Electrolyte and Blood Pressure最新文献

Unsupervised Clustering of Intradialytic Blood Pressure Patterns and Their Associations With Body Composition in Patients Undergoing Chronic Hemodialysis. 慢性血液透析患者的无监督聚类分析血压模式及其与身体成分的关系。

Electrolyte and Blood Pressure Pub Date : 2026-09-01 Epub Date: 2026-07-31 DOI: 10.5049/EBP.2026.24.e11

Hongtae Kim, Soie Kwon, Jin Ho Hwang, Jungho Shin

{"title":"Unsupervised Clustering of Intradialytic Blood Pressure Patterns and Their Associations With Body Composition in Patients Undergoing Chronic Hemodialysis.","authors":"Hongtae Kim, Soie Kwon, Jin Ho Hwang, Jungho Shin","doi":"10.5049/EBP.2026.24.e11","DOIUrl":"10.5049/EBP.2026.24.e11","url":null,"abstract":"Background: Intradialytic blood pressure (BP) abnormalities are common in patients undergoing chronic hemodialysis (HD), however, their relationship with body composition remains unclear. We investigated the association between intradialytic BP patterns and body composition using an unsupervised clustering approach.Methods: Adult outpatients receiving chronic HD who underwent segmental multifrequency bioelectrical impedance analysis were included. Systolic blood pressure (SBP) trajectories during HD were mapped to prespecified 30-minute time points from 0 to 240 minutes, and changes relative to predialysis SBP were clustered using k-means clustering. Body composition parameters were compared across BP clusters. Linear mixed-effects models with a random intercept for patient identifier were used to account for repeated HD sessions.Results: Among 928 HD sessions from 179 patients, three SBP patterns were identified: marked decreasing (16.8%), mild decreasing (46.2%), and rising (37.0%) patterns. Body mass index did not differ across clusters. However, fat-free mass index and skeletal muscle mass index increased from the marked decreasing to the mild decreasing and rising clusters, whereas percent body fat decreased. The extracellular water-to-total body water ratio was highest in the rising cluster, and visceral fat area showed a decreasing trend from the marked decreasing cluster to the rising cluster. These associations remained significant after adjustment. Similar findings were observed in sensitivity analyses.Conclusion: Unsupervised clustering identified reproducible intradialytic BP phenotypes that closely associated with volume status and body composition in patients undergoing chronic HD.","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"24 3","pages":"189-199"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620190/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149082072","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}

引用次数: 0

Dietary Salt Intake and Hypertension in Chronic Kidney Disease. 慢性肾病患者饮食盐摄入与高血压的关系。

Electrolyte and Blood Pressure Pub Date : 2026-09-01 Epub Date: 2026-07-31 DOI: 10.5049/EBP.2026.24.e10

Eunjin Bae

{"title":"Dietary Salt Intake and Hypertension in Chronic Kidney Disease.","authors":"Eunjin Bae","doi":"10.5049/EBP.2026.24.e10","DOIUrl":"10.5049/EBP.2026.24.e10","url":null,"abstract":"There is a high prevalence of hypertension, which is both a cause and consequence of kidney function decline, among patients with chronic kidney disease (CKD). Impaired sodium excretion and the activation of the renin-angiotensin-aldosterone system (RAAS) are central mechanisms underlying this relationship. In early CKD, compensatory increases in fractional sodium excretion help maintain the balance of sodium in the body; however, as kidney function deteriorates, this compensatory mechanism is overwhelmed, resulting in sodium retention, extracellular volume expansion, and predominantly volume-dependent hypertension. Furthermore, CKD is characterized by heightened salt sensitivity, owing to which blood pressure (BP) responds disproportionately to changes in dietary salt intake. Emerging evidence suggests that non-osmotic sodium storage in tissues, such as alterations in glycosaminoglycan networks, impaired lymphatic clearance, and endothelial glycocalyx dysfunction, further contributes to salt-sensitive hypertension. Together with RAAS activation, these mechanisms promote vascular dysfunction, BP variability, and adverse cardiovascular outcomes. Dietary salt intake is a key modifiable factor in the management of CKD and hypertension. Randomized controlled trials have shown that decreased salt intake lowers BP, reduces proteinuria, and enhances the efficacy of RAAS inhibitors, thereby slowing the progression of CKD and reducing cardiovascular risk. Conversely, increased salt intake is associated with resistant hypertension, increased BP variability, and higher mortality; therefore, current guidelines recommend limiting salt intake to 5 g/day. The role of dietary potassium is increasingly recognized; however, caution is required in patients with advanced CKD due to the risk of hyperkalemia.","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"24 3","pages":"158-165"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620185/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081349","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}

