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        <title>Frontiers in Nephrology | Glomerular disease section | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/nephrology/sections/glomerular-disease</link>
        <description>RSS Feed for Glomerular disease section in the Frontiers in Nephrology journal | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-05-14T13:34:26.628+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2026.1772736</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2026.1772736</link>
        <title><![CDATA[Successful use of obinutuzumab in focal segmental glomerulosclerosis with inadequate response to rituximab: a case report]]></title>
        <pubdate>2026-03-03T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Andreia Rita Henriques</author><author>João Venda</author><author>Emanuel Ferreira</author><author>Nuno Oliveira</author><author>Helena Sá</author>
        <description><![CDATA[IntroductionPodocytopathies such as minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) remain therapeutic challenges in adults. Although corticosteroids and rituximab (RTX), a chimeric anti-CD20 monoclonal antibody, are effective in most patients, up to 10% show resistance or relapse despite B-cell depletion. Obinutuzumab (OBZ), a humanized type II anti-CD20 monoclonal antibody, achieves deeper and more sustained B-cell depletion and may overcome RTX inadequate response.Case reportA 33-year-old woman presented with nephrotic syndrome (proteinuria 7.1 g/24 h, serum albumin 2.6 g/dL, preserved renal function). Kidney biopsy revealed primary FSGS. She achieved only partial remission with corticosteroids and cyclosporine. RTX (1 g × 2 doses) induced transient peripheral B-cell depletion but no complete remission. A second biopsy excluded chronic changes, and genetic testing for hereditary podocytopathy was negative. Thus 67 weeks after diagnosis and initial treatment with persistent proteinuria > 1g/24 h and hypoalbuminemia, the patient received OBZ (1 g × 2 doses, two weeks apart). Two months later, she achieved complete remission (proteinuria 0.2 g/24 h, serum albumin 3.7 g/dL), with sustained B-cell depletion and no adverse events. A repeat administration of OBZ (1 g) was performed 10 months later due to B-cell repopulation, rising proteinuria (0.6 g/24 h), and mild hypoalbuminemia (serum albumin 3.4 g/dL), successfully re-inducing complete remission (proteinuria 0.2 g/24 h, serum albumin 3.8 g/dL).DiscussionThis case illustrates the potential of OBZ as an effective therapeutic option in podocytopathies with RTX inadequate response. The superior efficacy of OBZ may result from enhanced antibody-dependent cellular cytotoxicity, depletion of tissue-resident B cells, and reduced immunogenicity compared with RTX. OBZ may thus offer an alternative in refractory MCD/FSGS.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2026.1648950</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2026.1648950</link>
        <title><![CDATA[Treatment practices, characteristics and outcome of immunoglobulin A nephropathy – a Swiss single center experience]]></title>
        <pubdate>2026-02-27T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Danny Thieny Taing</author><author>Bruno Vogt</author><author>Laila-Yasmin Mani</author>
        <description><![CDATA[IntroductionImmunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. Geographic differences in disease course and treatment response are well recognized. The purpose of this analysis was to study clinical and histological characteristics, treatment practices and outcome of IgAN cases from a Swiss tertiary center.MethodsThis retrospective cohort analysis identified 158 cases of adult biopsy-proven IgAN by chart review diagnosed between 1980 and 2016. Following detailed phenotyping, standard descriptive methods and univariate analysis were applied.ResultsThe majority of patients was male and of European ancestry. At diagnosis, mean estimated glomerular filtration rate (eGFR) was 55.7 ml/min/1.73 m2, mean proteinuria was 2.4 g/d and 69.9% of the patients were hypertensive. Clinical presentation varied according to age. Initial biopsies showed moderate to severe tubular atrophy and interstitial fibrosis (IFTA) in 29.1% and crescents in 36.7% of cases. Therapy included renin-angiotensin-aldosterone-inhibitors in 86.7% as well as immunosuppressive therapy in 46.8% including steroids and other immunosuppressive drugs (28.7%), mainly azathioprin. Outcome included 34.1% complete and 22.2% partial remissions, relapses in 32.0% of patients, while 43.0% of patients progressed to ESKD during follow-up (median 100.0 months). Recurrence rate after transplantation was 18.8%. Immunosuppressive therapy was more frequently used in patients with higher proteinuria level, higher hematuria grade, lower eGFR, more intense IgA and complement C3 staining and crescents. Predictors of progression were higher age, lower eGFR, higher proteinuria and blood pressure as well as crescents and higher extent of IFTA on the initial biopsy.ConclusionsThis retrospective cohort analysis gives insight into characteristics and outcome of patients with IgAN from a Swiss tertiary center, treatment practices as well as predictors of outcome and therapy choices. A comparatively high use of immunosuppressive treatment including non-steroid-based regimens was found along with a high rate of progression to ESKD.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2026.1747678</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2026.1747678</link>
