Andrea Bauer, R. M. Elias, Hugo Abensur, Marcelo Costa Batista, Angela Jansen, M. Riella
Background: Over the last three decades, over 700 million individuals worldwide have been diagnosed with chronic kidney disease (CKD). In a 2017 survey in southern Brazil, 11.4% of those surveyed had CKD. Early identification and effective therapy in Brazil may reduce chronic kidney disease's impact. This panel discusses the early diagnosis and treatment of CKD and the barriers and actions needed to improve the management of CKD in Brazil. A panel of Brazilian nephrologists was provided with relevant questions to address before a multi-day conference. During this meeting, each narrative was discussed and edited through several rounds until agreement on the relevant topics and recommendations was achieved. Summary: Panelists highlighted hurdles to early diagnosis and treatment of CKD. These include, but are not limited to, a lack of public and patient education, updated recommendations, multi-disciplinary CKD treatment, and a national CKD database. Key Messages: People-centered, physician-centered, and healthcare institution-centered actions can be taken to improve outcomes. Patient empowerment is needed via multiple channels of CKD education and access to health-monitoring wearables and apps. Primary care clinicians and non-specialists must be trained to screen and manage CKD-causing illnesses, including diabetes and hypertension. The healthcare system may implement a national health data gathering system, more screening tests, automated test result reporting, and telehealth. Increasing access to early diagnosis can provide a path to improving care for patients with CKD. Concerted efforts from all stakeholders are needed to overcome the barriers.
{"title":"Chronic Kidney Disease in Brazil: Current Status and Recommended Improvements","authors":"Andrea Bauer, R. M. Elias, Hugo Abensur, Marcelo Costa Batista, Angela Jansen, M. Riella","doi":"10.1159/000538068","DOIUrl":"https://doi.org/10.1159/000538068","url":null,"abstract":"Background: Over the last three decades, over 700 million individuals worldwide have been diagnosed with chronic kidney disease (CKD). In a 2017 survey in southern Brazil, 11.4% of those surveyed had CKD. Early identification and effective therapy in Brazil may reduce chronic kidney disease's impact. This panel discusses the early diagnosis and treatment of CKD and the barriers and actions needed to improve the management of CKD in Brazil. A panel of Brazilian nephrologists was provided with relevant questions to address before a multi-day conference. During this meeting, each narrative was discussed and edited through several rounds until agreement on the relevant topics and recommendations was achieved.\u0000Summary: Panelists highlighted hurdles to early diagnosis and treatment of CKD. These include, but are not limited to, a lack of public and patient education, updated recommendations, multi-disciplinary CKD treatment, and a national CKD database. \u0000Key Messages: People-centered, physician-centered, and healthcare institution-centered actions can be taken to improve outcomes. Patient empowerment is needed via multiple channels of CKD education and access to health-monitoring wearables and apps. Primary care clinicians and non-specialists must be trained to screen and manage CKD-causing illnesses, including diabetes and hypertension. The healthcare system may implement a national health data gathering system, more screening tests, automated test result reporting, and telehealth. Increasing access to early diagnosis can provide a path to improving care for patients with CKD. Concerted efforts from all stakeholders are needed to overcome the barriers.\u0000","PeriodicalId":17830,"journal":{"name":"Kidney Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140408641","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}
Jiaying Li, Fangxing Hou, Ning Lv, Ruohuan Zhao, Lei Zhang, Cai Yue, Min Nie, Limeng Chen
Background: Acute kidney injury (AKI) is a severe condition marked by rapid renal function deterioration and elevated mortality, with traditional biomarkers lacking sensitivity and specificity. Rare tubulointerstitial diseases encompass a spectrum of disorders, primarily including monogenic diseases, immune-related conditions, and drug-induced tubulointerstitial diseases. The clinical manifestations vary from the electrolyte and acid-base imbalance to kidney function insufficiency, which is associated with AKI in up to 20% of cases. Evidence indicated that rare tubulointerstitial diseases might provide new conceptual insights and perspectives for novel biomarkers and potential therapeutic strategies for AKI. Summary: Autosomal dominant tubulointerstitial kidney disease (ADTKD) and Fanconi syndrome (FS) are rare tubulointerstitial diseases. In ADTKD, UMOD and REN are closely related to AKI by affecting oxidative stress and tubuloglomerular feedback (TGF), which provide potential new biomarkers for AKI. Both rare tubulointerstitial diseases and AKI shared etiologies and treatment responses. From the mechanism standpoint, rare tubulointerstitial diseases and AKI involve tubular transporter injury, initially manifesting as tubular dysfunction in tubulointerstitial disorder and progressing to AKI because of the programmed cell death (PCD) with apoptosis, pyroptosis, or necroptosis of proximal tubule cells. Additionally, mitochondrial dysfunction has been identified as a common mechanism in both tubulointerstitial diseases and AKI induced by drugs, pSS, or monoclonal diseases. In the end, both AKI and FS patients and animal models responded well to the therapy of the primary diseases. Key messages: In this review, we describe an overview of ADTKD and FS to identify their associations with AKI. Mitochondrial dysfunction contributes to rare tubulointerstitial diseases and AKI, which might provide a potential therapeutic target.
