IF 2.3 4区医学

Nephron Pub Date : 2025-03-28 DOI: 10.1159/000543920

Allison M Paltzer, Allegra M Quadri, Carly Rasmussen, Raphael Schiffmann, Joel Charrow, Carlos E Prada

{"title":"Further Clinical and Biochemical Phenotype of GLA p.A143T: A Fabry Disease Newborn Screening Experience.","authors":"Allison M Paltzer, Allegra M Quadri, Carly Rasmussen, Raphael Schiffmann, Joel Charrow, Carlos E Prada","doi":"10.1159/000543920","DOIUrl":"10.1159/000543920","url":null,"abstract":"Background: In 2015, Illinois added Fabry disease to the newborn screening (NBS) panel, and numerous individuals who have the controversial p.A143T GLA variant were identified. Ann & Robert H. Lurie Children's Hospital of Chicago identified 80 individuals with this variant.Summary: Of the 80 individuals, 34/80 were identified by NBS, 2/80 were identified by gene panel testing, and 44/80 were identified by cascade testing. These individuals were from 36 families and ranged in age from 7 months to 71 years. Most individuals identified by NBS were male (90.9%) and 35.96% had the p.A143T variant. All newborns with known pathogenic or likely pathogenic variants in GLA had enzyme leukocyte activities below 20% of the percentage of mean of normal. This threshold could serve as a guideline for determining risk of symptom development for p.A143T and other variants of unknown significance. No person with p.A143T had significant lyso-GL3 elevation in this cohort.Key messages: These data suggest the variant impacts enzyme levels, but its effect on health outcomes remains unclear. We further characterize clinical and biochemical data on individuals with the p.A143T GLA variant to help provide guidance on its clinical significance.","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-7"},"PeriodicalIF":2.3,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753508","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}

引用次数: 0

Dapagliflozin Treatment Attenuates the Interaction between the Renal Sodium Chloride Co-Transporter and Ezrin in Hypertensive Diabetic db/db Mice. 达格列净治疗可减弱高血压糖尿病小鼠肾脏氯化钠共转运体与Ezrin的相互作用

IF 1.8 4区医学

Nephron Pub Date : 2025-03-21 DOI: 10.1159/000543336

Mohammed F Gholam, Abdel A Alli, Abdel Alli

{"title":"Dapagliflozin Treatment Attenuates the Interaction between the Renal Sodium Chloride Co-Transporter and Ezrin in Hypertensive Diabetic db/db Mice.","authors":"Mohammed F Gholam, Abdel A Alli, Abdel Alli","doi":"10.1159/000543336","DOIUrl":"10.1159/000543336","url":null,"abstract":"Introduction: Ezrin is a protein that links the actin cytoskeleton to membrane proteins. The sodium chloride cotransporter (NCC) plays a key role in regulating total body electrolyte homeostasis and systemic blood pressure. Dapagliflozin, an SGLT2 inhibitor, is used to manage type 2 diabetes mellitus. We hypothesize dapagliflozin reduces sodium reabsorption and blood pressure by inhibiting the interaction between NCC and ezrin in the distal convoluted tubules of salt-loaded hypertensive mice.Methods: Male diabetic db/db mice were salt loaded to induce hypertension and then given dapagliflozin or vehicle by oral gavage. The mice were subject to metabolic cage experiments and blood pressure was assessed using the tail-cuff method to study the impact of dapagliflozin compared to the vehicle. Protein expression of NCC and ezrin was evaluated using immunohistochemistry and Western blotting.Results: Treatment with dapagliflozin lowered systolic blood pressure, raised urine sodium excretion, and lowered urinary potassium excretion. A decrease in phospho-NCC and ezrin proteins was observed in db/db mice treated with dapagliflozin. There was less co-localization of ezrin and phosphorylated NCC in dapagliflozin treated mice.Conclusion: Collectively, we demonstrate that dapagliflozin reduces sodium retention and blood pressure via decreasing the density of renal NCC at the luminal membrane and the interaction between NCC and the actin cytoskeleton.","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-17"},"PeriodicalIF":1.8,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692574","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}