        <title><![CDATA[Primary membranoproliferative glomerulonephritis: natural history, pathogenesis, and treatment]]></title>
        <pubdate>2026-02-13T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Edward J. Filippone</author><author>John L. Farber</author>
        <description><![CDATA[Primary membranoproliferative glomerulonephritis (MPGN) is an ultrarare disease characterized by immunofluorescence microscopy as either immune-complex mediated (IC-MPGN) or C3 glomerulopathy (C3), the latter subdivided by electron microscopy to C3 glomerulonephritis (C3GN) and dense deposit disease (DDD). Both IC-MPGN and C3G typically have obvious C3 staining differentiating them from other causes of MPGN histology. Secondary causes must be excluded, including infections, autoimmune disease, and neoplasia. Clinical presentations are variable, including urinary sediment abnormalities, nephrotic syndrome, or a rapidly progressive course. The prognosis is unfavorable with about 50% reaching kidney failure by 10 years. Recurrence following transplantation is frequent, and allograft survival is shortened. The pathogenesis involves dysregulation of the alternate pathway (AP) of complement. Possibly 20% of patients harbor pathogenic mutations in AP proteins or their regulators, and up to 80% have autoantibodies impairing normal regulation. Paraproteins are found in 20 – 40% of otherwise primary MPGN, either directly detectable on biopsy (IC-MPGN) or as dysregulators of the AP. Therapy of MPGN begins with supportive care as for all glomerulopathies. Paraproteins require clone-directed therapy. When immunosuppression is considered, complement inhibition should be first line. Two agents are now FDA approved for C3G, the oral Factor B inhibitor iptacopan and the subcutaneous C3-inhibitor pegcetacoplan, the latter also approved for IC-MPGN. If complement inhibition is unavailable, MMF/steroids may be considered. Following transplantation, protocol biopsies are needed to detect early recurrence with the intent of complement inhibition.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1744454</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1744454</link>
        <title><![CDATA[Progression of immunoglobulin A nephropathy (IgAN) in a Hispanic/Latinx population in the United States]]></title>
        <pubdate>2026-01-09T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>John J. Sim</author><author>Nancy T. Cannizzaro</author><author>Qiaoling Chen</author><author>Sasikiran Nunna</author><author>Mohit Mathur</author><author>Cibele Pinto</author>
        <description><![CDATA[BackgroundImmunoglobulin A nephropathy (IgAN) is a leading cause of chronic kidney disease (CKD) worldwide. While racial and ethnic differences in disease progression are well documented, the Hispanic/Latinx populations remain understudied despite their elevated risk of kidney failure among other CKD populations.ObjectiveThis study aimed to evaluate the kidney function decline and progression in Hispanic/Latinx patients with biopsy-proven IgAN within a large, integrated healthcare system and to contextualize to other racial/ethnic groups.MethodsWe conducted a retrospective case series study of 259 Hispanic/Latinx adults with biopsy-proven IgAN from the Kaiser Permanente Southern California (KPSC) health system. Patients were followed from biopsy to ≥50% decline in the estimated glomerular filtration rate (eGFR), kidney failure, mortality, the study end date of November 30, 2022, or disenrollment. Annualized eGFR decline and the incidence of composite kidney outcomes were assessed.ResultsAt diagnosis, Hispanic/Latinx patients had significant CKD and a high risk of progression to kidney failure, indicated by a median eGFR of 56 ml min−1 1.73 m−2 and a median urine protein/creatinine ratio of 1.8 g/g. Common treatments included immunosuppressive agents (41%), angiotensin-converting enzyme (ACE) inhibitors (48%), and angiotensin receptor blockers (ARBs; 20%). The mean annual eGFR decline was −4.5 ml min−1 1.73 m−2, and 30.9% experienced rapid decline (>5 ml min−1 1.73 m−2 per year). The composite kidney outcome occurred at 73.3 events per 1,000 patient-years, with a median time to event of 2.8 years and a median age at event of 46 years.ConclusionHispanic/Latinx patients with IgAN demonstrate rapid kidney function decline and early-onset kidney failure. These findings underscore the need for earlier detection and targeted management in this underserved group.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1722582</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1722582</link>
        <title><![CDATA[Lower proteinuria is better for patients with IgA nephropathy: a systematic review]]></title>
        <pubdate>2026-01-07T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Ankit Shah</author><author>Manish Maski</author><author>Ogo Egbuna</author><author>Whitney Longstaff</author><author>Janice Stricker-Shaver</author><author>Beth Barber</author>