背景：急性肾损伤（AKI）是一种以肾功能急剧恶化和死亡率升高为特征的严重疾病，传统的生物标志物缺乏敏感性和特异性。罕见的肾小管间质疾病包括一系列疾病，主要包括单基因疾病、免疫相关疾病和药物诱发的肾小管间质疾病。其临床表现各不相同，从电解质和酸碱失衡到肾功能不全，多达 20% 的病例伴有 AKI。有证据表明，罕见的肾小管间质性疾病可能为新型生物标记物和潜在的 AKI 治疗策略提供新的概念见解和视角。摘要：常染色体显性肾小管间质性疾病（ADTKD）和范可尼综合征（FS）是罕见的肾小管间质性疾病。在 ADTKD 中，UMOD 和 REN 通过影响氧化应激和肾小管肾小球反馈（TGF）而与 AKI 密切相关，这为 AKI 提供了潜在的新生物标志物。罕见肾小管间质疾病和 AKI 有着共同的病因和治疗反应。从机制上看，罕见的肾小管间质性疾病和 AKI 都涉及肾小管转运体损伤，最初表现为肾小管间质性疾病中的肾小管功能障碍，后来由于近端肾小管细胞凋亡、热凋亡或坏死等程序性细胞死亡（PCD）而发展为 AKI。此外，线粒体功能障碍已被确定为肾小管间质疾病和由药物、PSS 或单克隆疾病诱发的 AKI 的共同机制。最终，AKI 和 FS 患者及动物模型对原发疾病的治疗均反应良好。关键信息：在这篇综述中，我们概述了 ADTKD 和 FS，以确定它们与 AKI 的关联。线粒体功能障碍导致了罕见的肾小管间质疾病和 AKI，这可能是一个潜在的治疗靶点。
{"title":"From Rare Disorders of Kidney Tubules to Acute Renal Injury: Progress and Prospective","authors":"Jiaying Li, Fangxing Hou, Ning Lv, Ruohuan Zhao, Lei Zhang, Cai Yue, Min Nie, Limeng Chen","doi":"10.1159/000536423","DOIUrl":"https://doi.org/10.1159/000536423","url":null,"abstract":"Background: Acute kidney injury (AKI) is a severe condition marked by rapid renal function deterioration and elevated mortality, with traditional biomarkers lacking sensitivity and specificity. Rare tubulointerstitial diseases encompass a spectrum of disorders, primarily including monogenic diseases, immune-related conditions, and drug-induced tubulointerstitial diseases. The clinical manifestations vary from the electrolyte and acid-base imbalance to kidney function insufficiency, which is associated with AKI in up to 20% of cases. Evidence indicated that rare tubulointerstitial diseases might provide new conceptual insights and perspectives for novel biomarkers and potential therapeutic strategies for AKI.\u0000Summary: Autosomal dominant tubulointerstitial kidney disease (ADTKD) and Fanconi syndrome (FS) are rare tubulointerstitial diseases. In ADTKD, UMOD and REN are closely related to AKI by affecting oxidative stress and tubuloglomerular feedback (TGF), which provide potential new biomarkers for AKI. Both rare tubulointerstitial diseases and AKI shared etiologies and treatment responses. From the mechanism standpoint, rare tubulointerstitial diseases and AKI involve tubular transporter injury, initially manifesting as tubular dysfunction in tubulointerstitial disorder and progressing to AKI because of the programmed cell death (PCD) with apoptosis, pyroptosis, or necroptosis of proximal tubule cells. Additionally, mitochondrial dysfunction has been identified as a common mechanism in both tubulointerstitial diseases and AKI induced by drugs, pSS, or monoclonal diseases. In the end, both AKI and FS patients and animal models responded well to the therapy of the primary diseases. \u0000Key messages: In this review, we describe an overview of ADTKD and FS to identify their associations with AKI. Mitochondrial dysfunction contributes to rare tubulointerstitial diseases and AKI, which might provide a potential therapeutic target.","PeriodicalId":17830,"journal":{"name":"Kidney Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139870148","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}
Jiaying Li, Fangxing Hou, Ning Lv, Ruohuan Zhao, Lei Zhang, Cai Yue, Min Nie, Limeng Chen
Background: Acute kidney injury (AKI) is a severe condition marked by rapid renal function deterioration and elevated mortality, with traditional biomarkers lacking sensitivity and specificity. Rare tubulointerstitial diseases encompass a spectrum of disorders, primarily including monogenic diseases, immune-related conditions, and drug-induced tubulointerstitial diseases. The clinical manifestations vary from the electrolyte and acid-base imbalance to kidney function insufficiency, which is associated with AKI in up to 20% of cases. Evidence indicated that rare tubulointerstitial diseases might provide new conceptual insights and perspectives for novel biomarkers and potential therapeutic strategies for AKI. Summary: Autosomal dominant tubulointerstitial kidney disease (ADTKD) and Fanconi syndrome (FS) are rare tubulointerstitial diseases. In ADTKD, UMOD and REN are closely related to AKI by affecting oxidative stress and tubuloglomerular feedback (TGF), which provide potential new biomarkers for AKI. Both rare tubulointerstitial diseases and AKI shared etiologies and treatment responses. From the mechanism standpoint, rare tubulointerstitial diseases and AKI involve tubular transporter injury, initially manifesting as tubular dysfunction in tubulointerstitial disorder and progressing to AKI because of the programmed cell death (PCD) with apoptosis, pyroptosis, or necroptosis of proximal tubule cells. Additionally, mitochondrial dysfunction has been identified as a common mechanism in both tubulointerstitial diseases and AKI induced by drugs, pSS, or monoclonal diseases. In the end, both AKI and FS patients and animal models responded well to the therapy of the primary diseases. Key messages: In this review, we describe an overview of ADTKD and FS to identify their associations with AKI. Mitochondrial dysfunction contributes to rare tubulointerstitial diseases and AKI, which might provide a potential therapeutic target.
