Clinical Kidney Journal最新文献

{"title":"ERA Registry Figure of the month Trends in kidney transplantation rate across countries.","authors":"Vianda S Stel, Alberto Ortiz, Anneke Kramer","doi":"10.1093/ckj/sfaf055","DOIUrl":"https://doi.org/10.1093/ckj/sfaf055","url":null,"abstract":"","PeriodicalId":10435,"journal":{"name":"Clinical Kidney Journal","volume":"18 3","pages":"sfaf055"},"PeriodicalIF":3.9,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11928784/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prophylactic proton pump inhibitor usage and new-onset acute kidney injury in critically ill patients: a retrospective analysis.","authors":"Jing Xu, Zhoucang Zhang, Yujing Pan, Xue Li, Jiaxiang Ding, Mei Wang","doi":"10.1093/ckj/sfaf037","DOIUrl":"10.1093/ckj/sfaf037","url":null,"abstract":"<p><strong>Background: </strong>Proton pump inhibitors (PPIs) are widely prescribed for stress ulcer prophylaxis (SUP) in intensive care unit (ICU) patients. However, the potential association between prophylactic PPIs and the development of new-onset acute kidney injury (AKI) remains unclear.</p><p><strong>Methods: </strong>Patients without AKI or end-stage renal disease and not undergoing renal replacement therapy upon admission to the ICU were identified from the Medical Information Mart for Intensive Care (MIMIC-IV) database. The exposure factor for the study was the initiation of prophylactic PPIs within 48 h of admission, with the primary outcome being the occurrence of new-onset AKI after 48 h. Multivariable regression models were employed to investigate the association between prophylactic PPIs and the risk of new-onset AKI. Various propensity score analyses, along with stratified and subgroup analyses and E-value calculations, were conducted to further evaluate the reliability of the results.</p><p><strong>Results: </strong>A total of 7498 ICU patients were analyzed. The multivariable analysis showed a higher incidence of new-onset AKI in the PPI group (30.7%) compared with the control group (24.1%), yielding an adjusted odds ratio (OR) of 1.43 (95% confidence interval 1.22-1.67). Propensity score analyses confirmed these results, with ORs ranging from 1.34 to 1.49 (<i>P</i> ≤ .005). Results from multiple sensitivity analyses further supported these findings, with an E-value of 2.34 indicating robustness against unmeasured confounders.</p><p><strong>Conclusions: </strong>Prophylactic PPI use is associated with an increased risk of new-onset AKI in ICU patients. Indiscriminate use of PPIs should be avoided.</p>","PeriodicalId":10435,"journal":{"name":"Clinical Kidney Journal","volume":"18 3","pages":"sfaf037"},"PeriodicalIF":3.9,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11932333/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathophysiology of chronic kidney disease-mineral bone disorder (CKD-MBD): from adaptive to maladaptive mineral homeostasis.","authors":"Davide Salera, Nathalie Merkel, Antonio Bellasi, Martin H de Borst","doi":"10.1093/ckj/sfae431","DOIUrl":"10.1093/ckj/sfae431","url":null,"abstract":"<p><p>Chronic kidney disease-mineral bone disorder (CKD-MBD) is a multifaceted condition commonly seen in people with reduced kidney function. It involves a range of interconnected issues in mineral metabolism, bone health and cardiovascular calcification, which are linked to a lower quality of life and shorter life expectancy. Although various epidemiological studies show that the laboratory changes defining CKD-MBD become more common as the glomerular filtration rate declines, the pathophysiology of CKD-MBD is still largely unexplained. We herein review the current understanding of CKD-MBD, provide a conceptual framework to understand this syndrome, and review the genetic and environmental factors that may influence the clinical manifestation of CKD-MBD. However, a deeper understanding of the pathophysiology of CKD-MBD is needed to understand the phenotype variability and the relative contribution to organ damage of factors involved in CKD-MBD to develop more effective interventions to improve outcomes in patients with CKD.