引用次数: 0

Lysosomal Storage-Independent Fabry Disease Variants with α-Galactosidase A Misprocessing-Induced ER Stress and the Unfolded Protein Response. α-半乳糖苷酶A错误加工诱导内质网应激和未折叠蛋白反应的溶酶体储存非依赖性法布里病变异

IF 2.3 4区医学

Nephron Pub Date : 2025-03-20 DOI: 10.1159/000545388

Martina Živná, Malte Lenders, Stanislav Kmoch

{"title":"Lysosomal Storage-Independent Fabry Disease Variants with α-Galactosidase A Misprocessing-Induced ER Stress and the Unfolded Protein Response.","authors":"Martina Živná, Malte Lenders, Stanislav Kmoch","doi":"10.1159/000545388","DOIUrl":"10.1159/000545388","url":null,"abstract":"Background: Clinical findings in Fabry disease have classically been attributed to loss-of-function variants in the GLA gene that result in α-galactosidase A deficiency, intracellular accumulation of globotriaosylceramides and clinical manifestations. However, over time, increasing number of patients have been identified with GLA variants causing either non-classic Fabry disease or having unclear clinical effects.Summary: Searching for additional etiologic and lysosomal storage-independent factors, investigators have recently identified that certain missense GLA variants not only affect enzymatic activity, but also encode for misfolded α-galactosidase A that itself induces chronic endoplasmic reticulum stress and the unfolded protein response. Thus, Fabry disease pathogenesis may be caused by decreased enzymatic activity as well as cellular toxicity from accumulation of the misfolded α-galactosidase A protein, with the contribution of each factor determined by the type of the genetic variant and host factors.Key messages: Defective proteostasis and misfolding of certain missense α-galactosidase A variants induce chronic endoplasmic reticulum stress and the unfolded protein response that may contribute to intra-familial and inter-familial variation in disease penetrance and clinical expressivity. Pharmacologic modulation of defective proteostasis may have therapeutic implications in Fabry disease.","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-11"},"PeriodicalIF":2.3,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12121966/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670531","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}

引用次数: 0

When Proteins Go Berserk: The Unfolded Protein Response and ER Stress. 当蛋白质发狂：未折叠的蛋白质反应和内质网应激。

IF 2.3 4区医学

Nephron Pub Date : 2025-03-04 DOI: 10.1159/000544971

Doria Meiseles, Narkis Arbeli, Moran Dvela-Levitt

{"title":"When Proteins Go Berserk: The Unfolded Protein Response and ER Stress.","authors":"Doria Meiseles, Narkis Arbeli, Moran Dvela-Levitt","doi":"10.1159/000544971","DOIUrl":"10.1159/000544971","url":null,"abstract":"Background: The cellular proteostasis machinery is essential for maintaining protein homeostasis by employing quality control systems that identify, sequester, and eliminate damaged or misfolded proteins. However, the accumulation of misfolded proteins can overwhelm these protective mechanisms, disrupting proteostasis. This phenomenon is a hallmark of numerous pathologies, including a variety of genetic disorders. In the secretory pathway, the buildup of misfolded proteins triggers endoplasmic reticulum (ER) stress, which activates the unfolded protein response (UPR). The UPR serves as an adaptive mechanism, aiming to alleviate stress and restore cellular homeostasis. However, if ER stress is prolonged or severe, the UPR may fail to restore balance and apoptosis is induced.Summary: This review introduces the intricate signaling pathways activated by the three UPR transmembrane sensors: protein-kinase R-like endoplasmic reticulum kinase (PERK), inositol requiring enzyme 1 (IRE1), and activating transcription factor 6 (ATF6). We briefly present the roles of the distinct transcriptional programs activated by each sensor in modulating the cellular response to protein stress and in determining cell fate. We discuss how genetic variants and environmental factors contribute to the heterogeneity observed in protein misfolding diseases. Finally, we critically evaluate select therapeutic strategies, specifically protein stabilization, trafficking modulation, and UPR sensor targeting approaches.Key messages: This review introduces the potential consequences of protein misfolding, which may not only impair protein function but can also lead to toxic protein accumulation and stress induction. Using Fabry disease as a compelling example, we suggest that future therapeutic intervention may require nuanced, combination approaches that address both loss and gain of protein function.","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-11"},"PeriodicalIF":2.3,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143557483","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}