背景：急性肾损伤（AKI）是一种以肾功能急剧恶化和死亡率升高为特征的严重疾病，传统的生物标志物缺乏敏感性和特异性。罕见的肾小管间质疾病包括一系列疾病，主要包括单基因疾病、免疫相关疾病和药物诱发的肾小管间质疾病。其临床表现各不相同，从电解质和酸碱失衡到肾功能不全，多达 20% 的病例伴有 AKI。有证据表明，罕见的肾小管间质性疾病可能为新型生物标记物和潜在的 AKI 治疗策略提供新的概念见解和视角。摘要：常染色体显性肾小管间质性疾病（ADTKD）和范可尼综合征（FS）是罕见的肾小管间质性疾病。在 ADTKD 中，UMOD 和 REN 通过影响氧化应激和肾小管肾小球反馈（TGF）而与 AKI 密切相关，这为 AKI 提供了潜在的新生物标志物。罕见肾小管间质疾病和 AKI 有着共同的病因和治疗反应。从机制上看，罕见的肾小管间质性疾病和 AKI 都涉及肾小管转运体损伤，最初表现为肾小管间质性疾病中的肾小管功能障碍，后来由于近端肾小管细胞凋亡、热凋亡或坏死等程序性细胞死亡（PCD）而发展为 AKI。此外，线粒体功能障碍已被确定为肾小管间质疾病和由药物、PSS 或单克隆疾病诱发的 AKI 的共同机制。最终，AKI 和 FS 患者及动物模型对原发疾病的治疗均反应良好。关键信息：在这篇综述中，我们概述了 ADTKD 和 FS，以确定它们与 AKI 的关联。线粒体功能障碍导致了罕见的肾小管间质疾病和 AKI，这可能是一个潜在的治疗靶点。
{"title":"From Rare Disorders of Kidney Tubules to Acute Renal Injury: Progress and Prospective","authors":"Jiaying Li, Fangxing Hou, Ning Lv, Ruohuan Zhao, Lei Zhang, Cai Yue, Min Nie, Limeng Chen","doi":"10.1159/000536423","DOIUrl":"https://doi.org/10.1159/000536423","url":null,"abstract":"Background: Acute kidney injury (AKI) is a severe condition marked by rapid renal function deterioration and elevated mortality, with traditional biomarkers lacking sensitivity and specificity. Rare tubulointerstitial diseases encompass a spectrum of disorders, primarily including monogenic diseases, immune-related conditions, and drug-induced tubulointerstitial diseases. The clinical manifestations vary from the electrolyte and acid-base imbalance to kidney function insufficiency, which is associated with AKI in up to 20% of cases. Evidence indicated that rare tubulointerstitial diseases might provide new conceptual insights and perspectives for novel biomarkers and potential therapeutic strategies for AKI.\u0000Summary: Autosomal dominant tubulointerstitial kidney disease (ADTKD) and Fanconi syndrome (FS) are rare tubulointerstitial diseases. In ADTKD, UMOD and REN are closely related to AKI by affecting oxidative stress and tubuloglomerular feedback (TGF), which provide potential new biomarkers for AKI. Both rare tubulointerstitial diseases and AKI shared etiologies and treatment responses. From the mechanism standpoint, rare tubulointerstitial diseases and AKI involve tubular transporter injury, initially manifesting as tubular dysfunction in tubulointerstitial disorder and progressing to AKI because of the programmed cell death (PCD) with apoptosis, pyroptosis, or necroptosis of proximal tubule cells. Additionally, mitochondrial dysfunction has been identified as a common mechanism in both tubulointerstitial diseases and AKI induced by drugs, pSS, or monoclonal diseases. In the end, both AKI and FS patients and animal models responded well to the therapy of the primary diseases. \u0000Key messages: In this review, we describe an overview of ADTKD and FS to identify their associations with AKI. Mitochondrial dysfunction contributes to rare tubulointerstitial diseases and AKI, which might provide a potential therapeutic target.","PeriodicalId":17830,"journal":{"name":"Kidney Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139810399","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}
Shuang Xu, Xinyuan Li, Qing Hou, Ning Xu, Qingmiao Lu, Sudan Wang, Chunsun Dai
Introduction: Unsaturated fatty acids play an essential role in the progression of diabetic nephropathy (DN). Previous studies were mainly focused on the role of individual unsaturated fatty acid. The serum unsaturated fatty acid patterns in patients with DN remains to be determined. Methods: A total of 135 patients with DN (DN group) and 322 patients with type II diabetes without nephropathy (non-DN group) were included in this study. Clinical data, serum levels of unsaturated fatty acids and other laboratory indicators were collected. Multivariate logistic regression was applied to identify risk factors for serum unsaturated fatty acids level in both groups. Serum unsaturated fatty acids were subjected to factor analysis to identify distinct fatty acid patterns (FAPs). Multivariable logistic regression was employed to assess the risk of DN associated with different serum FAPs. The role of FAPs major components was further validated at the cellular level. Results: After adjusting for confounders, three types of unsaturated fatty acid including C20:5 (eicosapentaenoic acid, EPA), C22:6 (docosahexaenoic, DHA) and C22:5 n-3 (docosapentaenoic acid, DPA n-3) were significantly associated with DN in the population. The odds ratios (ORs) (95% confidence interval [CI]) of DN were 0.583 (0.374, 0.908), 0.826 (0.716, 0.954) and 0.513 (0.298, 0.883), respectively. Factor analysis revealed five major FAPs, among of which, only FAP2 (enriched with EPA and DHA) exhibited a significant inverse association with DN. In the multivariate-adjusted model, the OR (95% CI) was 0.678 (0.493, 0.933). At the cellular level, DHA and EPA enriched in FAP2 reduced and a combination of which further decreased extracellular matrix production induced by transforming growth factor beta 1 (TGFβ1) in podocytes and tubular cells. Conclusions: Our findings suggest that FAP2, enriched with DHA and EPA, is associated with a reduced risk of DN. This highlights the potential of targeting FAP2 for the patients with DN.