        <description><![CDATA[BackgroundProteinuria is a well-established and recommended biomarker for disease activity in patients with IgAN. In the most recent version of the KDIGO guideline, the target level of proteinuria changed from < 1.0 g/day to < 0.5 g/day. The objective of this systematic literature review (SLR) is to identify, synthesize, and critically evaluate the evidence from peer-reviewed publications that inform the significance of achieving different proteinuria levels.MethodsWe searched PubMed and Embase (2005-2025) for studies in adult patients diagnosed with IgAN that examined the relationship between proteinuria measured by any method (e.g., uPCR, 24-hour protein excretion) and key kidney outcomes. The review used an a priori protocol following established methodological guidance for systematic reviews. Additionally, the quality of all studies included in the SLR was assessed based on standardized appraisal tools. The evidence was narratively synthesized reporting frequencies and percentages.ResultsTwenty-one unique studies were included (representing 13,006 patients with IgAN). The studies captured in the SLR were mostly observational and they encompassed diverse patient populations, timing of proteinuria assessment, methods of proteinuria measurement and classification, and clinical management strategies, reflecting real-world heterogeneity in IgAN. Despite the differences in individual study methods, results across studies consistently found that lower proteinuria was associated with better kidney outcomes. Specifically, it was clearly established that <0.5 g/day achieved better outcomes than higher proteinuria thresholds.ConclusionThe evidence identified in this SLR affirms the updated KDIGO recommendation to achieve at least a proteinuria level of < 0.5 g/day.Systematic Review Registrationhttps://www.crd.york.ac.uk/prospero/, identifier CRD420251062821.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1715546</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1715546</link>
        <title><![CDATA[Rituximab monotherapy versus glucocorticoid therapy for adult minimal change disease: a retrospective study on noninferiority]]></title>
        <pubdate>2025-12-09T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xiaoyun Li</author><author>Guoxiang Yao</author><author>Yujiao Sun</author><author>Na Li</author><author>Caifeng Gao</author><author>Haiping Wang</author><author>Rong Wang</author><author>Bing Chen</author>
        <description><![CDATA[IntroductionTo verify whether rituximab (RTX) monotherapy is noninferior to glucocorticoids in inducing and maintaining remission in adults with minimal change disease (MCD).MethodWe retrospectively analyzed the clinical data of 60 patients with minimal change disease (MCD) who were diagnosed with MCD by renal pathology biopsy and electron microscopy before their first visit to the Department of Nephrology of Shandong Provincial Hospital between 01/2020 and 01/2024, and were diagnosed with MCD at the first visit without acute kidney injury (AKI). Patients were divided into a RTX treatment group (RTX group, 20 cases) and glucocorticoids (GC) treatment group (GC group, 40 cases). None of the patients had previously received steroid/immunosuppressive therapy. The RTX group received rituximab monotherapy. At the 6-month follow-up, the RTX group received additional rituximab infusions as maintenance therapy. The primary endpoints were the time to induced remission, 12-month remission, and relapse rates in each group; the secondary endpoints were the safety and incidence of side effects.ResultsAfter treatment during the 12-month follow-up period, 57 out of 60 patients (95%) achieved remission, of which 48 (80%) achieved complete remission; and 9 (15%) patients relapsed during the follow-up period. A total of 24 (40%) patients experienced adverse events while receiving treatment. 19 (95%) patients in the RTX group and 38 (95%) patients in the GC group achieved remission within 12 months of follow-up, respectively [the difference in rates between the two groups was 0%, 95% confidence interval (0.08, 11.73)]. In the RTX group, 14 (70%) achieved complete remission. In the GC group, 34 (85%) achieved complete remission (p=0.304). In the RTX group, 2 (10%) patients relapsed, and in the GC group 7 (18%) patients relapsed (p=0.701). 1 (5%) patient in the RTX group and 23 (58%) patients in the GC group experienced adverse events (p=0.000), none of which were severe.ConclusionAdequate RTX monotherapy is noninferior to adequate glucocorticoids in inducing and maintaining remission in adult MCD patients without AKI, with fewer adverse effects and better adherence, and may be considered as a first-line treatment option for adult MCD patients without AKI.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1678502</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1678502</link>
        <title><![CDATA[Genetic and environmental factors associated with alteration of filtration slit proteins and their functions: a scoping review]]></title>
        <pubdate>2025-11-24T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Aolat Adepeju Adepoju</author><author>Mubarak Abubakar Muhammad</author><author>Mubashir Mayowa Adamson</author><author>Shakirudeen Abdulqodri Adewale</author><author>Adedeji Tayyib Adekunle</author><author>Lekan Sheriff Ojulari</author><author>Abdullateef Isiaka Alagbonsi</author>
