Pub Date : 2026-01-16DOI: 10.1016/j.kint.2025.11.009
Yuanhang Yang,Antoine Creon,Andrew S Levey,Anne-Laure Faucon,Aurora Caldinelli,Marie Evans,Arvid Sjölander,Alberto Ortiz,Edouard L Fu,Juan Jesus Carrero
INTRODUCTIONThere are currently no established strategies for early identification and primary prevention of chronic kidney disease (CKD). Automatic reporting of estimated glomerular filtration rate (eGFR) allows opportunistic CKD screening. Here, we hypothesized that comparison with population-based eGFR distributions may further help identify individuals at elevated risk.METHODSA population-based observational cohort study including adults aged 40 to 100 years with routine serum/plasma creatinine tests (Stockholm CREAtinine Measurements project) between 2006 and 2021 was conducted. The cohort captured 1,179,501 unique individuals (80% of the population in the region) with 6,914,993 repeated annual eGFR measurements. After computing eGFR distributions by age and sex, cause-specific Cox regressions evaluated the associations between eGFR percentiles and risks of kidney failure with replacement therapy (KFRT) and death.RESULTSMedian eGFR (2009 CKD-EPI) was lower at higher age, from 104-106 ml/min per 1.73 m2 (men-women) at age 40 to 45-50 ml/min per 1.73 m2 at age 100. Exclusion of individuals with selected comorbid conditions or adjustment for the non-tested population had minimal impact on eGFR distributions. Compared to the central percentiles (47.5-52.5th), eGFR percentiles below the 25th were significantly associated with increased risk of KFRT, and both low and high eGFR percentiles were associated with increased mortality. Associations were consistent across age groups. Among 421,547 individuals with eGFR 60 ml/min per 1.73 m2 or more who were below the 25th percentile, only 24% underwent albuminuria/proteinuria testing in the adjacent year and could have benefited from additional diagnostic work-up.CONCLUSIONSOur study shows that eGFR values below the 25th percentile of the population distribution are associated with increased risks of kidney failure and death. Population-based eGFR charts may complement current automatic reporting systems and provide opportunities for early identification and primary prevention of CKD.
{"title":"Population-based estimated Glomerular Filtration Rate distributions and associated health outcomes provide opportunities for early identification of and primary prevention of chronic kidney disease.","authors":"Yuanhang Yang,Antoine Creon,Andrew S Levey,Anne-Laure Faucon,Aurora Caldinelli,Marie Evans,Arvid Sjölander,Alberto Ortiz,Edouard L Fu,Juan Jesus Carrero","doi":"10.1016/j.kint.2025.11.009","DOIUrl":"https://doi.org/10.1016/j.kint.2025.11.009","url":null,"abstract":"INTRODUCTIONThere are currently no established strategies for early identification and primary prevention of chronic kidney disease (CKD). Automatic reporting of estimated glomerular filtration rate (eGFR) allows opportunistic CKD screening. Here, we hypothesized that comparison with population-based eGFR distributions may further help identify individuals at elevated risk.METHODSA population-based observational cohort study including adults aged 40 to 100 years with routine serum/plasma creatinine tests (Stockholm CREAtinine Measurements project) between 2006 and 2021 was conducted. The cohort captured 1,179,501 unique individuals (80% of the population in the region) with 6,914,993 repeated annual eGFR measurements. After computing eGFR distributions by age and sex, cause-specific Cox regressions evaluated the associations between eGFR percentiles and risks of kidney failure with replacement therapy (KFRT) and death.RESULTSMedian eGFR (2009 CKD-EPI) was lower at higher age, from 104-106 ml/min per 1.73 m2 (men-women) at age 40 to 45-50 ml/min per 1.73 m2 at age 100. Exclusion of individuals with selected comorbid conditions or adjustment for the non-tested population had minimal impact on eGFR distributions. Compared to the central percentiles (47.5-52.5th), eGFR percentiles below the 25th were significantly associated with increased risk of KFRT, and both low and high eGFR percentiles were associated with increased mortality. Associations were consistent across age groups. Among 421,547 individuals with eGFR 60 ml/min per 1.73 m2 or more who were below the 25th percentile, only 24% underwent albuminuria/proteinuria testing in the adjacent year and could have benefited from additional diagnostic work-up.CONCLUSIONSOur study shows that eGFR values below the 25th percentile of the population distribution are associated with increased risks of kidney failure and death. Population-based eGFR charts may complement current automatic reporting systems and provide opportunities for early identification and primary prevention of CKD.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"124 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145986566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.kint.2025.06.028
