GN in Ten

In this "Board Review Bonus" (BRB) episode, hosts Dr. Kenar Jhaveri and Dr. Koyal Jain break down the essential "must-knows" for Secondary Focal Segmental Glomerulosclerosis (FSGS). Geared toward board preparation and clinical practice, this bite-sized session covers everything from distinguishing secondary lesions from primary disease to navigating the modern cardiorenal toolkit.Key Discussion PointsPrimary vs. Secondary Differentiation: Primary FSGS typically presents with full-blown nephrotic syndrome (heavy proteinuria, hypoalbuminemia, edema) and diffuse foot process effacement (>80%). Secondary FSGS usually manifests with indolent nephrotic-range proteinuria, normal serum albumin, and focal or mild foot process effacement.Decoding Biopsy Variants & Pathology: While Columbia classification variants (perihilar, tip, cellular, collapsing, NOS) are not strictly diagnostic on their own, specific patterns offer critical clues:Perihilar & Glomerulomegaly: Point toward maladaptive, high-flow hyperfiltration states.Collapsing Variant: Prompts a rigorous search for viral triggers (HIV, COVID-19) or drug-induced etiologies driven by high local interferon activity.The "Global" Trap: Always distinguish true FSGS from secondary focal global glomerular sclerosis, which represents end-stage scarring rather than a primary podocytopathy.Pathogenesis: A mismatch between nephron mass and body mass causes glomerular hypertrophy, compensatory hyperfiltration, and increased intraglomerular pressure, leading to podocyte dropout and cytoskeletal damage.Comprehensive Causes: Spanning familial/genetic risk variants (APOL1), adaptive responses (reduced nephron mass, obesity, hypertension), viral triggers, and drug-induced injuries (lithium, CNIs, bisphosphonates).Management & The GDMT Era: Treatment focuses on reducing glomerular workload rather than immune suppression. Essential pillars include maximum RAAS blockade, SGLT2 inhibitors, GLP-1 receptor agonists, and sparsentan (backed by DUPLEX trial data for proteinuria reduction).Recommended Literature & Resources:De Vriese AS, et al. Differentiating Primary, Genetic, and Secondary FSGS in Adults: A Clinicopathologic Approach. J Am Soc Nephrol. 2018 Mar;29(3):759-774. PMID: 29321142Rheault MN, et al. Sparsentan versus Irbesartan in Focal Segmental Glomerulosclerosis. N Engl J Med. 2023 Dec 28;389(26):2436-2445. PMID: 37921461Concept Map: Focal Segmental  Glomerulosclerosis(FSGS): http://www.nephronpower.com/2011/12/concept-map-focal-segmental.html

Board Review Bonus 7: Membranous NephropathyIn this "Board Review Bonus" (BRB) episode, hosts Dr. Kenar Jhaveri and Dr. Koyal Jain deliver a high-yield clinical overview of membranous nephropathy (MN)—a classic, board-favorite cause of nephrotic syndrome. Utilizing a real-world case of a 50-year-old male presenting with heavy proteinuria and severe hypoalbuminemia, they walk through diagnostic dilemmas, pathological clues, and the modern therapeutic landscape. Whether you are studying for the boards or looking to "class-switch" your clinical knowledge from IgG1 to IgG4, this bite-sized episode is packed with essential clinical pearls.Key Topics Covered:Epidemiology & Biopsy Basics: Identifying MN as one of the most common causes of adult nephrotic syndrome. The hosts break down classic pathology features: diffuse GBM thickening on light microscopy, "spikes" on silver stain, granular IgG and C3 immunofluorescence, and subepithelial dense deposits on EM.The Antigen Revolution: A review of how the 2009 discovery of anti-PLA2R antibodies on podocytes transformed the diagnosis of primary MN. They also highlight newer antigens to know for the boards, including