Kidney & blood pressure research最新文献

{"title":"Long-Term Tolvaptan Administration in Chinese Patients with Autosomal Dominant Polycystic Kidney Disease: A Retrospective Study in Real Clinical Practice.","authors":"Mengfei Li, Mingyang Sun, Shaoyuan Cui, Xiaoxiao Liu, Ming Guo, Yunming Xiao, Yiyu Huang, Shaopeng Zhou, Hong Wang, Xiangmei Chen, Qinggang Li","doi":"10.1159/000550806","DOIUrl":"10.1159/000550806","url":null,"abstract":"<p><strong>Introduction: </strong>Tolvaptan is the first drug approved by the FDA for rapidly progressive polycystic kidney disease (PKD). However, there are no studies reporting real-world clinical practice using tolvaptan to treat Chinese patients with autosomal dominant polycystic kidney disease (ADPKD).</p><p><strong>Methods: </strong>This retrospective multicenter cohort study analyzed ADPKD patients diagnosed by genetic or imaging tests, comparing those treated with tolvaptan (15 mg, twice daily) to unmedicated patients. Clinical course, estimated glomerular filtration rate (eGFR), total kidney volume (TKV), Short-Form 36 (SF-36) score, and adverse events (AEs) were recorded for 83 patients, with 40 in the treatment group and 43 in the control group.</p><p><strong>Results: </strong>Compared with the control group, the tolvaptan treatment significantly delayed the increase in height-adjusted total kidney volume growth rate (htTKV%) in the 1st and 2nd years (1 year: difference: -5.58, 95% confidence interval [CI]: -8.39 to -2.78, p < 0.001; 2 years: difference: -9.75, 95% CI: -13.1 to -6.31, p < 0.001). Compared with the control group, the effect of tolvaptan on eGFR was more pronounced in the 2nd year of treatment (2 years: difference: 6.79, 95% CI: 5.10-8.48, p < 0.001). Tolvaptan attenuated the AEs, such as fatigue, back pain, and anxiety, to some extent, while the incidence of water-related AEs, such as thirst, polyuria, and urinary frequency, was significantly higher than that in the control group (p < 0.001, p = 0.006, p = 0.009, respectively). According to the SF-36 health survey, the physical component summary (PCS) score was significantly improved in the treatment group (p < 0.001).</p><p><strong>Conclusion: </strong>This real-world analysis showed that tolvaptan appears to be effective in delaying the clinical course of ADPKD patients in China, extending the results of previous clinical trials in other populations.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"178-187"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13065305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147348765","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":"Composite Phenotype: Recurrent Nephrolithiasis and Chronic Kidney Disease in an Adult with Biallelic <italic>SLC34A3</italic> and Monoallelic <italic>SLC3A1</italic> Pathogenic Variants - Who Is \"The Culprit\"?","authors":"Bukola A Olarewaju, Sonia Sabrowsky, Shaymaa Shurrab, Ann M Moyer, Mira T Keddis, Mayowa A Osundiji","doi":"10.1159/000551270","DOIUrl":"10.1159/000551270","url":null,"abstract":"<p><strong>Introduction: </strong>Kidney stones are common and can arise from many etiologies including genetic and environmental. Biallelic pathogenic variants in the solute carrier family 34-member 3 (SLC34A3) gene cause hereditary hypophosphatemic rickets with hypercalciuria, while both monallaelic and biallelic pathogenic variants in SLC3A1 cause cystinuria.</p><p><strong>Case presentation: </strong>We studied a 29-year-old man, who has a personal history of recurrent nephrolithiasis (with over 10 kidney stone episodes requiring lithotripsy and surgical interventions), medullary nephrocalcinosis, pyelonephritis, bilateral septate renal cysts, and chronic kidney disease. Genetic testing showed compound heterozygous pathogenic variants in SLC34A3 [NM_001177316.2, c.448+1G>A and c.575C>T (p.Ser192Leu)) and a heterozygous pathogenic variant in SLC3A1 (gain of exons 5-9). The renal calculi mostly comprised; 50% calcium oxalate monohydrate, and 30% calcium phosphate (hydroxy- and carbonate-apatite) as well as 20% calcium oxalate dihydrate.</p><p><strong>Conclusion: </strong>We report the clinical phenotype of a patient with concomitant biallelic and monoallelic pathogenic variants in SLC34A3 and SLC3A1, respectively.