Kidney & blood pressure research最新文献

{"title":"Do peritoneal dialysis patients with increased vascular stiffness measured by pulse wave velocity have reduced bone mineral density measured with dual energy X-ray absorptiometry.","authors":"Jamie Beverstock, Andrew Davenport","doi":"10.1159/000552051","DOIUrl":"https://doi.org/10.1159/000552051","url":null,"abstract":"<p><p>Introduction Vascular stiffness and osteoporosis are independently associated with increased cardiovascular morbidity. We investigated aortic pulse wave velocity (aoPWV), a measure of vascular stiffness, and bone mineral density (BMD) in peritoneal dialysis (PD) patients. Methods AaPWV was measured in patients who had dual energy X-ray absorptiometry (DXA) scans. Results The mean aoPWV was 10.0 ± 0.3 m/s in 118 established PD patients (57.6% male; mean age 64.5 ± 15.3 years. AoPWV was negatively associated with whole body T score r=-0.23, p=0.014, and Z score r=-0.21, p=0.031, left and right leg BMD (r= -0.22, p=0.019; -0.19, p=0.049), and femoral neck BMD (r=-0.18, p=0.047), but not after adjusting aoPWV for age and cardiovascular risk factors. Conclusions Vascular stiffness and osteoporosis increase with age. We report increased vascular stiffness associated with reduced BMD, but after adjusting for confounders, these associations were no longer significant, suggesting an overlapping connection rather than causality.  .</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-18"},"PeriodicalIF":2.1,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147775495","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":"Dapagliflozin may attenuate podocyte injury in diabetic kidney disease through inhibition of lactate-mediated H4K12 lactylation.","authors":"Caixia Cui, Ningying Fu, Shaoguo Tao, Jiasi Chen, Yuqi Shang, Xuan Peng, Qian Zhao, Haiyan Kang, Shanshan Wen, Hongbo Peng, Jie Xiao, Yonghua Peng, Guibao Ke","doi":"10.1159/000552052","DOIUrl":"https://doi.org/10.1159/000552052","url":null,"abstract":"<p><p>Introduction Podocyte injury is central to diabetic kidney disease (DKD). Metabolic reprogramming, particularly lactate accumulation, may drive podocyte injury via epigenetic mechanisms, yet this process remains poorly understood. This study aimed to clarify lactate's role in podocyte injury and explore the protective effects of dapagliflozin. Methods We retrospectively analyzed plasma lactate levels in healthy individuals, patients with diabetes, and DKD patients, and examined correlations with proteinuria. Subsequently, db/db mice and cultured podocytes were used to explore mechanisms of lactate-induced podocyte injury and potential protective effects of dapagliflozin in vivo and in vitro. Results Plasma lactate levels were analyzed in 66 healthy controls, 150 patients with diabetes, and 152 patients with DKD. Lactate concentrations were significantly higher in DKD patients compared with both diabetic patients and healthy controls. In DKD patients, lactate levels were positively correlated with serum creatinine and albuminuria. Logistic regression analysis identified hypertension, plasma lactate, white blood cell count, glycated hemoglobin, and serum creatinine as independent risk factors for DKD. Notably, dapagliflozin treatment significantly reduced plasma lactate levels in DKD patients. In diabetic mice and high-glucose-stimulated podocytes, marked lactate accumulation accompanied by increased histone H4 lysine 12 lactylation (H4K12la) was observed, indicating lactate-driven epigenetic regulation. In contrast, dapagliflozin treatment reduced lactate production and H4K12la levels, attenuated proteinuria, and ameliorated podocyte injury. Conclusions Lactate contributes to podocyte injury in DKD at least in part through promoting H4K12 lactylation. Dapagliflozin exerts renoprotective effects by attenuating this lactate-mediated epigenetic pathway, highlighting a potential therapeutic mechanism beyond glucose control.