NELL-1 (associated with malignancy, medications, and lipoic acid), THSD7A (associated with malignancy), and EXT1/EXT2 (associated with lupus).Investigating Secondary Causes: Why age-appropriate malignancy screening, medication reviews, and infectious workups (syphilis, hepatitis B and C) are essential even in PLA2R-positive cases. Key biopsy clues like "full house" staining or endothelial tubuloreticular inclusions can help tip you off to a secondary etiology.The "Koyal-Kenar" Risk Stratification: Why tracking immunological remission via anti-PLA2R titers is often far more predictive than following proteinuria alone. The hosts outline when to initiate immunosuppression based on GFR decline, severe proteinuria/complications, or stable/rising anti-PLA2R titers.Conservative Therapy (The CKD Toolkit): Standard management including low-sodium diets, maximal RAAS blockade, statins (mindful of CNI interactions), SGLT2 inhibitors, and prophylactic anticoagulation (using apixaban or warfarin) when albumin drops below 2.0–2.5 g/dL.The Immunosuppressive Toolkit: Navigating the "big three" regimens: the highly effective but complex 6-month Modified Ponticelli Regimen, first-line Rituximab (backed by the MENTOR trial), and Calcineurin Inhibitors (useful as a bridge, but limited by high relapse rates). Plus, a sneak peek at obinutuzumab (the Majesty trial) for deeper B-cell depletion.Recommended Literature:Fervenza FC, Appel GB, Barbour SJ, et al. Rituximab or Cyclosporine in the Treatment of Membranous NephropathyFernández-Juárez G, Rojas-Rivera J, van de Logt AE, et al. The STARMEN trial indicates that alternating treatment with corticosteroids and cyclophosphamide is superior to sequential treatment with tacrolimus and rituximab in primary membranous nephropathy. Scolari F, Delbarba E, Santoro D, et al. Rituximab or cyclophosphamide in the treatment of membranous nephropathy: the RI-CYCLO randomized trial.The MAJESTY Trial (Obinutuzumab vs Tacrolimus in Primary Membranous Nephropathy): ClinicalTrials.gov Identifier: NCT04629248.

Board Review Bonus 6: Alport Syndrome In this "Board Review Bonus" (BRB) episode, hosts Dr. Kenar Jhaveri and Dr. Koyal Jain provide a comprehensive clinical overview of hereditary nephritis—also known as Alport syndrome—a complex genetic condition with critical renal and extrarenal implications. From a sneaky real-world case of an 18-year-old female presenting with isolated microscopic hematuria to classic textbook syndromic features , our hosts break down the essential knowledge required for both board preparation and clinical practice.The discussion moves beyond the classic X-linked male phenotype to explore autosomal varieties and why thin basement membrane disease (TBMD) is increasingly viewed as part of the Alport spectrum rather than a purely benign entity. Dr. Jain and Dr. Jhaveri emphasize critical management strategies, highlighting why an accurate diagnosis is vital to protect patients from receiving unnecessary and ineffective immunosuppressive therapies.Key Topics Covered:The Hematuria Differential: Evaluating a young patient with a family history of hematuria, prioritizing Alport syndrome, thin basement membrane disease, and IgA nephropathy.Genetics and Inheritance Patterns: A detailed look at mutations in the alpha 3, 4, and 5 chains of type IV collagen, spanning X-linked, autosomal recessive, and autosomal dominant variants.Clinical and Extrarenal Manifestations: Identifying the classic trio of kidney involvement, high-pitched sensorineural hearing loss, and ocular abnormalities like anterior lenticonus.Biopsy and Pathology Pearls: Differentiating between simple glomerular basement membrane (GBM) thinning and advanced longitudinal splitting ("basket-weave" lamination) on electron microscopy, alongside the utility of pediatric skin biopsies.Clinical Management & Pitfalls: Navigating first-line RAAS inhibition and SGLT2 inhibitors while strictly avoiding immunosuppressive regimens for secondary FSGS lesions.Transplantation Outcomes: Understanding why Alport syndrome does not recur post-transplant, balanced against the 3% to 4% risk of developing de novo anti-GBM disease in the allograft.Recommended Literature:Consensus statement on guidelines for the care of children and adolescents with Alport syndrome.Early angiotensin-converting enzyme inhibition in Alport syndrome delays renal failure and improves life expectancy.Alport Syndrome: Classification and Management 

Episode 5: Board Review Bonus: Renal AmyloidosisIn this "Board Review Bonus" (BRB) episode, hosts Dr. Kenar Jhaveri and Dr. Koyal Jain provide a comprehensive clinical overview of amyloidosis—a complex and often enigmatic disease with significant renal implications. From the initial "mushy, smudgy" appearance on light microscopy to the precise measurements of electron microscopy, our hosts break down the essential knowledge required for both board preparation and clinical practice.The discussion moves beyond the common AL and AA variants to explore rare types like LECT2 and the hereditary forms. Dr. Jain and Dr. Jhaveri emphasize that "the tissue is the issue," highlighting the diagnostic necessity of biopsying the affected organ and the critical role of mass spectrometry in directing therapy.Key Topics Covered:Classification of Amyloidosis: A detailed look at AL, AA, LECT2, and the hereditary variants including ATTR, fibrinogen A alpha-chain, and Apolipoprotein.The Diagnostic Workup: Understanding the utility of Congo red staining, the significance of birefringence, and the institutional variability of fat pad biopsies.Electron Microscopy (EM) Pearls: A guide to differentiating amyloid fibrils from mimics such as fibrillary GN, immunotactoid GN, and cryoglobulinemia based on diameter and arrangement.Clinical Management: Navigating the multidisciplinary approach between nephrology, hematology, and cardiology, including the nuances of RAAS inhibition and diuretic therapy in proteinuric patients.Transplantation Outcomes: Evaluating recurrence rates and survival benefits for different amyloid types post-kidney transplant.Recommended Resources and Literature:Visual Aid: Concept Map: Causes of Renal Amyloidosis – A comprehensive resource for classifying amyloid variants and their underlying triggers (via NephronPower).Dandona P, et al. The amyloidoses: clinical features, diagnosis and treatment. Methodist Debakey Cardiovasc J. 2012 Jul-Sep;8(3):3-7. PMC3487569Panichella G, et al. Heart Failure Management in Cardiac Amyloidosis: Towards a Paradigm Shift. Heart Fail Rev. 2024. PMC12308146Moreno-Martínez P, et al. LECT2-associated renal amyloidosis (ALECT2): A case report. Nefrologia. 2018 Jan-Feb;38(1):97-99. PMID: 29254900Benson MD, et al. Hereditary renal amyloidosis associated with a mutant fibrinogen alpha-chain. Nat Genet. 1993 Mar;3(3):252-5. PMID: 8097946

