{"title":"Nephrogenic Diabetes Insipidus Presenting with Hypokalemic Paralysis in an Adolescent with Primary Sjögren's Syndrome: A Case Report.","authors":"Qiaofang Ke, Xinguang Ma, Zhiyong Xu, Gaoyan Dai, Feifei Li, Tenghui Wu, Yingqian Li, Hui Wu","doi":"10.1159/000552590","DOIUrl":"10.1159/000552590","url":null,"abstract":"<p><strong>Introduction: </strong>Diabetes insipidus is a rare disorder characterized by polyuria, polydipsia, and dilute urine. Nephrogenic diabetes insipidus (NDI) secondary to distal renal tubular acidosis (dRTA) in primary Sjögren's syndrome (pSS) is exceedingly rare in children.</p><p><strong>Case presentation: </strong>A 16-year-old girl presented with hypokalemic paralysis (potassium 1.89 mmol/L), polyuria (>5 L/day), and growth retardation (height 141 cm, <3rd percentile). Laboratory studies revealed dRTA with secondary NDI. Autoimmune workup confirmed pSS. A systematic literature review identified only 5 similar pediatric cases. Initial management with hydrochlorothiazide exacerbated hypokalemia and precipitated hypochloremic metabolic alkalosis. Switching to amiloride combined with glucocorticoids and potassium supplementation normalized electrolytes, reduced urine output to 1.5 L/day, and resulted in catch-up growth at the 6-month follow-up.</p><p><strong>Conclusion: </strong>This case highlights the pathophysiologic cascade of pSS-related dRTA causing secondary NDI and underscores the importance of early recognition and tailored diuretic selection in adolescents.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"790-797"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13585412/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669164","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}
María G Zavala-Cerna, Alma L Guzmán-Gurrola, Gabriela Asencio-Del Real, José A Novoa-Burquez, Julio A Díaz-Ramos, Gerardo Oliva-Armas, David Leal-Mora, Evelyn Yared Villanueva-Muñoz, Andrea Alejandra Sánchez-Soto, Urima Alejandra Castañeda-Lara, Aranza Gabriela Montoya-González, Jonathan S Chávez-Iñiguez
{"title":"Nutritional Status as Predictor for Mortality in Older Adults with Acute Kidney Injury.","authors":"María G Zavala-Cerna, Alma L Guzmán-Gurrola, Gabriela Asencio-Del Real, José A Novoa-Burquez, Julio A Díaz-Ramos, Gerardo Oliva-Armas, David Leal-Mora, Evelyn Yared Villanueva-Muñoz, Andrea Alejandra Sánchez-Soto, Urima Alejandra Castañeda-Lara, Aranza Gabriela Montoya-González, Jonathan S Chávez-Iñiguez","doi":"10.1159/000552588","DOIUrl":"10.1159/000552588","url":null,"abstract":"<p><strong>Introduction: </strong>Older adults (OAs) exhibit the highest incidence of acute kidney injury (AKI), with outcomes influenced by comorbidities, frailty, and malnutrition. Nutritional status, a potentially modifiable factor, has not been extensively evaluated as a mortality predictor in hospitalized OA with AKI. Our purpose was to report on the mortality risk provided by the nutritional status, comorbidities, and biochemical parameters in OA with AKI.</p><p><strong>Methods: </strong>In this prospective cohort study (July 2024-July 2025) conducted at a tertiary geriatric unit, hospitalized OA with AKI, diagnosed according to KDIGO criteria, underwent a comprehensive nutritional assessment within 48 h of admission. The Geriatric Nutritional Risk Index (GNRI), Mini Nutritional Assessment, anthropometric measurements, and biochemical markers were recorded. The primary outcome was in-hospital all-cause mortality; secondary outcomes included the analysis of all-cause mortality according to nutritional and clinical factors, such as dysphagia, hyporexia, and GNRI quartiles (Q1-Q4). Logistic regression models were used to identify independent predictors of mortality, and all models were adjusted for AKI severity.