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"280-284"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13193686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147480775","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":"TRPC6 Inhibition Attenuates Renal Tubulointerstitial Fibrosis via the Reactive Oxygen Species/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":"10.1159/000552129","url":null,"abstract":"<p><strong>Introduction: </strong>Chronic kidney disease 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. H&E and Masson staining were used to observe pathological changes. IHC staining was also conducted to measure the α-SMA, fibronectin (Fn), TRPC6, reactive oxygen species (ROS), and NLRP3 expressions. Scanning electron microscopy 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 markers and diminished levels of 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":"452-467"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13345608/pdf/","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":"OA","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":"10.1159/000552052","url":null,"abstract":"<p><strong>Introduction: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>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":"394-408"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13299129/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ten-Year Results of Therapeutic Intravascular Ultrasound Renal Denervation in Resistant Hypertension: A Prospective Single-Center Study.","authors":"Michael Jonas, Omar Ayyad, Mohammad Alnees, Alena Kirzhner, Tal Schiller, Christian Spaulding, Abdalaziz Darwish, Ameer Mahamid, Ortal Tuvali, Adam Hassan, Haitham Abu Khadija","doi":"10.1159/000551407","DOIUrl":"10.1159/000551407","url":null,"abstract":"<p><strong>Introduction: </strong>Renal denervation (RDN) is an emerging therapy for resistant hypertension. The therapeutic intravascular ultrasound (TIVUS) system offers a nonocclusive, multidirectional approach, but its long-term efficacy and safety remain unknown.</p><p><strong>Methods: </strong>We prospectively followed 12 patients with severe resistant hypertension who underwent bilateral ultrasound RDN as part of the TIVUS trial. Office BP was measured at baseline, 1, 3, 6, and 12 months; 24-h ambulatory BP at years 1, 2, 5, and 10. Estimated glomerular filtration rate (eGFR) and adverse events were tracked. BP changes were analyzed using mixed-effects models adjusted for baseline covariates.</p><p><strong>Results: </strong>Mean age was 65 ± 8 years; 75% had diabetes. Baseline office BP averaged 176/84 mm Hg. The procedure was completed in all patients without complications. Systolic office BP decreased by 22.1 mm Hg at 1 month and 36.2 mm Hg at 12 months (both p < 0.001). At 10 years, office BP reductions were -38.6/-13.3 mm Hg (p < 0.001). Ambulatory BP declined from 149.4 ± 9.8 to 128.4 ± 10.0 mm Hg (ASBP) and from 85.0 ± 8.5 to 74.4 ± 9.2 mm Hg (ADBP). The 10-year change in antihypertensive defined daily doses was -1.70 (95% CI -2.75 to -0.38; p = 0.002). eGFR declined modestly (68.6 to 60.2 mL/min/1.73 m2), consistent with aging. No procedure-related adverse events occurred.</p><p><strong>Conclusion: </strong>TIVUS ultrasound RDN achieved durable BP reduction with preserved renal function over 10 years.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"264-279"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13186550/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147390149","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":"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":"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-h 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% confidence interval [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":"340-353"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13262992/pdf/","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":"OA","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":"10.1159/000551664","url":null,"abstract":"<p><strong>Introduction: </strong>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 (global longitudinal strain [GLS], global circumferential strain [GCS], global radial strain [GRS]) and LV volumetry (left ventricular mass index [LVMi], left ventricular ejection fraction [LVEF], LV end-diastolic volume indexed [LVEDVi], and left ventricular end-systolic volume indexed [LVESVi]) measured by cardiac magnetic resonance (CMR) and echocardiography.