Pub Date : 2026-01-01Epub Date: 2025-11-13DOI: 10.1159/000548904
Romela Petrosyan, A Enrique Caballero, Tracey L Henry, Adam R Puchalski
Background: Diabetic kidney disease (DKD) is a serious complication arising from long-term diabetes, disproportionately affecting historically marginalized populations, such as racial and ethnic minority groups, populations with low socioeconomic status, or a lower level of education. This review explores the causes of these disparities and barriers to accessing DKD therapies and proposes solutions. Summary: Socioeconomic factors like lack of health insurance, low income, and limited health literacy significantly hinder access to DKD therapies for marginalized communities. Additionally, inadequate access to healthcare services further exacerbates the issue. Clinical factors also contribute to the inequity. Under-recognition of DKD, under-prescription of effective medications, and a lack of a patient-centered healthcare environment are prominent concerns. Implicit bias among healthcare professionals may also play a role. Patient factors include limited awareness of DKD, challenges with treatment adherence, and frequent healthcare interruptions. Policy interventions like the Inflation Reduction Act, expanding health insurance coverage, and increasing reimbursement for DKD therapies can improve affordability and access. Additionally, a shift toward preventive care models is crucial. Clinical interventions focus on improving early detection, accurate diagnosis, and proper management of DKD. Educating healthcare providers about the benefits of DKD therapies and implementing value-based kidney care programs are essential steps. Patient interventions involve raising awareness about DKD, implementing culturally appropriate educational programs, and fostering community-based support systems. Key Messages: Addressing these disparities requires a multipronged approach involving policy changes, improved healthcare delivery, and patient education. This collaborative effort can ensure equitable access to DKD therapies and improve health outcomes for all populations.
{"title":"Navigating Disparities and Overcoming Barriers to Access Diabetic Kidney Disease Therapies: A Proposed Multifactorial Approach.","authors":"Romela Petrosyan, A Enrique Caballero, Tracey L Henry, Adam R Puchalski","doi":"10.1159/000548904","DOIUrl":"10.1159/000548904","url":null,"abstract":"<p><p><p>Background: Diabetic kidney disease (DKD) is a serious complication arising from long-term diabetes, disproportionately affecting historically marginalized populations, such as racial and ethnic minority groups, populations with low socioeconomic status, or a lower level of education. This review explores the causes of these disparities and barriers to accessing DKD therapies and proposes solutions. Summary: Socioeconomic factors like lack of health insurance, low income, and limited health literacy significantly hinder access to DKD therapies for marginalized communities. Additionally, inadequate access to healthcare services further exacerbates the issue. Clinical factors also contribute to the inequity. Under-recognition of DKD, under-prescription of effective medications, and a lack of a patient-centered healthcare environment are prominent concerns. Implicit bias among healthcare professionals may also play a role. Patient factors include limited awareness of DKD, challenges with treatment adherence, and frequent healthcare interruptions. Policy interventions like the Inflation Reduction Act, expanding health insurance coverage, and increasing reimbursement for DKD therapies can improve affordability and access. Additionally, a shift toward preventive care models is crucial. Clinical interventions focus on improving early detection, accurate diagnosis, and proper management of DKD. Educating healthcare providers about the benefits of DKD therapies and implementing value-based kidney care programs are essential steps. Patient interventions involve raising awareness about DKD, implementing culturally appropriate educational programs, and fostering community-based support systems. Key Messages: Addressing these disparities requires a multipronged approach involving policy changes, improved healthcare delivery, and patient education. This collaborative effort can ensure equitable access to DKD therapies and improve health outcomes for all populations. </p>.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"131-140"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12707861/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145513636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-11-28DOI: 10.1159/000549795
Tanima Chatterjee, Joseph Rutkowski, Danielle E Soranno, Eibhlin Goggins, Mark Okusa, Stefania Prenna, Vincenzo Cantaluppi, Abolfazl Zarjou
Background: Acute kidney injury (AKI) represents a multifaceted clinical syndrome marked by precipitous loss of kidney function, high morbidity and mortality, and a strong propensity for progression to chronic kidney disease. Collectively, these challenges underscore the imperative to delineate conserved molecular and signaling networks that are uniformly engaged across diverse AKI etiologies.
Summary: Herein, we survey five emerging research domains poised to transform AKI pathophysiology and therapeutic paradigms. First, lymphatic network remodeling has been implicated as a critical determinant of renal immunodynamics and interstitial fluid homeostasis, whereby modulation of VEGF-C/D signaling reshapes immune cell trafficking and fibrogenic responses. Second, we will cover emerging evidence that positions macrophage ferritin heavy chain as a key regulator of macrophage phenotype and subsequent kidney ferroptosis susceptibility via coordinated regulation of synuclein-⍺, and Spic. Third, we will emphasize incorporating development as a biological variable into experimental design based on evidence that identifies age-dependent divergences in injury susceptibility, and progression of disease. Fourth, we cover mechanosensitive ion channels that are activated by therapeutic ultrasound offering novel opportunities to harness the cholinergic anti-inflammatory pathway for nephroprotection. Finally, targeting tubular epithelial cell senescence and mitochondrial bioenergetics as a promising approach to limit progression of kidney disease will be discussed.
