Kidney Medicine最新文献

{"title":"Daratumumab for Treatment of Refractory Podocytopathy: A Case Report","authors":"Andreia Curto ,&nbsp;Victor J. Martinez Leon ,&nbsp;Abdallah S. Geara","doi":"10.1016/j.xkme.2026.101253","DOIUrl":"10.1016/j.xkme.2026.101253","url":null,"abstract":"<div><div>Primary podocytopathies, manifesting as minimal change disease and primary focal and segmental glomerulosclerosis, previously had a debatable pathogenesis. However, with the recent discovery of antinephrin antibodies, these primary podocytopathies are now considered an antibody-mediated disease. As a result, the therapeutic approach targeting B-cells has become better justified. We present the case of a 30-year-old man who was evaluated for nephrotic syndrome and found to have minimal change disease on the kidney biopsy. He was initially treated with a prolonged course of steroids, achieving complete remission. But, shortly after starting the steroid tapering, the nephrotic syndrome relapsed, with a prolonged course of proteinuria that partially responded to the sequential resumption of corticosteroids, rituximab, calcineurin inhibitors, and obinutuzumab. A repeat kidney biopsy confirmed the primary podocytopathy with a histology of focal and segmental glomerulosclerosis, tip lesion. Then, the patient was treated with weekly subcutaneous daratumumab for 8 doses, resulting in improvement of proteinuria, albuminemia, and resolution of edema that was persistent for more than 2 years. A growing body of evidence supports the rationale of an anti-CD38 strategy in the treatment of immune-mediated kidney diseases resistant to anti-CD20 agents, highlighting the role of anti-B–cell therapy in primary podocytopathy.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 3","pages":"Article 101253"},"PeriodicalIF":3.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial DNA Analysis Should Be Considered in the Genetic Assessment of Focal Segmental Glomerulosclerosis or Unexplained Chronic Kidney Disease: A Case Report","authors":"Chloe Borden ,&nbsp;Iman Chaudhry ,&nbsp;Rhyan Maditz ,&nbsp;Sarah Mazzola ,&nbsp;Ronit Salomon Kent ,&nbsp;Kristen Tomaszewski ,&nbsp;Xiangling Wang","doi":"10.1016/j.xkme.2025.101233","DOIUrl":"10.1016/j.xkme.2025.101233","url":null,"abstract":"<div><div>Genetic testing is increasingly used to assist the precise diagnosis and clinical management of suspected genetic kidney diseases; however, mitochondrial DNA (mtDNA) analysis remains underutilized. Here we report a 61-year-old man who presented with chronic kidney disease (CKD), microscopic hematuria since childhood, bilateral sensorineural hearing loss (SNHL), and peripheral polyneuropathy. Laboratory reports showed serum creatinine 1.5 mg/dL with an estimated glomerular filtration rate of 55 mL/min/1.73m², no proteinuria, and a negative serological workup. Kidney biopsy demonstrated focal segmental glomerulosclerosis (FSGS) with segmental thinning of glomerular basement membrane and dysmorphic mitochondria. A 401 renal disease gene panel was negative, including type IV collagen genes. mtDNA analysis identified a pathogenic variant in the <em>MT-TV</em> gene (m.1642 G&gt;A; NC_012920.1) with 2% heteroplasmy in leukocyte-derived DNA, confirmed in urine-derived DNA at 5% heteroplasmy. Genetic counseling was offered along with systemic evaluation revealing left ventricular hypertrophy on echocardiogram. The patient was started on levocarnitine and coenzyme Q10 with multidisciplinary care. This is the first reported case of FSGS with dysmorphic mitochondria and a pathogenic <em>MT-TV</em> variant confirmed via both leukocyte-derived and urine-derived DNA. It supports the role of mitochondrial dysfunction in CKD and highlights the importance of mtDNA analysis in the evaluation of FSGS and unexplained CKD.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 3","pages":"Article 101233"},"PeriodicalIF":3.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146048953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ANCA-Negative Pauci-Immune Necrotizing Glomerulonephritis in the Setting of Multisystem Inflammatory Syndrome in Children","authors":"Christine A. VanBeek ,&nbsp;Naseem Alammar ,&nbsp;Qassim Abid","doi":"10.1016/j.xkme.2026.101254","DOIUrl":"10.1016/j.xkme.2026.101254","url":null,"abstract":"<div><div>Multisystem inflammatory syndrome in children (MIS-C) is a rare hyperinflammatory disorder that occurs in previously healthy pediatric patients after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) exposure or mild infection. MIS-C typically has mild kidney symptoms that resolve quickly. The kidney biopsy experience in pediatric coronavirus disease 2019 (COVID-19) and MIS-C is limited in the literature. Here, we describe a 17-year-old SARS-CoV-2 positive boy with features of MIS-C who presented with abdominal pain and gross hematuria. He developed acute kidney injury requiring dialysis. Kidney biopsy and serologic work-up documented antineutrophil cytoplasmic antibody (ANCA)-negative pauci-immune necrotizing glomerulonephritis (AN-PING). Treatment with steroids and intravenous immunoglobulin resulted in simultaneous resolution of the systemic inflammatory markers and kidney symptoms. Aggressive immune suppression and cytotoxic agents were avoided. The glomerulonephritis remained in remission at 3-year follow-up. Although most cases of AN-PING are thought to represent kidney involvement by a primary vasculitis, a subset can occur in association with other conditions. We propose that AN-PING could be a rare kidney manifestation of MIS-C.