Kidney & blood pressure research最新文献

{"title":"SIRT6 Attenuates Angiotensin II-Induced Podocyte Cholesterol Accumulation and Injury via Negative Modulation of SREBP2.","authors":"Yingjie Yang, Jingjing Ma, Danqi Chang, Shijing Ma, Lin Xu, Jianzhong Dang","doi":"10.1159/000552307","DOIUrl":"10.1159/000552307","url":null,"abstract":"<p><strong>Introduction: </strong>Angiotensin (Ang) II can cause podocyte injury and leads to chronic kidney disease (CKD), but the specific mechanism is not clear. In our previous study, we found that Ang II reduced the expression of cholesterol efflux-associated molecule by regulating sirtuin 6 (SIRT6), thereby inducing podocyte cholesterol accumulation and injury. However, the effect of SIRT6 on podocyte cholesterol synthesis is unclear. In this study, we evaluated the role of SIRT6 in the expression of cholesterol synthesis-associated molecular sterol regulatory element-binding protein 2 (SREBP2), cholesterol content, and apoptosis levels in podocytes.</p><p><strong>Methods: </strong>Ang II-infused rat model was constructed. Cholesterol quantification was examined using a cholesterol quantitation kit. The expression of SIRT6 and SREBP2 was examined by Western blot and immunofluorescence assay. The podocyte apoptotic level was detected by flow cytometry. Transfection of podocytes with pcDNA3.1 SIRT6 plasmid and the deacetylase-inactive SIRT6 mutant plasmid (pcDNA3.1 SIRT6 H133Y) was performed to investigate whether SIRT6 regulates SREBP2 expression and to further determine if this regulatory effect is dependent on SIRT6's deacetylase activity.</p><p><strong>Results: </strong>Ang II promoted lipid droplet and cholesterol accumulation in rat glomeruli, suppressed SIRT6 expression, and enhanced SREBP2 activation, evidenced by increased SREBP2 levels and nuclear translocation. Transfection of pcDNA3.1 SIRT6 into podocytes attenuated SREBP2 activation, reducing Ang II-induced cholesterol accumulation and apoptosis. Experiments using pcDNA3.1 SIRT6 and pcDNA3.1 SIRT6 H133Y plasmids indicate that SIRT6-mediated suppression of SREBP2 requires its histone deacetylase activity.</p><p><strong>Conclusion: </strong>We conclude that SIRT6 serves as a key protective regulator of podocytes against RAS activation, at least in part by suppressing SREBP2 expression and thereby alleviating cholesterol accumulation and associated podocyte injury. It provides a new target for clinical treatment of CKD.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"715-728"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13466445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148382313","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}

{"title":"ATHENA Study - The Role of Circulating Plasma MicroRNAs in Paediatric Patients with Untreated Primary Hypertension: Baseline Expression and Exercise-Induced Changes.","authors":"Michał Szyszka, Ceren Eyileten, Jolanta Małyszko, Karolina Skubisz, Radosław Pietrzak, Hubert Krysztofiak, Piotr Skrzypczyk","doi":"10.1159/000552984","DOIUrl":"10.1159/000552984","url":null,"abstract":"<p><strong>Introduction: </strong>The role of microRNA in primary hypertension (PH) remains unclear. This study examined the expression of microRNA-16, -21, -27a, -27b, -133a, and -145 in untreated hypertensive children, their response to aerobic exercise, and correlations with blood pressure (BP) and related parameters.</p><p><strong>Methods: </strong>A pre-post observational, hypothesis-generating study included 56 hypertensive (study group [SG]) and 59 healthy children (control group [CG]). Plasma microRNA levels and clinical, biochemical, BP, vascular, and hypertension-mediated organ damage (HMOD) parameters were assessed before and after one session of standardized aerobic exercise.</p><p><strong>Results: </strong>The baseline relative microRNA-27b (p < 0.001) and microRNA-133a (p = 0.018) expressions were significantly lower in the SG; similarly, after an exercise bout. After an exercise bout, the expression of microRNA-27b, -133a, and -145 increased in CG, whereas only the expression of microRNA-145 increased in SG. In SG, microRNA-16, -21, -27a, and -145 correlated positively with pre-exercise BP. There were no correlations between the analysed microRNA particles and parameters of HMOD. ROC analysis identified the best prognostic profile for relative microRNA-27b expression as a potential biomarker of the absence of PH. Multivariate analysis revealed the relative microRNA-16 expression as the only significant predictor of elevated diastolic BP.</p><p><strong>Conclusions: </strong>MicroRNA-27b and microRNA-133a are underexpressed in children with PH. These particles may represent potential markers of hypertension in children and may also be associated with a lower burden of hypertension-related alterations. MicroRNA-16 may serve as a marker of diastolic hypertension.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"468-487"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13363113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148211868","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}