        <description><![CDATA[BackgroundFiltration slit proteins are important for maintaining the integrity of the glomerular filtration barrier. Genetic mutations and environmental factors can disrupt their structure and functions, leading to proteinuria and kidney diseases. This scoping review aims to synthesize the available information on the genetic and environmental factors that affect the slit proteins to enhance our understanding of the (patho)physiology of glomerular filtration.MethodsOnline databases such as Wiley and PubMed were used. Relevant studies were selected focusing on genetic variations, environmental influences, and their impact on filtration slit proteins. Data extraction and synthesis were conducted to highlight key themes and knowledge gaps.ResultsWe summarized at least 20 proteins and their genes, including nephrin, podocin, phospholipase C Epsilon 1 (PLCE1), CD2-Associated Protein (CD2AP), ITGA 3, synaptopodin, myosin 1E (MYO1E), flotillin-2 (Flot2), podocalyxin, FAT1, Apo Hemoglobin-Haptoglobin (Apo Hb-Hp), spermidine, P-Cadherin, ephrin B1, Zo- 1 (Zona Occluden), MAGI 1&2 (MAGUK inverted), Par- complex, IP-10 (interferon-inducible protein), neurexin 1, and liver type fatty acid binding protein. We also reported at least 8 environmental factors, including oxidative stress, inflammation, heavy metals, air-bone pollutants, high-fat diets, vitamins and micronutrient deficiency, mechanical stretch, and nephrotoxic agents.ConclusionThis review highlights various filtration slit proteins and the mechanisms of their alterations by genetic and environmental factors. It contributes to efforts toward personalized therapeutic strategies for disorders of glomerular filtration.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1673799</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1673799</link>
        <title><![CDATA[Case Report: Maximizing the anti-proteinuric response: a multicenter real-world sparsentan case series in IgA disorders]]></title>
        <pubdate>2025-11-21T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Abhisekh Sinha Ray</author><author>Praveen Errabelli</author><author>Maulik Lathiya</author><author>Neeharik Mareedu</author>
        <description><![CDATA[Immunoglobulin A Nephropathy (IgAN) is a prevalent form of glomerulonephritis that leads to chronic kidney disease (CKD), typically marked by ongoing proteinuria, even when treated with standard therapies such as renin-angiotensin-aldosterone system (RAAS) blockers and occasionally immunosuppression. Proteinuria is a modifiable risk factor crucial for disease advancement. Sparsentan, a dual endothelin receptor and angiotensin receptor blocker (DEARA), has been introduced as a novel therapeutic option focusing on proteinuria. We present a case series featuring seven patients - five diagnosed with IgAN and two with IgA vasculitis (IgAV) - with severe proteinuria who were treated with Sparsentan, sometimes in combination with other medications such as targeted-release formulation (TRF) budesonide, sodium-glucose cotransporter-2 (SGLT2) inhibitors, or mycophenolate. Notable reductions in proteinuria and improvements in blood pressure regulation were observed in these cases. Sparsentan was well-tolerated overall, with no significant hyperkalemia or hepatotoxicity reported in this group. These cases emphasize the real-world experience, promising efficacy and safety of Sparsentan in reducing proteinuria in patients with IgA-mediated glomerular disorders, including its application in combination therapies and patients with concurrent or prior immunosuppression]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1667619</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1667619</link>
        <title><![CDATA[Case Report: Exostosin 1-associated membranous nephropathy and Guillain-Barré syndrome: a common autoimmune etiology?]]></title>
        <pubdate>2025-10-02T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Mariana León-Póo</author><author>Eva López-Melero</author><author>Amir Shabaka</author><author>Carmen Guerrero-Márquez</author><author>María Barcenilla-López</author><author>Clara Cases-Corona</author><author>Enrique Gruss</author><author>Deborah Roldán</author>
        <description><![CDATA[Membranous nephropathy is one of the most common causes of nephrotic syndrome in adults and is caused by the deposition of immune complexes in the subepithelial space of the glomerular basement membranes. On the other hand, Guillain-Barré syndrome is a type of acute, potentially fatal polyneuropathy, which is generally associated with an infection that serves as the initial immunological event and triggers immune-mediated disruption of the axon and/or myelin. We present the case of a 70-year-old patient with concurrent membranous nephropathy and Guillain-Barré syndrome, with subepithelial deposits in the renal biopsy positive for Exostosin 1, and who reached complete renal remission after treatment of Guillain-Barré syndrome with plasmapheresis and systemic corticosteroids, suggesting a common autoimmune origin for both entities.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1653595</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1653595</link>
        <title><![CDATA[From slit diaphragm to autoantigen formation: a SUMOylation-based perspective on minimal change disease]]></title>
        <pubdate>2025-09-18T00:00:00Z</pubdate>
        <category>Opinion</category>
        <author>Emre Leventoğlu</author><author>Bahar Büyükkaragöz</author><author>Sevcan A. Bakkaloğlu</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1667652</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1667652</link>
        <title><![CDATA[Epidemiological changes in anti-glomerular basement membrane disease in Madrid in the context of the COVID-19 pandemic]]></title>
        <pubdate>2025-09-10T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Lina León-Machado</author><author>Gonzalo Sierra-Torres</author><author>Amir Shabaka</author><author>Clara Cases-Corona</author><author>Cristina Vega</author><author>Begoña Rivas</author><author>Diana Ruiz Cabrera</author><author>Gema Fernandez-Juarez</author>