Key messages: Collectively, these emerging mechanisms deepen our understanding of AKI pathophysiology and unveil novel therapeutic targets with the potential to transform the treatment landscape.
{"title":"Discovery Pipeline for Acute Kidney Injury: Molecules, Mechanisms, Models, and Targets.","authors":"Tanima Chatterjee, Joseph Rutkowski, Danielle E Soranno, Eibhlin Goggins, Mark Okusa, Stefania Prenna, Vincenzo Cantaluppi, Abolfazl Zarjou","doi":"10.1159/000549795","DOIUrl":"10.1159/000549795","url":null,"abstract":"<p><strong>Background: </strong>Acute kidney injury (AKI) represents a multifaceted clinical syndrome marked by precipitous loss of kidney function, high morbidity and mortality, and a strong propensity for progression to chronic kidney disease. Collectively, these challenges underscore the imperative to delineate conserved molecular and signaling networks that are uniformly engaged across diverse AKI etiologies.</p><p><strong>Summary: </strong>Herein, we survey five emerging research domains poised to transform AKI pathophysiology and therapeutic paradigms. First, lymphatic network remodeling has been implicated as a critical determinant of renal immunodynamics and interstitial fluid homeostasis, whereby modulation of VEGF-C/D signaling reshapes immune cell trafficking and fibrogenic responses. Second, we will cover emerging evidence that positions macrophage ferritin heavy chain as a key regulator of macrophage phenotype and subsequent kidney ferroptosis susceptibility via coordinated regulation of synuclein-⍺, and Spic. Third, we will emphasize incorporating development as a biological variable into experimental design based on evidence that identifies age-dependent divergences in injury susceptibility, and progression of disease. Fourth, we cover mechanosensitive ion channels that are activated by therapeutic ultrasound offering novel opportunities to harness the cholinergic anti-inflammatory pathway for nephroprotection. Finally, targeting tubular epithelial cell senescence and mitochondrial bioenergetics as a promising approach to limit progression of kidney disease will be discussed.</p><p><strong>Key messages: </strong>Collectively, these emerging mechanisms deepen our understanding of AKI pathophysiology and unveil novel therapeutic targets with the potential to transform the treatment landscape.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"173-183"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12772422/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145636047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-08-13DOI: 10.1159/000547628
Hidenori Amaike, Masatoshi Kanda, Hirotsugu Yamazaki, Koki Nakamura, Li Ma, Ken Nagahata, Hiroyuki Nakamura, Arata Osanami, Naoya Yama, Masamitsu Hatakenaka, Masato Furuhashi, Hiroki Takahashi
Objectives: The aim of the study was to compare the efficacy of magnetic resonance imaging (MRI) with that of plain or contrast-enhanced computed tomography (CT) in the detection of renal parenchymal and pelvic lesions of immunoglobulin G4-related kidney disease (IgG4-RKD).
Methods: Patients with IgG4-RKD and controls, who performed plain, contrast-enhanced CT and MRI around the kidney region in our hospital, were enrolled. The diagnosis of IgG4-RKD was made by definite cases of IgG4-RKD diagnostic criteria in 2020. Five blinded observers independently assessed image datasets by confidence scores to assess diagnostic accuracy, sensitivity, specificity, areas under the receiver operating characteristic curve (AUROC), and Cronbach's alpha coefficient.
Results: A total of 31 patients were included in the study. Fourteen (45.2%) had IgG4-RKD. Five patients with IgG4-RKD had parenchymal lesions, 5 had renal pelvic lesions, and 4 had both. In the parenchymal lesions, there was no significant difference in diagnostic performance between contrast-enhanced CT and diffusion-weighted imaging (DWI)-b800. The AUROC and sensitivity were higher in DWI-b800 than in plain CT (p < 0.05). Cronbach's alpha coefficient was 0.44 for plain CT and over 0.80 for contrast-enhanced CT and DWI-b800. In the pelvic lesions, there were fewer differences in the performance among each sequence. Cronbach's alpha coefficient was over 0.80 for plain CT, contrast-enhanced CT, and DWI-b800.
Conclusion: Plain MRI, especially in DWI-b800, can effectively detect renal parenchymal lesions in IgG4-RKD. In cases where the use of a contrast agent of CT is difficult, DWI-b800 can be an alternative for the screening of IgG4-RKD.