In this episode, hosts Dr. Kenar Jhaveri and Dr. Koyal Jain are joined by Dr. Matt Sparks (co-creator of NephMadness) and Dr. Aarushi Varshney to discuss the evolving landscape of C3 Glomerulopathy (C3G). The conversation highlights the shift from traditional electron microscopy-based classifications to modern immunofluorescence-based diagnosis, as well as the groundbreaking arrival of two new FDA-approved targeted therapies.The NephMadness MatchupThis episode focuses on the C3G bracket pitting two critical aspects of C3G against each other:Team Diagnosis: Focusing on the challenges of distinguishing C3G from infection-related GN or monoclonal gammopathy.Team Treatment: Highlighting the new era of factor B and C3 inhibitors that are revolutionizing patient outcomes.Key Takeaways1. Challenges in DiagnosisThe "Two Orders of Magnitude" Rule: Modern diagnosis is based on immunofluorescence (IF) showing C3 deposition that is at least two orders of magnitude greater than any other immunoglobulin.C3G vs. PIGN: It can be difficult to distinguish C3G from Post-Infectious Glomerulonephritis (PIGN). Clinical clues include patient age, the persistence of low C3 levels after infection resolution, and the presence (or absence) of sub-epithelial humps on pathology.The Role of Monoclonal Gammopathy: In older patients, it is critical to rule out monoclonal gammopathy (using SPEP and free light chain assays) as a driver of complement activation.2. The New Therapeutic EraThe panel discussed two landmark drugs that have recently shifted the C3G treatment paradigm:Iptacopan: An oral factor B inhibitor that showed a 30% reduction in proteinuria at six months in the APPEAR trial.Pegcetacoplan: A subcutaneous infusion (twice weekly) C3 inhibitor that demonstrated a nearly 70% reduction in proteinuria and stabilization of eGFR in the VALIANT trial.A "Hammer" Approach: Pegcetacoplan is described as a "larger hammer" because it acts at the crux of all three complement pathways (Classical, Lectin, and Alternative).3. Safety & MonitoringVaccination: Because these drugs inhibit the complement cascade, patients MUST be vaccinated against Neisseria meningitidis and Streptococcus pneumoniae at least two weeks before starting therapy.Prophylaxis: If urgent treatment is required, patients should start prophylactic antibiotics (such as Penicillin, Augmentin, or Ciprofloxacin).Resources & Studies MentionedNephMadness: The annual educational "tournament" in nephrology that inspired this discussion.The APPEAR Trial (Iptacopan): Investigated the efficacy of the oral factor B inhibitor in patients with C3G.The VALIANT Trial (Pegcetacoplan): Evaluated the C3 inhibitor in patients with C3G and primary immune complex MPGN, including post-transplant patients.The hosts and guests of this GN in 10 episode do not have any disclosures to make relevant to the content of this episode.

It’s the "New England Journal of IgA" these days, and we’re just living in it! In this special NephMadness edition of GN in Ten, hosts Dr. Kenar Jhaveri and Dr. Koyal Jain are joined by NephMadness co-creator Dr. Matt Sparks and Duke Fellow Dr. Ale Tomasi to break down the heavy hitters in the IgA Nephropathy bracket. Matt’s dog also joins us for a special, possibly biased cameo.We’re moving past "ACE first, think later" and diving into the upstream battle: B-cell modulators (BAFF/APRIL inhibitors) versus Complement inhibitors. Whether you’re team "Hit Zero" or team "Alternative Pathway," this episode covers the latest trial data from ORIGIN, VISIONARY, and APPLAUSE to help you fill out your bracket. The "Hit Zero" HypothesisWhile we all know the classic four-hit hypothesis of IgAN, new therapies are targeting even further upstream—what some are calling "Hit Zero." Pathophysiology Recap: IgAN starts with galactose-deficient IgA1 (Hit 1), leading to autoantibody production (Hit 2), immune complex formation (Hit 3), and mesangial deposition/damage (Hit 4). B-Cell Modulators: These drugs target BAFF (B-cell activating factor) and/or APRIL (a proliferation-inducing ligand) to reduce the production of those pesky autoantibodies right at the source. The B-Cell Contenders: Sibeprenlimab & AtaciceptSibeprenlimab ("Sibi"): A monoclonal antibody directed at APRIL. The Data: Showed a 50% reduction in proteinuria at interim analysis and a nearly 98% reduction in APRIL levels. Status: Currently has conditional FDA approval. Atacicept: A fusion protein that dual-blocks both BAFF and APRIL. The Data (ORIGIN trials): Demonstrated a 45.7% proteinuria reduction at 36 weeks and, notably, stabilization of eGFR slope in long-term follow-up. Pronunciation Debate: Is it "Attack-a-cept" or "A-tassi-cept"? The investigators say "Attack," because it’s out for blood. The Complement Contender: IptacopanMechanism: A factor B inhibitor that specifically targets the alternative complement pathway, which is increasingly recognized as a key driver of IgAN damage. The APPLAUSE Study: This oral, twice-daily pill showed a 38% reduction in proteinuria at nine months. Safety First: Because complement blockade increases the risk of infections from encapsulated bacteria, patients must be up to date with vaccinations for meningitis, streptococcal and pneumococcal infections. The Verdict: Who Wins the Bracket?Tune in to find out what our experts think… then fill out your own bracket!ReferencesAtaciceptLafayette R, Barbour SJ, Brenner RM, Campbell KN, Doan T, Eren N, Floege J, Jha V, Kim BS, Liew A, Maes B, Pal A, Pecoits-Filho R, Phoon RKS, Rizk DV, Suzuki H, Tesař V, Trimarchi H, Wei X, Zhang H, Barratt J; ORIGIN Phase 3 Trial Investigators. A Phase 3 Trial of Atacicept in Patients with IgA Nephropathy. N Engl J Med. 2026 Feb 12;394(7):647-657. doi: 10.1056/NEJMoa2510198. Epub 2025 Nov 6. PMID: 41196369.Lafayette R, Barbour S, Israni R, Wei X, Eren N, Floege J, Jha V, Kim SG, Maes B, Phoon RKS, Singh H, Tesař V, Lin CJF, Barratt J. A phase 2b, randomized, double-blind, placebo-controlled, clinical trial of atacicept for treatment of IgA nephropathy. Kidney Int. 2024 Jun;105(6):1306-1315. doi: 10.1016/j.kint.2024.03.012. Epub 2024 Mar 27. PMID: 38552841.SibeprenlimabPerkovic V, Trimarchi H, Tesar V, Lafayette R, Wong MG, Barratt J, Suzuki Y, Liew A, Zhang H, Carroll K, Jha V, Quevedo A, Han SH, Praga M, Chacko B, Sahay M, Cheung CK, Kooienga L, Walsh M, Xia J, Fajardo C, Shah L, Hafkin J, Rizk DV; VISIONARY Trial Investigators Group. Sibeprenlimab in IgA Nephropathy - Interim Analysis of a Phase 3 Trial. N Engl J Med. 2026 Feb 12;394(7):635-646. doi: 10.1056/NEJMoa2512133. Epub 2025 Nov 8. PMID: 41211929.Mathur M, Barratt J, Chacko B, Chan TM, Kooienga L, Oh KH, Sahay M, Suzuki Y, Wong MG, Yarbrough J, Xia J, Pereira BJG; ENVISION Trial Investigators Group. A Phase 2 Trial of Sibeprenlimab in Patients with IgA Nephropathy. N Engl J Med. 2024 Jan 4;390(1):20-31. doi: 10.1056/NEJMoa2305635. Epub 2023 Nov 2. PMID: 37916620; PMCID: PMC7615905.IptacopanPerkovic V, Barratt J, Rovin B, Kashihara N, Maes B, Zhang H, Trimarchi H, Kollins D, Papachristofi O, Jacinto-Sanders S, Merkel T, Guerard N, Renfurm R, Hach T, Rizk DV; APPLAUSE-IgAN Investigators. Alternative Complement Pathway Inhibition with Iptacopan in IgA Nephropathy. N Engl J Med. 2025 Feb 6;392(6):531-543. doi: 10.1056/NEJMoa2410316. Epub 2024 Oct 25. PMID: 39453772.Zhang H, Rizk DV, Perkovic V, Maes B, Kashihara N, Rovin B, Trimarchi H, Sprangers B, Meier M, Kollins D, Papachristofi O, Milojevic J, Junge G, Nidamarthy PK, Charney A, Barratt J. Results of a randomized double-blind placebo-controlled Phase 2 study propose iptacopan as an alternative complement pathway inhibitor for IgA nephropathy. Kidney Int. 2024 Jan;105(1):189-199. doi: 10.1016/j.kint.2023.09.027. Epub 2023 Oct 31. PMID: 37914086. The hosts and guests of this GN in 10 episode do not have any disclosures to make relevant to the content of this episode.