</p><p><strong>Results: </strong>Of 742 admissions, 187 patients met the inclusion criteria. The median age was 76.8 years, and 50% were male. GNRI quartile analysis demonstrated a progressive deterioration in anthropometric and biochemical markers from Q4 to Q1. Mortality was higher in the high-risk GNRI group (42.2% vs. 30.1%); however, this difference did not reach statistical significance (p = 0.098). In adjusted analyses, dysphagia (adjusted odds ratio [aOR] 6.11; 95% CI: 1.82-20.51; p = 0.003), hyporexia (aOR 2.24; 95% CI: 1.02-4.92; p = 0.044), and lower GNRI (aOR 1.07 per unit decrease; 95% CI: 1.02-1.13; p = 0.004) were independently associated with increased mortality. In contrast, a higher mid-upper arm circumference was independently associated with a protective effect (aOR 0.78; 95% CI: 0.67-0.91; p = 0.001).</p><p><strong>Conclusions: </strong>In OA hospitalized with AKI, poor nutritional status, particularly dysphagia, hyporexia, and lower GNRI, was independently associated with increased in-hospital mortality, whereas preserved muscle mass was protective. Early, simple, bedside nutritional assessments may help guide targeted interventions to improve outcomes in this high-risk population.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"813-826"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13608887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148764731","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":"Association of the C-Reactive Protein-Albumin-Lymphocyte Index with Chronic Kidney Disease: A Comprehensive Assessment Based on Inflammation, Nutrition, and Immune Status.","authors":"Xiujun Zhang, Fan Zhang, Wenjian Li","doi":"10.1159/000551082","DOIUrl":"10.1159/000551082","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to examine the relationship between the C-reactive protein-albumin-lymphocyte (CALLY) index, a composite measure of inflammation, nutritional status, and immune function, and chronic kidney disease (CKD).</p><p><strong>Methods: </strong>The study employed a population-based cohort retrospective analysis design, integrating the NHANES dataset (n = 24,538) and the clinical cohort of China (n = 7,102). The present study sought to assess the association and predictive efficacy of the CALLY index for CKD. To this end, multistage logistic regression modeling, receiver operating characteristic (ROC) analysis, and restricted cubic spline analysis were employed. The analysis controlled for demographic factors, lifestyle, and metabolic diseases.</p><p><strong>Results: </strong>The study indicated a negative correlation between the CALLY index and CKD, with a 1% reduction (odds ratio [OR] = 0.99, 95% confidence interval [CI] = 0.99-0.99) and a 3% reduction (OR = 0.97, 95% CI = 0.96-0.98) in CKD risk for every 1-unit increase in the index, respectively, in the US and Chinese cohorts. The ROC analyses yielded a multifactorial-adjusted AUC for the US cohort of 0.803 (95% CI: 0.795-0.810), and the Chinese cohort was 0.676 (95% CI: 0.657-0.695). Threshold effect analyses demonstrated that the risk significantly reduced when CALLY<2.313 (OR = 0.77 for the US cohort and OR = 0.63 for the Chinese cohort), and the association disappeared above the threshold. Subgroup analyses indicated that hypertension and obesity status modified the predictive efficacy of the CALLY index.</p><p><strong>Conclusion: </strong>The CALLY index demonstrates a negative correlation with CKD. Its cross-cohort robustness and threshold effect provide a foundation for implementing early screening and stratified intervention strategies. However, the index's clinical translational value remains to be validated in future studies.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"225-242"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13134843/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147344583","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":"Urinary Sclerostin and Renal Magnesium Handling in Proteinuric Nondiabetic Chronic Kidney Disease.","authors":"Ching-Fang Wu, Te-Hui Kuo, An-Bang Wu, Wei-Hung Lin, Jo-Yen Chao, Shih-Yuan Hung, Chin-Chung Tseng, Hung-Hsiang Liou, Ming-Cheng Wang","doi":"10.1159/kbr/adjag003","DOIUrl":"10.1159/kbr/adjag003","url":null,"abstract":"<p><strong>Introduction: </strong>Sclerostin is involved in chronic kidney disease-mineral and bone disorder (CKD-MBD), but its relation to renal magnesium handling remains unclear. We investigated whether urinary and serum sclerostin were associated with fractional excretion of magnesium (FeMg) in proteinuric nondiabetic chronic kidney disease (CKD).