{"title":"The Effectiveness of Lesion Detection for Immunoglobulin G4-Related Kidney Diseases by Diffusion-Weighted Imaging.","authors":"Hidenori Amaike, Masatoshi Kanda, Hirotsugu Yamazaki, Koki Nakamura, Li Ma, Ken Nagahata, Hiroyuki Nakamura, Arata Osanami, Naoya Yama, Masamitsu Hatakenaka, Masato Furuhashi, Hiroki Takahashi","doi":"10.1159/000547628","DOIUrl":"10.1159/000547628","url":null,"abstract":"<p><strong>Objectives: </strong>The aim of the study was to compare the efficacy of magnetic resonance imaging (MRI) with that of plain or contrast-enhanced computed tomography (CT) in the detection of renal parenchymal and pelvic lesions of immunoglobulin G4-related kidney disease (IgG4-RKD).</p><p><strong>Methods: </strong>Patients with IgG4-RKD and controls, who performed plain, contrast-enhanced CT and MRI around the kidney region in our hospital, were enrolled. The diagnosis of IgG4-RKD was made by definite cases of IgG4-RKD diagnostic criteria in 2020. Five blinded observers independently assessed image datasets by confidence scores to assess diagnostic accuracy, sensitivity, specificity, areas under the receiver operating characteristic curve (AUROC), and Cronbach's alpha coefficient.</p><p><strong>Results: </strong>A total of 31 patients were included in the study. Fourteen (45.2%) had IgG4-RKD. Five patients with IgG4-RKD had parenchymal lesions, 5 had renal pelvic lesions, and 4 had both. In the parenchymal lesions, there was no significant difference in diagnostic performance between contrast-enhanced CT and diffusion-weighted imaging (DWI)-b800. The AUROC and sensitivity were higher in DWI-b800 than in plain CT (p < 0.05). Cronbach's alpha coefficient was 0.44 for plain CT and over 0.80 for contrast-enhanced CT and DWI-b800. In the pelvic lesions, there were fewer differences in the performance among each sequence. Cronbach's alpha coefficient was over 0.80 for plain CT, contrast-enhanced CT, and DWI-b800.</p><p><strong>Conclusion: </strong>Plain MRI, especially in DWI-b800, can effectively detect renal parenchymal lesions in IgG4-RKD. In cases where the use of a contrast agent of CT is difficult, DWI-b800 can be an alternative for the screening of IgG4-RKD.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-11"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144855851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-11-13DOI: 10.1159/000548254
Mijie Guan, Haofei Hu, Haiying Song, Qijun Wan
Introduction: Oxalate nephropathy, characterized by calcium oxalate crystal deposition in renal tissue, represents an underrecognized etiology of acute and chronic kidney injury. Secondary hyperoxaluria can emerge from diverse pathogenetic mechanisms, including excessive oxalate precursor intake, augmented intestinal absorption, or iatrogenic interventions. The therapeutic potential of glucocorticoids in managing this condition remains incompletely elucidated.
Case presentation: A 66-year-old man with no significant prior medical history developed acute kidney injury (AKI), manifesting as a profound serum creatinine elevation from 81 µmol/L to 1,140.4 µmol/L. The patient had consumed a "corn germ powder" supplement containing lactitol for five consecutive months, concurrently experiencing persistent diarrhea. Initial laboratory investigations revealed severe renal dysfunction without notable proteinuria or hematuria. Renal ultrasonography demonstrated normal kidney morphology and dimensions. Definitive kidney biopsy revealed extensive calcium oxalate crystal deposition within renal tubular structures, conclusively diagnosing oxalate nephropathy. Therapeutic intervention comprised prednisone (60 mg daily) and comprehensive supportive management. Following a 3-month treatment protocol with gradual corticosteroid dose reduction, the patient's renal function demonstrated substantial improvement, with serum creatinine declining to 118.2 µmol/L.
Conclusion: This case underscores lactitol-induced secondary oxalate nephropathy as a rare yet clinically significant contributor to AKI. Prompt diagnostic recognition and targeted therapeutic intervention, potentially incorporating glucocorticoid therapy, may substantially facilitate renal functional recovery. Clinicians should maintain heightened awareness of nephrotoxic risks associated with over-the-counter laxative supplements and consider oxalate nephropathy in cryptogenic renal dysfunction scenarios.