</p>","PeriodicalId":10435,"journal":{"name":"Clinical Kidney Journal","volume":"18 Suppl 1","pages":"i3-i14"},"PeriodicalIF":3.9,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903091/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathophysiology and therapies of CKD-associated secondary hyperparathyroidism.","authors":"Sandro Mazzaferro, Lida Tartaglione, Martine Cohen-Solal, Minh Hoang Tran, Marzia Pasquali, Silverio Rotondi, Pablo Ureña Torres","doi":"10.1093/ckj/sfae423","DOIUrl":"10.1093/ckj/sfae423","url":null,"abstract":"<p><p>Uremic secondary hyperparathyroidism (SHP) refers to the biochemical abnormalities that characterize CKD-MBD. However, historically parathyroid hormone (PTH) is identified as the key culprit hormone and the essential biomarker of secondary hyperparathyroidism. SHP represents the adaptive response to several mineral abnormalities that initiate and maintain increased PTH secretion through classical mineral derangements and more recently elucidated hormonal dysregulations. Among classic factors involved in the pathogenesis of SHP, phosphate, calcium, and calcitriol have a prominent role. The discovery of new pathogenetic factors involved in the development of SHP (and the eventual CKD-MBD) including fibroblast growth factor-23 (FGF23) and klotho provides new hypothesis and perspectives to our understanding of this complex metabolic disturbance. Recently more than serum phosphate a critical role in regulating FGF23 synthesis and the progression of CKD is ascribed to phosphate pool, reflected by production of glycerol-3-phosphate and the formation of excessive CPP-2. Finally, also skeletal resistance to PTH action, due to dysregulation of the Wnt-β-catenin system and intestinal dysbiosis, affecting the PTH actions on bone are causal factor of SHP. Identifying all the actors at play is mandatory to allow the most precise therapeutic prescription in the individual patient. This paper aims to review, in particular, the pathophysiology of SHP, which is essential to envisage the eventual therapeutic options for the associated MBD.</p>","PeriodicalId":10435,"journal":{"name":"Clinical Kidney Journal","volume":"18 Suppl 1","pages":"i15-i26"},"PeriodicalIF":3.9,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903092/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New perspectives on chronic kidney disease-mineral bone disorder.","authors":"Mario Cozzolino, Jordi Bover","doi":"10.1093/ckj/sfae432","DOIUrl":"10.1093/ckj/sfae432","url":null,"abstract":"","PeriodicalId":10435,"journal":{"name":"Clinical Kidney Journal","volume":"18 Suppl 1","pages":"i1-i2"},"PeriodicalIF":3.9,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903090/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Valvular calcification in chronic kidney disease: new insights from recent clinical and preclinical studies.","authors":"Lucie Hénaut, Alexandre Candellier, Sharon Huish, Nervana Issa, Smeeta Sinha, Ziad A Massy","doi":"10.1093/ckj/sfae421","DOIUrl":"10.1093/ckj/sfae421","url":null,"abstract":"<p><p>Valvular calcification, developing either in the mitral or the aortic valve, is highly prevalent in patients suffering from chronic kidney disease (CKD), in whom their presence correlates with higher cardiovascular and all-cause mortality risk. To date, the exact mechanisms that promote heart valve calcification remain unclear, and none of the treatments tested so far have shown efficacy in preventing valvular fibrocalcific remodelling. It is therefore essential to improve our understanding of the mechanisms involved in the pathological process if we are to find new, effective therapies. The purpose of this review is to (i) summarize our current knowledge of the mechanisms by which CKD and related therapies affect valvular cell activity, (ii) present the latest therapeutic targets identified in preclinical studies, and (iii) discuss the most recent clinical trials evaluating the efficacy of therapies aimed at preventing valvular calcification in CKD.