</p><p><strong>Methods: </strong>In this cross-sectional study, 70 adults with proteinuric nondiabetic CKD stages 1-5 at a tertiary medical center were enrolled. Urinary sclerostin normalized to urine creatinine (Uscl/Ucre) and serum sclerostin were measured. Their associations with ln-transformed FeMg [ln(FeMg)] were examined using multivariable linear regression with sequential adjustment for age, sex, estimated glomerular filtration rate (eGFR), proteinuria, electrolytes, serum sclerostin, and CKD-MBD markers including plasma intact parathyroid hormone, serum fibroblast growth factor 23, and soluble alpha-Klotho.</p><p><strong>Results: </strong>Urinary sclerostin (Uscl/Ucre) increased across CKD stages, and higher Uscl/Ucre tertiles were associated with higher FeMg. Uscl/Ucre was positively associated with ln(FeMg) in crude analysis (β 0.652; p < 0.001), and this association still existed after adjustment for age, sex, eGFR, serum magnesium, and CKD-MBD markers (β 0.366; p < 0.001). Compared with the lowest tertile, the highest urinary sclerostin tertile was significantly associated with higher ln(FeMg) (β 0.662; p = 0.007). In contrast, serum sclerostin was not associated with ln(FeMg) after adjustment.</p><p><strong>Conclusion: </strong>In proteinuric nondiabetic CKD, urinary but not serum sclerostin is independently associated with fractional excretion of magnesium. Urinary sclerostin may reflect intrarenal processes relevant to tubular magnesium handling.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"953-962"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13688352/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148906607","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}
Alessandro Domenico Quercia, Beatrice Cavigiolo, Chiara Mele
{"title":"Chronic Kidney Disease, Sarcopenia, and Hormonal-Metabolic Alterations: An Intriguing Association.","authors":"Alessandro Domenico Quercia, Beatrice Cavigiolo, Chiara Mele","doi":"10.1159/000551499","DOIUrl":"10.1159/000551499","url":null,"abstract":"<p><strong>Background: </strong>Sarcopenia is a common yet underrecognized complication of chronic kidney disease (CKD), often affecting younger patients and progressing more rapidly than age-related muscle loss. It is driven by a combination of metabolic, hormonal, and inflammatory abnormalities associated with declining renal function.</p><p><strong>Summary: </strong>This review outlines the key mechanisms linking CKD to sarcopenia, including metabolic acidosis, uremic toxin accumulation, hormonal dysregulation, insulin resistance, and chronic inflammation. These factors impair muscle protein turnover and promote protein-energy wasting. The review also discusses diagnostic limitations and emerging therapeutic strategies, such as individualized nutrition, resistance training, and gut microbiota modulation.</p><p><strong>Key messages: </strong>Sarcopenia in CKD contributes to increased morbidity and mortality. Early identification and personalized, multidisciplinary interventions are essential to preserve muscle health and improve patient outcomes.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"312-325"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13221173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147474428","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}
Martina Cacciapuoti, Ilaria Caputo, Giulia Driussi, Paul A Davis, Federico Nalesso, Lorenzo A Calò
{"title":"Higher Expression of miR-155 and miR-103 in Patients with Gitelman Syndrome: Potential Implications for Angiotensin II-Induced Cardiovascular Remodeling in Hypertension.","authors":"Martina Cacciapuoti, Ilaria Caputo, Giulia Driussi, Paul A Davis, Federico Nalesso, Lorenzo A Calò","doi":"10.1159/000552985","DOIUrl":"10.1159/000552985","url":null,"abstract":"<p><strong>Introduction: </strong>miR-155 and miR-103 are multifunctional miRNAs known to be involved in angiotensin II (Ang II) signaling linked with hypertension and cardiovascular remodeling, although their role is controversial and not completely clarified. Gitelman syndrome (GS), rare genetic tubulopathy, represents a human model of an endogenous Ang II signaling antagonism and GS patients are in fact protected from Ang II-mediated cardiovascular remodeling. This study aimed to compare the expression of miR-155 and miR-103 in patients with GS vs. healthy controls.