{"title":"Association of serum unsaturated fatty acid patterns with the risk of diabetic nephropathy","authors":"Shuang Xu, Xinyuan Li, Qing Hou, Ning Xu, Qingmiao Lu, Sudan Wang, Chunsun Dai","doi":"10.1159/000536532","DOIUrl":"https://doi.org/10.1159/000536532","url":null,"abstract":"Introduction: Unsaturated fatty acids play an essential role in the progression of diabetic nephropathy (DN). Previous studies were mainly focused on the role of individual unsaturated fatty acid. The serum unsaturated fatty acid patterns in patients with DN remains to be determined.\u0000Methods: A total of 135 patients with DN (DN group) and 322 patients with type II diabetes without nephropathy (non-DN group) were included in this study. Clinical data, serum levels of unsaturated fatty acids and other laboratory indicators were collected. Multivariate logistic regression was applied to identify risk factors for serum unsaturated fatty acids level in both groups. Serum unsaturated fatty acids were subjected to factor analysis to identify distinct fatty acid patterns (FAPs). Multivariable logistic regression was employed to assess the risk of DN associated with different serum FAPs. The role of FAPs major components was further validated at the cellular level.\u0000Results: After adjusting for confounders, three types of unsaturated fatty acid including C20:5 (eicosapentaenoic acid, EPA), C22:6 (docosahexaenoic, DHA) and C22:5 n-3 (docosapentaenoic acid, DPA n-3) were significantly associated with DN in the population. The odds ratios (ORs) (95% confidence interval [CI]) of DN were 0.583 (0.374, 0.908), 0.826 (0.716, 0.954) and 0.513 (0.298, 0.883), respectively. Factor analysis revealed five major FAPs, among of which, only FAP2 (enriched with EPA and DHA) exhibited a significant inverse association with DN. In the multivariate-adjusted model, the OR (95% CI) was 0.678 (0.493, 0.933). At the cellular level, DHA and EPA enriched in FAP2 reduced and a combination of which further decreased extracellular matrix production induced by transforming growth factor beta 1 (TGFβ1) in podocytes and tubular cells. \u0000Conclusions: Our findings suggest that FAP2, enriched with DHA and EPA, is associated with a reduced risk of DN. This highlights the potential of targeting FAP2 for the patients with DN.\u0000","PeriodicalId":17830,"journal":{"name":"Kidney Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140483592","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}
Bo Chen, Ling Chen, Qiao Yang, Xue-jing Gao, Qi-quan Lai, B. Tu, Ziming Wan
Introduction: Venous valve–related stenosis (VVRS) is an uncommon type of failure of arteriovenous fistula (AVF) among patients with end-stage renal disease (ESRD). There is a paucity of data on the long-term efficacy of ultrasound-guided percutaneous transluminal angioplasty (PTA) for VVRS. Methods: ESRD patients who underwent PTA because of VVRS between January 2017 and December 2021 at the First Affiliated Hospital of Chongqing Medical University were enrolled. Patients were classified into three cohorts (cohort1, VVRS located within 3 cm of the vein adjacent to the anastomosis; cohort2, VVRS located over 3 cm away from the anastomosis; cohort3, multiple stenoses). The patency rates were assessed by the Kaplan-Meier method and compared using the log-rank test. Univariate and multivariate Cox analyses were performed to identify the risk factors. Results: A total of 292 patients were enrolled, including 125 (42.8%), 111 (38.0%), and 56 (19.2%) patients in cohort1, cohort2 and cohort3, respectively. The median follow-up was 34.8 months. The 6-month, 1-year, 2-year, and 3-year primary patency rates were 86.0%, 69.4%, 47.5%, and 35.3%, respectively. The secondary patency rates were 94.5%, 89.4%, 75.5%, and 65.3%, respectively. Cohort1 showed a relatively better primary patency compared to cohort2 and cohort3. The secondary patency rates were comparable in the three cohorts. Duration of dialysis and VVRS type were potential factors associated with primary patency. Conclusions: This study showed acceptable long-term primary and secondary patency rates after PTA for VVRS in ESRD patients, especially for those with VVRS located within 3 cm of the vein adjacent to the anastomosis.