</p>","PeriodicalId":10435,"journal":{"name":"Clinical Kidney Journal","volume":"18 Suppl 1","pages":"i27-i45"},"PeriodicalIF":3.9,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903095/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin D: are all compounds equal?","authors":"Lorenza Magagnoli, Matthias Cassia, Andrea Galassi, Paola Ciceri, Elisabet Massó, Rosana Gelpi, Jordi Bover, Mario Cozzolino","doi":"10.1093/ckj/sfae417","DOIUrl":"10.1093/ckj/sfae417","url":null,"abstract":"<p><p>Vitamin D is a pre-hormone essential for maintaining mineral homeostasis and also plays significant roles in bone, cardiovascular and renal health. Vitamin D deficiency is prevalent in the general population, and even more so in chronic kidney disease (CKD) patients, in which it contributes to the development and progression of mineral and bone disorder. The landscape of vitamin D treatment has evolved, with several analogues now available, each possessing distinct pharmacokinetic and pharmacodynamic properties, efficacies and safety profiles. This diversity allows for tailored, personalized approaches to treatment in CKD patients. This review aims to provide a comprehensive overview of vitamin D, including its natural sources and metabolism, and examines the main available pharmacological vitamin D products. Particular emphasis is placed on their application in CKD management, highlighting how these compounds can be strategically used to address both vitamin D deficiency and secondary hyperparathyroidism, while also acknowledging the ongoing debate about their impact on bone health and other clinical outcomes.</p>","PeriodicalId":10435,"journal":{"name":"Clinical Kidney Journal","volume":"18 Suppl 1","pages":"i61-i96"},"PeriodicalIF":3.9,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The true cost of phosphate control in chronic kidney disease.","authors":"Cristian Rodelo-Haad, María E Rodríguez-Ortiz, Raquel Garcia-Sáez, Antonio Rivas-Domínguez, Daniel Jurado-Montoya, Alejandro Martín-Malo, Mariano Rodríguez, M Victoria Pendón-Ruiz de Mier, Juan Rafael Muñoz-Castañeda","doi":"10.1093/ckj/sfae434","DOIUrl":"10.1093/ckj/sfae434","url":null,"abstract":"<p><p>The loss of kidney function entails the development of a positive phosphate balance. The burden of addressing elevated phosphate levels is high. Both parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) are increased to promote phosphaturia, thereby preventing the rise in serum phosphate. However, if the phosphate load is excessive, the corresponding phosphaturia is maximal, kidney function deteriorates and hyperphosphataemia becomes clinically evident in advanced stages of chronic kidney disease (CKD). In addition to its role in CKD progression, hyperphosphataemia has been linked to a multitude of adverse outcomes, including overt inflammation, vascular calcifications, endothelial dysfunction, cardiovascular disease, renal osteodystrophy and secondary hyperparathyroidism. Collectively, these factors contribute to the markedly elevated mortality rates observed among individuals with CKD. Furthermore, hyperphosphataemia has been identified as a significant contributor to the development of inflammatory processes, oxidative stress and fibrosis, which underlie the aetiology of numerous comorbidities. Additionally, elevated levels of PTH and FGF23 have been demonstrated to independently induce organ and tissue injury, which is associated with poor outcomes in CKD. This article provides a concise overview of the current understanding of phosphate handling by the kidney in the context of CKD. It outlines the detrimental effects of phosphate on various organs and the mechanisms through which it contributes to CKD progression. Additionally, we discuss the tools available for clinicians to identify patients at risk of an excessive phosphate load.</p>","PeriodicalId":10435,"journal":{"name":"Clinical Kidney Journal","volume":"18 Suppl 1","pages":"i46-i60"},"PeriodicalIF":3.9,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevalence and determinants of chronic kidney disease among community-dwelling adults, 50 years and older in Ireland.","authors":"Meera Tandan, Leonard D Browne, Amir Jalali, Colm Rowan, Frank Moriarty, Austin G Stack","doi":"10.1093/ckj/sfaf065","DOIUrl":"10.1093/ckj/sfaf065","url":null,"abstract":"<p><strong>Background: </strong>Using the Irish Longitudinal Study on Ageing (TILDA), we evaluated the prevalence and distribution of chronic kidney disease (CKD), and its determinants in order to identify risk groups for population health planning in Ireland.