Advances in kidney disease and health最新文献

{"title":"Social Determinants of Health and Primary Hypertension in Children and Adolescents: Proposed Solutions Using a Socioecological Model of Health","authors":"Sean Connolly,&nbsp;Abbas Zaidi,&nbsp;Carissa M. Baker-Smith","doi":"10.1053/j.akdh.2026.05.001","DOIUrl":"10.1053/j.akdh.2026.05.001","url":null,"abstract":"<div><div>Pediatric hypertension is prevalent in 4% of children and is mainly of primary origin. Risk factors for primary pediatric hypertension extend beyond individual risk and include the social determinants of health. Addressing the presence of pediatric hypertension in the United States and globally requires careful attention to the social determinants of health, including socioecological models of health and their multiple domains and levels of influence.</div></div><div>Pediatric hypertension is prevalent in 4% of children and is mainly of primary origin. Risk factors for primary pediatric hypertension extend beyond individual risk and include the social determinants of health. Addressing the presence of pediatric hypertension in the United States and globally requires careful attention to the social determinants of health, including socioecological models of health and their multiple domains and levels of influence.</div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":"33 2","pages":"Pages 160-167"},"PeriodicalIF":3.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148378335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endocrine Hypertension in Children and Adults: Beyond Primary Aldosteronism","authors":"Stefanie Parisien-La Salle,&nbsp;Athira Puthukara,&nbsp;Anand Vaidya,&nbsp;G. Chandra Bhatt","doi":"10.1053/j.akdh.2026.04.002","DOIUrl":"10.1053/j.akdh.2026.04.002","url":null,"abstract":"<div><div>Endocrine hypertension refers to elevated blood pressure resulting from an identifiable hormonal cause that is potentially treatable. Endocrine hypertension occurs in ∼30% of young adults with hypertension (18-40 years), in 30-50% of patients with resistant hypertension, most commonly due to primary aldosteronism, and can occur in a small yet clinically significant subset of children with hypertension. Other causes of endocrine hypertension include excess mineralocorticoid production, cortisol excess or impaired cortisol metabolism, disorders of the mineralocorticoid receptor or epithelial sodium channel, catecholamine-secreting tumors, thyroid or parathyroid disorders, and growth hormone excess. Early recognition is crucial, as many of these conditions are amenable to targeted medical or surgical therapies. This review focuses on endocrine causes of hypertension in both pediatric and adult populations, excluding primary aldosteronism.</div></div><div>Endocrine hypertension refers to elevated blood pressure resulting from an identifiable hormonal cause that is potentially treatable. Endocrine hypertension occurs in ∼30% of young adults with hypertension (18-40 years), in 30-50% of patients with resistant hypertension, most commonly due to primary aldosteronism, and can occur in a small yet clinically significant subset of children with hypertension. Other causes of endocrine hypertension include excess mineralocorticoid production, cortisol excess or impaired cortisol metabolism, disorders of the mineralocorticoid receptor or epithelial sodium channel, catecholamine-secreting tumors, thyroid or parathyroid disorders, and growth hormone excess. Early recognition is crucial, as many of these conditions are amenable to targeted medical or surgical therapies. This review focuses on endocrine causes of hypertension in both pediatric and adult populations, excluding primary aldosteronism.</div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":"33 2","pages":"Pages 143-152"},"PeriodicalIF":3.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148378077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oncohypertension: Unraveling the Link Between Cancer and Hypertension","authors":"Prakash Gudsoorkar,&nbsp;Paul E. Hanna,&nbsp;Priti Meena,&nbsp;Sabine Karam","doi":"10.1053/j.akdh.2026.06.002","DOIUrl":"10.1053/j.akdh.2026.06.002","url":null,"abstract":"<div><ul><li><span>•</span><span><div>Vascular endothelial growth factor inhibitors: reduce nitric oxide and increase endothelin-1.</div></span></li><li><span>•</span><span><div>Bruton tyrosine kinase inhibitors: impair nitric oxide signaling and increase blood pressure.</div></span></li><li><span>•</span><span><div>BRAF and mitogen-activated activated protein kinase inhibitors: reduce vasodilation by inhibiting cyclic guanosine monophosphate.</div></span></li><li><span>•</span><span><div>Abiraterone and enzalutamide: cause hypertension through mineralocorticoid excess.</div></span></li><li><span>•</span><span><div>Home blood pressure monitoring: detects early, often asymptomatic, blood pressure rises.