{"title":"Long-term efficacy of ultrasound-guided percutaneous transluminal angioplasty for arteriovenous fistula outflow stenosis caused by venous valve","authors":"Bo Chen, Ling Chen, Qiao Yang, Xue-jing Gao, Qi-quan Lai, B. Tu, Ziming Wan","doi":"10.1159/000536309","DOIUrl":"https://doi.org/10.1159/000536309","url":null,"abstract":"Introduction: Venous valve–related stenosis (VVRS) is an uncommon type of failure of arteriovenous fistula (AVF) among patients with end-stage renal disease (ESRD). There is a paucity of data on the long-term efficacy of ultrasound-guided percutaneous transluminal angioplasty (PTA) for VVRS.\u0000Methods: ESRD patients who underwent PTA because of VVRS between January 2017 and December 2021 at the First Affiliated Hospital of Chongqing Medical University were enrolled. Patients were classified into three cohorts (cohort1, VVRS located within 3 cm of the vein adjacent to the anastomosis; cohort2, VVRS located over 3 cm away from the anastomosis; cohort3, multiple stenoses). The patency rates were assessed by the Kaplan-Meier method and compared using the log-rank test. Univariate and multivariate Cox analyses were performed to identify the risk factors.\u0000Results: A total of 292 patients were enrolled, including 125 (42.8%), 111 (38.0%), and 56 (19.2%) patients in cohort1, cohort2 and cohort3, respectively. The median follow-up was 34.8 months. The 6-month, 1-year, 2-year, and 3-year primary patency rates were 86.0%, 69.4%, 47.5%, and 35.3%, respectively. The secondary patency rates were 94.5%, 89.4%, 75.5%, and 65.3%, respectively. Cohort1 showed a relatively better primary patency compared to cohort2 and cohort3. The secondary patency rates were comparable in the three cohorts. Duration of dialysis and VVRS type were potential factors associated with primary patency.\u0000Conclusions: This study showed acceptable long-term primary and secondary patency rates after PTA for VVRS in ESRD patients, especially for those with VVRS located within 3 cm of the vein adjacent to the anastomosis.\u0000","PeriodicalId":17830,"journal":{"name":"Kidney Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139601646","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}
B. Ma, A. Tam, Kam Wa Chan, Ivan Fan Ngai Hung, Sydney Chi Wai Tang, Tak Mao Chan, D. Y. Yap
Background A three-dose regimen is the current standard for COVID-19 vaccination, but systematic data on immunogenicity and safety in CKD patients remains limited. Objectives We conducted a meta-analysis on the immunogenicity and safety of three-dose COVID-19 vaccination in patients on renal replacement therapy (RRT). Methods Systematic literature search in four electronic databases yielded twenty eligible studies (2117 patients, 94% received mRNA vaccines) for meta-analysis. Results The overall seropositivity rate of anti-SARS-CoV-2 was 74.2% (95% CI: 65.0%-83.4%) after three-dose COVID-19 vaccination. The seropositivity rate of anti-SARS-CoV-2 in kidney transplant recipients (KTRs) was 64.6% (95% CI: 58.7%-70.5%), and 43.5% (95% CI: 38.5%-48.6%) of non-responders after second dose became seropositive after third dose. The seropositivity rate of anti-SARS-CoV-2 was 92.9% (95% CI: 89.5%-96.2%) in dialysis patients, and 64.6% (95% CI: 46.8%-82.3%) of non-responders after second dose became seropositive after third dose. In KTRs, each year increase in transplant vintage was associated with 35.6% increase in anti-SARS-CoV-2 seropositivity (95% CI: 15.9%-55.4%, p=0.01). There were no serious adverse events attributed to vaccination in KTRs and the commonest local and systemic adverse events were injection site pain and fatigue respectively.