{"title":"Verapamil Reduces Collagen Synthesis to Alleviate Ureteral Scar Formation by Inhibiting KDM1A-Mediated Epigenetic Silencing of SESN2.","authors":"Junhuan He, Jun Li, Xuecheng Wu, Zhiwei Zhu, Junjie Chen, Qiang Lu, Zhengyan Tang, Yuanwei Li, Mingqiang Zeng","doi":"10.1159/000553434","DOIUrl":"10.1159/000553434","url":null,"abstract":"<p><strong>Introduction: </strong>Ureteral scar formation is a fibrotic process linked with collagen synthesis. Although autophagy prevents collagen synthesis, its role in ureteral scarring remains unclear. Therefore, this study investigated the modulation of SESN2-mediated autophagy by verapamil during ureteral scar formation.</p><p><strong>Methods: </strong>An in vitro fibrosis model was constructed using transforming growth factor-β1 (TGF-β1)-stimulated primary fibroblasts. We established a rat model of ureteral stricture (US), and KN-93 was used to inhibit the phosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaMK II). Histopathological alterations and collagen accumulation in rat ureteral tissues were examined using hematoxylin-eosin and Masson staining. The levels of vimentin, α-SMA, and LC3 were determined using immunofluorescence. Autophagic flux was assessed using an mCherry-GFP-LC3 assay. mRNA and protein levels were assessed by quantitative real-time PCR and Western blot, respectively. Additionally, co-immunoprecipitation and GST pull-down assays were used to detect the binding relationship between CaMK II and lysine-specific histone demethylase 1A (KDM1A). The interaction of H3K4me2 and KDM1A with the SESN2 promoter in fibroblasts was verified using chromatin immunoprecipitation.</p><p><strong>Results: </strong>Verapamil increased autophagy in TGF-β1-stimulated fibroblasts and alleviated ureteral fibrosis in US rats by inhibiting CaMK II phosphorylation (p-CaMK II) to reduce collagen synthesis. Moreover, p-CaMK II promoted the nuclear translocation of KDM1A by phosphorylating KDM1A. Additionally, the effects of KDM1A knockdown on the autophagy and collagen synthesis in TGF-induced fibroblasts were reversed by SESN2 knockdown. Finally, KDM1A knockdown further enhanced the effect of verapamil in promoting SESN2-mediated fibroblast autophagy and suppressed collagen synthesis.</p><p><strong>Conclusion: </strong>Verapamil reduced collagen synthesis during ureteral scar formation by inhibiting the phosphorylation of KDM1A by p-CaMK II, thus, decreasing the demethylation of H3K4me2 on the SESN2 promoter to enhance SESN2-mediated autophagy.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"749-765"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13498315/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148471387","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}

{"title":"Endothelial-to-Mesenchymal Transition in Chronic Kidney Disease: Mechanisms and Therapeutic Targets.","authors":"Abdul H Khan, Pratheesh D Mankuzhy, Linto Thomas, Adebowale Adebiyi","doi":"10.1159/kbr/adjag001","DOIUrl":"10.1159/kbr/adjag001","url":null,"abstract":"<p><strong>Background: </strong>Renal fibrosis is the final common pathological outcome of chronic kidney disease (CKD) and a major driver of progression to end-stage kidney disease. Endothelial-to-mesenchymal transition (EndMT) is a phenotypic process in which endothelial cells lose their endothelial identity and acquire mesenchymal or myofibroblast-like characteristics, thereby contributing to extracellular matrix accumulation, capillary rarefaction, microvascular dysfunction, and fibrotic remodeling.</p><p><strong>Summary: </strong>Transforming growth factor-β (TGF-β) is a central inducer of EndMT through canonical Smad-dependent and noncanonical Smad-independent signaling pathways. Additional pathways, including Wnt/β-catenin, Notch, Hedgehog, inflammatory cytokine signaling, autophagy dysregulation, oxidative stress, and metabolic reprogramming, further regulate EndMT in the diseased kidney. This review summarizes the cellular and molecular mechanisms underlying EndMT in CKD, highlights interactions among major regulatory pathways, and discusses emerging pharmacological strategies to inhibit EndMT, preserve renal microvascular integrity, and attenuate fibrogenesis.</p><p><strong>Key messages: </strong>Growing evidence supports an important role for EndMT in renal fibrosis and CKD progression. However, the quantitative contribution of EndMT to human kidney fibrosis, the biological significance of partial or hybrid EndMT states, and the most effective approaches for therapeutically targeting this process remain incompletely defined. Advances in lineage-tracing, single-cell and spatial transcriptomics, biomarker development, and pathway-selective therapies will be essential for translating EndMT-directed interventions into clinical practice.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"860-872"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148604452","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}