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 3","pages":"Article 101254"},"PeriodicalIF":3.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147399973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Estimating Short-Term and Long-Term Survival for Patients With Kidney Failure Using a Mixture Survival Model","authors":"Nathan Meyer ,&nbsp;Maxwell Donelan ,&nbsp;Hossein Moradi Rekabdarkolaee ,&nbsp;Brandon M. Varilek ,&nbsp;Surachat Ngorsuraches ,&nbsp;Patti Brooks ,&nbsp;Jerry Schrier ,&nbsp;Semhar Michael","doi":"10.1016/j.xkme.2025.101232","DOIUrl":"10.1016/j.xkme.2025.101232","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Rationale &amp; Objective&lt;/h3&gt;&lt;div&gt;Traditional survival models assume all patients receiving kidney replacement therapy (KRT) may be grouped into one population, overlooking long-term survivors, particularly successful transplant recipients, and may fail to appreciate the disparities in minority populations. On the other hand, a mixture survival model allows for the estimation of hazard and odds ratios of all-cause mortality in patients with kidney failure undergoing either dialysis or transplantation.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Study Design&lt;/h3&gt;&lt;div&gt;This retrospective cohort study analyzed survival outcomes using a proportional hazards mixture survival model, comparing results to a traditional Cox proportional hazards model with time-varying modality of treatment.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Setting &amp; Participants&lt;/h3&gt;&lt;div&gt;Data from the United States Renal Data System included 2,228,693 patients initiating KRT between 2000 and 2020.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Predictors&lt;/h3&gt;&lt;div&gt;Key predictors included demographics, comorbid conditions, socioeconomic status, geographic location, and rurality.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Outcomes&lt;/h3&gt;&lt;div&gt;The primary outcome was all-cause mortality. The mixture survival model distinguishes between patients’ characteristics associated with long-term survival (ie, primarily those with successful transplants) and short-term survival (ie, those at a greater risk of mortality over time, such as patients treated with dialysis).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Analytical Approach&lt;/h3&gt;&lt;div&gt;Both a Cox proportional hazards model and a proportional hazards mixture survival model were applied to all patients.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Findings from both models were largely consistent, but the mixture survival model revealed new insights into racial disparities. In the Cox model, American Indian individuals had an adjusted hazard ratio of 0.63 compared with White individuals (95% CI. 0.62-0.63) and 0.74 for Black individuals compared with White (95% CI, 0.74-0.74). The mixture model confirmed these trends but also showed that American Indian individuals were 1.59 times more likely to not have a long-term survival than White individuals (95% CI, 1.415-1.797) and Black individuals were 1.35 times more likely to not be in the long-term surviving group than White individuals (95% CI, 1.310-1.397). Additional disparities were observed by socioeconomic and geographic factors.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Limitations&lt;/h3&gt;&lt;div&gt;Data collected at the beginning of dialysis may not fully capture patients’ health trajectories.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;The mixture survival model provides a more comprehensive understanding of mortality disparities for patients with kidney failure receiving KRT by distinguishing between short-term and long-term survivability. The findings highlight the need for targeted interventions to improve long-term outcomes for minority patients.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Plain-language Summary&lt;/h3&gt;&lt;div&gt;Kidney failure affects minority ","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 3","pages":"Article 101232"},"PeriodicalIF":3.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146081368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Incremental Hemodialysis Practices and Impact on Survival: Systematic Review and Meta-Analysis","authors":"Adil M. Hazara ,&nbsp;Abdullah Abdullah ,&nbsp;Victoria Allgar ,&nbsp;Maureen Twiddy ,&nbsp;Sunil Bhandari","doi":"10.1016/j.xkme.2025.101238","DOIUrl":"10.1016/j.xkme.2025.101238","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Starting hemodialysis (HD) incrementally may help reduce the burden of treatment in patients with established kidney failure. A systematic review has been conducted to describe variations in the practice of incremental HD worldwide and to study its impact on mortality.