{"title":"Immunogenicity and safety of the three-dose COVID-19 vaccine regimen in patients receiving renal replacement therapy: a systematic review and meta-analysis","authors":"B. Ma, A. Tam, Kam Wa Chan, Ivan Fan Ngai Hung, Sydney Chi Wai Tang, Tak Mao Chan, D. Y. Yap","doi":"10.1159/000536308","DOIUrl":"https://doi.org/10.1159/000536308","url":null,"abstract":"Background \u0000A three-dose regimen is the current standard for COVID-19 vaccination, but systematic data on immunogenicity and safety in CKD patients remains limited. \u0000\u0000Objectives \u0000We conducted a meta-analysis on the immunogenicity and safety of three-dose COVID-19 vaccination in patients on renal replacement therapy (RRT).\u0000\u0000Methods\u0000Systematic literature search in four electronic databases yielded twenty eligible studies (2117 patients, 94% received mRNA vaccines) for meta-analysis. \u0000\u0000Results \u0000The overall seropositivity rate of anti-SARS-CoV-2 was 74.2% (95% CI: 65.0%-83.4%) after three-dose COVID-19 vaccination. The seropositivity rate of anti-SARS-CoV-2 in kidney transplant recipients (KTRs) was 64.6% (95% CI: 58.7%-70.5%), and 43.5% (95% CI: 38.5%-48.6%) of non-responders after second dose became seropositive after third dose. The seropositivity rate of anti-SARS-CoV-2 was 92.9% (95% CI: 89.5%-96.2%) in dialysis patients, and 64.6% (95% CI: 46.8%-82.3%) of non-responders after second dose became seropositive after third dose. In KTRs, each year increase in transplant vintage was associated with 35.6% increase in anti-SARS-CoV-2 seropositivity (95% CI: 15.9%-55.4%, p=0.01). There were no serious adverse events attributed to vaccination in KTRs and the commonest local and systemic adverse events were injection site pain and fatigue respectively.\u0000","PeriodicalId":17830,"journal":{"name":"Kidney Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139613936","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}
Currently, renal malignancies and some diseases accompanied by renal impairment, such as multiple myeloma (MM), systemic lupus erythematosus (SLE), and acquired immunodeficiency syndrome (AIDS) are characterized by encouraging benefits from immunotherapy that have led to significantly improved outcomes. In this regard, the chimeric antigen receptor (CAR)-T represents a further step forward in the field of immunotherapy, which is becoming a hot issue and revealing potential in these diseases. Additionally, with numerous novel targets and indications being discovered and tried for clinical practice, the nephrotoxicity associated with CAR-T cell therapy also needs attention. In this review, we focused on discussing the effects and drawbacks of CAR-T cell therapy in several common diseases involving kidneys, as well as how we might enhance it.
{"title":"CAR-T Cell Therapy: Advances in Kidney-Related Diseases","authors":"Longyuan Wu, Youqin Feng, Yue Huang, Jingjing Feng, Yong-xian Hu, He Huang","doi":"10.1159/000536194","DOIUrl":"https://doi.org/10.1159/000536194","url":null,"abstract":"Currently, renal malignancies and some diseases accompanied by renal impairment, such as multiple myeloma (MM), systemic lupus erythematosus (SLE), and acquired immunodeficiency syndrome (AIDS) are characterized by encouraging benefits from immunotherapy that have led to significantly improved outcomes. In this regard, the chimeric antigen receptor (CAR)-T represents a further step forward in the field of immunotherapy, which is becoming a hot issue and revealing potential in these diseases. Additionally, with numerous novel targets and indications being discovered and tried for clinical practice, the nephrotoxicity associated with CAR-T cell therapy also needs attention. In this review, we focused on discussing the effects and drawbacks of CAR-T cell therapy in several common diseases involving kidneys, as well as how we might enhance it.","PeriodicalId":17830,"journal":{"name":"Kidney Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139441233","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}
Background: Anemia is one of the common complications of chronic kidney disease (CKD), and its prevalence has been arising globally. The key cause of anemia in CKD patients is the diseased kidney's reduced ability to synthesize endogenous erythropoietin, yet this is not the sole reason. Inflammatory elements, functional iron deficiency, and uremic toxins together participate in the development of anemia. According to research data, anemia is an independent risk factor for cardiovascular events, all-cause mortality and worsening renal function, and affects the clinical prognosis and quality of life of CKD patients. Regular treatments for anemia in CKD patients include the use of erythropoietin stimulators (ESA), iron supplements, and blood transfusions. Summary：Hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHIs) is a novel and small molecule pharmacological compound that targets the HIF pathway and is another option for improving anemia in CKD patients. HIF-PHIs simulates hypoxia, stabilizes HIF protein, stimulates EPO synthesis, reduces hepcidin level and boosts iron utilization, induces the creation of red blood cells and alleviates anemia. The results of several HIF-PHIs phase III trials indicated that HIF-PHIs are similarly effective as ESA at raising hemoglobin (Hb) concentration. Key Messages: This article summarizes the structure of HIF and the mechanism of stabilizing HIF to improve anemia, discusses the efficacy of HIF-PHIs in CKD patients with or without dialysis, as well as emphasizes the potential safety concerns with HIF-PHIs.