</p><p><strong>Methods: </strong>Sixteen patients with GS and 21 age- and sex-matched healthy controls were recruited from an active cohort at the Nephrology Unit of Padua University Hospital and among volunteers, respectively. The specific miRNA population was isolated from plasma, and miR-155 and miR-103 were then quantified using droplet PCR and TaqMan miRNA assays and compared using the Mann-Whitney U test.</p><p><strong>Results: </strong>In GS patients, expression of miR-155 (528.7 vs. 64.40 copies/sample, p = 0.0015) and miR-103 (80.25 vs. 23.94 copies/sample, p = 0.0034) were significantly higher compared to the control group.</p><p><strong>Conclusion: </strong>This is the first study investigating circulating miRNAs in GS patients. The difference in expression levels of miR-155 and miR-103 in these patients compared to healthy subjects suggests that these miRNAs may be associated with mechanisms contributing to their well-established protection from Ang II-mediated cardiovascular remodeling.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"606-613"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13427314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148218278","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}
Luka Varda, Nino Vreča, Robert Ekart, Sebastjan Bevc, Nejc Piko
{"title":"Diabetic Kidney Disease: From Pathophysiology to Treatment Perspectives.","authors":"Luka Varda, Nino Vreča, Robert Ekart, Sebastjan Bevc, Nejc Piko","doi":"10.1159/000550085","DOIUrl":"10.1159/000550085","url":null,"abstract":"<p><strong>Background: </strong>Chronic kidney disease (CKD) presents an extensive healthcare burden globally. Diabetes mellitus (DM) is the most prevalent cause of CKD and end-stage kidney disease, requiring renal replacement therapy. Type II DM remains the most prevalent subtype, as it is closely related to metabolic syndrome, whose prevalence is also rising with a sedentary lifestyle and with consumption of energy-dense, highly processed foods, including excess sodium, high-fat dairy products, added sugars, saturated fats, and processed meats. Therefore, understanding the pathophysiology of diabetic kidney disease (DKD), its early recognition and early initiation of the currently available therapy remains an important measure to slow the progression of the disease.</p><p><strong>Summary: </strong>Pathophysiology of DKD is a complex process, where all the mechanisms are still being elucidated on preclinical animal and in vitro models as well as in clinical studies. Changes in glomerular hemodynamics, glomerular and tubular hypertrophy, hyperfiltration, overactivation of the renin-angiotensin-aldosterone system, podocyte injury, inflammation, oxidative stress, renal hypoxia, mitochondrial injury, and epigenetic changes are the main mechanisms leading to albuminuria, glomerulosclerosis, and fibrosis. In the latter years, the importance of gut microbiota in DKD has also been shown. Understanding the mechanisms behind DKD is important, especially for researching current and possibly future pharmacological treatment of DKD. While angiotensin convertase enzyme inhibitors and angiotensin receptor blockers alongside nonpharmacological measures have been the pillars of DKD treatment and reduction of albuminuria for many decades, novel pharmacological agents are emerging, starting with sodium-glucose transporter 2 (SGLT2) inhibitors, which have been proven to affect many of the pathophysiological mechanisms, continuing with novel non-steroidal mineralocorticoid receptor antagonists, which are a new anti-inflammatory and antifibrotic possibility, and finishing with glucagon-like peptide 1 receptor antagonists (GLP1RAs), which have recently joined the therapeutic options for DKD.</p><p><strong>Key messages: </strong>This comprehensive review focuses on the main pathophysiological mechanisms of DKD and current available pharmacological and non-pharmacological possibilities.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"107-127"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12962719/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146113533","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}