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-18"},"PeriodicalIF":2.1,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147775500","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":"TRPC6 inhibition attenuates renal tubulointerstitial fibrosis via the ROS/TXNIP/NLRP3 signaling pathway.","authors":"Linting Wei, Chenkai Cui, Yan Li, Pengbo Ge, Ke Li, Haodong Wang, Weihao Zhao, Yinhong Wang, Jianpeng Zhang, Rongguo Fu","doi":"10.1159/000552129","DOIUrl":"https://doi.org/10.1159/000552129","url":null,"abstract":"<p><strong>Introduction: </strong>Chronic kidney disease (CKD) is a worldwide public health issue primarily characterized by glomerulosclerosis and the renal tubulointerstitial fibrosis. Recent studies have shown that TRPC6 is essential in renal interstitial fibrosis, although the precise mechanisms involved are not yet fully understood.</p><p><strong>Methods: </strong>UUO model was established using C57BL/6 male mice in which HK-2 cells were stimulated with TGF-β1. HE and Masson staining were used to observe pathological changes. IHC staining was also conducted to measure the α-SMA, Fibronectin (Fn), TRPC6, ROS and NLRP3 expressions. Scanning electron microscopy (SEM) was used to observe morphological changes in the tubular cell membrane, and flow cytometry was utilized to measure ROS levels. In addition, western blotting was performed to detect Fn, α-SMA, TRPC6, TXNIP, NLRP3 and the downstream pyroptosis related molecule levels.</p><p><strong>Results: </strong>TRPC6 protein levels were enhanced in UUO mice and HK-2 cells upon TGF-β1 stimulation, which coincided with noticeable morphological changes associated with pyroptosis. Treatment with the TRPC6 inhibitor SAR7334 effectively reduced renal fibrosis markersand diminished levels of reactive oxygen species (ROS), TXNIP, and proteins related to NLRP3-mediated pyroptosis (including NLRP3, cGSDMD, and IL-1β). Furthermore, application of the NLRP3 inhibitor MCC950 in HK-2 cells reinforced our findings, as it attenuated renal fibrosis related proteins and counteracted the elevated levels of Fn, α-SMA and NLRP3-mediated pyroptosis proteins observed in TGF-β1 stimulated HK-2 cells. Additionally, inhibiting TRPC6 appeared to dampen the activity of the ROS/TXNIP/NLRP3 pathway.</p><p><strong>Conclusion: </strong>TRPC6 may represent a promising target for mitigating renal interstitial fibrosis, potentially through its effects on the ROS/TXNIP regulatory pathway involving NLRP3-mediated pyroptosis.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-17"},"PeriodicalIF":2.1,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147774596","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":"Divergent renal benefits of SGLT2 inhibitors and mineralocorticoid receptor antagonists in non-diabetic kidney disease.","authors":"Rulong Chen, Jinxin Zhang, Jiating Chen, Tingfei Xie, Yunpeng Xu, Zhaoyong Hu, Jihong Chen","doi":"10.1159/000552201","DOIUrl":"https://doi.org/10.1159/000552201","url":null,"abstract":"<p><strong>Introduction: </strong>Non-diabetic kidney disease (NDKD) is a major contributor to chronic kidney disease (CKD) worldwide. Although renin-angiotensin system inhibitors (RASi) remain standard therapy, sodium-glucose cotransporter-2 inhibitors (SGLT2i), non-steroidal mineralocorticoid receptor antagonists (non-steroidal MRA), and glucagon-like peptide-1 receptor agonists (GLP-1 RA) are now recommended in clinical guidelines. However, direct comparative evidence to guide their prioritization in NDKD is limited.</p><p><strong>Methods: </strong>We performed a systematic review and Bayesian network meta-analysis of randomized controlled trials enrolling adults with NDKD. The primary endpoint was the annualized change in estimated glomerular filtration rate (eGFR) slope; secondary endpoints included urine protein-to-creatinine ratio (UPCR), blood pressure, and biochemical safety parameters.</p><p><strong>Results: </strong>Eighteen trials were included. SGLT2i, as add-on to RASi, produced the greatest preservation of kidney function compared with RASi alone (mean difference [MD] 12.1 mL/min/1.73 m²/year; 95% credible interval [CrI] 3.9 to 20.4). non-steroidal MRA achieved the largest reduction in proteinuria versus RASi (UPCR MD -0.4 g/g; 95% CrI -1.0 to -0.2). SGLT2i also yielded the greatest systolic blood pressure reduction versus RASi (MD -9.1 mmHg vs RASi; 95% CrI -11.7 to -6.5). Surface under the cumulative ranking (SUCRA) probabilities identified SGLT2i as most effective for eGFR slope preservation (99.8%) and non-steroidal MRA as most effective for proteinuria reduction (98.8%). Safety analyses showed a mild, expected hemoglobin decrease with SGLT2i and a non-significant creatinine rise with non-steroidal MRA.