In this episode of GN in Ten, hosts Dr. Kenar Jhaveri and Dr. Koyal Jain break down the essential "must-knows" for ANCA-associated vasculitis (AAV). Geared toward board preparation and clinical practice, this bite-sized session covers everything from the initial diagnosis and the role of kidney biopsy to the latest advancements in induction and maintenance therapy.Key Discussion PointsDiagnosis & Biopsy Strategy: Why checking specific MPO and PR3 titers is more reliable than general C/P-ANCA. The hosts also discuss the value of biopsy in older patients to assess chronicity and guide treatment duration.Induction Therapy: Comparing the "three pillars" of induction: Rituximab, Cyclophosphamide (IV vs. oral), and the increasingly popular combination therapy for organ-threatening disease.The Steroid Taper: A shift toward "less is more." Following the PEXIVAS protocol, the hosts explain how to aggressively taper steroids to minimize toxicity, especially when using adjunctive therapies.Plasma Exchange (PLEX): Does it still have a role? A nuanced look at the PEXIVAS trial results and why PLEX is now largely reserved for severe pulmonary hemorrhage or rapidly worsening AKI.Avacopan (C5a Receptor Inhibitor): Insights from the ADVOCATE trial on how this steroid-sparing agent is changing the landscape of AAV treatment.Maintenance: Long-term strategies using Rituximab (typically up to 18 months) or Azathioprine, and when to consider switching agents for refractory cases.Essential Reading & ResourcesTo master ANCA vasculitis, the hosts recommend reviewing these landmark studies:PEXIVAS: Plasma Exchange and Glucocorticoids in ANCA-Associated Vasculitis — Evaluated PLEX and reduced-dose steroids.ADVOCATE: Avacopan for the Treatment of ANCA-Associated Vasculitis — The landmark trial for C5a receptor inhibition.RAVE: Rituximab versus Cyclophosphamide for ANCA-Associated Vasculitis — Established rituximab as a standard for induction.MAINRITSAN: Rituximab versus Azathioprine for Maintenance in ANCA-Associated Vasculitis — Compared maintenance strategies.RITUXVAS: Rituximab versus Cyclophosphamide in ANCA-Associated Renal Vasculitis — Induction in patients with severe renal involvement.RITAZAREM: Rituximab as Maintenance Therapy in Relapsing ANCA-Associated Vasculitis — Focus on maintenance for relapsing disease.

In this episode of GN in Ten, hosted by Dr. Kenar Jhaveri and Dr. Koyal Jain, takes a deep dive into the specialized world of pediatric glomerular disease. Joining the show are world-renowned pediatric nephrologists Dr. Louise Oni (Great Ormond Street Hospital, London) and Dr. Jun Oh (University of Hamburg, Germany) to discuss the "pediatric lag" in drug development and the massive global efforts currently underway to bring targeted therapies to children.Key HighlightsThe C3G Breakthrough: Discussion on the "wave of excitement" following adult trials for iptacopan and pegcetacoplan, and how these results are paving the way for pediatric use.SGLT2 Inhibitors in Children: Insights into the collaborative global effort that overcame initial industry waivers to launch a landmark clinical trial for SGLT2 inhibitors in children aged 2–17.Challenges in Rare Disease: Why international collaboration and registries are vital for treating ultra-rare conditions like Anti-GBM disease and C3G in small pediatric populations.The Future of Genetics: A look toward the next 15 years, where genetic screening may shift the focus from treating active disease to early prevention.Managing Long-term Immunosuppression: The delicate balance of using B-cell depletion (Rituximab) in developing immune systems to preserve "childhood" and avoid dialysis.Featured GuestsDr. Louise Oni: Professor of Pediatric Nephrology at Great Ormond Street and Chair of the ESPN Glomerular Disease Working Group.Dr. Jun Oh: Professor of Pediatrics at the University of Hamburg and a leader in the ISGD Pediatric Committee.Resources & Mentioned StudiesInternational Society of Glomerular Disease (ISGD): Learn more about the society’s mission and join for free!ESPN Glomerular Disease Working Group: Clinical research and educational resources for pediatric nephrologists.NephCure: A key partner in driving global pediatric clinical trials and supporting families affected by rare kidney disease.APPEAR-C3G Trial (Iptacopan): Phase 3 study evaluating the first approved treatment for C3G.VALIANT Trial (Pegcetacoplan):  Recent Phase 3 results showing success in both adult and adolescent patients (12+), published in the New England Journal of Medicine. 