</p><p><strong>Methods: </strong>A systematic search was performed on PubMed for articles published through November 2025. 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.</p><p><strong>Results: </strong>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 = 0.005), 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 < 0.00001).</p><p><strong>Conclusion: </strong>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":"299-311"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13218700/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effect of Renal Ischemia/Reperfusion on the Renal Expression of Epithelial Sodium Channels in Rat: Possible Role of Neural Precursor Cell-Expressed Developmentally Down-Regulated Protein (Nedd4-2).","authors":"Slava Malatiali, Rana Fahel, Rola H Ali, Zoran Redzic","doi":"10.1159/000551003","DOIUrl":"10.1159/000551003","url":null,"abstract":"<p><strong>Introduction: </strong>The epithelial sodium channel (ENaC) expressed in renal collecting duct epithelia plays a key role in regulating sodium balance. ENaC is regulated by the ubiquitin ligase Nedd4-2, which binds to ⍺ENaC and causes its retrieval, under low energy conditions due to the activation of AMP activated protein kinase (AMPK). Acute kidney injury (AKI) after ischemia/reperfusion (I/R) disrupts sodium balance. In this study, we examined the impact of acute renal I/R on renal Na+ handling, ENaC subunits expression in renal membranes and the potential role of AMPK-Nedd4-2 pathway in this process.</p><p><strong>Methods: </strong>Adult Sprague-Dawley rats were randomized into two groups; I/R group, in which both renal arteries were occluded for 30 min, and sham group. Data were collected 48 h post-I/R. To confirm AKI, tubular damage and serum creatinine levels were assessed. Serum Na+ concentration and urinary sodium excretion rate were measured. Renal gene expression of α-, β-, and γ-ENaC subunits was studied using RT-PCR with hydroxymethylbilane synthase as a housekeeping gene. Protein expression of α-, β-, and γ-ENaC in renal homogenates and membrane fractions and protein expression of Nedd4-2, phospho-Nedd4-2, AMPK, and p-AMPK in renal homogenates were assessed by Western blot. Results were expressed as mean ± SEM. Control groups were compared to I/R groups using student t test and p < 0.05 was set as significant.</p><p><strong>Results: </strong>AKI after I/R was confirmed by revealing a significant tubular cell damage and the rise in serum creatinine levels (1.66 ± 0.14 in I/R vs. 0.64 ± 0.09 in sham group, p < 0.001). Serum Na+ concentration and Na+ excretion rate were not altered after I/R. Gene expression of ENaC subunits was not affected by I/R; however, protein expression of α-ENaC was decreased in renal membranes (0.03 ± 0.003 in I/R vs. 0.05 ± 0.01 in sham group, p < 0.05), with no change in β or γ expression. There were increases in the expressions of Nedd4-2 (0.27 ± 0.04 vs. 0.09 ± 0.03, p < 0.05), p-Nedd4-2 (0.15 ± 0.04 vs. 0.04 ± 0.01, p < 0.05), AMPK (0.09 ± 0.01 vs. 0.03 ± 0.02, p < 0.05), and p-AMPK (1.05 ± 0.2 vs. 0.6 ± 0, p < 0.05), indicating the activation of AMPK-Nedd4-2 pathway.</p><p><strong>Conclusion: </strong>Ischemia reperfusion caused renal injury, however, did not affect renal sodium handling. A decrease in membrane expression of α-ENaC was detected without a change in total α-ENaC suggesting ENaC trafficking into the cell. This occurred with the concomitant activation of AMPK-Nedd4-2 pathway, which is known to cause retrieval of ENaC and decrease its membrane expression.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"188-199"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13068382/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146227311","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":"Inflammatory Biomarkers in the Assessment of Kidney Function Decline in Long COVID Syndrome.","authors":"Margherita Borriello, Roberta Ranieri, Annapaola Coppola, Patrizia Lombari, Riccardo Nevola, Aldo Marrone, Giuseppe Signoriello, Luigi Elio Adinolfi, Nicola Coppola, Diana Ingrosso, Flavia Maria Longo, Christian Di Maro, Carlo Maria Alfieri, Diego Ingrosso, Mariadelina Simeoni, Alessandra Perna","doi":"10.1159/000552904","DOIUrl":"10.1159/000552904","url":null,"abstract":"<p><strong>Introduction: </strong>Long COVID (LC) is an inflammatory condition, affecting multiple organs, including kidneys. This study aims to identify a signature of inflammatory biomarkers that can predict, describe, and monitor kidney function decline in LC patients.