Stefan Erfurt, Johanna Gruzla, Karsten-Henrich Weylandt, Oliver Ritter, Meike Hoffmeister, Daniel Patschan
{"title":"Lipids and Lipid Metabolites in the Diagnosis, Risk Prediction and Treatment of Chronic Kidney Disease and Acute Kidney Injury: A Narrative Review.","authors":"Stefan Erfurt, Johanna Gruzla, Karsten-Henrich Weylandt, Oliver Ritter, Meike Hoffmeister, Daniel Patschan","doi":"10.1159/000552568","DOIUrl":"10.1159/000552568","url":null,"abstract":"<p><strong>Background: </strong>Acute kidney injury (AKI) and chronic kidney disease (CKD) represent the principal nephrological conditions encountered globally. Despite the diverse etiologies and pathogeneses associated with these disorders, both are characterized by disruptions in lipid metabolism, largely due to the frequent involvement of inflammatory mechanisms in the onset and progression of acute and chronic renal dysfunction. This review will examine two key areas: the diagnostic and prognostic relevance of lipids and their metabolites, particularly fatty acids (FAs), in AKI and CKD; and the potential therapeutic application or external modulation of lipid components in the management of these diseases. The following databases were utilized for reference identification: PubMed, Web of Science, Cochrane Library, and Scopus. The search period spanned from 2010 to 2025. The search terms employed in various combinations included \"CKD,\" \"AKI,\" \"CRP,\" \"inflammation,\" \"serum fatty acids,\" \"lipids,\" \"lipid profile.\"</p><p><strong>Summary: </strong>A total of 28 studies were selected for further analysis. Twelve studies focused on diagnostics and prognostics in CKD, while nine addressed treatment strategies for CKD. The number of studies performed in AKI 5 (diagnostics/prognostics) and 2 (therapy). In CKD, free FAs may help predict three clinical outcomes: mortality, progression of CKD, and cardiovascular risk. However, therapy-related references remain inconsistent, anti-proteinuric effects of omega-3 FAs have been reported sporadically. The current data on lipids in AKI diagnostics, prognostics, and therapy are still too limited to draw any definitive conclusions.</p><p><strong>Key messages: </strong>Free FAs enable the prediction of significant outcomes associated with CKD. Omega-3 FAs may exhibit anti-proteinuric properties. Evidence regarding FA-based diagnostics and therapies in acute kidney injury remain limited.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"567-588"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13423319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148005658","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}
XiaoWen Ha, XiYuan Gao, Wei Teng, JiaLi Zhang, Zuolamu Maimaiti, Dilina Yalikun, ShuFen Yang, Lu Bai, Takexi Caoke, Hong Jiang
{"title":"Pharmacogenomics-Guided Precision Therapy for Chronic Kidney Disease with Resistant Hypertension: A Prospective Cohort Study.","authors":"XiaoWen Ha, XiYuan Gao, Wei Teng, JiaLi Zhang, Zuolamu Maimaiti, Dilina Yalikun, ShuFen Yang, Lu Bai, Takexi Caoke, Hong Jiang","doi":"10.1159/000549936","DOIUrl":"10.1159/000549936","url":null,"abstract":"<p><strong>Introduction: </strong>Managing blood pressure in patients with chronic kidney disease (CKD) complicated by resistant hypertension (RH) remains a major clinical challenge. The clinical utility of pharmacogenomics (PGx) in this high-risk population has not been well established. This study aimed to evaluate the effectiveness of PGx-guided precision therapy on blood pressure control, medication optimization, and treatment safety in CKD patients with RH.