引用次数: 0

The Inflammatory Pathogenetic Pathways of Fabry Nephropathy and Agalopathy: GLA Variant Induction of Endoplasmic Reticulum Stress. 法布里肾病和无脂病的炎症发病途径Gla变异体诱导内质网应激。

IF 2.3 4区医学

Nephron Pub Date : 2025-02-20 DOI: 10.1159/000544760

Sandro Feriozzi, Paula Rozenfeld

{"title":"The Inflammatory Pathogenetic Pathways of Fabry Nephropathy and Agalopathy: GLA Variant Induction of Endoplasmic Reticulum Stress.","authors":"Sandro Feriozzi, Paula Rozenfeld","doi":"10.1159/000544760","DOIUrl":"10.1159/000544760","url":null,"abstract":"Background: Fabry disease (FD) is a monogenic disease with highly variable clinical features. This variability suggests that additional pathogenetic pathways may exist besides the intra-lysosomal deposition of globotriaosylceramide (Gb3) and its deacylated form globotriaosylsphingosine (LysoGb3) caused by an enzyme deficiency.Summary: It has been demonstrated that intralysosomal accumulation of Gb3 and LysoGb3 triggers an inflammatory response. Monocytes, macrophages, and dendritic cells overexpress the adhesion molecules, and cytokines release occurs, including interleukin β, tumor necrosis factor-alpha (TNFα), and transforming growth factor beta. These processes determine the activation of inflammation processes associated with chronic inflammation and tissue fibrosis. The pathogenetic mechanisms stimulated by Gb3 and LysoGb3 deposition could break free from the original activation, causing an irreversible effect, in which Fabry disease-specific therapy can play a limited role. A new disease mechanism, \"Agalopathy\" would coexist with enzyme deficiency. Missense variants in the coding sequence of the GLA gene would generate the misfolding of the altered protein alpha-galactosidase A. Emergence of misfolded proteins may generate stress of the endoplasmic reticulum, leading to induction of the unfolded protein response (UPR). The UPR causes the release of pro-inflammatory cytokines and contributes to inflammatory status. This mechanism could be activated independently of glycolipid deposition, and its relationship with inflammatory pathways deserves more research. Strikingly, a zebrafish GLA knockout model that naturally lacks the enzyme that synthesizes Gb3 shows many alterations in lysosomal functions.Key messages: These pieces of evidence suggest the involvement of alternative pathways independent of Gb3 in FD pathogenesis. This review aims to describe these processes' role in the pathogenesis of renal damage in FD or Agalopathy nephropathies.","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-6"},"PeriodicalIF":2.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468638","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}

引用次数: 0

Subclinical Inflammation and Renal Allograft Dysfunction: Myth or Reality? 亚临床炎症和肾移植功能障碍：神话还是现实？

IF 2.3 4区医学

Nephron Pub Date : 2025-02-17 DOI: 10.1159/000544762

Carlos Couceiro, Maria Visent, Josep M Cruzado

{"title":"Subclinical Inflammation and Renal Allograft Dysfunction: Myth or Reality?","authors":"Carlos Couceiro, Maria Visent, Josep M Cruzado","doi":"10.1159/000544762","DOIUrl":"10.1159/000544762","url":null,"abstract":"Background: Since the implementation of the Banff classification, the diagnosis and treatment of transplant rejection have been standardised. However, the rigid categorisation of transplant pathology has limited our perspective on allograft inflammation, particularly disregarding those inflammatory infiltrates who do not reach the category of rejection.Summary: The term subclinical inflammation was introduced to designate the inflammation found in protocol biopsies, without significant renal function deterioration. Following the introduction of modern immunosuppression with tacrolimus and mycophenolate, subclinical rejection rate decreased, and less attention was paid to this entity. However, in the last decades, several studies have evaluated the impact of lower levels of inflammation and demonstrated its negative consequences on long-term outcomes. Although, in some patients, this subclinical inflammation is not permanent and can spontaneously disappear. The uncomplete definition of subclinical inflammation, which only considers renal function stability, and the evaluation of the biopsy as a definitive diagnosis, and not as a picture of an evolving process, are the main reasons why managing this inflammation represents a challenge, especially when there is no pathogenic mechanism identified.Key messages: In this review, we revise the \"natural\" history of inflammation in the kidney allograft and its possible origins based on cellular composition and transcriptomic expression changes in kidney biopsies. In addition, we propose an updated definition and an approach to manage it.","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-6"},"PeriodicalIF":2.3,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143441530","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}