{"title":"Lactitol-Induced Acute Kidney Injury with Oxalate Nephropathy: A Case Report.","authors":"Mijie Guan, Haofei Hu, Haiying Song, Qijun Wan","doi":"10.1159/000548254","DOIUrl":"10.1159/000548254","url":null,"abstract":"<p><strong>Introduction: </strong>Oxalate nephropathy, characterized by calcium oxalate crystal deposition in renal tissue, represents an underrecognized etiology of acute and chronic kidney injury. Secondary hyperoxaluria can emerge from diverse pathogenetic mechanisms, including excessive oxalate precursor intake, augmented intestinal absorption, or iatrogenic interventions. The therapeutic potential of glucocorticoids in managing this condition remains incompletely elucidated.</p><p><strong>Case presentation: </strong>A 66-year-old man with no significant prior medical history developed acute kidney injury (AKI), manifesting as a profound serum creatinine elevation from 81 µmol/L to 1,140.4 µmol/L. The patient had consumed a \"corn germ powder\" supplement containing lactitol for five consecutive months, concurrently experiencing persistent diarrhea. Initial laboratory investigations revealed severe renal dysfunction without notable proteinuria or hematuria. Renal ultrasonography demonstrated normal kidney morphology and dimensions. Definitive kidney biopsy revealed extensive calcium oxalate crystal deposition within renal tubular structures, conclusively diagnosing oxalate nephropathy. Therapeutic intervention comprised prednisone (60 mg daily) and comprehensive supportive management. Following a 3-month treatment protocol with gradual corticosteroid dose reduction, the patient's renal function demonstrated substantial improvement, with serum creatinine declining to 118.2 µmol/L.</p><p><strong>Conclusion: </strong>This case underscores lactitol-induced secondary oxalate nephropathy as a rare yet clinically significant contributor to AKI. Prompt diagnostic recognition and targeted therapeutic intervention, potentially incorporating glucocorticoid therapy, may substantially facilitate renal functional recovery. Clinicians should maintain heightened awareness of nephrotoxic risks associated with over-the-counter laxative supplements and consider oxalate nephropathy in cryptogenic renal dysfunction scenarios.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"99-106"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145513623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-08-02DOI: 10.1159/000547796
Gabriel Sartori Pacini, Renato George Eick, Renata Asnis Schuchmann, Mário Sergio Fernandes, Lucas Gobetti da Luz, Illan George Balestrin, Karla Lais Pêgas, Milton Kalil, Maurício Lutzky
Background: Thrombotic microangiopathy (TMA) encompasses a group of rare, life-threatening disorders characterized by microangiopathic hemolytic anemia, thrombocytopenia, and organ damage, most commonly affecting the kidneys. Complement-mediated TMA (CM-TMA), a subtype of TMA, is often associated with dysregulation of the complement system due to genetic mutations. Dengue virus has been recognized as a potential trigger of secondary TMA and may precipitate CM-TMA in genetically predisposed individuals.
Case presentation: We report the case of a 47-year-old woman with a history of thrombotic thrombocytopenic purpura (TTP) who presented with fever, gastrointestinal symptoms, anemia, thrombocytopenia, and acute kidney injury. Dengue infection was confirmed by a positive NS1 antigen. Laboratory and peripheral smear findings indicated TMA. Therapeutic plasma exchange was started due to previous history of TTP, with partial clinical response. ADAMTS13 activity was preserved at 60.7%. Kidney biopsy demonstrated features of TMA. Genetic testing identified a heterozygous pathogenic variant in the CD46 gene, supporting the diagnosis of CM-TMA. Notably, the patient showed sustained clinical improvement without the use of eculizumab.
Conclusion: This case illustrates the diagnostic challenges of TMA in patients with overlapping clinical features and potential infectious triggers. In dengue-endemic regions, the virus should be recognized as a possible precipitating factor for TMA, particularly in individuals harboring complement gene mutations. A multidisciplinary approach - integrating clinical, laboratory, histopathological, and genetic data - is essential for accurate diagnosis and personalized management of TMA syndromes.