</div></span></li></ul></div><div><div>Cancer therapies have reshaped survival, but have also unmasked hypertension as a common and clinically significant complication with distinct underlying mechanisms. This review uniquely integrates mechanistic insights, particularly those related to vascular signaling pathway inhibition, alongside emerging pathways implicated in other molecularly targeted therapies, with practical therapeutic considerations specific to oncology populations. We examine how cancer biology and treatment-related factors converge to drive hypertension, with a primary focus on agents targeting vascular signaling, while also highlighting the prevalence and mechanisms associated with other targeted therapies. In the absence of dedicated guidelines, we critically appraise current management strategies and propose a framework for individualized care. By bridging pathophysiology with treatment approaches, this review identifies key knowledge gaps and underscores the need for multidisciplinary, oncology-specific hypertension management.</div></div><div>Cancer therapies have reshaped survival, but have also unmasked hypertension as a common and clinically significant complication with distinct underlying mechanisms. This review uniquely integrates mechanistic insights, particularly those related to vascular signaling pathway inhibition, alongside emerging pathways implicated in other molecularly targeted therapies, with practical therapeutic considerations specific to oncology populations. We examine how cancer biology and treatment-related factors converge to drive hypertension, with a primary focus on agents targeting vascular signaling, while also highlighting the prevalence and mechanisms associated with other targeted therapies. In the absence of dedicated guidelines, we critically appraise current management strategies and propose a framework for individualized care. By bridging pathophysiology with treatment approaches, this review identifies key knowledge gaps and underscores the need for multidisciplinary, oncology-specific hypertension management.</div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":"33 2","pages":"Pages 186-198"},"PeriodicalIF":3.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148392570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute Severe Hypertension in Children","authors":"Esraa Elsamny,&nbsp;Joyce P. Samuel","doi":"10.1053/j.akdh.2026.06.005","DOIUrl":"10.1053/j.akdh.2026.06.005","url":null,"abstract":"<div><div>Acute severe hypertension, historically referred to as hypertensive crisis, is an infrequent but important condition in children and adolescents. It is characterized by an abrupt and severe increase in blood pressure from baseline, which may be symptomatic and could produce life-threatening damage to target organs. The prevalence of this condition is difficult to quantify given largely outdated data with disparate diagnostic criteria. A wide range of causes can be implicated, which occur with varying frequency by age group. The diagnostic criteria are not well-defined due to a lack of progress in identifying outcome-based blood pressure thresholds and therapeutic targets. Future studies are needed to address these knowledge gaps and reduce the likelihood of long-term morbidity and mortality in children.</div></div><div>Acute severe hypertension, historically referred to as hypertensive crisis, is an infrequent but important condition in children and adolescents. It is characterized by an abrupt and severe increase in blood pressure from baseline, which may be symptomatic and could produce life-threatening damage to target organs. The prevalence of this condition is difficult to quantify given largely outdated data with disparate diagnostic criteria. A wide range of causes can be implicated, which occur with varying frequency by age group. The diagnostic criteria are not well-defined due to a lack of progress in identifying outcome-based blood pressure thresholds and therapeutic targets. Future studies are needed to address these knowledge gaps and reduce the likelihood of long-term morbidity and mortality in children.</div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":"33 2","pages":"Pages 178-185"},"PeriodicalIF":3.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148622745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypertension Board Review","authors":"Sam Kant,&nbsp;Jeffrey William","doi":"10.1053/j.akdh.2026.07.002","DOIUrl":"10.1053/j.akdh.2026.07.002","url":null,"abstract":"<div><div>This current issue of <em>Hypertension</em> introduces a new series on Board Review questions. After the success of the previous issues dedicated to Board Review,<span><span>¹</span></span>^,<span><span>²</span></span> the editors of <em>Advances in Kidney Disease and Health</em> are pleased to introduce this new series that will accompany many of the future issues. These series of articles are meant to reinforce established practice and bring forward new advances that are becoming mainstream in nephrology. These will not only provide Continuing Medical Education credits but also enhance our daily practice.