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Study Design&lt;/h3&gt;&lt;div&gt;Systematic review.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Setting &amp; Population&lt;/h3&gt;&lt;div&gt;Patients with established kidney failure starting HD.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Selection Criteria for Studies&lt;/h3&gt;&lt;div&gt;Medline and Academic Search Premier were searched from inception to July 20, 2020, for observational and interventional studies comparing incremental or twice weekly treatments with conventional treatment, with mortality as one of the outcome measures.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Predictor&lt;/h3&gt;&lt;div&gt;Incremental (or twice-weekly) HD therapy versus thrice-weekly treatments.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Outcomes&lt;/h3&gt;&lt;div&gt;Mortality.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Fourteen studies were included (combined 91,928 participants; 5,075 [5.5%] in the intervention, 86,853 [94.5%] in standard treatment groups). Large variations in the practice of incremental HD were noted with treatments differing in HD frequency, treatment goals, monitoring schedules, duration of the incremental program, and cointerventions. Larger studies with lowest risk of bias demonstrated equivalent survival between incremental and conventional treatment groups. Meta-analysis of mortality hazards showed an overall hazard ratio of 0.97 (95% CI 0.76-1.19). Centers which screened patients for adequacy of residual kidney function at baseline and pursued prespecified treatment goals have demonstrated better outcomes in incremental HD recipients compared with conventional treatment. There is evidence of publication bias in the literature.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Limitations&lt;/h3&gt;&lt;div&gt;Studies from diverse settings, searches limited to English language.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;There is wide variation in the interpretation of incremental HD treatments and therefore primary studies of incremental HD must be examined in the context of their settings, population, and available resources. Optimal method of implementing incremental HD remains controversial; available data indicate that incremental HD is at least noninferior to conventional HD.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Plain-language Summary&lt;/h3&gt;&lt;div&gt;The conventional way of starting dialysis in people with kidney failure is to deliver thrice-weekly sessions from the outset. In incremental dialysis, people receive fewer sessions at the start, and their treatment is gradually increased. We have analyzed studies comparing incremental with conventional dialysis treatments. We show that practices vary widely across the world, including how incremental dialysis is given and how patients are monitored. Overall, survival was similar between incremental and conventional programs. Some centers have shown that incremental dialysis may be better when","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 3","pages":"Article 101238"},"PeriodicalIF":3.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147326584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"C3 Glomerulopathy Diagnosis, Current Treatments, and Emerging Therapies","authors":"Mahtab Mashayekhi ,&nbsp;Jonathan E. Zuckerman ,&nbsp;Jonathan Barratt ,&nbsp;Richard J. Glassock ,&nbsp;Fernando Caravaca-Fontán ,&nbsp;Raymond K. Hsu ,&nbsp;Arun Rajasekaran ,&nbsp;Edgar Lerma ,&nbsp;Sahibzadi Mahrukh Noor ,&nbsp;Amir Abdipour ,&nbsp;Sayna Norouzi","doi":"10.1016/j.xkme.2026.101258","DOIUrl":"10.1016/j.xkme.2026.101258","url":null,"abstract":"<div><div>C3 glomerulopathy (C3G) is characterized by prominent deposition of complement component C3 in the kidney glomeruli, leading to glomerular inflammation. C3G is a rare and complex pattern of injury caused by dysregulation of the alternative pathway of complement system and occurs in both children and adults. It can happen because of genetic and acquired factors. Kidney biopsy is the gold standard for diagnosing C3G. About 50% of cases progress to kidney failure, and traditional treatment strategies, including immunosuppression and supportive care, have demonstrated variable efficacy. In this review, we aim to provide a comprehensive overview of pathophysiology, clinical presentations, and diagnostic criteria of C3G. Additionally, we will discuss current treatment guidelines and ongoing clinical trials.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 3","pages":"Article 101258"},"PeriodicalIF":3.