{"title":"Stabilizing hypoxia-inducible factor manage anemia in chronic kidney disease：From basic theory to clinical study","authors":"Yudian Wang, Xiaoyong Yu","doi":"10.1159/000536039","DOIUrl":"https://doi.org/10.1159/000536039","url":null,"abstract":"Background: Anemia is one of the common complications of chronic kidney disease (CKD), and its prevalence has been arising globally. The key cause of anemia in CKD patients is the diseased kidney's reduced ability to synthesize endogenous erythropoietin, yet this is not the sole reason. Inflammatory elements, functional iron deficiency, and uremic toxins together participate in the development of anemia. According to research data, anemia is an independent risk factor for cardiovascular events, all-cause mortality and worsening renal function, and affects the clinical prognosis and quality of life of CKD patients. Regular treatments for anemia in CKD patients include the use of erythropoietin stimulators (ESA), iron supplements, and blood transfusions. Summary：Hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHIs) is a novel and small molecule pharmacological compound that targets the HIF pathway and is another option for improving anemia in CKD patients. HIF-PHIs simulates hypoxia, stabilizes HIF protein, stimulates EPO synthesis, reduces hepcidin level and boosts iron utilization, induces the creation of red blood cells and alleviates anemia. The results of several HIF-PHIs phase III trials indicated that HIF-PHIs are similarly effective as ESA at raising hemoglobin (Hb) concentration. Key Messages: This article summarizes the structure of HIF and the mechanism of stabilizing HIF to improve anemia, discusses the efficacy of HIF-PHIs in CKD patients with or without dialysis, as well as emphasizes the potential safety concerns with HIF-PHIs.\u0000\u0000","PeriodicalId":17830,"journal":{"name":"Kidney Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139451695","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}
Background: Peripheral neuropathy (PN), one of the commonest neurological complications of chronic kidney disease (CKD), was associated with physical limitation. Studies showed that a decrease in physical capability in patients with CKD is related with an increased risk of mortality. The objective of our research is directly exploring the relationship between PN and risk of mortality in patients with CKD. Method: 1836 participants with CKD and 6036 participants without CKD, which were classified by peripheral neuropathy based on monofilament examination in National Health and Nutrition Examination Survey (NHANES), were collected from the 1999 to 2004 National Health and Nutrition Examination Surveys. Multi-variable Cox proportional hazards models was conducted to assess the relationships of peripheral neuropathy and deaths in patients with CKD and non-CKD. Results: During 14 years of a median follow up from 1999 to 2015 and 2004 to 2015, 1072 (58.4%) and 1389 (23.0%) deaths were recorded in participants with CKD and without CKD, respectively. PN was related with increased all-cause mortality even after adjusting possible confounding factors in population with CKD (HR 1.34, 95% confidence interval [CI] 1.17-1.53) and without CKD (HR 1.27 95% CI 1.12-1.43). And the adjusted HRs (95% CI) for cardiovascular mortality of the people with CKD and without CKD who suffering from peripheral neuropathy were 1.42 (1.07, 1.90) and 1.23 (0.91, 1.67), respectively, versus those without peripheral neuropathy. Conclusion: PN was related with a higher risk of all-cause and cardiovascular death in people with CKD, which clinically suggests that the adverse prognostic impact of PN in the CKD population deserve attention and are an important target for intervention.