{"title":"Erratum.","authors":"","doi":"10.1159/kbr/adjag008","DOIUrl":"https://doi.org/10.1159/kbr/adjag008","url":null,"abstract":"&lt;p&gt;&lt;p&gt;In the article \"Lipids and Lipid Metabolites in the Diagnosis, Risk Prediction, and Treatment of Chronic Kidney Disease and Acute Kidney Injury: A Narrative Review\" [Kidney Blood Press Res. 2026;51:567-588. https://doi.org/10.1159/000552568] by Erfurt et al. Table 1 was incorrectly transferred during the production process. A corrected version of Table 1 is available below.Table 1.Summaries of all studies discussed, including design and outcomesReferenceDesignMethodologyMain findingsConclusionDiagnostic and prognostic role of fatty acids and their metabolites in CKDShearer et al. [36] (2012)Comparison of plasma fatty acid (FA) profiles in patients with stage 3-4 CKD (n = 10), stage 5 CKD near dialysis initiation (n = 20; one excluded for poor FA recovery), and 10 non-CKD controls from Karolinska prospective cohorts (mean follow-up for stage 5 = 2.7±1.7 years)FAs measured by gas chromatography; eGFR (MDRD) and FA relationships assessed using Deming orthogonal regression and Cox models (age-adjusted)Stage 5 CKD patients had lower relative abundances of polyunsaturated Fas - especially arachidonate synthesis intermediates - and lower stearic acid; EPA was lower in stage 5 vs. stage 3-4 and controls. Monounsaturated FAs showed opposing trends with declining eGFR (palmitate decreased, oleic acid increased). Nervonic acid abundance was a strong age-adjusted predictor of mortality in dialysis patientsMetabolic intermediates of arachidonic acid synthesis are reduced in CKDNervonic acid significantly predicts all-cause mortalityAfshinnia et al. [39] (2016)Nested case-control study used fasting serum from a subcohort of the CRIC cohort to identify lipidomic predictors of progression to end-stage kidney disease (ESKD)LC-MS shotgun lipidomics510 lipids detected (382 after filtering); 49 showed nominal differences between progressors and nonprogressors. Statistical selection combined t tests with FDR correction, PLS-DA, and Random Forest, and candidates were tested in logistic regression models adjusted for eGFR, UPCR, demographics, diabetes, hypertension, and heart failure. Two diacylglycerols (DAG 36:0 and DAG 32:0) were lower in progressors and each 1-SD higher level was associated with substantially reduced progression risk; monoacylglycerol MAG 16:0 was higher in progressors and associated with increased risk. Class-level findings showed enrichment and differential regulation of cholesterol esters, DAGs, and phosphatidylethanolamines, with chain length and unsaturation patterns differing between groupsMultimarker lipid panels significantly improve discrimination vs. a base model (eGFR + UPCR)Gollasch et al. [37] (2020)Comparison of fatty acid profiles in 15 healthy volunteers and 15 end-stage kidney disease (ESKD) patients on maintenance hemodialysis (HD)Venous blood collected from controls and pre-/post-HD from patients; RBC and plasma fatty acids measured by HPLC-MSESRD patients showed altered RBC and plasma fatty acid patterns: reduced EPA (C20:","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":"51 1","pages":"915-922"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149111571","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}