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Incidence and Risk Factors of Gout in Non-dialysis Chronic Kidney Disease Patients With Asymptomatic Hyperuricemia","authors":"Ilia Beberashvili ,&nbsp;Hamza Abu Marsa ,&nbsp;Keren Doenyas-Barak ,&nbsp;Ilya Maslakov ,&nbsp;Shai Efrati","doi":"10.1016/j.xkme.2025.101197","DOIUrl":"10.1016/j.xkme.2025.101197","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Rationale &amp; Objective&lt;/h3&gt;&lt;div&gt;Gout frequently complicates chronic kidney disease (CKD), yet the incidence and specific risk factors for gout in patients with CKD and asymptomatic hyperuricemia remain unclear. We aimed to determine gout incidence and risk factors in nondialysis patients with CKD and asymptomatic hyperuricemia.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Study Design&lt;/h3&gt;&lt;div&gt;Retrospective cohort study.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Setting &amp; Participants&lt;/h3&gt;&lt;div&gt;Analysis of 771 ambulatory nondialysis patients with CKD (stages 3-5) with asymptomatic hyperuricemia (serum urate level, ≥7.0 mg/dL), without prior gout, followed from 2010 to 2023 at a single center.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Predictors&lt;/h3&gt;&lt;div&gt;Multiple clinical and laboratory factors were evaluated, including demographics, comorbidities, medications, and biochemical markers.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Outcomes&lt;/h3&gt;&lt;div&gt;Incident gout diagnosis confirmed by rheumatology specialists.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Analytical Approach&lt;/h3&gt;&lt;div&gt;Cox proportional hazards models and receiver operating characteristic curve analyses. A composite weighted index was derived from regression-based predictors.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Over a median follow-up of 47 months, gout developed in 140 (18.2%) patients (incidence rate, 41.9 cases per 1,000 person-years). Independent predictors of gout included younger age (per year; hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.96-0.99), higher serum urate (per 1 mg/dL; HR, 1.29; 95% CI, 1.14-1.46), lower serum creatinine levels (per 1 mg/dL; HR, 0.81; 95% CI, 0.65-0.99), and diuretic use (HR, 1.86; 95% CI, 1.00-3.45). Higher composite weighted index (per 1 unit; HR, 2.19; 95% CI, 1.70-2.83) was associated with increased gout risk.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Limitations&lt;/h3&gt;&lt;div&gt;Single-center, retrospective study design limits generalizability and causal inference.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;Incident gout is common among patients with CKD and asymptomatic hyperuricemia. Younger age, elevated serum urate levels, lower creatinine levels, and diuretic use significantly predict gout onset. Identifying high-risk patients using these predictors could guide preventive therapeutic decisions.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Plain-Language Summary&lt;/h3&gt;&lt;div&gt;People with chronic kidney disease often have high levels of uric acid in their blood, but not all of them develop gout. We wanted to understand which patients are more likely to develop gout so that preventive steps could be considered. We studied a large group of patients with chronic kidney disease who had high uric acid levels but no history of gout. We found that younger age, higher uric acid levels, use of diuretics, and earlier stages of kidney disease were linked to a higher chance of developing gout. We combined these factors into a weighted risk index to help identify high-risk patients. Identifying high-risk patients may help guide future treatment strategies aimed at preventing gout and improving quality of l","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 2","pages":"Article 101197"},"PeriodicalIF":3.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145978512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Renal Technician Programs at US Postsecondary Institutions","authors":"Laura C. Plantinga PhD ,&nbsp;Danilo Concepcion CBNT, CCHT-A ,&nbsp;Megan Urbanski PhD, MSW ,&nbsp;Christin Iroegbu PhD, RN ,&nbsp;Delphine Tuot MD ,&nbsp;Bernard G. Jaar MD, MPH","doi":"10.1016/j.xkme.2025.101224","DOIUrl":"10.1016/j.xkme.2025.101224","url":null,"abstract":"","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 2","pages":"Article 101224"},"PeriodicalIF":3.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145978508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association Between Transportation and Home Dialysis Transition: Retrospective Cohort Study","authors":"Na’amah Razon ,&nbsp;Yi Zhang ,&nbsp;Bethney Bonilla-Herrera ,&nbsp;Lorien S. Dalrymple ,&nbsp;Amanda K. Stennett ,&nbsp;Baback Roshanravan ,&nbsp;Daniel Tancredi ,&nbsp;Joshua J. Fenton","doi":"10.1016/j.xkme.2025.101199","DOIUrl":"10.1016/j.xkme.2025.101199","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Rationale &amp; Objective&lt;/h3&gt;&lt;div&gt;Transportation insecurity is a social risk factor of particular importance to individuals with end-stage kidney disease (ESKD), as most individuals need to travel multiple times a week to dialysis treatment. Advancing home modalities for individuals with ESKD experiencing transportation insecurity may be beneficial by reducing travel burden and improving access.