{"title":"Differential Diagnosis of Thrombotic Microangiopathy: Overlapping Features of Thrombotic Thrombocytopenic Purpura and Complement-Mediated Thrombotic Microangiopathy in a Dengue-Infected Patient.","authors":"Gabriel Sartori Pacini, Renato George Eick, Renata Asnis Schuchmann, Mário Sergio Fernandes, Lucas Gobetti da Luz, Illan George Balestrin, Karla Lais Pêgas, Milton Kalil, Maurício Lutzky","doi":"10.1159/000547796","DOIUrl":"10.1159/000547796","url":null,"abstract":"<p><strong>Background: </strong>Thrombotic microangiopathy (TMA) encompasses a group of rare, life-threatening disorders characterized by microangiopathic hemolytic anemia, thrombocytopenia, and organ damage, most commonly affecting the kidneys. Complement-mediated TMA (CM-TMA), a subtype of TMA, is often associated with dysregulation of the complement system due to genetic mutations. Dengue virus has been recognized as a potential trigger of secondary TMA and may precipitate CM-TMA in genetically predisposed individuals.</p><p><strong>Case presentation: </strong>We report the case of a 47-year-old woman with a history of thrombotic thrombocytopenic purpura (TTP) who presented with fever, gastrointestinal symptoms, anemia, thrombocytopenia, and acute kidney injury. Dengue infection was confirmed by a positive NS1 antigen. Laboratory and peripheral smear findings indicated TMA. Therapeutic plasma exchange was started due to previous history of TTP, with partial clinical response. ADAMTS13 activity was preserved at 60.7%. Kidney biopsy demonstrated features of TMA. Genetic testing identified a heterozygous pathogenic variant in the CD46 gene, supporting the diagnosis of CM-TMA. Notably, the patient showed sustained clinical improvement without the use of eculizumab.</p><p><strong>Conclusion: </strong>This case illustrates the diagnostic challenges of TMA in patients with overlapping clinical features and potential infectious triggers. In dengue-endemic regions, the virus should be recognized as a possible precipitating factor for TMA, particularly in individuals harboring complement gene mutations. A multidisciplinary approach - integrating clinical, laboratory, histopathological, and genetic data - is essential for accurate diagnosis and personalized management of TMA syndromes.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"41-46"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-10-18DOI: 10.1159/000549074
Yamini Mallisetty, Ahmed Kabeil, Cameron Jackson Bergeron, Zhongji Han, Chi-Yang Chiu, Csaba P Kovesdy, Keiichi Sumida
Introduction: Elevated monocyte to lymphocyte ratio (MLR) represents a pro-inflammatory immune microenvironment and has been associated with poor clinical outcomes such as cardiovascular disease. However, little is known about its association with outcomes among patients on hemodialysis.
Methods: In a nationwide prospective cohort of 952 patients receiving maintenance hemodialysis from 2011-2013, we examined the association of baseline MLR with subsequent risk of cardiovascular events (cardiovascular-related hospitalization and cardiovascular death) and all-cause mortality, using multivariable Cox proportional-hazards models with adjustment for potential confounders. We also examined the mediation effect of inflammatory markers on the association between MLR and cardiovascular events and all-cause mortality, respectively.
Results: Overall, patients were 60.1 ± 13.4 years old; 53.3% were male; 39.7% were African American; and 56.9% were diabetic. The median dialysis vintage was 3.1 years. During a median follow-up of 2.1 years, 184 and 207 cases experienced cardiovascular events and all-cause death, respectively. A higher MLR was incrementally associated with higher risk of cardiovascular events and all-cause mortality. The multivariable-adjusted hazard ratios (95% confidence interval) of cardiovascular events and all-cause mortality for 0.1-unit increase in MLR were 1.22 (1.09-1.37) and 1.18 (1.07-1.30), respectively. There was a modest but significant mediation effect of plasma interleukin-6 (IL-6) on the association between MLR and cardiovascular events (28.2%) and all-cause mortality (24.1%).
Conclusion: A higher MLR was independently associated with higher risk of cardiovascular events and all-cause mortality in patients on hemodialysis. Our findings suggest the potential of MLR as a simple, cost-effective prognostic biomarker and support IL-6-targeted therapeutic interventions to improve clinical outcomes in patients with ESKD.
{"title":"Association of Monocyte-Lymphocyte Ratio with Cardiovascular Events and All-Cause Mortality in Patients Undergoing Hemodialysis: A Prospective Cohort Study.","authors":"Yamini Mallisetty, Ahmed Kabeil, Cameron Jackson Bergeron, Zhongji Han, Chi-Yang Chiu, Csaba P Kovesdy, Keiichi Sumida","doi":"10.1159/000549074","DOIUrl":"10.1159/000549074","url":null,"abstract":"<p><strong>Introduction: </strong>Elevated monocyte to lymphocyte ratio (MLR) represents a pro-inflammatory immune microenvironment and has been associated with poor clinical outcomes such as cardiovascular disease. However, little is known about its association with outcomes among patients on hemodialysis.</p><p><strong>Methods: </strong>In a nationwide prospective cohort of 952 patients receiving maintenance hemodialysis from 2011-2013, we examined the association of baseline MLR with subsequent risk of cardiovascular events (cardiovascular-related hospitalization and cardiovascular death) and all-cause mortality, using multivariable Cox proportional-hazards models with adjustment for potential confounders. We also examined the mediation effect of inflammatory markers on the association between MLR and cardiovascular events and all-cause mortality, respectively.</p><p><strong>Results: </strong>Overall, patients were 60.1 ± 13.4 years old; 53.3% were male; 39.7% were African American; and 56.9% were diabetic. The median dialysis vintage was 3.1 years. During a median follow-up of 2.1 years, 184 and 207 cases experienced cardiovascular events and all-cause death, respectively. A higher MLR was incrementally associated with higher risk of cardiovascular events and all-cause mortality. The multivariable-adjusted hazard ratios (95% confidence interval) of cardiovascular events and all-cause mortality for 0.1-unit increase in MLR were 1.22 (1.09-1.37) and 1.18 (1.07-1.30), respectively. There was a modest but significant mediation effect of plasma interleukin-6 (IL-6) on the association between MLR and cardiovascular events (28.2%) and all-cause mortality (24.1%).</p><p><strong>Conclusion: </strong>A higher MLR was independently associated with higher risk of cardiovascular events and all-cause mortality in patients on hemodialysis. Our findings suggest the potential of MLR as a simple, cost-effective prognostic biomarker and support IL-6-targeted therapeutic interventions to improve clinical outcomes in patients with ESKD.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"76-86"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145318518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-08-23DOI: 10.1159/000547798
Liyin Guo, Tian Wang
Introduction: This study examined the relationship between the dietary inflammatory index (DII) and anemia in patients with diabetic kidney disease (DKD).