</p><p><strong>Methods: </strong>A single-center observational study was carried out at the COVID Center of University of Campania \"L. Vanvitelli.\" Patients who survived the acute phase were invited for a follow-up visit at least 12 months after discharge. Based on the estimated glomerular filtration rate (eGFR), patients were categorized in three groups: group 1: eGFR >90 mL/min × 1.73 m2, group 2: eGFR 30-89 mL/min × 1.73 m2, and group 3: eGFR <30 mL/min × 1.73 m2. The multiplex ELLA platform was employed to quantify serum levels of inflammatory biomarkers including IL-6, IL-17, IL-10, IL-1β, PTX3, TNF-α, VCAM-1, ICAM-1, and E-selectin. Associations between each biomarker level and eGFR were analyzed.</p><p><strong>Results: </strong>A decline in the eGFR at follow-up compared to that at admission was observed. IL-6 levels increased significantly as the eGFR decreased across the groups. IL-17, IL-10, and VCAM1 levels were markedly elevated in group 3.</p><p><strong>Conclusions: </strong>According to our results, IL-6, IL-17, IL-10, and VCAM1 constitute a biomarker signature associated with poorer renal prognosis in LC patients. The rise in IL-6 could drive an increase in IL-17, IL-10, and VCAM1, contributing to kidney function decline. These findings may help establish a clinical and laboratory framework to predict chronic kidney disease risk in LC. Furthermore, ELLA platform appears as a useful tool for inflammatory biomarker quantification in the clinical setting.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"542-552"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13412225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148176329","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":"Impact of Renal Replacement Therapy on Severe Lactic Acidosis in Intensive Care Unit Patients: A MIMIC-IV Retrospective Replication Analysis.","authors":"Alexander Jerman, Luka Petravić, Vanja Peršič","doi":"10.1159/000553085","DOIUrl":"10.1159/000553085","url":null,"abstract":"<p><strong>Introduction: </strong>Severe lactic acidosis (SLA), defined as lactate ≥5 mmol/L, is a critical condition in intensive care unit (ICU) patients and is associated with high mortality. Despite the broad use of renal replacement therapy (RRT) to manage metabolic derangements, its impact on outcomes in SLA remains uncertain. Implementing a replication analysis, we aimed to validate the previous findings by Van de Ginste et al. regarding the association between RRT initiation and patient outcomes for patients with SLA in ICU.</p><p><strong>Methods: </strong>We conducted a retrospective cohort analysis using the MIMIC-IV database (2008-2019). Adult ICU patients with SLA (lactate ≥5 mmol/L) during their first ICU stay were included. Patients on maintenance dialysis, with prior RRT, or do-not-resuscitate status were excluded. RRT was considered if initiated within 24 h of reaching the lactate threshold. Logistic regression was used to assess the association between RRT and 90-day mortality.</p><p><strong>Results: </strong>Of 5,317 screened patients, 4,450 met inclusion criteria; 314 (7.1%) received early RRT. Overall 90-day mortality was 51.3%. The propensity to receive RRT was related to the lactate level and to the SOFA renal score. Higher age, serum lactate, lower pH, and greater organ dysfunction were associated with mortality. After adjustment, RRT remained associated with increased 90-day mortality (OR 1.51; 95% CI: 1.05-2.20).</p><p><strong>Discussion: </strong>Replicating previous work using a large, independent database (MIMIC-IV), our findings align with the observation that early initiation of RRT in patients with SLA is associated with a poor prognosis, even after adjustment for illness severity. However, given the inherent and severe limitations of this study design, the causal effect of RRT in SLA remains largely speculative. The results thus highlight the necessity for prospective studies to clarify the role of RRT in this critical patient population.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"827-835"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13608886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148818734","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}