Deep Dive Into World Congress of Nephrology 2026 (WCN’26): Transforming Kidney Care and Innovation
May 04, 2026
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The World Congress of Nephrology 2026 (WCN’26) is the flagship event of the International Society of Nephrology (ISN). The Congress was co-hosted by the Japanese Society of Nephrology (JSN) and the Asian Pacific Society of Nephrology (APSN). This conference marked a pivotal moment in the evolution of kidney disease research, with over 3,000 abstracts presented across a wide spectrum of clinical and translational science. Among these, late-breaking abstracts stood out as the most impactful, offering early signals of practice-changing therapies and next-generation treatment paradigms.
When and Where: March 28–31, 2026 | Yokohama, Japan
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Key Theme of WCN 2026: From Symptom Management to Mechanism-Driven, Disease-Modifying Therapies in Nephrology
Quick Highlights of WCN2026
The World Congress of Nephrology 2026 reinforced its role as a key platform for advancing kidney research, precision medicine, and mechanism-driven therapies, with a strong focus on CKD, IgA nephropathy, lupus nephritis, and rare glomerular diseases. Scientific attention centered on targeted immunological pathways (APRIL inhibition, B-cell modulation), metabolic approaches (GLP-1 and SGLT2), and emerging modalities such as complement inhibition and cell-based therapies.
Major players, including Novo Nordisk, Roche/Genentech, Jiangsu Hengrui Medicine, Novartis, and AstraZeneca, highlighted growing commercial prioritization of nephrology. Overall, WCN 2026 underscored a clear shift toward molecularly driven, disease-modifying treatments and improved patient stratification.
Semaglutide Moves Upstream: Expanding from Metabolic Control to Kidney Protection
One of the most discussed late-breaking abstracts was the REMODEL trial (NCT04865770), which evaluated the mechanistic effects of semaglutide in patients with Type 2 Diabetes (T2D) and CKD. About 40% of individuals with T2D also have CKD, making T2D the primary cause of kidney failure worldwide. Although several pathways are implicated, the exact mechanism of action for semaglutide’s kidney-protective properties is yet unknown. REMODEL study (52-week, randomized (2:1), parallel-group trial comparing once-weekly SC semaglutide 1 mg treatment with placebo) used a pathophysiologically integrated approach to evaluate the kidney-protective effects of semaglutide. REMODEL was developed as a follow-up study to the important FLOW trial (led to FDA approval of semaglutide in chronic kidney disease), which showed that semaglutide significantly improved cardiorenal outcomes, whereas the FLOW trial confirmed the treatment’s effectiveness. REMODEL aimed to explore a different question: The underlying reasons behind these benefits.
Key Findings
- The REMODEL trial did not show an improvement in kidney oxygenation (its primary imaging endpoint).
- However, it demonstrated direct renal protective mechanisms, beyond glucose-lowering. The drug showed an impact on
- Reduction in perirenal and hilar fat
- Improvements in markers of fibrosis and inflammation
- Evidence of changes in endothelial cell biology
- Decreases in inflammatory cell activity within the kidney
- Complemented findings from FLOW-related analyses showing improved kidney outcomes across patient subgroups
Impact on Treatment Paradigm
- The findings shift focus from “does semaglutide work in CKD?” (Already shown in FLOW) to “how does it protect the kidney?” (addressed by REMODEL).
- Strengthens the concept of semaglutide as a kidney-directed therapy, not only a metabolic drug.
- Supports earlier use in CKD patients even beyond strict glycemic indications
- Opens the door for combination metabolic renal therapeutic strategies. Combining GLP-1 receptor agonists with SGLT2 inhibitors may offer complementary kidney protection.
Conclusion: While those findings established clinical efficacy, they did not fully elucidate the underlying biology. This development represents a pivotal shift in the therapeutic positioning of GLP-1 receptor agonists, transitioning from a predominantly metabolic-focused role to a broader, multi-system application. Notably, emerging evidence highlights their direct nephroprotective benefits, reinforcing their potential as integral agents in renal disease management beyond glycemic control.