Adrian P. Schug , Lam-Thanh Ly , Kai-Uwe Eckardt , Michael S. Balzer
{"title":"The Case | The sweet twirl—chorea as a diabetic complication: an elderly patient with CKD, hyperglycemia, and chorea","authors":"Adrian P. Schug , Lam-Thanh Ly , Kai-Uwe Eckardt , Michael S. Balzer","doi":"10.1016/j.kint.2025.06.028","DOIUrl":"10.1016/j.kint.2025.06.028","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"109 1","pages":"Pages 235-236"},"PeriodicalIF":12.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145880293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.kint.2025.09.024
Rukshana Shroff , Franz Schaefer
Dialysis is a life-sustaining treatment but comes with a very high burden of cardiovascular (CV) morbidity and mortality risk. CV events account for almost 30% of deaths in children receiving dialysis. Multiple risk factors for CV disease, both traditional and uremia-related, are present in children before they even start kidney replacement therapy and increase in prevalence and severity on dialysis. Peritoneal dialysis, as well as the conventional 3 times per week regimen of hemodialysis, offers only suboptimal clearance of uremic toxins and fluid removal. Intensified dialysis regimens, in the form of adding in convective clearance with hemodiafiltration or increasing dialysis time with longer or more frequent sessions in home hemodialysis, may offer some cardioprotective effect, but data in children are scarce. Importantly, several risk factors for CV damage are modifiable and their early diagnosis and management are crucial to mitigate CV damage. Intensified dialysis may attenuate the progression of subclinical CV disease, but no treatment to date has shown that the inexorable progression of CV disease can be reversed. Children on dialysis have a lifetime of kidney replacement therapy ahead of them, so our management must focus on early diagnosis and robust preventive strategies to give them the best chance of optimal CV health and survival. In this mini review, we discuss the key risk factors for CV disease and how to optimize CV outcomes in children receiving dialysis.
{"title":"Optimizing cardiovascular outcomes in pediatric dialysis","authors":"Rukshana Shroff , Franz Schaefer","doi":"10.1016/j.kint.2025.09.024","DOIUrl":"10.1016/j.kint.2025.09.024","url":null,"abstract":"<div><div>Dialysis is a life-sustaining treatment but comes with a very high burden of cardiovascular (CV) morbidity and mortality risk. CV events account for almost 30% of deaths in children receiving dialysis. Multiple risk factors for CV disease, both traditional and uremia-related, are present in children before they even start kidney replacement therapy and increase in prevalence and severity on dialysis. Peritoneal dialysis, as well as the conventional 3 times per week regimen of hemodialysis, offers only suboptimal clearance of uremic toxins and fluid removal. Intensified dialysis regimens, in the form of adding in convective clearance with hemodiafiltration or increasing dialysis time with longer or more frequent sessions in home hemodialysis, may offer some cardioprotective effect, but data in children are scarce. Importantly, several risk factors for CV damage are modifiable and their early diagnosis and management are crucial to mitigate CV damage. Intensified dialysis may attenuate the progression of subclinical CV disease, but no treatment to date has shown that the inexorable progression of CV disease can be reversed. Children on dialysis have a lifetime of kidney replacement therapy ahead of them, so our management must focus on early diagnosis and robust preventive strategies to give them the best chance of optimal CV health and survival. In this mini review, we discuss the key risk factors for CV disease and how to optimize CV outcomes in children receiving dialysis.</div></div>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"109 1","pages":"Pages 73-80"},"PeriodicalIF":12.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145382746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.kint.2025.07.034
Benoît Brilland , Maïa Despré , Robin Khatri , Thomas Quéméneur , Cyrille Vandenbussche , Nathalie Merillon , Andrea Boizard-Moracchini , Maëva Roy , Laurence Preisser , Jérémie Riou , Giorgina Barbara Piccoli , Assia Djema , Nicolas Henry , Odile Blanchet , Stefan Bonn , Céline C. Berthier , Peter Grayson , Yves Delneste , Viviane Gnemmi , Patrick Blanco , Samuel Wacrenier
Introduction
Anti-neutrophil cytoplasmic antibody (ANCA)–associated vasculitis (AAV) causes severe multisystemic organ damage. The main phenotypes, microscopic polyangiitis (MPA) and granulomatosis with polyangiitis (GPA), share similarities but differ in clinical presentation and outcome. To uncover their molecular differences, we performed transcriptomic profiling of kidney tissue, then focused on type I interferon (IFN-I) pathway activation in kidney and blood and its clinical implications.