</p><p><strong>Methods: </strong>A single-center prospective cohort study was conducted using the Yidu Cloud big data platform at People's Hospital of Xinjiang Uygur Autonomous Region. Sixty-five patients with CKD and RH were enrolled and randomized into either an empirical treatment group (Empirical group, n = 22) or a PGx-guided group (PGx group, n = 43). Patients in the PGx group received individualized therapy based on genetic testing covering 21 antihypertensive drugs, whereas the Empirical group received conventional empirical treatment. The primary endpoint was the rate of achieving target blood pressure (systolic BP <140 mm Hg, diastolic BP <90 mm Hg) at 24 months. Secondary endpoints included medication optimization, incidence of adverse events, and changes in kidney function.</p><p><strong>Results: </strong>The PGx group demonstrated earlier and greater improvement in blood pressure control compared with the Empirical group. At 0.5 months, the proportion of patients achieving systolic BP targets was significantly higher in the PGx group (20.93% vs. 0%, p = 0.021). By 3 months, the diastolic BP target achievement rate had markedly increased (72.09% vs. 27.27%, p = 0.001) and was sustained through 24 months (systolic BP target rate 44.18% vs. 13.63%, p = 0.014). Medication optimization analysis showed a 46.5% reduction in the proportion of patients requiring four to 5 antihypertensive agents in the PGx group, compared with 31.8% in the Empirical group, alongside a 41% lower risk of adverse events (34.88% vs. 59.09%, p = 0.016). Genotyping revealed high responsiveness to angiotensin II receptor blockers (candesartan 86.05%, telmisartan 79.07%, irbesartan 76.74%) and calcium channel blockers (amlodipine, nitrendipine, and felodipine all 81.40%), whereas angiotensin-converting enzyme inhibitors showed generally poor efficacy. Moreover, the decline in estimated glomerular filtration rate at 24 months was significantly less pronounced in the PGx group compared with the Empirical group (8.82% vs. 30.00%, p < 0.001), indicating a potential renal-protective effect.</p><p><strong>Conclusion: </strong>PGx-guided precision therapy enables more rapid and sustained blood pressure control, reduces polypharmacy and adverse events, and slows kidney function decline in CKD patients with RH. This study represents the first PGx-based clinical trial in a multi-ethnic population from Northwest China, providing valuable evidence to support personalized treatment strategies for CKD with RH in East Asian ","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"36-49"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145708173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Do Peritoneal Dialysis Patients with Increased Vascular Stiffness Measured by Pulse Wave Velocity Have Reduced Bone Mineral Density Measured with Dual Energy X-Ray Absorptiometry?","authors":"Jamie Beverstock, Andrew Davenport","doi":"10.1159/000552051","DOIUrl":"10.1159/000552051","url":null,"abstract":"<p><strong>Introduction: </strong>Vascular stiffness and osteoporosis are independently associated with increased cardiovascular morbidity. We investigated the relationship between pulse wave velocity (aoPWV), a measure of vascular stiffness, and bone mineral density (BMD) in peritoneal dialysis (PD) patients.</p><p><strong>Methods: </strong>AoPWV was measured in patients who had dual energy X-ray absorptiometry (DXA) scans.</p><p><strong>Results: </strong>The mean aoPWV was 9.9 ± 0.2 m/s in 113 established PD patients (59.3% male; mean age 64.1 ± 15.3 years. AoPWV was negatively associated with whole body T score r = -0.24, p = 0.016, and Z score r = -0.23, p = 0.021, total body BMD, r = 0.21, p = 0.029, and left leg BMD, r = -0.19, p = 0.044, However, these associations were no longer significant after adjusting aoPWV for age and cardiovascular risk factors.</p><p><strong>Conclusion: </strong>Vascular stiffness and osteoporosis increase with age. Although increased vascular stiffness was associated with reduced BMD on unadjusted analysis, this relationship was no longer significant after adjustment for confounding factors. This suggests that the association between vascular stiffness and reduced BMD may reflect shared factors rather than a direct causal relationship.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"421-428"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13322684/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147775495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}