In this Board Review Bonus episode of GN in Ten, hosts Dr. Kenar Jhaveri (Northwell Health/Hofstra University) and Dr. Koyal Jain (UNC Chapel Hill) dive into the crucial topic of Lupus Nephritis. Special guest, Northwell fellow Dr. Mahmoud Abdelaziz, asks Kenar and Koyal the tough questions about key topics in diagnosing and managing LN. Tune in to learn about diagnosis and initial suspicion of kidney involvement in Systemic Lupus Erythematosus (SLE), the six histological classifications (Class I-VI) of lupus nephritis, and an overview of induction and maintenance treatment algorithms for Class III and IV (proliferative) and Class V (membranous) lupus nephritis, including the use of reduced-dose glucocorticoids, MMF, cyclophosphamide (Euro-lupus vs. NIH protocols), and newer agents like voclosporin and belimumab. The GN in Ten hosts also discuss essential supportive care, like pneumocystic pneumonia prophylaxis (and the associated controversy with sulfamethoxazole/trimethoprim), multidisciplinary management, and management of special situations like pregnancy and Thrombotic Microangiopathy (TMA).Referenced Resources and Studies:KDIGO 2024 Clinical Practice Guideline for the Management of Lupus NephritisAmerican College of Rheumatology (ACR) Guidelines for Lupus Nephritis and Systemic Lupus Erythematosus Euro-Lupus Nephritis Trial and ProtocolNIH Lupus Nephritis Trial and ProtocolLUNAR Trial

In this episode, world-renowned complement expert Carla Nester (University of Iowa) joins Koyal and Kenar to discuss the state of the art in C3 glomerulopathy and other complement-mediated kidney diseases, the opportunities and unknowns of targeted treatments, the recent advances in understanding of all things complement, and how her med/peds specialization brings additional superpowers to her clinical practice.Dr. Nester is an adult and pediatric nephrologist, currently serving as Professor of Pediatrics and Internal Medicine in the Carver College of Medicine at the University of Iowa, where she also directs or co-directs the Molecular Otolaryngology and Renal Research Laboratory, Pediatric Glomerular Disease Clinic, Rare Renal Disease Clinic, and nephrology fellowship program. She specializes in the diagnosis, clinical management, and transplantation of complement-mediated kidney diseases, including C3 Glomerulopathy (C3G) and Atypical Hemolytic Uremic Syndrome (aHUS), and is a leading authority on the successful renal transplant protocol for aHUS patients. Her basic science research focuses on using unique complement functional assays to define complement dysregulation in patients with complement-mediated renal disease.Dr. Nester is co-chair of the SEISMIC Cross-Stakeholder Summit (AddreSsing accEss Issues in diagnoSis and treatMent of C3G nephropathy and IC-MPGN, July 17-19 2025), hosted by ISGD, NephCure and CompCure. To stay informed of the meeting results, sign up for the ISGD mailing list.Disclosures:Dr. Nester has disclosed the following relationships:Novartis: Research Grant Site Principal Investigator, Novartis: Consultant, Apellis: Research Grant Site Principal Investigator, Apellis: Consultant, Biocryst: Research Grant Site Principal Investigator, Biocryst: Consultant, Vertex: Scientific/Medical Advisory Board Member, Retrophin/Travere: Research Grant Site Principal Investigator, AstraZeneca: Consultant