Methods
We analyzed two independent cohorts (Maine-Anjou and RENVAS registries) totaling 193 patients with AAV and glomerulonephritis. NanoString nCounter transcriptomic profiling, and serum inflammatory molecules quantification were conducted. Comparative analyses of MPA vs. GPA (and MPO-AAV vs. PR3-AAV) were validated using independent public datasets (including kidney spatial transcriptomic datasets, European cDNA Renal Biobank and blood from the RAVE trial).
Results
The kidney IFN-I signature found in AAV-GN is upregulated in MPA/MPO-AAV compared to GPA/PR3-AAV and controls. Quantitative PCR, MxA immunohistochemistry, and analysis of external datasets confirmed these findings. This IFN-I signature, close to the one found in lupus nephritis, is linked to the extent of pDC infiltration. Kidney IFN-I activation correlated with increased kidney fibrosis, independently of kidney function. High kidney IFN-I signatures were linked to lower kidney survival, independently of kidney function and pathological scores. MPA kidneys also exhibited higher mast cell and T-cell infiltration. Systemic analyses showed elevated IFNα and interferon related inflammatory molecules in all patients with AAV, but a stronger IFN-I gene signature was found in immune cells from MPA.
Conclusions
Our study identifies an IFN-I signature in AAV, especially in MPA/MPO-AAV, underscoring its potential role in disease heterogeneity and kidney pathology. IFN-I emerges as a potential prognostic biomarker and therapeutic target in AAV, particularly for MPA. Further studies are needed to clarify its mechanisms and explore IFN-I modulation in clinical trials.
{"title":"A stronger type I interferon signature distinguishes ANCA-associated vasculitis phenotypes and predicts kidney prognosis","authors":"Benoît Brilland , Maïa Despré , Robin Khatri , Thomas Quéméneur , Cyrille Vandenbussche , Nathalie Merillon , Andrea Boizard-Moracchini , Maëva Roy , Laurence Preisser , Jérémie Riou , Giorgina Barbara Piccoli , Assia Djema , Nicolas Henry , Odile Blanchet , Stefan Bonn , Céline C. Berthier , Peter Grayson , Yves Delneste , Viviane Gnemmi , Patrick Blanco , Samuel Wacrenier","doi":"10.1016/j.kint.2025.07.034","DOIUrl":"10.1016/j.kint.2025.07.034","url":null,"abstract":"<div><h3>Introduction</h3><div>Anti-neutrophil cytoplasmic antibody (ANCA)–associated vasculitis (AAV) causes severe multisystemic organ damage. The main phenotypes, microscopic polyangiitis (MPA) and granulomatosis with polyangiitis (GPA), share similarities but differ in clinical presentation and outcome. To uncover their molecular differences, we performed transcriptomic profiling of kidney tissue, then focused on type I interferon (IFN-I) pathway activation in kidney and blood and its clinical implications.</div></div><div><h3>Methods</h3><div>We analyzed two independent cohorts (Maine-Anjou and RENVAS registries) totaling 193 patients with AAV and glomerulonephritis. NanoString nCounter transcriptomic profiling, and serum inflammatory molecules quantification were conducted. Comparative analyses of MPA vs. GPA (and MPO-AAV vs. PR3-AAV) were validated using independent public datasets (including kidney spatial transcriptomic datasets, European cDNA Renal Biobank and blood from the RAVE trial).</div></div><div><h3>Results</h3><div>The kidney IFN-I signature found in AAV-GN is upregulated in MPA/MPO-AAV compared to GPA/PR3-AAV and controls. Quantitative PCR, MxA immunohistochemistry, and analysis of external datasets confirmed these findings. This IFN-I signature, close to the one found in lupus nephritis, is linked to the extent of pDC infiltration. Kidney IFN-I activation correlated with increased kidney fibrosis, independently of kidney function. High kidney IFN-I signatures were linked to lower kidney survival, independently of kidney function and pathological scores. MPA kidneys also exhibited higher mast cell and T-cell infiltration. Systemic analyses showed elevated IFNα and interferon related inflammatory molecules in all patients with AAV, but a stronger IFN-I gene signature was found in immune cells from MPA.</div></div><div><h3>Conclusions</h3><div>Our study identifies an IFN-I signature in AAV, especially in MPA/MPO-AAV, underscoring its potential role in disease heterogeneity and kidney pathology. IFN-I emerges as a potential prognostic biomarker and therapeutic target in AAV, particularly for MPA. Further studies are needed to clarify its mechanisms and explore IFN-I modulation in clinical trials.</div></div>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"109 1","pages":"Pages 139-159"},"PeriodicalIF":12.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145035803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.kint.2025.08.034
Behzad Najafian , Maria Luiza Caramori , Michele Dalla Vestra , Alois Saller , Mehrdad Noruzinia , Michael Mauer , Paola Fioretto
Introduction
Kidney structural-functional relationship studies have been critical in understanding diabetic kidney disease (DKD) evolution. However, most such studies were performed in persons with type 1 diabetes, where diabetic glomerular lesions are strongly associated with albumin excretion rate (AER). Here, we compare DKD structural-functional relationships in type 1 and type 2 diabetes.