{"title":"Peritoneal Dialysis-Associated Peritonitis in 2 Patients with Bartter Syndrome and End-Stage Kidney Disease: A Case Report.","authors":"Caterina Vitagliano, Giulia Florio, Giovanni Piscopo, Francesca Silvestri, Roberto Russo, Ida Molfino, Anna Iervolino, Flavia Maria Longo, Roberta Ranieri, Miriam Zacchia, Alessandra F Perna, Loreto Gesualdo, Francesco Trepiccione","doi":"10.1159/kbr/adjag004","DOIUrl":"10.1159/kbr/adjag004","url":null,"abstract":"<p><strong>Introduction: </strong>Bartter syndrome (BS) is a rare inherited salt-wasting disorder affecting the thick ascending limb of the loop of Henle. It is characterized by hypokalemic metabolic alkalosis, polyuria, and secondary normotensive hyperaldosteronism. A minority of patients may progress to end-stage kidney disease while maintaining polyuria and normokalemia. Peritoneal dialysis (PD) may represent a suitable option for these patients when kidney transplantation is not available. However, due to its rarity, there are no data on PD-related outcomes.</p><p><strong>Methods: </strong>Here, we report 2 cases of PD treatment in BS from two Italian referral centers.</p><p><strong>Results: </strong>In both cases, PD was discontinued early because of peritonitis.</p><p><strong>Conclusion: </strong>Although no causal relationship can be established, these observations highlight the need for heightened vigilance regarding infectious complications in this population.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"873-876"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13688361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795119","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}

{"title":"Mortality and Cardiovascular Outcomes Associated with Statin Use in Dialysis Patients with Atherosclerotic Cardiovascular Disease: A Systematic Review and Meta-Analysis.","authors":"Kittiphan Chienwichai, Pannawat Mongkolrattanakul, Arunchai Chang, Sorawat Sangkaew","doi":"10.1159/kbr/adjag006","DOIUrl":"10.1159/kbr/adjag006","url":null,"abstract":"<p><strong>Introduction: </strong>Dialysis patients with established atherosclerotic cardiovascular disease (ASCVD) face exceptionally high risks of mortality and recurrent cardiovascular events yet remain substantially underrepresented in major statin trials. We aimed to synthesize evidence from studies restricted to this population to evaluate the association between statin therapy and clinical outcomes.</p><p><strong>Methods: </strong>We systematically searched Embase, MEDLINE, Web of Science, Scopus, and CENTRAL databases from inception through February 20, 2025, for randomized controlled trials and observational studies evaluating statin therapy in adults receiving maintenance dialysis with documented ASCVD. Hazard ratios were pooled using random-effects models. Risk of bias was assessed using the ROBINS-I tool. The primary outcome was all-cause mortality.</p><p><strong>Results: </strong>Fourteen cohort studies comprising 242,118 patients were included in the meta-analysis. Statin therapy was associated with a significant reduction in all-cause mortality (HR 0.85, 95% CI: 0.74-0.98; p = 0.027; I2 = 53.1%). Associations with cardiac mortality (HR 0.88, 95% CI: 0.66-1.16; I2 = 79.6%) and major adverse cardiovascular events (HR 0.85, 95% CI: 0.59-1.21; I2 = 61.8%) were not statistically significant. Leave-one-out sensitivity analyses supported the robustness of the primary finding. Among dialysis patients with established ASCVD, the proportion of statin-treated patients was 35% and increased over time.</p><p><strong>Conclusion: </strong>Among dialysis patients with established ASCVD, statin therapy is associated with lower all-cause mortality; however, its effect on cardiovascular outcomes remains uncertain. Substantial heterogeneity and a predominance of observational evidence limit causal inference. Well-designed prospective trials in this high-risk population are warranted.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"923-935"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13688380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897517","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}

{"title":"Multi-Omics Analysis Identified ADAM7 as a Biomarker and Therapeutic Target for End-Stage Renal Disease.","authors":"Xiaoqi Deng, Yu Luo, Lin Mei, Jinlan Wu, Mengxi He, Li Ma, Yun Lin","doi":"10.1159/000550025","DOIUrl":"10.1159/000550025","url":null,"abstract":"<p><strong>Introduction: </strong>Sarcopenia is a common comorbidity in end-stage renal disease (ESRD) and is associated with increased risk of adverse clinical outcomes. The genetic mechanisms underlying sarcopenia in ESRD remain largely unclear. This study employed multi-omics bioinformatics approaches to elucidate potential genetic determinants.</p><p><strong>Methods: </strong>Gene expression datasets GSE1428 and GSE142153 were retrieved from the Gene Expression Omnibus database to identify shared differentially expressed genes. Machine learning approaches were applied to pinpoint hub genes, followed by Mendelian randomization (MR) analyses to assess their associations with ESRD. Candidate therapeutic agents were subsequently predicted based on these hub genes.</p><p><strong>Results: </strong>ADAM7 emerged as the principal hub gene, with MR analyses suggesting a protective role against ESRD and sarcopenia. Predicted therapeutics included arbutin, metribolone, and phenethyl isothiocyanate. Molecular docking studies revealed favorable interactions, with binding free energies consistently below 5.0 kcal/mol between ADAM7 and these compounds.</p><p><strong>Conclusion: </strong>Our findings identify ADAM7 as a potential biomarker and therapeutic target for ESRD-associated sarcopenia, offering insights for future intervention strategies.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"61-71"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12863727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145757053","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}