Methods: All the data were obtained from the National Health and Nutrition Examination Survey (NHANES) from 2007 to 2018. The final analysis included 1918 DKD patients, with 500 experiencing anemia. Weighted multivariate logistic regression models were used to assess the association between DII and anemia, with results expressed as odds ratios.
Results: Elevated DII scores correlated with an increased incidence of anemia (OR = 1.13, 95% CI: 1.02-1.25). When analyzed as categorical variables, DII scores of 1.57-2.64 (OR = 1.77, 95% CI: 1.13-2.77) and >2.64 (OR = 1.78, 95% CI: 1.12-2.85) were linked to higher anemia risk. Subgroup analyses revealed consistent associations in individuals aged 65 and older (OR = 1.92, 95% CI: 1.16-3.17), those with serum iron levels <73 μg/dL (OR = 2.01, 95% CI: 1.11-3.62), and males (OR = 2.23, 95% CI: 1.21-4.11). Higher DII scores correlated with greater odds of moderate-severe anemia (OR = 1.22, 95% CI: 1.07-1.38).
Conclusion: The results indicate that elevated DII scores are associated with an increased occurrence of anemia in DKD patients, emphasizing the importance of lowering pro-inflammatory food consumption as a potential strategy to prevent anemia in this group.
{"title":"The Relationship of Dietary Inflammatory Index with Anemia in Diabetic Kidney Disease: A Cross-Sectional Study of the NHANES.","authors":"Liyin Guo, Tian Wang","doi":"10.1159/000547798","DOIUrl":"10.1159/000547798","url":null,"abstract":"<p><strong>Introduction: </strong>This study examined the relationship between the dietary inflammatory index (DII) and anemia in patients with diabetic kidney disease (DKD).</p><p><strong>Methods: </strong>All the data were obtained from the National Health and Nutrition Examination Survey (NHANES) from 2007 to 2018. The final analysis included 1918 DKD patients, with 500 experiencing anemia. Weighted multivariate logistic regression models were used to assess the association between DII and anemia, with results expressed as odds ratios.</p><p><strong>Results: </strong>Elevated DII scores correlated with an increased incidence of anemia (OR = 1.13, 95% CI: 1.02-1.25). When analyzed as categorical variables, DII scores of 1.57-2.64 (OR = 1.77, 95% CI: 1.13-2.77) and >2.64 (OR = 1.78, 95% CI: 1.12-2.85) were linked to higher anemia risk. Subgroup analyses revealed consistent associations in individuals aged 65 and older (OR = 1.92, 95% CI: 1.16-3.17), those with serum iron levels <73 μg/dL (OR = 2.01, 95% CI: 1.11-3.62), and males (OR = 2.23, 95% CI: 1.21-4.11). Higher DII scores correlated with greater odds of moderate-severe anemia (OR = 1.22, 95% CI: 1.07-1.38).</p><p><strong>Conclusion: </strong>The results indicate that elevated DII scores are associated with an increased occurrence of anemia in DKD patients, emphasizing the importance of lowering pro-inflammatory food consumption as a potential strategy to prevent anemia in this group.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"52-62"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144962187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-11-26DOI: 10.1159/000549041
In the article by Jeon et al. entitled "The Impact of C-Reactive Protein-To-Albumin Ratio on Mortality in Patients with Acute Kidney Injury Requiring Continuous Renal Replacement Therapy: A Multicenter Retrospective Study" [Nephron. 2024;148:379-389; https://doi.org/10.1159/000534970], the license type has been changed to CC-BY-NC.The original article has been updated.