Methods
To better understand the evolution of DKD in type 2 diabetes, analyses of glomerular structure/albuminuria relationships were performed in 133 research volunteers with type 2 and 161 with type 1 diabetes matched for AER compared to 95 living donor kidney biopsies as controls.
Results
Morphometric measures of DKD glomerular lesions were more advanced and showed stronger relationships with AER in persons with type 1 vs type 2 diabetes. K-means cluster analysis based on distance from a structural-functional relationship model derived from data of research participants with type 1 diabetes yielded two clusters: 74% of participants with type 2 diabetes were in Cluster 1, which also included most participants with type 1 diabetes, while 26% of participants with type 2 diabetes (39% of type 2 cases with increased AER) were in Cluster 2 and showed greater AER than predicted by their DKD glomerular lesions based on the model. Among those with type 2 diabetes, despite excessive AER in Cluster 2, DKD glomerular lesions and podocyte structural parameters were similar between the two clusters. However, adjusted for AER, individuals with type 2 diabetes in Cluster 1 had more severe DKD lesions and approximately four-fold greater rates of glomerular filtration rate decline over nine to ten years follow up than those in Cluster 2.
Conclusions
Kidney structural-functional relationships are heterogeneous in individuals with type 2 diabetes, and this heterogeneity is linked to glomerular filtration rate loss over time. Our investigation calls for further studies to better understand factors involved in this heterogeneity.
{"title":"Heterogeneity in the relationships between albuminuria and glomerular structure in type 1 and type 2 diabetes","authors":"Behzad Najafian , Maria Luiza Caramori , Michele Dalla Vestra , Alois Saller , Mehrdad Noruzinia , Michael Mauer , Paola Fioretto","doi":"10.1016/j.kint.2025.08.034","DOIUrl":"10.1016/j.kint.2025.08.034","url":null,"abstract":"<div><h3>Introduction</h3><div>Kidney structural-functional relationship studies have been critical in understanding diabetic kidney disease (DKD) evolution. However, most such studies were performed in persons with type 1 diabetes, where diabetic glomerular lesions are strongly associated with albumin excretion rate (AER). Here, we compare DKD structural-functional relationships in type 1 and type 2 diabetes.</div></div><div><h3>Methods</h3><div>To better understand the evolution of DKD in type 2 diabetes, analyses of glomerular structure/albuminuria relationships were performed in 133 research volunteers with type 2 and 161 with type 1 diabetes matched for AER compared to 95 living donor kidney biopsies as controls.</div></div><div><h3>Results</h3><div>Morphometric measures of DKD glomerular lesions were more advanced and showed stronger relationships with AER in persons with type 1 vs type 2 diabetes. K-means cluster analysis based on distance from a structural-functional relationship model derived from data of research participants with type 1 diabetes yielded two clusters: 74% of participants with type 2 diabetes were in Cluster 1, which also included most participants with type 1 diabetes, while 26% of participants with type 2 diabetes (39% of type 2 cases with increased AER) were in Cluster 2 and showed greater AER than predicted by their DKD glomerular lesions based on the model. Among those with type 2 diabetes, despite excessive AER in Cluster 2, DKD glomerular lesions and podocyte structural parameters were similar between the two clusters. However, adjusted for AER, individuals with type 2 diabetes in Cluster 1 had more severe DKD lesions and approximately four-fold greater rates of glomerular filtration rate decline over nine to ten years follow up than those in Cluster 2.</div></div><div><h3>Conclusions</h3><div>Kidney structural-functional relationships are heterogeneous in individuals with type 2 diabetes, and this heterogeneity is linked to glomerular filtration rate loss over time. Our investigation calls for further studies to better understand factors involved in this heterogeneity.</div></div>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"109 1","pages":"Pages 119-128"},"PeriodicalIF":12.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145246804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.kint.2025.10.005