引用次数: 0

Recurrence of Glomerular Diseases after Kidney Transplantation: What Do We Know New? 肾移植后肾小球疾病的复发：我们有什么新发现？

IF 2.3 4区医学

Nephron Pub Date : 2025-01-08 DOI: 10.1159/000543268

Emilio Rodrigo, Lara Belmar, José Luis Pérez-Canga

{"title":"Recurrence of Glomerular Diseases after Kidney Transplantation: What Do We Know New?","authors":"Emilio Rodrigo, Lara Belmar, José Luis Pérez-Canga","doi":"10.1159/000543268","DOIUrl":"10.1159/000543268","url":null,"abstract":"Background: The recurrence of primary glomerulonephritis (GN) following kidney transplantation poses a significant threat to graft survival. To enhance kidney transplant outcomes, we must lessen the burden of recurrence. In recent years, there has been progress in understanding the incidence, risk factors for recurrence, pathophysiology, biomarkers, and therapeutics, making it worthwhile to conduct an update on primary GN that may recur following kidney transplantation.Summary: We conducted a narrative review of the literature on the novel discoveries of primary GN that can recur following kidney transplantation. To summarize, developing a broad consensus on recurrence diagnosis would greatly advance our understanding, and its development would be a valuable collaborative effort. The key risk factors for recurrence have been better understood, particularly in individuals with complement-related or monoclonal gammopathy-related recurrent membranoproliferative GN. Furthermore, we can identify better recurrent IgA nephropathy patients who are more likely to experience graft loss. New biomarkers for membranous nephropathy (anti-PLA2R-Ab) and focal and segmental glomerulosclerosis (anti-nephrin-Ab) can assist in identifying and monitoring patients at risk of recurrence. Regarding therapy, the focal and segmental glomerulosclerosis consensus will enhance recurrence treatment. Some complement inhibitors and anti-CD38 monoclonal antibodies are already promising in treating and healing recurrent C3 glomerulopathy and focal and segmental glomerulosclerosis, respectively. Finally, new drugs developed specifically to treat IgA nephropathy in the native kidney will also change the outcome of IgA nephropathy recurrence.Key messages: Although there has been progress in understanding the recurrence of primary GN following kidney transplantation, a worldwide effort should be undertaken to gather research that will allow for improved diagnosis, monitoring, and management of these patients.","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-12"},"PeriodicalIF":2.3,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142952054","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}

引用次数: 0

Exploring the Critical Role of Tight Junction Proteins in Kidney Disease Pathogenesis. 探索紧密连接蛋白在肾病发病机制中的关键作用

