrotoxicity is largely avoided.PMID 18685574 (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 defining kidney lesion — its #1 signature. Cited incidence is shown where a citable figure exists; otherwise the tier stands qualitatively.
Collapsing FSGS (podocytopathy) with nephrotic-range proteinuria; dose-dependent, seen mainly with high/escalated IV doses (>90 mg/mo). Rare at standard 90 mg dosing — no population incidence rate established (index case series of 7 patients). PMID 11373339 (opens PubMed in a new tab)
§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
Direct podocyte injury produces collapsing focal segmental glomerulosclerosis — the first drug ever causally linked to this lesion. It presents with new, often nephrotic-range proteinuria and progressive renal failure rather than a tubular creatinine bump, and clustered in patients given supratherapeutic doses (180–360 mg) or shortened infusions. The injury is frequently irreversible — many reported patients progressed to dialysis-dependent ESKD despite withdrawal — so a rising urine protein, not just creatinine, is the earliest actionable signal.
Clinical presentation
Nephrotic-range proteinuria, edema and progressive renal failure.
Management
Discontinue; supportive nephrotic care.Lesion-level management framework
Risk factors
- High dose
- Prolonged use
- Pre-existing CKD
Prevention
- Use approved doses
Anticancer mechanism· how it treats cancer
Nitrogen-containing bisphosphonate inhibiting osteoclasts. Hypercalcemia of malignancy and myeloma bone disease.
Note · Pamidronate → podocyte/FSGS; zoledronate → tubule/ATN. A useful contrast pair.
§04
Clinical depth
Renal dose adjustment
No formal renal-function dosing algorithm exists for the oncology (hypercalcemia/myeloma/bone-metastasis) indications because pamidronate was not adequately studied in renal impairment; the label advises against use in severe renal impairment and recommends holding therapy if renal function deteriorates. Nephrotoxicity is dose-dependent — in the landmark collapsing-FSGS series five of the seven patients had been escalated above the approved dose (180 mg monthly in two, 360 mg in three), and at the recommended 90 mg monthly renal toxicity is infrequent — so adhere to the labeled 90 mg over no less than 2-4 hours, not exceeding 90 mg per dose.
Dialyzability & ESKD dosing
Pamidronate is not meaningfully dialyzable — roughly half of an absorbed dose is rapidly taken up and sequestered in bone, and the remainder is renally excreted unchanged, so it is not given to "treat" with HD removal in mind. There are limited data to guide dosing in dialysis-dependent ESKD; given the severity of the glomerular lesion at presentation and the lack of renal clearance, use in advanced CKD/ESKD is generally avoided in favor of denosumab.
Differential diagnosis
Pamidronate's lesion is collapsing FSGS with heavy (often nephrotic-range) proteinuria and progressive renal failure, distinguishing it from zoledronate, whose signature is dose/infusion-rate-dependent acute tubular necrosis with bland sediment and modest proteinuria. Differentiate from idiopathic/HIV-associated collapsing glomerulopathy and APOL1-driven collapsing FSGS by the temporal link to high-dose IV pamidronate; biopsy showing collapsing tufts plus tubular degeneration supports a drug etiology, but APOL1 risk genotype and viral causes should be excluded.
Monitoring
- Check serum creatinine before each pamidronate dose and hold the next dose for any deterioration from baseline (label-recommended interruption threshold).
- Screen for proteinuria (urine protein/creatinine ratio or dipstick) at baseline and serially — new nephrotic-range proteinuria is the hallmark of collapsing FSGS and warrants stopping the drug and nephrology referral.
- Monitor serum calcium, phosphate, magnesium, and potassium, since correcting hypercalcemia can unmask hypocalcemia and electrolyte shifts.
- Verify infusion duration and dose against the order each cycle — rapid or supratherapeutic infusion is the dominant modifiable nephrotoxicity risk.
Key trials & series
- Markowitz et al. (J Am Soc Nephrol 2001, PMID 11373339) — the landmark clinicopathologic case series establishing high-dose pamidronate as the first drug definitively linked to collapsing focal segmental glomerulosclerosis with nephrotic-range proteinuria and podocyte injury.