</p><p><strong>Conclusions: </strong>SGLT2i and non-steroidal MRA confer distinct renal benefits in NDKD-SGLT2i primarily preserve kidney function, whereas non-steroidal MRA most effectively reduce proteinuria. These results support a phenotype-driven therapeutic framework and highlight the need for head-to-head trials to validate precision-guided treatment strategies in NDKD.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-17"},"PeriodicalIF":2.1,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147775481","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":"An Integrated, Evidence-Guided Framework for CKD Self-Management: Behavioral Mechanisms, Implementation Strategies, and Real-World Application.","authors":"Janet Diaz-Martinez, Staci Leon-Morris, Iván Delgado-Enciso, Gustavo A Hernández-Fuentes, Osiris G Delgado-Enciso, Gilda Stanco, Laura Kallus, Aydeivis Jean-Pierre, Carlos Duran, Yoel Madruga-Reyes, Brenda Lopez, Jessica Mancilla, Lazaro Parra-Vidal, Michelle Hospital","doi":"10.1159/000552085","DOIUrl":"https://doi.org/10.1159/000552085","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Chronic kidney disease (CKD) affects over 850 million people worldwide and contributes substantially to cardiovascular complications, reduced quality of life, and high healthcare utilization. Self-management support can improve patient activation, self-management behaviors, and quality of life, yet application in routine CKD care remains inconsistent. Many existing programs lack explicit specification of behavioral mechanisms and implementation-relevant delivery approaches, limiting reproducibility and real-world scale-up.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We conducted a structured narrative review with framework development. A systematic database search (PubMed, Embase, CINAHL, Scopus) identified English-language studies published January 2010-March 2025 addressing CKD self-management behaviors, behavioral mechanisms/theory, and/or delivery approaches and evaluation measures. Quantitative, qualitative, and mixed-methods studies were included, along with systematic reviews/meta-analyses to characterize evidence patterns. Supplementary sources (clinical guidelines, foundational theory frameworks, and measurement instruments) were used to define constructs and evaluation measures and were not treated as intervention-effect evidence. Findings were extracted into a structured evidence matrix and synthesized using a combined deductive-inductive approach to develop a practice-oriented framework.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;We synthesized 144 included records into an integrated framework linking domain-specific barriers, strategies/delivery supports, and evaluation measures. Seven priority CKD self-management domains were identified: (1) medication adherence; (2) dietary and fluid management; (3) clinical and home monitoring; (4) lifestyle modification; (5) patient activation; (6) emotional, psychological, and symptom burden; and (7) preparation for kidney failure treatment pathways (dialysis, transplant, or conservative kidney management). Cross-domain strategy clusters were mapped to behavioral mechanisms (e.g., self-efficacy strengthened through mastery experiences, observational learning, motivational communication, and management of emotional/physiological feedback). Implementation guidance was organized into a six-step, adaptable process: (1) identify and prioritize behaviors; (2) link targets to behavioral mechanisms and specify components; (3) co-design and adapt content to patient priorities and context; (4) implement multimodal delivery (clinic, digital, and community reinforcement) with structured follow-up; (5) evaluate and refine using behavioral, clinical, patient-reported, utilization, and implementation outcomes; and (6) plan for scalability, sustainability, and system alignment.