引用次数: 0

Overcorrection of Hyponatremia: A Complicated Story. 低钠血症矫治过度：一个复杂的故事。

Electrolyte and Blood Pressure Pub Date : 2026-09-01 Epub Date: 2026-08-07 DOI: 10.5049/EBP.2026.24.e12

Gheun-Ho Kim

{"title":"Overcorrection of Hyponatremia: A Complicated Story.","authors":"Gheun-Ho Kim","doi":"10.5049/EBP.2026.24.e12","DOIUrl":"10.5049/EBP.2026.24.e12","url":null,"abstract":"Overcorrection is a frequently encountered issue in the treatment of severe hyponatremia, which is defined as a serum sodium concentration below 120-125 mmol/L in symptomatic patients. Severe hyponatremic symptoms, including persistent vomiting, cardiorespiratory arrest, seizures, and reduced consciousness, clearly indicate the use of hypertonic (e.g., 3%) saline infusion to immediately elevate serum sodium levels. In the chronic phase, however, overcorrection is a major concern because an overly rapid increase in serum sodium concentration is an important cause of osmotic demyelination syndrome (ODS). Although risk groups for ODS are well known, saline infusion and water diuresis are 2 common factors underlying the overcorrection of hyponatremia. We propose that isotonic saline initially be infused (1 mL/kg/h) when encountering hyponatremic patients with moderately severe symptoms, such as confusion, headache, or nausea. Although this empirical therapy may not be consistent with current guidelines, it may reduce the risk of overcorrection and be effective in cases with unrecognized hypovolemia or waning vasopressin hyperactivity. We believe that hypertonic saline should be reserved for patients with severely symptomatic hyponatremia. In practice, urine sodium and osmolality should then be measured, along with follow-up serum sodium levels. Subsequent intravenous fluids can be selected according to the response of serum sodium levels and the differential diagnosis of hyponatremia. Because water diuresis is a critical contributor to overcorrection, urine output and urine sodium, potassium, and osmolality should be monitored during fluid therapy. Appropriate use of 5% dextrose in water and/or desmopressin may be necessary to re-lower serum sodium levels.","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"24 3","pages":"166-174"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620182/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149082105","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}

引用次数: 0

Impact of the Four Pillars on Electrolyte Derangements during State-of-the-Art Therapy for Diabetic Kidney Disease. 在最新的糖尿病肾病治疗中，四大支柱对电解质紊乱的影响

Electrolyte and Blood Pressure Pub Date : 2026-09-01 Epub Date: 2026-08-07 DOI: 10.5049/EBP.2026.24.e13

Mie Jung Yoo, Shina Lee

{"title":"Impact of the Four Pillars on Electrolyte Derangements during State-of-the-Art Therapy for Diabetic Kidney Disease.","authors":"Mie Jung Yoo, Shina Lee","doi":"10.5049/EBP.2026.24.e13","DOIUrl":"10.5049/EBP.2026.24.e13","url":null,"abstract":"The pharmacological management of diabetic kidney disease (DKD) has shifted toward a \"four-pillar\" approach that offers robust cardiorenal protection. While traditional renin-angiotensin system (RAS) inhibitors carry well-documented electrolyte risks, the distinct electrolyte profiles of novel therapies-sodium-glucose cotransporter-2 (SGLT2) inhibitors, glucagon-like peptide-1 receptor agonists (GLP-1 RAs), and non-steroidal mineralocorticoid receptor antagonists (nsMRAs)-warrant a comprehensive understanding. This review examines these drug-induced electrolyte derangements. SGLT2 inhibitors demonstrate a highly favorable safety profile; despite inducing osmotic diuresis, they are notably associated with a reduced risk of hyperkalemia. Similarly, GLP-1 RAs possess an exceptionally low risk of direct renal electrolyte wasting, with imbalances occurring primarily secondary to severe gastrointestinal intolerance. Conversely, nsMRAs, such as finerenone, introduce a mild risk of hyperkalemia, though their unique receptor selectivity significantly diminishes this risk compared to traditional steroidal mineralocorticoid receptor antagonists. Crucially, combining SGLT2 inhibitors and nsMRAs creates a physiological synergy that attenuates hyperkalemic adverse effects while maximizing antiproteinuric benefits. By integrating these complementary mechanisms alongside routine electrolyte monitoring, clinicians can safely sustain these indispensable combination therapies and optimize clinical outcomes in DKD.","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"24 3","pages":"175-188"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149082077","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}