</p><p><strong>Methods: </strong>Data were analysed from Wave 1 (2009-2011) of the TILDA, a national cohort of participants aged 50+ years who had both plasma creatinine and cystatin C measured at baseline. Kidney function was estimated using the 2012 and 2021 Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equations. CKD was defined as estimated glomerular filtration rate <60 mL/min/1.73 m². Multivariable logistic regression explored associations using adjusted odds ratios (OR).</p><p><strong>Results: </strong>Prevalence of CKD was significantly higher using the CKD-EPI 2012_(Scr-CysC) compared with the CKD-EPI 2021_(Scr-CysC) (14.7% vs 11.3%, respectively). The prevalence was highest in patients with cardiovascular disease (CVD) (33.9%), diabetes (28.0%), cancer (25.5%), urinary incontinence (23.7%), bone diseases (21.5%), hypertension (19.8%) and obesity (19.5%). In multivariable analysis, individuals with hypertension (OR 1.78), diabetes (OR 1.45), CVD (OR 1.43), cancer (OR 1.53), overweight (OR 1.37) and obesity (OR 2.33) experienced greater likelihood of CKD. In addition, individuals with a history of previous hospitalization (OR 1.50), free or subsidized healthcare (OR 1.31), and unemployed individuals (OR 1.86) were also significantly more likely to have CKD.</p><p><strong>Conclusion: </strong>Compared with the national average, the burden of CKD is far greater in older individuals with major chronic conditions and socioeconomic deprivation. The identification and targeting of these groups through national surveillance programmes is likely to yield substantial benefits from more effective disease management and proactive population health planning.</p>","PeriodicalId":10435,"journal":{"name":"Clinical Kidney Journal","volume":"18 3","pages":"sfaf065"},"PeriodicalIF":3.9,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11932339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy and safety of endothelin A receptor antagonists in IgA nephropathy: a systematic review and meta-analysis.","authors":"Zhonghua Tian, Yalin Yang, Jixiong Mei, Mingchun Huang, Yanyan Li, Zhie Fang, Yunyi Li, Ling Tang, Yuxia Li","doi":"10.1093/ckj/sfaf066","DOIUrl":"10.1093/ckj/sfaf066","url":null,"abstract":"<p><strong>Background: </strong>Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. Endothelin A receptor activation is a key driver of proteinuria, inflammation and fibrosis in IgAN. This systematic review and meta-analysis aimed to comprehensively evaluate the efficacy and safety of endothelin A receptor antagonists (EARAs) in IgAN patients.</p><p><strong>Methods: </strong>PubMed, Embase, Web of Science and Cochrane Library were searched from inception to 31 October 2024. All randomized controlled trials were identified according to the inclusion criteria. Data were analyzed by RevMan 5.4.</p><p><strong>Results: </strong>Four high-quality studies were included, comprising 1346 IgAN patients. Compared with the control group, EARAs group achieved a greater reduction in urine protein-creatinine ratio (UPCR) [mean difference (MD) -31.89, 95% confidence interval (CI) -37.50 to -26.28], systolic blood pressure (BP) (MD -2.78, 95% CI -4.11 to -1.44) and diastolic BP (MD -4.12, 95% CI -5.24 to -2.99), and a smaller reduction in estimated glomerular filtration rate (eGFR) (MD 4.10, 95% CI -0.76 to 8.96). However, the EARAs group had higher risk of anemia [odds ratio (OR) 2.38, 95% CI 1.54 to 3.69], cough (OR 2.27, 95% CI 1.24 to 4.15), dizziness (OR 2.37, 95% CI 1.51 to 3.71), hypotension (OR 2.39, 95% CI 1.56 to 3.67), fluid retention (OR 1.46, 95% CI 1.04 to 2.05) and acute kidney injury (OR 3.12, 95% CI 1.31 to 7.42).</p><p><strong>Conclusion: </strong>EARAs can significantly reduce UPCR, lower both systolic and diastolic BP, and delay eGFR decline in IgAN patients. However, they may cause anemia, cough, dizziness, hypotension, fluid retention and acute kidney injury.</p>","PeriodicalId":10435,"journal":{"name":"Clinical Kidney Journal","volume":"18 3","pages":"sfaf066"},"PeriodicalIF":3.9,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11932335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}