</div></div><div>This current issue of <em>Hypertension</em> introduces a new series on Board Review questions. After the success of the previous issues dedicated to Board Review,<span><span>¹</span></span>^,<span><span>²</span></span> the editors of <em>Advances in Kidney Disease and Health</em> are pleased to introduce this new series that will accompany many of the future issues. These series of articles are meant to reinforce established practice and bring forward new advances that are becoming mainstream in nephrology. These will not only provide Continuing Medical Education credits but also enhance our daily practice.</div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":"33 2","pages":"Pages 199-203"},"PeriodicalIF":3.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148992677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"When the Bottle Lies: Advances in Detecting Medication Adherence in Hypertension","authors":"Januvi Jegatheswaran,&nbsp;Indranil Dasgupta","doi":"10.1053/j.akdh.2026.06.006","DOIUrl":"10.1053/j.akdh.2026.06.006","url":null,"abstract":"<div><div>Medication nonadherence is common among patients with chronic conditions including hypertension, contributing to increased cardiovascular risk and health care costs. Although indirect methods of assessing adherence are simple and inexpensive, they lack the accuracy of direct methods like direct observed therapy or chemical assays, which are more precise but less feasible, resource-intensive and costly for routine use. Identifying nonadherence is only the first step, effectively addressing it remains a significant challenge. This review explores current methods for detecting adherence in hypertension and outlines strategies to approach both intentional and unintentional nonadherence.</div></div><div>Medication nonadherence is common among patients with chronic conditions including hypertension, contributing to increased cardiovascular risk and health care costs. Although indirect methods of assessing adherence are simple and inexpensive, they lack the accuracy of direct methods like direct observed therapy or chemical assays, which are more precise but less feasible, resource-intensive and costly for routine use. Identifying nonadherence is only the first step, effectively addressing it remains a significant challenge. This review explores current methods for detecting adherence in hypertension and outlines strategies to approach both intentional and unintentional nonadherence.</div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":"33 2","pages":"Pages 129-134"},"PeriodicalIF":3.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148802259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic Testing in Nephrology: Policy, Health Economics, and Implications for Clinical Practice","authors":"Asheeta Gupta ,&nbsp;Gráinne Butler ,&nbsp;Catherine Quinlan","doi":"10.1053/j.akdh.2026.03.004","DOIUrl":"10.1053/j.akdh.2026.03.004","url":null,"abstract":"<div><div>This article explores the intersection of policy-informed study design and the cost-effectiveness of integrating genetic testing into nephrology, focusing on its potential to enhance diagnostic precision, optimize management strategies, and guide evidence-based policymaking. In Australia, early-stage CKD contributes an estimated AUD 1.6 billion annually to health care costs, highlighting the economic imperative for preventive and diagnostic strategies. Real-world and modeled cost analyses have clearly demonstrated that early genomic sequencing reduces health care expenditure and improves diagnostic yield, particularly in conditions such as glomerular diseases. Genomic testing not only accelerates accurate diagnoses and avoids invasive procedures but also informs treatment plans and reproductive decisions, delivering substantial long-term cost savings and improved patient outcomes. The article emphasizes the importance of tailoring study designs to address policy priorities and engaging stakeholders, including policymakers and patients, to advocate for equitable access to genomic testing. Implementation challenges, such as funding limitations and low genomic literacy, are addressed alongside enablers like embedding genetic counselors and upskilling clinicians. Practical recommendations include aligning evidence-based narratives with policymakers' personal drivers and leveraging patient stories to drive awareness and influence health policy for genetic testing. This article offers clinicians a practical framework to influence health policy, ensuring the transformative potential of genomic medicine is realized in nephrology.</div></div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":"33 1","pages":"Pages 118-126"},"PeriodicalIF":3.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148304273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ethical Perspectives in Renal Genetic Testing and Counseling","authors":"Heather Gardiner ,&nbsp;Dena Werner ,&nbsp;Jessica Barker ,&nbsp;Ilene L. Hollin ,&nbsp;Melody Slashinski ,&nbsp;Laura Siminoff ,&nbsp;Sarah Bauerle Bass ,&nbsp;Ryan Blunt ,&nbsp;Avrum Gillespie","doi":"10.1053/j.akdh.2026.03.005","DOIUrl":"10.1053/j.akdh.2026.03.005","url":null,"abstract":"<div><div>This report examines ethical considerations surrounding genetic testing in nephrology. More than 14% of the U.S. population lives with CKD, including approximately 800,000 individuals receiving treatment for end-stage kidney disease, and an estimated 20% of CKD cases have a genetic etiology. As genetic testing becomes integrated into routine care, careful evaluation of its risks and benefits is essential. Using the Georgetown principles—autonomy, beneficence, nonmaleficence, and justice—as a framework, we analyze contemporary ethical challenges in renal genetics. We emphasize the importance of shared decision-making, culturally and linguistically appropriate risk communication, and access to genetic counseling. Finally, we offer practical recommendations to strengthen ethical implementation and advance equitable integration of genomic medicine in nephrology.