引用次数: 0

From Specialty Silos to Integrated Care: A Korean Initiative for Cardiovascular-Kidney-Metabolic Health. 从专业孤岛到综合护理：韩国心血管-肾脏-代谢健康倡议。

Electrolyte and Blood Pressure Pub Date : 2026-09-01 Epub Date: 2026-09-03 DOI: 10.5049/EBP.2026.24.e16

Sungjin Chung, Jihyun Yang, Jungho Shin, Tae Hyun Ban, Hyung Duk Kim, Yeoree Yang, Sangmo Hong, Eun Joo Cho

引用次数: 0

Long-Standing Hypokalemia and Hypomagnesemia in a 61 Year-Old Woman: A Delayed Diagnosis of Gitelman Syndrome. 长期低钾血症和低镁血症在61岁妇女：延迟诊断吉特曼综合征。

Electrolyte and Blood Pressure Pub Date : 2026-09-01 Epub Date: 2026-08-13 DOI: 10.5049/EBP.2026.24.e14

Shin Young Lee, Sang-Woong Han, Jiwon Lee, Mi-Yeon Yu

{"title":"Long-Standing Hypokalemia and Hypomagnesemia in a 61 Year-Old Woman: A Delayed Diagnosis of Gitelman Syndrome.","authors":"Shin Young Lee, Sang-Woong Han, Jiwon Lee, Mi-Yeon Yu","doi":"10.5049/EBP.2026.24.e14","DOIUrl":"10.5049/EBP.2026.24.e14","url":null,"abstract":"Background: Gitelman syndrome (GS) is an autosomal recessive renal tubular disorder characterized by a distinct biochemical profile, including hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria. Due to its often mild or nonspecific clinical presentation, GS is frequently misdiagnosed as idiopathic hypokalemia, leading to prolonged symptomatic treatment without a definitive etiologic diagnosis.Case presentation: We report the case of a 61-year-old female with a one-year history of unexplained, refractory hypokalemia and hypomagnesemia. The diagnosis had been delayed as clinical efforts were primarily focused on escalating electrolyte supplementation. Systematic evaluation of renal electrolyte handling revealed inappropriate urinary potassium and magnesium wasting in conjunction with marked hypocalciuria. In addition, a symptom-oriented family history, documenting chronic fatigue and muscle cramps in her sibling, served as a critical diagnostic clue. Genetic testing confirmed the diagnosis by identifying compound heterozygous variants in the SLC12A3 gene. Following diagnosis, the patient was enrolled in the Korean National Medical Expense Support Program for rare diseases, ensuring structured long-term management.Conclusions: This case underscores the importance of an etiologic approach over a purely treatment-focused one in patients with recurrent electrolyte imbalances. GS may be more prevalent than currently recognized, particularly among adults receiving empirical therapy for hypokalemia. Early clinical suspicion, grounded in urinary electrolyte indices and careful family history, is essential for timely diagnosis.","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"24 3","pages":"200-204"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620180/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149082046","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}

引用次数: 0

Monogenic Kidney Disorders as Hidden Drivers of Electrolyte Imbalance and Hypertension. 单基因肾病是电解质失衡和高血压的潜在驱动因素。