        <description><![CDATA[IntroductionRecent studies in Europe have reported a rising incidence in anti-glomerular basement membrane (anti-GBM) disease, potentially linked to demographic shifts or environmental factors. This study aimed to assess temporal trends in incidence, clinical presentation, and outcomes of anti-GBM disease in two urban areas of Madrid over the past two decades.Materials and methodsWe conducted a retrospective observational study of patients diagnosed with anti-GBM disease between 2006 and 2022 at two urban areas covering 884,000 residents in Madrid. Inclusion required confirmed anti-GBM antibodies with clinical manifestations. Incidence was calculated per 1,000,000 person-years. Data were analyzed across six time periods and compared pre- and post-COVID-19 onset.ResultsA total of 26 cases were identified (mean age 52 ± 26 years; 54% female). Incidence increased from 1.13 cases per million persons-year before 2020, to 4.53 cases per million persons-year after 2020 (p<0.001). No differences were observed in demographic data or environmental exposures over time. Post-COVID-19 cases had lower serum creatinine at presentation (5.09 ± 4 vs. 8.7 ± 3.9 mg/dL, p=0.037), more pulmonary involvement (83.3% vs. 35.7%, p=0.039), and better 1-year renal survival (50% vs. 14.3%, p=0.049). Overall patient survival did not differ between groups.ConclusionsIncidence of anti-GBM disease has increased in Madrid, particularly after the COVID-19 pandemic. Improved renal survival appears linked to earlier diagnosis and management, rather than changes in environmental exposure. These findings highlight the importance of heightened clinical awareness for early detection and treatment of this aggressive disease.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1591512</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1591512</link>
        <title><![CDATA[Case Report: Anti-glomerular basement membrane disease following COVID-19 infection]]></title>
        <pubdate>2025-09-02T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Justin David Tse</author><author>Jackson Wang</author><author>Adarsh Bhat</author><author>Rajib Kumar Gupta</author>
        <description><![CDATA[Anti-glomerular basement membrane (anti-GBM) disease is a rare autoimmune disorder characterized by circulating autoantibodies targeting type IV collagen, leading to rapidly progressive glomerulonephritis. We report a case of a 44-year-old African American female with a history of hypertension who presented with acute kidney injury, hematuria, and shortness of breath. She tested positive for COVID-19 and received antiviral therapy; however, her renal function rapidly deteriorated, with serum creatinine rising from 3.4 to 10 mg/dL. Serologic testing ruled out common autoimmune conditions, but elevated CH50 levels suggested ongoing immune activation. Renal biopsy demonstrated diffuse necrotizing crescentic glomerulonephritis with linear IgG staining, consistent with anti-GBM disease. Despite aggressive therapy, including plasmapheresis, corticosteroids, and dialysis, renal recovery was not achieved. Immunosuppressive therapy was deferred in light of her active COVID-19 infection and the risk of immunosuppression-related complications. This case highlights a potential association between COVID-19 and anti-GBM disease, suggesting viral-induced endothelial injury and aberrant immune activation as possible mechanisms. Given emerging reports of autoimmune kidney diseases following COVID-19, further research is needed to clarify this relationship and guide optimal management. This is particularly important for patients who present with severe renal dysfunction in the context of an active infection.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1594639</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1594639</link>
        <title><![CDATA[IgA nephropathy with crescent cell lesions in a human brucellosis patient: a case report]]></title>
        <pubdate>2025-08-26T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Dongli Qi</author><author>Ricong Yu</author><author>Qijun Wan</author><author>Yi Xu</author>
        <description><![CDATA[Brucellosis is known to impact multiple organ systems in humans, including the urogenital system; however, the occurrence of glomerular diseases is relatively uncommon. In this study, we present the case of a 45-year-old man with no prior history of renal disease who developed gross hematuria, proteinuria, acute kidney injury, anemia, hypoproteinemia, pleural effusion, arthralgia, and lymphadenopathy following an acute Brucella infection. Renal biopsy revealed mesangial proliferative immunoglobulin A (IgA) nephropathy with partial crescents, classified as M1E0S0T0C2 according to the Oxford classification, in conjunction with Brucella spondylitis. The patient achieved complete remission after 4 months of anti-brucellosis therapy with doxycycline, levofloxacin, and rifampicin. In this paper, we present a case study of IgA nephropathy complicated by cellular crescent lesions resulting from acute Brucella infection, which completely resolved following anti-Brucella therapy. In addition, we review previously documented cases of Brucella-associated glomerular disease confirmed through renal biopsy, aiming to offer a reference for clinical diagnosis and treatment.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1593927</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1593927</link>