- Berenson 'Aredia' pivotal myeloma/bone-metastasis trial (Berenson et al., N Engl J Med 1996) — the registrational randomized trial of 90 mg pamidronate that established efficacy for skeletal events and the labeled dose/infusion that nephrotoxicity recommendations are anchored to.
Clinical pearls
- Pamidronate was the first drug ever causally linked to collapsing FSGS — a true sentinel association in drug-induced nephrotoxicity.
- Patients in the landmark series presented already in renal failure — mean creatinine 3.6 mg/dL and 12.4 g/d of protein after 15-48 months of therapy — so prevention (correct dose, slow infusion, hydration) outweighs rescue.
- New or rising proteinuria — not just a creatinine bump — is the earliest actionable signal; a falling albumin with edema should prompt discontinuation rather than dose continuation.
- In patients needing antiresorptive therapy with established glomerular injury or advanced CKD, the RANKL antibody denosumab is the kidney-sparing alternative (watch for hypocalcemia instead).
Where it strikes· nephron segments & injury signatures
Nephron segments
Glomerulus
Filtration barrier (podocytes + endothelium)
Injury signatures
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
4 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
4 references · 2001–2008 · 2 since 2006Primary (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.Renal safety of 1-hour pamidronate infusion for breast cancer and multiple myeloma patients: comparison between clinical trials and population-based database.de Lemos ML et al. · Journal of Oncology Pharmacy Practice · 2006 · PMID 17156591Source of the stored incidence: Renal deterioration occurred in 7.7% of 169 patients with multiple myeloma and metastatic breast cancer.
- 2.LandmarkCollapsing focal segmental glomerulosclerosis following treatment with high-dose pamidronate.Markowitz GS et al. · J Am Soc Nephrol · 2001 · PMID 11373339Landmark series — first association of collapsing FSGS with a therapeutic agent.
- 3.Collapsing glomerulopathy.Schwimmer JA et al. · Semin Nephrol · 2003 · PMID 12704581Review of collapsing glomerulopathy and its pamidronate association.
- 4.Bisphosphonate nephrotoxicity.Perazella MA et al. · Kidney Int · 2008 · PMID 18685574Details pamidronate collapsing FSGS versus zoledronate ATN.
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 · ModerateProliferating cells in HIV and pamidronate-associated collapsing focal segmental glomerulosclerosis are parietal epithelial cells.Dijkman HB et al. · Kidney Int 2006 · PMID 16761013Histopathologic study including a patient with pamidronate-associated collapsing FSGS, characterizing the proliferating glomerular epithelial cells driving the podocytopathic lesion.CaseB · ModerateNephrotic syndrome induced by pamidronate.ten Dam MA et al. · Med Oncol 2011 · PMID 20865462Two patients developed nephrotic syndrome and progressive renal failure with biopsy-proven collapsing FSGS after intravenous pamidronate.
FDA label — boxed warning & renal dosing· renal impairment
Quoted verbatim from this agent's current FDA label (Dec 2025) — not paraphrased or interpreted. Full label on DailyMed .