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;This structured narrative synthesis integrates behavioral mechanisms with implementation-relevant strategies to provide a practice-oriented framework for designing, implementing, and evaluating","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-34"},"PeriodicalIF":2.1,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147729414","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":"Clarifying Molecular Mechanisms and Novel Strategies for Intervention Uremia and Cognitive Decline.","authors":"Yang Liang, Lingyan Ren, Yu Deng, Misbah Ullah Khan","doi":"10.1159/000550688","DOIUrl":"https://doi.org/10.1159/000550688","url":null,"abstract":"<p><p>Uremia is now considered to be one of the most relevant causes of dementia, but at that time, it was defined as a sign of the failure of the kidney. The condition of CKD patients is cognitive impairment, which sometimes progresses to dementia; that condition was mentioned very often in cases on dialysis. However, it is still uncertain whether uremia is directly connected with cognitive dysfunction. More recent studies indicate that factors associated with uremic toxicity are affected by changes in protein and metabolic waste products in plasma along with inflammatory cytokines. The presence of these toxins, inflammation, oxidation damage, and alteration in vascular properties of the brain could at least affect the quality of neuronal integrity in the affected cerebral system. This review provides an overview of molecular aspects contributing to neuro-cognition in uremia about the brain's vulnerability to exposure to toxins. Emerging treatment strategies include prevention by way of biomarker identification and early intervention in addition to the help of innovative imaging approaches as well as precision medicine strategies. Certainly, regarding the problem of cognitive impairment, one can discuss the creation of new therapeutic approaches, which include the queries of neuroprotective drugs and the improvement of the methods of hemodialysis and renal transplantation. This study calls for a multifaceted approach to both the understanding and treatment process of cognitive decline in uremic patients, bridging nephrology with neurology and proposing future directions for research and practice.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-30"},"PeriodicalIF":2.1,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147690914","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":"New Anticomplement Drugs in Nephrology - Mechanism and Indication.","authors":"Lucia Macciò, Elisa Russo, Francesca Costigliolo, Yuri Battaglia, Francesca Viazzi, Pasquale Esposito","doi":"10.1159/000551965","DOIUrl":"https://doi.org/10.1159/000551965","url":null,"abstract":"<p><strong>Background: </strong>The complement system is a key component of innate immunity, critical for pathogen defense, inflammation, and immune regulation. Dysregulation or overactivation of complement pathways contributes to the pathogenesis of numerous kidney diseases, including atypical hemolytic uremic syndrome (aHUS), C3 glomerulopathy (C3G), membranous nephropathy, systemic lupus erythematosus (SLE), antiphospholipid antibody syndrome (APS), ANCA-associated vasculitis (AAV), diabetic nephropathy, and focal segmental glomerulosclerosis (FSGS). In these conditions, uncontrolled complement activation drives renal inflammation, microvascular injury, and fibrosis.</p><p><strong>Summary: </strong>Recent advances in complement biology have enabled the development of targeted anticomplement therapies. These include C5 inhibitors (eculizumab, ravulizumab, crovalimab, nomacopan), C3 inhibitors (pegcetacoplan), factor B and D inhibitors (iptacopan, danicopan, vemircopan), C5a receptor antagonists (avacopan), and MASP-2 inhibitors (narsoplimab). This review outlines their mechanisms of action, current clinical indications, and evidence from clinical trials and real-world experience. It also addresses challenges such as safety, cost, and optimization of treatment strategies, while considering future directions in biomarker-driven, personalized approaches.</p><p><strong>Key messages: </strong>Anticomplement therapies represent a transformative advance in nephrology, offering targeted interventions that can improve outcomes for patients with complement-mediated kidney diseases. Their strategic use may reduce disease progression, manage inflammation, and mitigate organ damage, highlighting the potential of personalized treatment approaches in complement-driven renal disorders.