Electrolyte and Blood Pressure Pub Date : 2026-09-01 Epub Date: 2026-08-31 DOI: 10.5049/EBP.2026.24.e15

Yo Han Ahn

{"title":"Monogenic Kidney Disorders as Hidden Drivers of Electrolyte Imbalance and Hypertension.","authors":"Yo Han Ahn","doi":"10.5049/EBP.2026.24.e15","DOIUrl":"10.5049/EBP.2026.24.e15","url":null,"abstract":"Hypertension is the leading modifiable risk factor for cardiovascular disease, stroke, and chronic kidney disease worldwide. Although most cases are essential hypertension, a subset of patients harbors monogenic disorders that disrupt how the kidneys control electrolyte balance and blood pressure regulation. These rare conditions provide important insights into the fundamental physiological mechanisms that link tubular sodium transport, extracellular volume homeostasis, and systemic hemodynamics. The distal nephron is crucial in fine-tuning sodium and potassium balance through tightly regulated transport systems, such as the sodium-chloride cotransporter (NCC) in the distal convoluted tubule and the epithelial sodium channel (ENaC) in the collecting duct. Genetic perturbations of these pathways can markedly disrupt electrolyte balance and blood pressure. Monogenic hypertensive disorders exemplify these mechanisms. Liddle syndrome results from gain-of-function mutations in ENaC subunits, resulting in sodium retention, hypokalemia, and suppressed renin-aldosterone levels. Conversely, Gordon syndrome (pseudohypoaldosteronism type II) is caused by the dysregulation of the with-no-lysine (K) kinase-SPS1-related proline/alanine-rich kinase signaling pathway, resulting in NCC overactivation and the paradoxical concurrence of hypertension and hyperkalemia. Apparent mineralocorticoid excess results from deficiency of 11β-hydroxysteroid dehydrogenase type 2, resulting in the inappropriate activation of the mineralocorticoid receptor by cortisol and subsequent sodium retention. Together, these disorders illustrate how discrete defects in distal nephron transport pathways induce characteristic electrolyte signatures while converging on the shared phenotype of hypertension. Understanding these genetic mechanisms may provide insight into fundamental renal physiology and facilitate the use of precision diagnostic and therapeutic approaches for patients with atypical or treatment-resistant hypertension.","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"24 3","pages":"147-157"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620189/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149082129","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}

引用次数: 0

The Role of Extracellular Vesicles in the Pathogenesis of Hypertension. 细胞外囊泡在高血压发病中的作用。

Electrolyte and Blood Pressure Pub Date : 2026-06-01 Epub Date: 2026-06-08 DOI: 10.5049/EBP.2026.24.e8

Seung Hee Jeong, In O Sun

{"title":"The Role of Extracellular Vesicles in the Pathogenesis of Hypertension.","authors":"Seung Hee Jeong, In O Sun","doi":"10.5049/EBP.2026.24.e8","DOIUrl":"10.5049/EBP.2026.24.e8","url":null,"abstract":"Hypertension is one of the most common health problems and a leading global risk factor for cardiovascular, cerebrovascular, and renal diseases. The pathogenesis of essential hypertension is complex, and many organs, such as the heart, kidneys, arteries, and immune system, are involved in its pathophysiology. Extracellular vesicles (EVs) are membrane-bound nanosized structures that are generated and released into the extracellular fluid by all cell types. They mediate cell-to-cell communication in various physiological and pathophysiological processes. Therefore, EVs may play pivotal roles in the pathogenesis and systemic progression of diverse pathological conditions, including inflammatory, vascular, neoplastic, infectious, and neurodegenerative disorders. Emerging evidence has underscored their involvement in the development and progression of hypertension. Circulating and urinary EVs are promising diagnostic, prognostic, and therapeutic biomarkers of cardiovascular diseases, including hypertension. Moreover, EV-mediated therapies, particularly engineered EVs designed for precise drug delivery, are currently being developed for the treatment of various cardiovascular disorders, including hypertension and myocardial infarction. This review explores the role of EVs in the pathogenesis of hypertension and summarizes their potential as diagnostic and prognostic biomarkers.","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"24 2","pages":"120-128"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13338640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148406091","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}