Iptacopan Redefines IgA Nephropathy: 2-Year APPLAUSE Data Signal a Paradigm Shift Toward Disease Modification
Iptacopan (FABHALTA), developed by Novartis, is an oral complement factor B inhibitor targeting the alternative complement pathway, a key driver of kidney injury in IgA Nephropathy (IgAN). The pivotal APPLAUSE-IgAN trial (NCT04578834) is a Phase III, randomized, double-blind, placebo-controlled study evaluating iptacopan on top of standard-of-care (including RAAS blockade) to assess its impact on proteinuria reduction and long-term kidney function decline. The drug received FDA accelerated approval in 2024 for IgAN based on proteinuria reduction, with ongoing efforts toward full approval driven by confirmatory eGFR outcomes. Novartis is positioning iptacopan as a first-in-class complement inhibitor franchise, with expansion across multiple complement-mediated renal diseases. At WCN 2026, new 2-year data from the Phase III APPLAUSE-IgAN trial showed that iptacopan significantly slowed kidney function decline in high-risk IgA nephropathy patients. Novartis described plans to use these data to support regulatory submissions for iptacopan in 2026.
Key Findings
- In a severe disease population, placebo patients had rapid eGFR loss (~6 mL/min/1.73 m²/year), while iptacopan reduced decline to just over three, about a 50% slowing of disease progression.
- The drug also reduced the risk of the composite outcome of ≥30% eGFR decline or kidney failure by 43%, supporting meaningful long-term kidney protection.
- Earlier results showed a 38% reduction in proteinuria, now reinforced by evidence of sustained benefit on kidney function.
- Safety: Overall, adverse events were similar between groups. There was a small increase in infections with iptacopan, but they were generally manageable, with no deaths or severe infection signals.
Impact on Treatment Paradigm
- Foundational therapies (Renin-angiotensin system inhibitors and SGLT2 inhibitors) remain essential
- Add-on benefit: Even in patients already receiving SGLT2 inhibitors, iptacopan provided additional kidney protection, supporting a combination therapy strategy rather than substitution.
- Combination treatment is likely required to achieve optimal outcomes, especially in patients with high proteinuria, and will probably require multiple therapies with complementary mechanisms.
- Iptacopan showed a linear eGFR decline without an initial acute drop, making treatment effects easier to interpret compared with drugs that have early hemodynamic changes.
- Earlier intervention may become increasingly important, including earlier diagnosis, earlier initiation of treatment, and reconsideration of biopsy thresholds and optimal timing of therapy.
Conclusion: The findings suggest a shift toward multi-drug (combination-based therapy), mechanism-based treatment strategies in IgAN, especially for high-risk patients, with earlier and more aggressive intervention likely to become increasingly important.
Targeted Gut–Kidney Axis Therapy: HR19042 (Budesonide) in IgAN
A key highlight from the High Impact Clinical Trials session at the WCN’26 was a late-breaking Phase II/III (NCT05016323) randomized, double-blind, placebo-controlled study evaluating HR19042 (targeted budesonide delivery to distal ileum) in patients with primary IgA nephropathy. HR19042 is a targeted-release formulation of budesonide being developed by Jiangsu Hengrui Pharmaceuticals, a leading China-based pharma player expanding its footprint in immunology and nephrology. The therapy is designed to deliver corticosteroid activity to the distal ileum, targeting mucosal immune dysregulation along the gut–kidney axis in IgAN.
Key Findings
The study met its primary endpoints, demonstrating
- Significant reduction in proteinuria by ~41–48% at 9 months
- Slowing of kidney function decline (eGFR preservation), showing a smaller eGFR drop at 12 months
- Favorable safety and tolerability profile
Impact on Treatment Paradigm
- Trial findings strengthen the concept that targeting gut mucosal immunity is a viable disease pathway in IgAN. Unlike traditional systemic steroids, HR19042 is designed to
- Deliver budesonide locally to the Gut-associated Lymphoid Tissue (GALT)
- Target the source of pathogenic IgA production
- Trial findings strengthen the concept that targeting gut mucosal immunity is a viable disease pathway in IgA nephropathy.
- Supports HR19042 as a potential early disease-modifying therapy, not just symptomatic proteinuria control
- Adds to the growing shift toward mechanism-based, targeted therapies in IgAN.