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-19"},"PeriodicalIF":2.1,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147654399","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":"Isolated non-albumin proteinuria was associated with the progression of chronic kidney disease in hypertensive patients: a retrospective cohort study.","authors":"GianLuca Colussi, Nicholas Fiorini, Stefania Rondinella, Paolo De Martin, Marco F Cola, Maurizio Tonizzo, Benedetta Boari, Roberto Manfredini, Giulio Romano","doi":"10.1159/000551406","DOIUrl":"https://doi.org/10.1159/000551406","url":null,"abstract":"<p><strong>Objectives: </strong>Isolated non-albumin proteinuria (iNAP) has been linked to kidney function decline in diabetes, but its prognostic role in hypertensive patients with chronic kidney disease (CKD) and normal albuminuria remains uncertain. We evaluated whether baseline iNAP predicts longitudinal estimated glomerular filtration rate (eGFR) decline and kidney events in this setting.</p><p><strong>Methods: </strong>In a retrospective cohort of 166 hypertensive CKD outpatients with normal albuminuria, iNAP was defined as total 24-hour proteinuria ≥150 mg/day with albuminuria <30 mg/day. Kidney function change was assessed as (i) eGFR trajectory over 6 years using linear mixed-effects models and (ii) a composite kidney endpoint (≥30% eGFR decline or incident end-stage kidney disease) using cumulative incidence and Fine-Gray competing-risk regression (death as competing event). Confounding control was guided by a directed acyclic graph (DAG), yielding a minimal adjustment set (age, sex, diabetes, on-treatment mean arterial pressure, baseline eGFR). Sensitivity analyses examined alternative model specifications and endpoint definitions.</p><p><strong>Results: </strong>Median follow-up was 5.4 years (interquartile range 4.5-6.0). iNAP was present in 41/166 participants; 32 reached the composite kidney endpoint and 25 died. Baseline eGFR was similar in iNAP versus normal proteinuria (57±24 vs 61±24 mL/min/1.73 m²; p=0.318). In mixed-effects models, eGFR declined by -0.61 mL/min/1.73 m²/year (95% CI -0.96 to -0.25) in normal proteinuria and by -1.53 mL/min/1.73 m²/year (95% CI -2.15 to -0.91) in iNAP, with a between-group slope difference of -0.92 mL/min/1.73 m²/year (95% CI -1.63 to -0.22; time×iNAP interaction p=0.011). In competing-risk analyses, iNAP was associated with a higher risk of the composite kidney endpoint (Fine-Gray subdistribution hazard ratio 3.15, 95% CI 1.58-6.31; p=0.001), while cumulative incidence of death without prior kidney endpoint (the competing event) did not differ between groups (Gray's test p=0.920). Findings were consistent after DAG-minimal adjustment and across sensitivity analyses.</p><p><strong>Conclusions: </strong>In hypertensive CKD patients with normal albuminuria, baseline iNAP is associated with faster eGFR decline and a higher risk of kidney events, independent of key baseline risk factors in DAG-guided analyses.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-19"},"PeriodicalIF":2.1,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645773","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":"A comprehensive report on the self-reported chronic kidney disease patients in the NHANES cross-sectional cohort from 2001-2020.","authors":"Muhammad Sohaib Asghar, Muhammad Nadeem Ahsan, Sadia Iqbal, Afsana Ansari Shaik, Maria Duharte, Mohammed Mahmmoud Fadelallah Eljack, Moustafa Hegazi, Chad K Brands","doi":"10.1159/000551875","DOIUrl":"https://doi.org/10.1159/000551875","url":null,"abstract":"<p><p>Background This study was a comprehensive review of the Centers for Disease Control and Prevention (CDC) National Health and Nutrition Examination (NHANES) databases. The primary objectives were to ascertain patterns of demographic and clinical data among chronic kidney disease (CKD) and dialysis patients. Methods This study examines participants from the CDC NHANES database to identify the population diagnosed with chronic kidney disease or dialysis patients from 2001-2020. The total cohort of 51,743 patients were included in each group, i.e., CKD group included 1509 patients (out of which 173 patients have received dialysis in the past 12 months), while non-CKD group included 50,234 patients. Exclusion criteria included age >85 