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Study Design&lt;/h3&gt;&lt;div&gt;Retrospective cohort study.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Setting &amp; Participants&lt;/h3&gt;&lt;div&gt;Individuals with ESKD treated with in-center hemodialysis (HD) at a large, national dialysis organization.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Exposures&lt;/h3&gt;&lt;div&gt;The main transportation mode to HD is categorized into private transportation (individuals who drive themselves or have a family member/friend drive) or those who lack private transportation (Medicaid non-emergency medical transportation, paratransit, public transportation, private pay non-emergency medical transportation, and other).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Outcomes&lt;/h3&gt;&lt;div&gt;Transition to home dialysis is defined as an individual who has completed at least 1 training treatment for home therapies or at least 1 dialysis treatment at home.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Analytic Approach&lt;/h3&gt;&lt;div&gt;Log-binomial multivariate regression models to estimate adjusted incidence rate ratios of home dialysis transition by transportation mode.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Individuals who lacked private transportation were significantly less likely to transition to home dialysis compared with those who drove themselves or had a family member/friend drive them to HD. Adjusted incidence rate ratios for home dialysis transition were 47%-58% lower in nonprivate transportation groups compared with those with private transportation, ranging from 0.42 in individuals relying on Medicaid transportation benefits (95% confidence interval, 0.35-0.50; &lt;em&gt;P&lt;/em&gt; &lt; 0.001) to 0.53 (95% confidence interval, 0.41-0.67; &lt;em&gt;P&lt;/em&gt; &lt; 0.001) among paratransit users.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Limitations&lt;/h3&gt;&lt;div&gt;Single transportation assessment, exclusion of individuals already on home dialysis, and absence of caregiver data.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;Individuals with ESKD receiving in-center HD who lack private transportation may have reduced access to home dialysis, even though this group may benefit from home modalities. Better identifying transportation barriers and targeting home modalities for those with transportation insecurity may reduce the adverse consequences of missed dialysis related to transportation barriers and be an additional opportunity to increase home dialysis uptake.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Plain-Language Summary&lt;/h3&gt;&lt;div&gt;Transportation is a key barrier for many individuals receiving in-center dialysis care. Nonetheless, the majority of individuals in the United States receive their dialysis treatment at an in-center facility. In a study of patients with end-stage kidney disease treate","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 2","pages":"Article 101199"},"PeriodicalIF":3.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146023299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rituximab-Induced Remission in Proliferative Glomerulonephritis With Monoclonal Immunoglobulin G Deposits: A Case Report With Serial Kidney Biopsies","authors":"Jeong-Hoon Lim ,&nbsp;Youn-Sik Oh ,&nbsp;Man-Hoon Han ,&nbsp;You Hyun Jeon ,&nbsp;Hee-Yeon Jung ,&nbsp;Ji-Young Choi ,&nbsp;Jang-Hee Cho ,&nbsp;Sun-Hee Park ,&nbsp;Chan-Duck Kim ,&nbsp;Yong-Lim Kim ,&nbsp;Yong-Jin Kim","doi":"10.1016/j.xkme.2025.101212","DOIUrl":"10.1016/j.xkme.2025.101212","url":null,"abstract":"<div><div>Proliferative glomerulonephritis with monoclonal IgG deposits (PGNMID) is a rare form of monoclonal gammopathy of renal significance (MGRS). The natural history and optimal treatment are poorly defined, particularly when circulating monoclonal proteins or hematologic clones are undetectable. We report a 57-year-old woman with biopsy-confirmed PGNMID who underwent 3 sequential kidney biopsies. The initial biopsy showed a classic membranoproliferative pattern with monotypic IgG-kappa deposits, whereas bone marrow examination showed no clonal plasma cell or B-cell proliferation. Despite corticosteroid-based immunosuppression, proteinuria persisted, and histology worsened on the second biopsy. Rituximab was administered 10 months after diagnosis; a third biopsy 3 months later showed resolution of immune deposits and glomerular proliferation. At 8 months post-rituximab, the patient remained in clinical remission with stable kidney function. This case underscores the value of sequential kidney biopsies to monitor disease activity and treatment response in PGNMID. Rituximab can induce clinical and histologic remission, even when circulating monoclonal proteins are undetectable.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 2","pages":"Article 101212"},"PeriodicalIF":3.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145978510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}