        <title><![CDATA[Case Report: Full-house renal-limited lupus-like nephritis in pregnancy]]></title>
        <pubdate>2025-06-30T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Lucille Jane Wilkinson</author><author>Sally Stauder</author><author>Brady Culpepper</author><author>Jalal Ibrahim</author><author>Vivekanand Pantangi</author><author>Prathap Kumar Simhadri</author>
        <description><![CDATA[Lupus nephropathy is a common manifestation of systemic lupus erythematosus (SLE), with immune-mediated inflammatory damage to the glomerulus leading to acute kidney injury, chronic kidney disease, and end-stage renal disease. Occasionally, patients present with renal-limited lupus nephropathy with classic full-house staining on immunofluorescence and no signs of systemic lupus. Limited data are available on renal-limited “lupus-like nephropathy” in pregnancy. A 24-year-old G1P0 woman at 14 weeks of gestation was referred to nephrology for further evaluation of 8.4g proteinuria. She was found to be ANA negative with a decreased C1q level and a renal biopsy revealing membranous nephropathy. Immunofluorescence staining was positive for IgG, IgA, IgM, C3, and C1Q, consistent with full-house pattern. She was started on 500 mg pulse dose methylprednisolone for 3 days, which was gradually tapered to 5 mg daily, and cyclosporine 75 mg BID. She delivered a healthy baby via induction at 36 weeks. Six-month follow-up revealed 1g protein on 24-hour urine collection, normal C3/C4 levels, and no signs of SLE. This case report adds to the literature discussing renal-limited “lupus-like nephropathy” in pregnancy and helps guide further management of this condition.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1599316</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1599316</link>
        <title><![CDATA[ANCA-related vasculitis incidence and features before and during the COVID-19 pandemic in Los Angeles, Biobio Province, Chile: an observational retrospective analysis]]></title>
        <pubdate>2025-06-16T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Daniel Enos</author><author>Mariel Hernández</author><author>Gonzalo P. Méndez</author><author>Lysis Cáceres</author><author>Ignacia Bravo</author><author>Josefina Jobet</author><author>Simón Castro</author><author>Lorena Cornejo</author><author>Catalina Vega</author><author>Andrés Salazar</author>
        <description><![CDATA[IntroductionRenal vasculitis is a rare disease, the incidence of which increased markedly during the COVID-19 pandemic in our center. The aim of this study is to compare the incidence and the clinical and histopathological characteristics of anti-neutrophil cytoplasm antibodies (ANCA)-associated vasculitis patients before and during the COVID-19 pandemic.MethodsA single-center observational retrospective analysis of 61 patients with ANCA-associated vasculitis who were divided into two groups according to date of diagnosis: pre-pandemic from 2008 to 2020 (n=37) and during the pandemic from 2020 to the middle of 2022 (n=24). The annual incidence rate was compared, as were characteristics such as age, gender, Birmingham Vasculitis Activity Score (BVAS) score, renal clinic, organ involvement, and ANCA serotype. Biopsy findings, such as optical microscopy glomerular characteristics, crescents, interstitium, immunofluorescence, and electron microscopy findings, were analyzed. Mortality and renal replacement therapy needs were also compared.ResultsThe annual incidence rate was higher in the pandemic group compared to the pre-pandemic group, with 9.6 cases per year vs. 3.1 cases per year [incidence rate ratio (IRR)=3.11, 95% CI 1.86 to 5.20]. No significant differences between the groups were found for clinical characteristics, except for greater hemoptysis frequency in the pandemic group. Significant differences in immunofluorescence and electronic microscopy were observed, with a higher IgG deposit and C3 in the pandemic group (37.5% vs 8.1%, p=0.0064; 43.5% vs 10.8%, p=0.009, respectively), whereas the incidence of pauci-immune patterns was higher in the pre-pandemic group (81.1% vs 54.1%, p=0.016). Mortality and the need for renal replacement therapy were significant higher in the pandemic group (IRR=3.56, CI 95% 1.27–9.98 and IRR=4.24, CI 95% 2.08–8.65, respectively)ConclusionThe incidence of ANCA vasculitis increased during the COVID-19 pandemic and was associated with higher rates of IgG deposit and C3 in the immunofluorescence findings and with higher rates of deaths and dialysis in the pandemic group compared with the pre-pandemic group.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1548679</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1548679</link>
        <title><![CDATA[Efficacy and safety of rituximab for membranous nephropathy in adults: a meta-analysis of RCT]]></title>
        <pubdate>2025-04-29T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Baike Mao</author><author>Jiahui Han</author><author>Jia Wang</author><author>Kan Ye</author>