years (n=624), pregnancy (n=1375), and history of malignancy (n=5575). Logistic regression was performed to identify conditions that were more frequently observed with CKD and those on dialysis with reported odds ratios (OR). Receiver operating characteristics (ROC) analysis was used to calculate diagnostic accuracies of different cut-offs for urinary albumin-to-creatinine ratio (UACR). Results The mean age of study participants (n=51,743) was 48.50±17.43 years. Age was significantly higher in CKD group but there was no difference in dialysis versus non-dialysis patients (P=0.833). There was no gender predisposition in CKD patients however, males were more likely to undergo dialysis with 13.3% vs 9.8% in females (P=0.032). Among racial differences, Non Hispanic Whites were predominantly affected by CKD (37.0%) followed by non-Hispanic Blacks (29.3%) but non-Hispanic Blacks are mostly undergoing dialysis (48.6% vs 17.3%). BMI (kg/m2) was significantly higher in CKD group (P<0.001), but lower in dialysis group (P=0.039). Among urinary complaints, history of kidney stones was prevalent in CKD patients (7.7% vs 2.6%, P<0.001). Frequent coexisting comorbidities were congestive heart failure (OR: 9.8), diabetes (OR: 5.4), Coronary artery disease (OR: 5.0), and hypertension (OR: 4.7). UACR (>30 mg/g) is able to categorize CKD patients (AUC: 0.73), at a sensitivity of 44.9% and a specificity of 88.8%. Conclusion Certain clinical factors were identified as highly associated with CKD, as disseminated by the NHANES database findings. These findings emphasize the need for targeted interventions to address CKD disparities and inform public health strategies.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-14"},"PeriodicalIF":2.1,"publicationDate":"2026-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147619020","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":"Reversal of uraemic cardiomyopathy following kidney transplantation: systematic review and meta-analysis of myocardial strain compared to left ventricular volumetry as a potential early marker.","authors":"Daniek van der Kaaij, Begawan A Siadari, Aiko P J de Vries, Hildo J Lamb, Ilona A Dekkers","doi":"10.1159/000551664","DOIUrl":"https://doi.org/10.1159/000551664","url":null,"abstract":"<p><p>Introduction Adverse cardiovascular changes associated with end-stage kidney disease (ESKD), referred to as uraemic cardiomyopathy, can potentially be reversed by kidney transplantation (KTx). Myocardial strain is hypothesized to be a more sensitive marker for reversal of uraemic cardiomyopathy following KTx than conventional left ventricle (LV) volumetric measurements. This meta-analysis study compared post-KTx changes in myocardial strain (GLS, GCS, GRS) and left ventricular (LV) volumetry (LVMi, LVEF, LVEDVi, and LVESVi) measured by cardiac magnetic resonance (CMR) and echocardiography. Methods A systematic search was performed on PubMed for articles published through November 2025, and studies meeting the inclusion criteria-assessing paired myocardial strain pre- and post-KTx in adult ESKD patients using echocardiography or CMR-were included in the meta-analysis. Results Ten echocardiographic and three CMR studies were included, with follow-up durations ranging from 1 to 36 months. Strain measurements improved across all parameters, LV GLS [Standardized Mean Difference (SMD) -1.57 (95%CI -2.66, -0.48); p=0.0.005], LV GCS [SMD -1.63 (95%CI -2.33, -0.93); p<0.00001] and LV GRS [SMD 3.34 (95%CI 1.08, 5.59); p=0.004]. Conventional LV volumetric measurements also improved, LVMi [SMD -17.93 (95%CI -26.19, -9.68); p<0.0001], LVEF [SMD 5.45 (95%CI 0.17, 10.72); p=0.04], LVEDVi [SMD -12.72 (95%CI -17.59, -7.84); p<0.00001] and LVESVi [SMD -8.79 (95%CI -11.72, -5.86); p<0.0001. Conclusion These findings indicate a reversal of uraemic cardiomyopathy following KTx. However, since both strain and volumetric measurements showed similar patterns of improvement across CMR and echocardiography, myocardial strain could not be confirmed as a more sensitive marker of uraemic cardiomyopathy reversal than LV volumetry.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-22"},"PeriodicalIF":2.1,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147513349","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}