{"title":"Cystine-Binding Medication Is Poorly Accessible for the Treatment of Cystinuria.","authors":"Xuemi Peng, Bart Penninx, Roos F Marsman, Giovanna Capolongo, Marie Courbebaisse, Bertrand Knebelmann, Francesco Trepiccione, Francesco Emma, Aude Servais, Carla E M Hollak, Elena N Levtchenko, Rik H G Olde Engberink","doi":"10.1159/000553298","DOIUrl":"10.1159/000553298","url":null,"abstract":"<p><strong>Introduction: </strong>Cystinuria is a rare inherited disorder characterized by recurrent cystine stone formation. When lifestyle modification and urine alkalinization fail, cystine-binding medication such as tiopronin and D-penicillamine are indicated. Despite proven benefit, their accessibility across Europe appears limited. We hypothesized that access to this medication is restricted and varies substantially between European countries.</p><p><strong>Methods: </strong>We surveyed physicians affiliated with the European Reference Network for Rare Kidney Diseases (ERKNet) regarding access barriers and prescribing practices. The online questionnaire was completed by 40 clinicians from 15 countries.</p><p><strong>Results: </strong>Eighty-five percent of respondents had prescribed cystine-binding medication in the past 2 years, with tiopronin being the preferred agent. However, 30% reported having no access to tiopronin at all, and 83% of recent prescribers experienced accessibility problems, including high costs and unfilled prescriptions. Substantial differences were observed both between and within countries. Prescription rates correlated with physicians' cystinuria caseload.</p><p><strong>Discussion: </strong>Cystine-binding medication is poorly and inconsistently accessible across Europe. Coordinated efforts are urgently needed to stabilize supply and ensure equitable, affordable access.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"729-736"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13472590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148361489","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}

{"title":"Association of Physical Activity with Abdominal Aortic Calcification in Chronic Kidney Disease: A Cross-Sectional Study.","authors":"Yang Kong, Aihua Zhang","doi":"10.1159/000552553","DOIUrl":"10.1159/000552553","url":null,"abstract":"<p><strong>Introduction: </strong>Limited studies have investigated the impact of physical activity (PA) on vascular calcification (VC) in patients with chronic kidney disease (CKD). Therefore, this cross-sectional study aimed to investigate the link between PA and abdominal aortic calcification (AAC) in CKD patients.</p><p><strong>Methods: </strong>This study involved 571 participants with CKD from the 2013-2014 National Health and Nutrition Examination Survey (NHANES). PA was measured by total weekly time (hours) and metabolic equivalent task (MET) levels. Weighted Poisson regression analyses (both univariate and multivariable) were conducted to investigate the associations between PA and AAC. Subgroup analyses were performed to detect interaction effects, and restricted cubic splines were applied to assess potential nonlinear relationships.</p><p><strong>Results: </strong>Longer weekly PA time and higher MET levels were associated with reduced AAC prevalence and severity. Each 1-h increase in PA was associated with a 1% lower prevalence of AAC (PR = 0.99, 95% CI 0.98-0.99, p = 0.002), while the high MET group showed a 29% lower prevalence compared to the inactive group (PR = 0.71, 95% CI: 0.55-0.92, p = 0.01). These associations were independent of traditional and CKD-specific risk factors. Subgroup analyses revealed no significant interaction effects, and restricted cubic spline models did not indicate a nonlinear association.</p><p><strong>Conclusion: </strong>Our study demonstrated that PA was independently and inversely associated with AAC burden in patients with CKD. These findings highlight the potential value of PA as a modifiable lifestyle factor in the comprehensive management of CKD.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"553-566"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13412230/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148005656","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}