Conclusion: Overall results indicate clinically meaningful and consistent disease-modifying effects within a relatively short treatment period. From a clinical and market perspective, this represents a meaningful inflection point: it signals the entry of a disease-modifying therapy in IgAN, moving beyond conventional standards such as RAAS blockade and nonspecific steroids, and positioning targeted budesonide as a foundational component of treatment algorithms. At the same time, it introduces competitive pressure on emerging pipeline therapies, including complement inhibitors and BAFF/APRIL-targeting agents, given its oral administration, targeted mechanism, and improved safety profile versus systemic immunosuppression. Taken together, HR19042 is likely to be adopted as a first-line add-on therapy before biologics, anchoring a more stepwise, mechanism-driven treatment paradigm in IgAN.
Paradigm Shift in Idiopathic Nephrotic Syndrome (INS): Precision Immunology Moves Center Stage
A key highlight from WCN’26 underscored the rapid evolution of precision medicine in idiopathic nephrotic syndrome, with Phase III global data evaluating cell-targeted approaches such as obinutuzumab-based, B-cell directed therapies in combination with next-generation immunomodulators. Obinutuzumab, developed by Roche/Genentech, is a next-generation anti-CD20 monoclonal antibody designed for enhanced B-cell depletion. The Phase III, randomized, open-label INShore trial (NCT05627557) compared obinutuzumab with Mycophenolate Mofetil (MMF) in patients with INS.
Key Findings
- Targeted depletion/modulation of pathogenic B-cells
- Improved
- Proteinuria remission rates
- Relapse prevention
- Reduced reliance on broad, non-specific immunosuppression
Impact on Treatment Paradigm
- Reinforces that B-cell targeting is a viable, mechanism-driven strategy in idiopathic nephrotic syndrome
- Enables precision immunology approaches, moving beyond steroid-dependent management
- Supports stratified, patient-specific treatment, addressing disease heterogeneity
- Reduces the long-term toxicity burden associated with generalized immunosuppressant
- Positions B-cell directed therapies as potential foundational or early-line options in treatment algorithms.
Conclusion: Overall, the findings highlight a significant shift toward targeted, immune pathway-specific intervention in idiopathic nephrotic syndrome. This marks a transition from conventional, broad immunosuppression to precision-driven disease control, with the potential for more durable remissions, improved safety, and optimized long-term outcomes. Collectively, these advances signal the emergence of a more refined, mechanism-based treatment paradigm in nephrology.
| WCN 2026: Key Trial Highlights and Therapeutic Breakthroughs | ||||||
| Drug Name | Company | NCT ID | Abstract Number | Patient Segment | Results | Conclusion |
| Semaglutide | Novo Nordisk | NCT04865770(REMODEL) | 3792 | T2D and CKD | Reduction in RARI observed across both groups (SGLT2i users and non-users)No significant interaction effect (p-int = 0.29) consistent benefit irrespective of SGLT2i useRenal Fibrosis Markers (MRI-based)Increase in cortical ADC and delta ADC with semaglutide vs placeboOxygenation Markers (R2 Cortical and Medullary)No significant differences between semaglutide and placebo across subgroups (p-int = 0.88 and 0.84)Glomerular Kidney Perfusion (GKP)Effect consistent regardless of SGLT2i use (p-int = 0.42) | Consistent renal benefit independent of SGLT2i use, with signals toward antifibrotic effects; however, underlying mechanisms remain incompletely defined. |