{"title":"Erratum.","authors":"","doi":"10.1159/000549041","DOIUrl":"10.1159/000549041","url":null,"abstract":"<p><p>In the article by Jeon et al. entitled \"The Impact of C-Reactive Protein-To-Albumin Ratio on Mortality in Patients with Acute Kidney Injury Requiring Continuous Renal Replacement Therapy: A Multicenter Retrospective Study\" [Nephron. 2024;148:379-389; https://doi.org/10.1159/000534970], the license type has been changed to CC-BY-NC.The original article has been updated.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"63-64"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145636100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-09-19DOI: 10.1159/000548245
Fernando Caravaca-Fontán, Fadi Fakhouri, Matthew C Pickering, Vikte Lionikaite, Alison Baird, Regina Horneff, Luis López-Lázaro, Lucia Quintana-Gallardo, Carly Rich
Introduction: Knowledge gaps and controversies remain regarding the natural history and variability of C3 glomerulopathy (C3G) and primary immune complex membranoproliferative glomerulonephritis (IC-MPGN). The objectives were to provide an overview of these diseases for the following outcomes of interest: clinical presentation, treatment patterns, and disease burden, including the association between proteinuria and kidney outcomes.
Methods: This systematic literature review (SLR) included studies of adults and children with C3G or primary IC-MPGN investigating outcomes of interest. Embase and MEDLINE were searched from January 2012 to February 22, 2024, combining terms for C3G or IC-MPGN and outcomes of interest. Supplementary congress searches and reference list checking of relevant articles were conducted. Study details, outcomes of interest, and key findings were extracted, and data were narratively summarized.
Results: In total, 148 articles were included. No clear trend for differences between C3G and primary IC-MPGN were observed for clinical presentation. Treatments included immunosuppressive therapies and off-label anti-complement agents. Kidney failure occurred in up to 50% and 37% of patients with C3G and primary IC-MPGN, respectively, and kidney transplantation was required in up to 32% and 24% of patients, respectively. Mortality was reported in up to 21% of patients. No clear trend of complete remission across treatments was observed. In longitudinal studies, proteinuria was associated with increasing risk of kidney failure. No articles reported on patient quality of life or caregiver burden. Several articles reported an economic burden according to length of hospital stay. Possible limitations include that terms used for electronic searches limited which articles were identified, many studies were retrospective and small (<10 participants), and risk of bias was not performed.
Conclusions: This SLR provides insights into C3G and primary IC-MPGN, emphasizing the need for new targeted and effective treatments. Proteinuria was identified to be an acceptable marker in assessing the efficacy of treatments on long-term kidney outcomes.
{"title":"Clinical Presentation, Treatment Patterns, Burden of Disease, and the Association of Proteinuria with Clinical Outcomes in C3 Glomerulopathy and Primary Immune Complex Membranoproliferative Glomerulonephritis: A Systematic Review.","authors":"Fernando Caravaca-Fontán, Fadi Fakhouri, Matthew C Pickering, Vikte Lionikaite, Alison Baird, Regina Horneff, Luis López-Lázaro, Lucia Quintana-Gallardo, Carly Rich","doi":"10.1159/000548245","DOIUrl":"10.1159/000548245","url":null,"abstract":"<p><strong>Introduction: </strong>Knowledge gaps and controversies remain regarding the natural history and variability of C3 glomerulopathy (C3G) and primary immune complex membranoproliferative glomerulonephritis (IC-MPGN). The objectives were to provide an overview of these diseases for the following outcomes of interest: clinical presentation, treatment patterns, and disease burden, including the association between proteinuria and kidney outcomes.</p><p><strong>Methods: </strong>This systematic literature review (SLR) included studies of adults and children with C3G or primary IC-MPGN investigating outcomes of interest. Embase and MEDLINE were searched from January 2012 to February 22, 2024, combining terms for C3G or IC-MPGN and outcomes of interest. Supplementary congress searches and reference list checking of relevant articles were conducted. Study details, outcomes of interest, and key findings were extracted, and data were narratively summarized.</p><p><strong>Results: </strong>In total, 148 articles were included. No clear trend for differences between C3G and primary IC-MPGN were observed for clinical presentation. Treatments included immunosuppressive therapies and off-label anti-complement agents. Kidney failure occurred in up to 50% and 37% of patients with C3G and primary IC-MPGN, respectively, and kidney transplantation was required in up to 32% and 24% of patients, respectively. Mortality was reported in up to 21% of patients. No clear trend of complete remission across treatments was observed. In longitudinal studies, proteinuria was associated with increasing risk of kidney failure. No articles reported on patient quality of life or caregiver burden. Several articles reported an economic burden according to length of hospital stay. Possible limitations include that terms used for electronic searches limited which articles were identified, many studies were retrospective and small (<10 participants), and risk of bias was not performed.</p><p><strong>Conclusions: </strong>This SLR provides insights into C3G and primary IC-MPGN, emphasizing the need for new targeted and effective treatments. Proteinuria was identified to be an acceptable marker in assessing the efficacy of treatments on long-term kidney outcomes.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"25-40"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12795539/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145092201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-11-27DOI: 10.1159/000549072
Olav Rivero Martín, Raúl Morales Febles, Patricia I Delgado Mallén, Elia Reseghetti, Rosa M Miquel Rodríguez, Sara Estupiñán Torres, María A Cobo Caso, Coriolano Cruz, Laura Díaz Martín, Amelia R González Martín, Daniel J Sánchez Báez, Domingo J Hernández Marrero, Sergio Luis Lima, Esteban Porrini
Introduction: In patients with chronic kidney disease (CKD) of diverse causes, obesity and metabolic syndrome (MS) accelerate disease progression. Therapeutic exercise could be effective in treating obesity and MS in patients with CKD. However, the evidence in this area is limited. The aim of this research was to evaluate the effect of an individualized exercise program on major metabolic and renal outcomes in patients with CKD, obesity, and MS.