Renal impairment — from the label
The renal clearance of pamidronate was reduced in patients with reduced creatinine clearance. Because pamidronate disodium is administered on a monthly basis, drug accumulation is not expected. No changes in pamidronate disodium dosing regimen are recommended for patients with mild to moderate renal impairment (creatinine clearance > 30 mL/min). Limited pharmacokinetic data exist in patients with creatinine clearance < 30 mL/min [see Warnings and Precautions (5.1) and Clinical Pharmacology (12.3) ] . 8.7 Patients with
What gets reported — FAERS
Everything below is FAERS — adverse events someone chose to report, about 3,387 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 10.58 — on the terms that name the lesion (ROR 19.06)
Glomerular Injury / Proteinuria
ROR 10.5895% CI 7.98–14.03· 49 reports
Electrolyte Disturbance
ROR 6.4395% CI 5.55–7.45· 189 reports
Acute Tubular Necrosis
ROR 5.6895% CI 2.95–10.94· 9 reports
Crystal / Obstructive Nephropathy
ROR 3.2495% CI 2.25–4.67· 29 reports
SIADH / Hyponatremia
ROR 2.4095% CI 1.68–3.41· 31 reports
Hypertension
ROR 1.4295% CI 1.15–1.76· 88 reports
FAERS outcomes & reporting trend· 12.6% of reports w/ death · 31.1% w/ hospitalization
12.6%
Reported with a death outcome
428 of 3,387 reports
31.1%
Reported with hospitalization
1,052 of 3,387 reports
Reports per year
- 2015: 54 reports
- 2016: 78 reports
- 2017: 100 reports
- 2018: 125 reports
- 2019: 216 reports
- 2020: 185 reports
- 2021: 108 reports
- 2022: 91 reports
- 2023: 100 reports
- 2024: 105 reports
- 2025: 60 reports
- 2026: 30 reports
Yearly FAERS report volume · most recent year is partial.
FAERS adverse-event signal — all organ systems· 7 systems · 3,387 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 1.3995% CI 0.99–1.94· 34 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).
General / constitutional
Pain421Fatigue154Pyrexia139Weight Decreased112Asthenia111
Musculoskeletal
Osteonecrosis534Osteonecrosis Of Jaw435Pain In Jaw115Femur Fracture80
Gastrointestinal
Nausea170Diarrhoea149Vomiting118
Immune / infection
Infection133Pneumonia125
Nervous system
Headache100
Blood & lymphatic
Anaemia88
Respiratory
Dyspnoea86
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 Pamidronate 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
Belantamab mafodotin
Blenrep · Antibody-drug conjugate (BCMA/MMAF)
Myeloma ADC; renal data emerging.
GLOM
Mild#2 · 78% phenotype match
Interferon-α
Intron A · Cytokine
Collapsing FSGS in APOL1 carriers.
GLOMTMA
Severe#3 · 65% phenotype match
Fruquintinib
Fruzaqla · VEGFR TKI
2023 colorectal VEGFR-TKI; hypertension and proteinuria, class effect.
HTNGLOMTMA
Moderate#4 · 48% phenotype match
Avelumab
Bavencio · Anti-PD-L1 antibody
ICI-associated AIN.
AINGLOM
Moderate#5 · 48% phenotype match
Cabozantinib
Cabometyx · VEGFR/MET TKI
Hypertension and proteinuria; nephrotic case reports.
HTNGLOM
Moderate#6 · 48% 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 acidATN — Acute Tubular NecrosisFAERS AKIModerate
- 4Pamidronate· this agentGLOM — 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 Pamidronate’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 Pamidronate; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.
- Markowitz, Glen S — their work on Pamidronate, on PubMed (opens in a new tab)4 papers · 1,000 citesPMID 18685574 (opens PubMed in a new tab)PMID 12787420 (opens PubMed in a new tab)PMID 12704581 (opens PubMed in a new tab)
- D'Agati, Vivette D — their work on Pamidronate, on PubMed (opens in a new tab)2 papers · 606 citesPMID 12787420 (opens PubMed in a new tab)PMID 11373339 (opens PubMed in a new tab)
- Perazella, Mark A — their work on Pamidronate, on PubMed (opens in a new tab)3 papers · 497 citesPMID 18685574 (opens PubMed in a new tab)PMID 12811231 (opens PubMed in a new tab)PMID 12087588 (opens PubMed in a new tab)
- Raje, Noopur — their work on Pamidronate, on PubMed (opens in a new tab)4 papers · 398 citesPMID 29341831 (opens PubMed in a new tab)PMID 23690408 (opens PubMed in a new tab)PMID 23073123 (opens PubMed in a new tab)
- Terpos, Evangelos — their work on Pamidronate, on PubMed (opens in a new tab)2 papers · 261 citesPMID 30285492 (opens PubMed in a new tab)PMID 23690408 (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 97 clinical records among all 144 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.