引用次数: 0

From Ion Channels to Blood Pressure: Genetic Disorders of Renal Tubular Transport. 从离子通道到血压：肾小管运输的遗传性疾病。

Electrolyte and Blood Pressure Pub Date : 2026-06-01 Epub Date: 2026-06-02 DOI: 10.5049/EBP.2026.24.e5

Hayne Cho Park

{"title":"From Ion Channels to Blood Pressure: Genetic Disorders of Renal Tubular Transport.","authors":"Hayne Cho Park","doi":"10.5049/EBP.2026.24.e5","DOIUrl":"10.5049/EBP.2026.24.e5","url":null,"abstract":"Blood pressure regulation is fundamentally dependent on renal sodium and electrolyte handling. Genetic disorders of renal tubular transport provide representative evidences that illuminate the molecular mechanisms linking ion channels to systemic hemodynamics. Monogenic conditions such as Bartter syndrome, Gitelman syndrome, Liddle syndrome, and Gordon syndrome demonstrate how specific alterations in tubular sodium, potassium, chloride, and magnesium transport translate into distinct blood pressure phenotypes. Salt-wasting disorders are characterized by hypokalemic metabolic alkalosis and low or normal blood pressure despite activation of the renin-angiotensin-aldosterone system, underscoring the dominant role of tubular sodium loss. In contrast, gain-of-function mutations enhancing distal sodium reabsorption produce volume expansion, suppressed renin levels, and hypertension, often accompanied by characteristic electrolyte abnormalities. These conditions highlight the tight coupling between sodium and potassium handling and reveal how small perturbations in distal nephron transport can exert disproportionate effects on blood pressure. Insights from these rare genetic syndromes extend beyond monogenic disease. Variants in genes regulating Na+-Cl- cotransporter, epithelial sodium channel, and with-no-lysine signaling pathways contribute to salt sensitivity and low-renin hypertension in the general population. Understanding tubular channelopathies thus provides a mechanistic framework for precision diagnosis and targeted therapy in hypertension. The current review examines how renal ion channel dysfunction translates from molecular defects to systemic blood pressure regulation.","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"24 2","pages":"85-94"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13338639/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148406079","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}

引用次数: 0

Glomerulo-Tubular Crosstalk in Diabetic Kidney Disease: From Pathophysiology to Novel Therapeutics. 糖尿病肾病的肾小球-小管串扰：从病理生理学到新疗法。

Electrolyte and Blood Pressure Pub Date : 2026-06-01 Epub Date: 2026-06-02 DOI: 10.5049/EBP.2026.24.e7

Il Young Kim

{"title":"Glomerulo-Tubular Crosstalk in Diabetic Kidney Disease: From Pathophysiology to Novel Therapeutics.","authors":"Il Young Kim","doi":"10.5049/EBP.2026.24.e7","DOIUrl":"10.5049/EBP.2026.24.e7","url":null,"abstract":"Diabetic kidney disease (DKD) remains the leading cause of chronic kidney disease and kidney failure worldwide despite advances in glycemic and blood pressure control. Although DKD has traditionally been viewed as a primarily glomerular disorder, growing evidence suggests that its progression is shaped by complex communication between the glomerulus and the tubulointerstitium. Under diabetic conditions characterized by persistent hyperglycemia, oxidative stress, and metabolic imbalance, signaling networks among glomerular endothelial cells, podocytes, and mesangial cells become disrupted. Glomerular injury may generate downstream signals, including proteinuria and loss of protective mediators, that impose inflammatory and metabolic stress on proximal tubular epithelial cells and may activate profibrotic pathways. Conversely, injured tubular cells release cytokines, chemokines, and extracellular vesicles that may influence glomerular cells and further contribute to structural damage. In addition, metabolic disturbances within tubular cells, such as lipid accumulation, mitochondrial dysfunction, and cellular stress responses, may promote tubulointerstitial fibrosis. Viewing DKD as a disorder of disrupted glomerulo-tubular communication provides an integrated framework linking pathophysiological mechanisms with emerging therapeutic strategies aimed at slowing disease progression.","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"24 2","pages":"106-119"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13338642/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148406160","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}

引用次数: 0