        <description><![CDATA[BackgroundMembranous nephropathy (MGN) represents a significant challenge in nephrology, with Rituximab emerging as a potential therapeutic intervention.MethodsA comprehensive systematic review was conducted using PubMed, EMBASE, and Web of Science databases, focusing exclusively on randomized controlled trials (RCTs) from January 2002 to November 2024. Stringent eligibility criteria were applied, including studies with at least ten participants, with data extracted by two independent reviewers. The meta-analysis utilized fixed and random effects models to assess Rituximab’s efficacy and safety across multiple outcome measures.ResultsThe meta-analysis revealed nuanced findings across different follow-up periods. At 6 months, complete remission rates showed non-significant odds ratios ranging from 2.12 to 2.48. By 12 months, the pooled odds ratio was 0.8085 (95% CI: 0.2238-2.9213), with complete remission rates varying between 13.8% and 19.4%. Notably, at 24 months, the common effects model demonstrated a statistically significant odds ratio of 5.0792 (95% CI: 2.2609-11.4107, p < 0.0001). Proteinuria reduction showed consistent improvement, with a median difference of 4.3225. Adverse event analysis indicated a relatively low risk, with an odds ratio of 0.9706 (95% CI: 0.5781-1.6297).ConclusionRituximab demonstrates potential efficacy in treating MGN, with promising long-term outcomes and a favorable adverse event profile.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1574239</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1574239</link>
        <title><![CDATA[Real-world challenges associated with the use of four common systemic glucocorticoids in a United States IgAN cohort]]></title>
        <pubdate>2025-04-24T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Giancarlo Pesce</author><author>Mit Patel</author><author>Gaelle Gusto</author><author>Ananth Kadambi</author><author>Aastha Chandak</author><author>Terri Madison</author>
        <description><![CDATA[ObjectivesTo understand the difference in adverse events (AEs), healthcare resource utilization (HCRU), and kidney failure rates in immunoglobulin A nephropathy (IgAN) patients who initiated systemic glucocorticoid (SGC) treatment compared with those who did not.MethodsThe overall cohort was selected from patients with IgAN (ICD-10 codes N02.8 and N04.1) identified in the TriNetX Dataworks database between January 2011 and May 2022. New initiators of dexamethasone, prednisone, prednisolone, or methylprednisolone (SGC cohort) were propensity score (PS) matched 1:1 with patients who did not receive SGC (non-SGC cohort) based on their characteristics at diagnosis. The index date was the date of SGC initiation; for the non-SGC cohort, a pseudo-index date was assigned using the same lag from diagnosis to index date as their PS-matched pairs. Patients with kidney failure before the index/pseudo-index date and their 1:1 PS-matched pairs were excluded.ResultsThe final analysis was conducted in 802 patients (401 PS-matched pairs, mean age 41.2 years, 55% male). Median duration of follow-up was 3.5 and 3.1 years for the SGC and non-SGC cohorts, respectively. Compared with the non-SGC cohort, patients in the SGC cohort had greater frequency of several AEs, including severe infections, greater annualized HCRU and costs, and greater incidence of kidney failure.ConclusionsThis study found that SGC therapy may increase adverse reactions and HCRU in IgAN patients, while comparatively providing no beneficial effects on preserving kidney function.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1542475</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1542475</link>
        <title><![CDATA[Case Report: a novel variant in WT1 leads to focal segmental glomerulosclerosis and uterovaginal anomalies through exon skipping]]></title>
        <pubdate>2025-04-01T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Jonathan Marquez</author><author>Lauren O’Sullivan</author><author>Audrey E. Squire</author><author>Ginny L. Ryan</author><author>Katherine E. Debiec</author><author>Anne-Marie Amies Oelschlager</author><author>Margaret P. Adam</author>
        <description><![CDATA[BackgroundPodocytopathies are a varied set of renal diseases in which podocytes are unable to perform their typical filtration function within the glomerulus. This typically leads to edema, proteinuria, and hypoalbuminemia early in life. Among podocytopathies, focal segmental glomerulosclerosis (FSGS) is characterized by histology demonstrating segmental and focal sclerosis of the glomerular tuft. FSGS affects an estimated 1–20 per one million individuals and leads to significant morbidity and mortality related to renal failure. While FSGS can be attributed to many causes, such as drug reactions and infections, underlying pathogenic genetic variants play an increasingly well-recognized role in this disease.CaseA 38-year-old 46,XX female patient of self-reported Cambodian ancestry was evaluated due to her history of atypical uterovaginal morphology. She had a history of hypertension and nephrotic range proteinuria that was diagnosed early in adulthood. A kidney biopsy at that time revealed FSGS. Following worsening renal function and subsequent end-stage renal disease (ESRD), she underwent a kidney transplant at 33 years of age. After kidney transplant, she presented with hematocolpos and was found to have distal vaginal atresia and an arcuate uterus. She underwent vaginoplasty and then had regular menses. She was noted to have persistently elevated follicle stimulating hormone levels, consistent with primary ovarian insufficiency, but with normal anti-Müllerian hormone levels. Assessment of her family history was suggestive of other individuals in her family with similar renal disease and uterine differences. Genetic analysis identified a WT1 variant (c.1338A>C; p. =) of uncertain