| Finerenone + Empagliflozin | Bayer | NCT05254002(CONFIDENCE) | 4303 | Effecton the urine proteome | Finerenone Monotherapy (Month 6)236/239 significantly altered urinary proteins were decreased vs baselineOnly three proteins increasedImproved tubular reabsorptionTransferrin was the most upregulated markerEmpagliflozin Monotherapy177/264 proteins decreased, while 87 proteins increasedCombination Therapy (finerenone + empagliflozin)697 proteins decreased, 57 increasedAmplified suppression of complement and coagulation pathways compared to either agent alone | Combination therapy demonstrates synergistic, multi-pathway renal protection with enhanced suppression of inflammatory and complement pathways versus monotherapy. |
| Budesonide(HR19042) | Jiangsu Hengrui | NCT05016323 | 5099 | Primary IgAN | Proteinuria Reduction (UPCR) at Month 9HR19042 12 mg: −40.9% vs. placeboHR19042 16 mg: −47.7% vs. placeboBoth doses showed highly significant reductions (p<0.0001)Kidney Function (eGFR) at Month 12HR19042 12 mg: +3.30 mL/min/1.73 m² vs. placebo (p = 0.0105)HR19042 16 mg: +5.22 mL/min/1.73 m² vs. placebo (p = 0.0001)Indicates significantly slower decline in kidney function vs placeboSafety ProfileSerious Adverse Events: 12 mg: 8.5%; 16 mg: 10.5%; Placebo: 3.8%Discontinuations due to TEAEs: 12 mg: 0.9%; 16 mg: 3.8%; Placebo: 1%No deaths reported | Demonstrates strong, dose-dependent proteinuria reduction with meaningful eGFR preservation, supporting its role as a targeted, disease-modifying therapy in IgAN with a manageable safety profile. |
| Finerenone + Empagliflozin | Bayer | NCT05254002(CONFIDENCE) | 4303 | Patients with initialdecline in eGFR | eGFR Change (Day 14, Least-squares Mean): Combination: −6.1; Finerenone: −1.3; Empagliflozin: −4Acute eGFR decline (>10%): Combination: 58.5%; Empagliflozin: 47.3%; Finerenone: 30%Predictors of Acute eGFR Decline (>10%)Higher baseline eGFR: OR 1.09Higher systolic blood pressure: OR 1.07Combination vs. empagliflozin: OR 1.6Combination vs. finerenone: OR 2.9 | Combination therapy is associated with a greater initial eGFR dip, reflecting enhanced hemodynamic effects, with identifiable predictors guiding patient selection and monitoring |
| Obinutuzumab | Roche | NCT05627557(INShore) | 7699 | Idiopathicnephrotic syndrome (INS) | Sustained CR at Week 52: OBI: 95.5%; MMF: 73.2% (p = 0.0031)RFS: 75% reduction in risk of relapse or death with OBI; hazard ratio: 0.25 (p = 0.0074)Glucocorticoid Exposure: Lower cumulative dose with OBI; median difference: −8.86 mg/kg (p = 0.0391)Relapse Rates (Baseline to Week 52): OBI: four relapses; MMF: 23 relapses (p = 0.0015)Sustained CR at Week 76: Numerically higher with OBI (p = 0.1399)Safety ProfileTreatment Discontinuation (up to Week 52): OBI: 2.3% (one patient); MMF: 22% (9 patients)Grade ≥3 AEs: OBI: 25.0%; MMF: 7.3%One patient in each arm discontinued | Superior efficacy in sustaining remission and preventing relapse with reduced steroid exposure, positioning B-cell targeting as a highly effective strategy in INS despite higher AE rates. |
| Iptacopan | Novartis | NCT04578834(APPLAUSE-IgAN) | Primary IgAN | Kidney Function (eGFR Slope): –3.10 vs. –6.12 mL/min/1.73 m²/year (49.3% slower decline)Composite Kidney Failure Events: 21.4% vs. 33.5%; HR: 0.57Proteinuria (24-h UPCR <1 g/g): 40.7% vs. 23.7%; achieved target | Delivers robust and clinically meaningful renal protection, significantly slowing disease progression and reinforcing complement inhibition as a disease-modifying approach in IgAN. | |
| Atrasentan | Novartis | NCT05834738(ASSIST) | 1868 | IgAN | Primary Endpoint: Change in proteinuria (24-h UPCR) from baseline to Week 12 (Treatment Period 1)Secondary Endpoint: Change in proteinuria at Week 24 (Treatment Period 2) | Ongoing study evaluating proteinuria reduction, aiming to establish endothelin receptor antagonism as a targeted therapeutic strategy in IgAN. |