Menno Pruijm , Nicolas Belmar , Petter Bjornstad , David Z.I. Cherney , Vivek Das , Thomas Gunnarsson , Jeffrey B. Hodgin , Philip A. Schytz , Katherine R. Tuttle , Matthias Kretzler
Chronic kidney disease poses a major global health burden and is one of the most common complications of type 2 diabetes. Drug trials have demonstrated that treatments, including sodium-glucose cotransporter-2 inhibitors, a glucagon-like peptide-1 receptor agonist, and a nonsteroidal mineralocorticoid receptor antagonist, mitigate chronic kidney disease progression, but the underlying nephroprotective mechanisms of action remain incompletely understood, partly ascribed to their pleiotropic actions. New innovative trial designs are needed to tackle simultaneously the hemodynamic and structural effects induced by these drugs. The REMODEL trial (REnal MODE of action of semagLutide in patients with type 2 diabetes and chronic kidney disease; ClinicalTrials.gov identifier: NCT04865770) is designed to explore the mechanisms of action of semaglutide with a novel multiparametric approach, integrating functional magnetic resonance imaging and research kidney biopsies for structural and molecular interrogation and blood and urine biomarker analysis. Better understanding of these mechanisms will help explain semaglutide's beneficial effects on kidney disease outcomes, reported in the FLOW (Evaluate Renal Function with Semaglutide Once Weekly; ClinicalTrials.gov identifier: NCT03819153) trial, and may identify patient subpopulations to optimize treatment strategies. By combining diverse and state-of-the-art methods, REMODEL aims to pave the way to a larger use of mechanism of action trials in the near future. To this purpose, this article describes the REMODEL framework, methods, technical challenges, and lessons learned as a platform for future mechanistic trials of chronic kidney disease therapies and beyond.
{"title":"REMODELing mechanistic trials for kidney disease: a multimodal, tissue-centered approach to understand the renal mechanism of action of semaglutide","authors":"Menno Pruijm , Nicolas Belmar , Petter Bjornstad , David Z.I. Cherney , Vivek Das , Thomas Gunnarsson , Jeffrey B. Hodgin , Philip A. Schytz , Katherine R. Tuttle , Matthias Kretzler","doi":"10.1016/j.kint.2025.10.005","DOIUrl":"10.1016/j.kint.2025.10.005","url":null,"abstract":"<div><div>Chronic kidney disease poses a major global health burden and is one of the most common complications of type 2 diabetes. Drug trials have demonstrated that treatments, including sodium-glucose cotransporter-2 inhibitors, a glucagon-like peptide-1 receptor agonist, and a nonsteroidal mineralocorticoid receptor antagonist, mitigate chronic kidney disease progression, but the underlying nephroprotective mechanisms of action remain incompletely understood, partly ascribed to their pleiotropic actions. New innovative trial designs are needed to tackle simultaneously the hemodynamic and structural effects induced by these drugs. The REMODEL trial (REnal MODE of action of semagLutide in patients with type 2 diabetes and chronic kidney disease; ClinicalTrials.gov identifier: NCT04865770) is designed to explore the mechanisms of action of semaglutide with a novel multiparametric approach, integrating functional magnetic resonance imaging and research kidney biopsies for structural and molecular interrogation and blood and urine biomarker analysis. Better understanding of these mechanisms will help explain semaglutide's beneficial effects on kidney disease outcomes, reported in the FLOW (Evaluate Renal Function with Semaglutide Once Weekly; ClinicalTrials.gov identifier: NCT03819153) trial, and may identify patient subpopulations to optimize treatment strategies. By combining diverse and state-of-the-art methods, REMODEL aims to pave the way to a larger use of mechanism of action trials in the near future. To this purpose, this article describes the REMODEL framework, methods, technical challenges, and lessons learned as a platform for future mechanistic trials of chronic kidney disease therapies and beyond.</div></div>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"109 1","pages":"Pages 6-16"},"PeriodicalIF":12.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145461316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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