{"title":"Peripheral Neuropathy Associated with Higher Mortality in Population with Chronic Kidney Disease: National Health and Nutrition Examination Surveys","authors":"Wei-Lan Li, X-Y Cai, Shu-Wang Ge, Gang Xu","doi":"10.1159/000535481","DOIUrl":"https://doi.org/10.1159/000535481","url":null,"abstract":"Background: Peripheral neuropathy (PN), one of the commonest neurological complications of chronic kidney disease (CKD), was associated with physical limitation. Studies showed that a decrease in physical capability in patients with CKD is related with an increased risk of mortality. The objective of our research is directly exploring the relationship between PN and risk of mortality in patients with CKD. Method: 1836 participants with CKD and 6036 participants without CKD, which were classified by peripheral neuropathy based on monofilament examination in National Health and Nutrition Examination Survey (NHANES), were collected from the 1999 to 2004 National Health and Nutrition Examination Surveys. Multi-variable Cox proportional hazards models was conducted to assess the relationships of peripheral neuropathy and deaths in patients with CKD and non-CKD. Results: During 14 years of a median follow up from 1999 to 2015 and 2004 to 2015, 1072 (58.4%) and 1389 (23.0%) deaths were recorded in participants with CKD and without CKD, respectively. PN was related with increased all-cause mortality even after adjusting possible confounding factors in population with CKD (HR 1.34, 95% confidence interval [CI] 1.17-1.53) and without CKD (HR 1.27 95% CI 1.12-1.43). And the adjusted HRs (95% CI) for cardiovascular mortality of the people with CKD and without CKD who suffering from peripheral neuropathy were 1.42 (1.07, 1.90) and 1.23 (0.91, 1.67), respectively, versus those without peripheral neuropathy. Conclusion: PN was related with a higher risk of all-cause and cardiovascular death in people with CKD, which clinically suggests that the adverse prognostic impact of PN in the CKD population deserve attention and are an important target for intervention.","PeriodicalId":17830,"journal":{"name":"Kidney Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2023-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139163135","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}
Background: Acute kidney injury (AKI) is kidney damage that leads to a rapid decline in function. AKI primarily occurs when the tubular epithelium is damaged, causing swelling, loss of brush margin, and eventual apoptosis. Research has shown that tubular epithelial cell damage in AKI is linked to cell cycle arrest, autophagy, and regulation of cell death. Summary: Pyroptosis, a type of programmed cell death triggered by inflammation, is believed to play a role in the pathophysiology of AKI. Cumulative evidence has shown that pyroptosis is the main cause of tubular cell death in AKI. Thus, targeted intervention of pyroptosis may be a promising therapeutic approach for AKI. In this review, we delve deep into the cutting-edge research surrounding pyroptosis in the context of AKI, shedding light on its intricate mechanisms and potential implications for clinical practice. Additionally, we explore the exciting realm of potential pre-clinical treatment options for AKI, aiming to pave the way for future therapeutic advancements. Key Messages: Pyroptosis, a highly regulated form of cell death, plays a crucial role in determining the fate of cells during the development of AKI. This intricate process involves the activation of inflammasomes, which are multi-protein complexes that initiate pyroptotic cell death. By understanding the mechanisms underlying pyroptosis, researchers aim to gain insights into the pathogenesis of AKI and potentially identify new therapeutic targets for this condition.
背景：急性肾损伤（AKI）是指导致肾功能急剧下降的肾损伤。AKI 主要发生在肾小管上皮细胞受损时，导致肿胀、刷状缘脱落和最终凋亡。研究表明，AKI 中的肾小管上皮细胞损伤与细胞周期停滞、自噬和细胞死亡调控有关。摘要：炎症引发的一种程序性细胞死亡--嗜热症，被认为在 AKI 的病理生理学中发挥作用。累积的证据表明，肾小管炎症中肾小管细胞死亡的主要原因是嗜热细胞增多。因此，有针对性地干预热蛋白沉积可能是治疗 AKI 的一种很有前景的方法。在这篇综述中，我们深入探讨了围绕 AKI 中热蛋白沉积的前沿研究，揭示了其复杂的机制和对临床实践的潜在影响。此外，我们还探索了令人兴奋的 AKI 潜在临床前治疗方案，旨在为未来的治疗进展铺平道路：在发生 AKI 的过程中，决定细胞命运的关键因素是细胞热解，这是一种受到高度调控的细胞死亡形式。这一错综复杂的过程涉及炎性体的激活，炎性体是一种多蛋白复合物，可启动细胞的裂解死亡。研究人员希望通过了解热凋亡的内在机制，深入了解 AKI 的发病机理，并找到治疗这种疾病的新靶点。
{"title":"Pyroptosis: The Determinator of Cell Death and Fate in Acute Kidney Injury","authors":"Jiachuan Xiong, Jinghong Zhao","doi":"10.1159/000535894","DOIUrl":"https://doi.org/10.1159/000535894","url":null,"abstract":"Background: Acute kidney injury (AKI) is kidney damage that leads to a rapid decline in function. AKI primarily occurs when the tubular epithelium is damaged, causing swelling, loss of brush margin, and eventual apoptosis. Research has shown that tubular epithelial cell damage in AKI is linked to cell cycle arrest, autophagy, and regulation of cell death.\u0000Summary: Pyroptosis, a type of programmed cell death triggered by inflammation, is believed to play a role in the pathophysiology of AKI. Cumulative evidence has shown that pyroptosis is the main cause of tubular cell death in AKI. Thus, targeted intervention of pyroptosis may be a promising therapeutic approach for AKI. In this review, we delve deep into the cutting-edge research surrounding pyroptosis in the context of AKI, shedding light on its intricate mechanisms and potential implications for clinical practice. Additionally, we explore the exciting realm of potential pre-clinical treatment options for AKI, aiming to pave the way for future therapeutic advancements.\u0000Key Messages: Pyroptosis, a highly regulated form of cell death, plays a crucial role in determining the fate of cells during the development of AKI. This intricate process involves the activation of inflammasomes, which are multi-protein complexes that initiate pyroptotic cell death. By understanding the mechanisms underlying pyroptosis, researchers aim to gain insights into the pathogenesis of AKI and potentially identify new therapeutic targets for this condition.\u0000","PeriodicalId":17830,"journal":{"name":"Kidney Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2023-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138947418","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}
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