Methods: This was an interventional exploratory study that included patients with established CKD - estimated glomerular filtration rate (GFR) ≥30 mL/min, obesity, and MS treated by therapeutic exercise (aerobic and resistance) for 6 months. We evaluated changes in renal outcomes - measured glomerular filtration rate (mGFR) with iohexol-DBS and albuminuria, and metabolic outcomes - weight and MS traits. Biochemical, anthropometric, and renal function were performed every 3 months.
Results: Forty patients were evaluated. All were overweight or obese, mGFR was 58 ± 20 mL/min, and the urine albumin-creatinine ratio (UACR) was 256 mg/g [IQR: 38-774]. Based on weight reduction (>5%), patients were classified as "responders" (n = 30) and "nonresponders" (n = 10). Responders had a major reduction in body mass index from 35 ± 4 to 31 ± 4 kg/m2 (p < 0.001), triglycerides, HbA1c, systolic and diastolic blood pressure, and UACR from 222 [20-610] to 89 [17-413] mg/g (p < 0.01), whereas mGFR diminished (≥7%) in half of them and remained stable in the other half. Nonresponders experienced no changes. No major side effects were observed.
Conclusion: In patients with CKD, obesity, and MS, exercise is an effective treatment to reduce weight, MS traits, and albuminuria. Changes in mGFR are heterogeneous. Understanding the impact of weight reduction on GFR changes is crucial in CKD. The role of exercise in nephrological care deserves further attention. The study trial registration number is NCT06576518.
{"title":"Exercise Intervention in Patients with Metabolic Syndrome and Renal Disease: A Prospective Study (EXRED).","authors":"Olav Rivero Martín, Raúl Morales Febles, Patricia I Delgado Mallén, Elia Reseghetti, Rosa M Miquel Rodríguez, Sara Estupiñán Torres, María A Cobo Caso, Coriolano Cruz, Laura Díaz Martín, Amelia R González Martín, Daniel J Sánchez Báez, Domingo J Hernández Marrero, Sergio Luis Lima, Esteban Porrini","doi":"10.1159/000549072","DOIUrl":"10.1159/000549072","url":null,"abstract":"<p><strong>Introduction: </strong>In patients with chronic kidney disease (CKD) of diverse causes, obesity and metabolic syndrome (MS) accelerate disease progression. Therapeutic exercise could be effective in treating obesity and MS in patients with CKD. However, the evidence in this area is limited. The aim of this research was to evaluate the effect of an individualized exercise program on major metabolic and renal outcomes in patients with CKD, obesity, and MS.</p><p><strong>Methods: </strong>This was an interventional exploratory study that included patients with established CKD - estimated glomerular filtration rate (GFR) ≥30 mL/min, obesity, and MS treated by therapeutic exercise (aerobic and resistance) for 6 months. We evaluated changes in renal outcomes - measured glomerular filtration rate (mGFR) with iohexol-DBS and albuminuria, and metabolic outcomes - weight and MS traits. Biochemical, anthropometric, and renal function were performed every 3 months.</p><p><strong>Results: </strong>Forty patients were evaluated. All were overweight or obese, mGFR was 58 ± 20 mL/min, and the urine albumin-creatinine ratio (UACR) was 256 mg/g [IQR: 38-774]. Based on weight reduction (>5%), patients were classified as \"responders\" (n = 30) and \"nonresponders\" (n = 10). Responders had a major reduction in body mass index from 35 ± 4 to 31 ± 4 kg/m2 (p < 0.001), triglycerides, HbA1c, systolic and diastolic blood pressure, and UACR from 222 [20-610] to 89 [17-413] mg/g (p < 0.01), whereas mGFR diminished (≥7%) in half of them and remained stable in the other half. Nonresponders experienced no changes. No major side effects were observed.</p><p><strong>Conclusion: </strong>In patients with CKD, obesity, and MS, exercise is an effective treatment to reduce weight, MS traits, and albuminuria. Changes in mGFR are heterogeneous. Understanding the impact of weight reduction on GFR changes is crucial in CKD. The role of exercise in nephrological care deserves further attention. The study trial registration number is NCT06576518.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"141-155"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145636098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}