| HSK39297 | Haisco Pharmaceutical | NCT06670352 | 5558 | Primary IgAN | Proteinuria Reduction (24 h-UPCR at Week 12): –52.3% (50 mg BID), –52.5% (100 mg BID), –48.2% (200 mg QD) vs. –5.3% (placebo)Placebo-adjusted Reduction: –49.6%, –49.8%, –45.3% (all statistically significant). All secondary proteinuria-related endpoints met.Kidney function (eGFR) remained stable over time.Mechanism (AP Activity Inhibition): –64% (50 mg BID), –85% (100 mg BID), –79% (200 mg QD)Common TEAEs (≥5% incidence): Upper respiratory tract infection: 9.1% vs. 0% | Shows potent proteinuria reduction with stable kidney function and strong pathway inhibition, supporting its potential as an effective complement-targeted therapy in IgAN. |
| Atacicept | Vera Therapeutics | NCT04716231(ORIGIN 3) | 6572 | IgAN | Proteinuria Reduction (UPCR): –45.7% (atacicept) vs. –6.8% (placebo)Treatment Difference: –41.8% (95% CI: 28.9–52.3%; P<0.001)Biomarker Impact (Serum Gd-IgA1): –68.3% (atacicept) vs. –2.9% (placebo)Hematuria Resolution: 81% (atacicept) vs. 20.7% (placebo)Safety Profile: Comparable to placebo | Demonstrates significant proteinuria reduction and biomarker improvement with favorable safety, reinforcing BAFF/APRIL inhibition as a promising disease-modifying strategy. |
| Iptacopan | Novartis | NCT04817618(APPEAR-C3G) | 4069 | C3G | Proteinuria Reduction (FMV UPCR): 35.9% at Month 12; 34.2% sustained at Month 24 (iptacopan arm)Placebo: Iptacopan switch: 34% (Month 12): 29.7% at Month 24Kidney Function (eGFR slope)Pre-treatment decline: –7.22 mL/min/1.73 m²/yearPost-iptacopan: –0.29 mL/min/1.73 m²/year | Sustained proteinuria reduction and marked stabilization of eGFR highlight its strong disease-modifying potential in C3G. |
| NOTE: RARI: Relative Area of Renal Injury (RARI); p-int: p interaction; UPCR: Urine Protein-Creatinine Ratio; eGFR: Estimated Glomerular Filtration Rate; CR: complete remission; RFS: Relapse-free survival; FMV: First Morning Void | ||||||
Spotlight on Emerging Excellence: Award-winning Top Scored Abstracts Shaping the Future of Nephrology
WCN’26 award-winning abstracts emphasized disease biology over clinical endpoints. Advanced understanding of glomerular disease mechanisms and podocyte injury.
Key Drivers Identified
- Cytoskeletal signaling (GIT1/GIT2 axis) in glomerular integrity
- Autoantibody-mediated pathways in FSGS and podocytopathies
- Disease Complexity: Presence of slit diaphragm–targeting autoantibodies and age-specific immune signatures highlights heterogeneity
- Strategic Impact: Strong push toward mechanism-driven, precision approaches
- Future Direction: Enables biomarker-led diagnosis, risk stratification (including transplant), and personalized therapy selection.
Major Trends Shaping Future Nephrology
- Paradigm Shift in Care: Moving from uniform, symptom-driven approaches to mechanism-based, layered treatment strategies
- Convergence of Science: Integration of immunology, metabolism, and molecular biology into a unified therapeutic framework
Rise of Combination Therapy
- RAAS + SGLT2 inhibitors as backbone
- Increasing addition of targeted agents (complement inhibitors, endothelin antagonists, gut-directed therapies)
- Driving multi-pathway disease control, especially in complex diseases like IgAN
- Focus on root biology: Transition from downstream markers (e.g., proteinuria) to upstream disease drivers.
- Emphasis on immune modulation, metabolic reprogramming, and structural kidney effects
- Reinforces heterogeneity in diseases like FSGS and podocytopathies
Emergence of Precision Nephrology
- Enabled by biomarkers, immune profiling, and autoantibody signatures
- Supporting patient stratification and personalized therapy selection
Evolving Treatment Sequencing
- Oral targeted therapies moving earlier due to favorable safety
- Biologics and intensive therapies reserved for high-risk or refractory patients
- Shift toward a stepwise, mechanism-aligned treatment paradigm.
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