significance that is also present in her similarly affected mother. To help clarify the potential impact of this variant, we completed a mini-gene assay to detect in vitro splicing changes in the presence of the WT1 variant sequence uncovered in this individual. This demonstrated resultant aberrant splicing that further supports the pathogenicity of the uncovered variant for this individual.ConclusionsTo our knowledge, this represents the first case of a podocytopathy with co-occurring uterovaginal anomalies due to exon skipping in WT1. The patient exhibited a severe course of chronic kidney dysfunction requiring a kidney transplant. Clinical RNA sequencing to clarify variants impacting splicing remains challenging due to tissue- specific gene expression for genes such as WT1, thus, research-based assays may be beneficial to understand the consequence of rare or previously uncharacterized variants.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1545329</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1545329</link>
        <title><![CDATA[The road ahead: emerging therapies for primary IgA nephropathy]]></title>
        <pubdate>2025-02-04T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Edward J. Filippone</author><author>Rakesh Gulati</author><author>John L. Farber</author>
        <description><![CDATA[Primary IgA nephropathy (IgAN) is the most common form of primary glomerulopathy. A slowly progressive disease presenting in the young to middle-aged, most patients with reduced eGFR or proteinuria will progress to end-stage kidney disease (ESKD) in their lifetimes. The pathogenesis involves increased production of galactose-deficient IgA1 (Gd-IgA1) that forms immune complexes that deposit in the glomerulus, eliciting mesangial cell proliferation, inflammation, and complement activation. The backbone of therapy is supportive, including lifestyle modifications, strict blood pressure control, and renin-angiotensin system inhibition targeting proteinuria < 300 mg/day. Sodium-glucose transporter 2 inhibitors are indicated for persisting proteinuria or declining eGFR. Sparsentan is indicated for persisting proteinuria. Immunosuppression should be considered for all patients at risk for progression (persisting proteinuria and/or declining eGFR). To reduce Gd-IgA1 production, targeted-release budesonide is approved. Agents targeting B cell survival factors APRIL or BAFF/APRIL have significantly reduced Gd-IgA1 production and proteinuria in phase 2 trials but await phase 3 data for approval. To reduce inflammation, high-dose steroids are ineffective and toxic in Caucasian patients, although lower-dose regimens may be effective in Chinese patients. Complement inhibition is being actively studied. The factor B inhibitor iptacopan has conditional approval. The terminal pathway inhibitors cemdisiran and ravulizumab show promise in phase 2 studies. Our current approach for those requiring immunosuppression involves combining the reduction of Gd-IgA1 (nefecon) with suppressing the effects of inflammation (iptacopan). The optimal duration of such therapy is uncertain. Clearly, there is more to be learned with many trials underway.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1519481</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1519481</link>
        <title><![CDATA[Global and national public awareness and interest in glomerular diseases from 2004 to 2024]]></title>
        <pubdate>2025-01-23T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Suryanarayanan Balakrishnan</author><author>Charat Thongprayoon</author><author>Iasmina M. Craici</author><author>Wisit Cheungpasitporn</author><author>Jing Miao</author>
        <description><![CDATA[BackgroundGlomerular diseases significantly impact global health. This study investigated public interest in five common glomerular diseases.MethodsGoogle Trends™ were used to analyze search activity from January 2004 to December 2024 for IgA nephropathy (IgAN), membranous glomerulonephritis (MN), focal segmental glomerulosclerosis (FSGS), lupus nephritis (LN), and diabetic nephropathy (DN). Data were retrieved both globally and in English-speaking countries, including the United States. Monthly and yearly relative search activity were assessed and compared.ResultsGlobally, IgAN had the highest average relative search activity, followed by DN, FSGS, LN, and MN. Both IgAN and FSGS exhibited declining trends, while LN showed an upward pattern. MN and DN experienced a modest decline before 2016, preceded by a slight increase. Among English-speaking countries, search interest was predominantly concentrated in five countries, primarily including the United States, United Kingdom, Canada, and Australia, with the United States consistently ranking as the leading country. For IgAN, LN, and MN, the trends observed in the United States appeared to align with global data. In contrast, search interest for FSGS exceeded global levels, while interest in DN was slightly lower than global activity. In the United States, IgAN, FSGS, and LN were most prominent in North Dakota, Massachusetts, and Delaware, respectively, while DN and MN saw peak activity in West Virginia.ConclusionPublic engagement with glomerular diseases has not uniformly grown, at least in English-speaking countries, emphasizing the need for enhanced awareness efforts. Future analysis should prioritize search terms in the predominant language of each country.]]></description>
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