IF 2.3 4区医学

Nephron Pub Date : 2025-01-01 Epub Date: 2024-11-12 DOI: 10.1159/000542498

David Jayne, Corentin Herbert, Vincent Anquetil, Geoffrey Teixeira

{"title":"Exploring the Critical Role of Tight Junction Proteins in Kidney Disease Pathogenesis.","authors":"David Jayne, Corentin Herbert, Vincent Anquetil, Geoffrey Teixeira","doi":"10.1159/000542498","DOIUrl":"10.1159/000542498","url":null,"abstract":"Background: Kidney disease poses a significant global health challenge, marked by a rapid decline in renal function due to a variety of causative factors. A crucial element in the pathophysiology of kidney disease is the dysregulation of epithelial cells, which are vital components of renal tissue architecture. The integrity and functionality of these cells are largely dependent on tight junctions (TJ) proteins, complex molecular structures that link adjacent epithelial cells. These TJ not only confer cellular polarity and maintain essential barrier functions but also regulate epithelial permeability.Summary: TJ proteins are pivotal in their traditional role at cell junctions and in their non-junctional capacities. Recent research has shifted the perception of these proteins from mere structural elements to dynamic mediators of kidney disease, playing significant roles in various renal pathologies. This review explores the multifaceted roles of TJ proteins, focusing on their functions both within and external to the renal epithelial junctions. It highlights how these proteins contribute to mechanisms underlying kidney disease, emphasizing their impact on disease progression and outcomes.Key messages: TJ proteins have emerged as significant players in the field of nephrology, not only for their structural role but also for their regulatory functions in disease pathology. Their dual roles in maintaining epithelial integrity and mediating pathological processes make them promising therapeutic targets for kidney disease. Understanding the intricate contributions of TJ proteins in kidney pathology offers potential for novel therapeutic strategies, aiming to modulate these proteins to halt or reverse the progression of kidney disease.","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"240-250"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11991748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624128","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}

引用次数: 0

Comments regarding "Adoption of CKD-EPI (2021) for Glomerular Filtration Rate Estimation: Implications for UK Practice". 关于“采用CKD-EPI（2021）估算GFR -对英国实践的影响”的评论。

IF 1.8 4区医学

Nephron Pub Date : 2025-01-01 Epub Date: 2025-03-11 DOI: 10.1159/000545104

Paul T Williams

引用次数: 0

Correlation between Plasma Aldosterone Concentrations and Simple Renal Cyst in Hypertensive Patients. 高血压患者血浆醛固酮浓度与单纯性肾囊肿的相关性研究。

IF 1.8 4区医学

Nephron Pub Date : 2025-01-01 Epub Date: 2025-03-21 DOI: 10.1159/000545105

Huimin Ma, Xintian Cai, Shuaiwei Song, Qing Zhu, Junli Hu, Di Shen, Wenbo Yang, Yingying Zhang, Rui Ma, Pan Zhou, Delian Zhang, Qin Luo, Jing Hong, Nanfang Li, Nanfang Li

{"title":"Correlation between Plasma Aldosterone Concentrations and Simple Renal Cyst in Hypertensive Patients.","authors":"Huimin Ma, Xintian Cai, Shuaiwei Song, Qing Zhu, Junli Hu, Di Shen, Wenbo Yang, Yingying Zhang, Rui Ma, Pan Zhou, Delian Zhang, Qin Luo, Jing Hong, Nanfang Li, Nanfang Li","doi":"10.1159/000545105","DOIUrl":"10.1159/000545105","url":null,"abstract":"Background: Previous studies have linked primary aldosteronism to simple renal cysts (SRCs), but the relationship between plasma aldosterone concentration (PAC) and SRC remains unclear. This study aimed to investigate the association between PAC and SRC in hypertensive patients.Methods: A total of 30,135 hypertensive patients who visited our hospital from January 2014 to December 2023 were included. Logistic regression analyses were conducted to explore the relationship between PAC and SRC, while restricted cubic splines (RCS) assessed the dose-response relationship. SRC were further categorized by size (≥2 cm) and number ≥2). Subgroup analyses were performed to evaluate PAC effects across different conditions.Results: Multivariate logistic regression showed a positive association between PAC levels (per 5-ng/dL increase) and SRC (OR: 1.20, 95% CI: 1.17-1.23) after adjusting for confounders. Compared to the lowest PAC quartile (Q1), the Q2, Q3, and Q4 groups had progressively higher risks of SRC, with ORs of 1.03 (95% CI: 0.95-1.12), 1.25 (95% CI: 1.15-1.35), and 1.65 (95% CI: 1.52-1.78), respectively. Combining Q3 and Q4 (PAC ≥14.92) yielded an OR of 1.41 compared to Q1 and Q2 (<14.92). Similar trends were observed for SRC size ≥2 cm and number ≥2. RCS analysis confirmed a linear dose-response relationship between PAC and SRC risk. Subgroup and sensitivity analyses consistently supported these findings.Conclusions: Elevated PAC levels have been linked to an increased risk of SRC in hypertensive patients. Regulating PAC levels may help mitigate SRC formation; however, further prospective studies are required to confirm this causal relationship.","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"505-518"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692567","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}

引用次数: 0

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