</div></div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":"33 1","pages":"Pages 110-117"},"PeriodicalIF":3.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148304144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autosomal Dominant Polycystic Kidney Disease: Genetic Insights, Phenotypic Spectrum, and Advances in Prognosis and Treatment","authors":"Ru Sin Lim,&nbsp;Becky Mingyao Ma,&nbsp;Kitty St Pierre,&nbsp;Erik Biros,&nbsp;Andrew J. Mallett","doi":"10.1053/j.akdh.2025.12.003","DOIUrl":"10.1053/j.akdh.2025.12.003","url":null,"abstract":"<div><div>Autosomal dominant polycystic kidney disease is a leading cause of inherited kidney failure, primarily due to pathogenic variants in <em>PKD1</em> (80%) and <em>PKD2</em> (15%), with rare contributions from genes like <em>GANAB</em> and <em>DNAJB11</em>. This review summarizes the understanding of autosomal dominant polycystic kidney disease's genetic and phenotypic diversity, emphasizing genotype–phenotype correlations that influence disease severity and progression. Truncating <em>PKD1</em> variants are linked to earlier kidney failure (median onset in the fifth to sixth decade) and a faster estimated glomerular filtration rate decline (−4.7 to −1.44 mL/min/1.73 m²/year) than nontruncating variants or <em>PKD2</em> variants. Atypical presentations, such as nonenlarged kidneys and absent family history, often relate to phenocopy genes or cases with no mutation detected, exhibiting milder phenotypes. Prognostic tools, such as the Mayo Imaging Classification and the Predicting Renal Outcomes in autosomal dominant polycystic kidney disease score, use height-adjusted total kidney volume in conjunction with clinical and genetic data to assess progression risk. Tolvaptan, the only disease-modifying therapy, slows total kidney volume growth and estimated glomerular filtration rate decline in rapidly progressing cases, although it may have adverse effects. Emerging therapies, like metformin and sodium-glucose co-transporter 2 inhibitors, are under investigation. This review highlights the importance of integrating genetic, imaging, and clinical data for personalized management of autosomal dominant polycystic kidney disease.</div></div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":"33 1","pages":"Pages 15-26"},"PeriodicalIF":3.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148304206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fabry Disease: Current Perspectives on Diagnosis and Management Strategies","authors":"Sayna Norouzi ,&nbsp;Zohreh Gholizadeh Ghozloujeh ,&nbsp;Edgar Lerma ,&nbsp;Michelle R. Hwang ,&nbsp;Anjay Rastogi","doi":"10.1053/j.akdh.2026.04.004","DOIUrl":"10.1053/j.akdh.2026.04.004","url":null,"abstract":"<div><div>Fabry disease is a rare, X-linked lysosomal storage disorder caused by deficient α-galactosidase A activity, leading to progressive accumulation of globotriaosylceramide in multiple tissues. Its estimated incidence ranges from 1 in 40,000 to 1 in 117,000 live births. Fabry disease manifests primarily as 2 phenotypes: classic (type 1), presenting in childhood with neuropathic pain, fatigue, thermal intolerance, and early multiorgan involvement; and late onset (type 2), typically manifesting in adulthood with predominant cardiac or renal complications. Timely diagnosis requires clinical suspicion combined with enzymatic assays and genetic testing; however, atypical presentations and variability in female patients often delay recognition, underscoring the necessity for heightened clinical vigilance. Current therapeutic approaches primarily focus on enzyme replacement therapy and pharmacologic chaperones, aimed at enhancing quality of life and delaying organ dysfunction. Optimal management necessitates an individualized, multidisciplinary strategy encompassing nephrology, cardiology, genetics, clinical pharmacy, and pain management. Emerging treatments, including next-generation enzyme replacement therapies, substrate reduction therapy, gene therapy, and mRNA-based therapeutics, offer promising avenues for more effective and durable outcomes. Ongoing clinical trials and comprehensive long-term outcome studies are crucial for refining these innovative therapeutic strategies and further advancing patient care.</div></div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":"33 1","pages":"Pages 92-102"},"PeriodicalIF":3.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148304305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}