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Search Results (1,808)

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Keywords = diabetic kidney disease

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13 pages, 1096 KiB  
Article
Fibrosis-4 Score Is Associated with Mortality in Hemodialysis Patients with Chronic Viral Hepatitis: A Retrospective Study
by Hao-Hsuan Liu, Chieh-Li Yen, Wen-Juei Jeng, Cheng-Chieh Hung, Ching-Chung Hsiao, Ya-Chung Tian and Kuan-Hsing Chen
Diagnostics 2024, 14(18), 2048; https://doi.org/10.3390/diagnostics14182048 - 15 Sep 2024
Viewed by 289
Abstract
BACKGROUND: Chronic hepatitis B and C infections are major causes of morbidity and mortality in end-stage kidney disease (ESKD) patients on hemodialysis (HD). The Fibrosis-4 (FIB-4) score is a non-invasive method to evaluate chronic liver disease. However, it is unclear whether there is [...] Read more.
BACKGROUND: Chronic hepatitis B and C infections are major causes of morbidity and mortality in end-stage kidney disease (ESKD) patients on hemodialysis (HD). The Fibrosis-4 (FIB-4) score is a non-invasive method to evaluate chronic liver disease. However, it is unclear whether there is a connection between the FIB-4 score and major adverse cardiovascular events (MACEs) and mortality in patients on HD. This study investigates the relationship between FIB-4 scores, MACEs, and mortality in HD patients. METHODS: A 5-year retrospective study included 198 HD patients with chronic hepatitis B and C from Chang Gung Memorial Hospital. FIB-4 scores were categorized into high (>2.071), middle (1.030~2.071), and low (<1.030) tertiles for cross-sectional analyses. MACEs and mortality were tracked longitudinally. RESULTS: Patients with high FIB-4 scores had lower hemoglobin and albumin levels. Cox multivariate analysis showed that high FIB-4 scores (aHR: 1.589) and diabetes mellitus (aHR: 5.688) were significant factors for all-cause mortality. The optimal FIB-4 score for 5-year mortality was 2.942. FIB-4 scores were not significant for predicting 5-year MACEs. CONCLUSIONS: High FIB-4 scores are associated with increased 5-year all-cause mortality risk in HD patients with chronic hepatitis virus infection. Full article
(This article belongs to the Section Diagnostic Microbiology and Infectious Disease)
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<p>Flowchart of included patients in this study.</p>
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<p>ROC curve and AUC of the FIB-4 score for identifying 5-year mortality. ROC curve: receiver operating characteristic curve; AUC: area under the curve; FIB-4 score: Fibrosis-4 score.</p>
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<p>Kaplan–Meier plot with the diagnostic point of the FIB-4 score (2.942) for identifying 5-year mortality. Group 1: FIB-4 score ≥ 2.942; Group 2: FIB-4 score &lt; 2.942.</p>
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16 pages, 336 KiB  
Review
Low-Protein Diets, Malnutrition, and Bone Metabolism in Chronic Kidney Disease
by Cidália D. Pereira, Carla Guimarães, Vânia S. Ribeiro, Daniela C. Vaz and Maria João Martins
Nutrients 2024, 16(18), 3098; https://doi.org/10.3390/nu16183098 - 13 Sep 2024
Viewed by 575
Abstract
Chronic kidney disease (CKD) has a high prevalence worldwide, with increasing incidence in low- and middle-income countries, and is associated with high morbidity and mortality, particularly from cardiovascular disease. Protein-restricted diets are one of the most widely used non-pharmacological approaches to slow the [...] Read more.
Chronic kidney disease (CKD) has a high prevalence worldwide, with increasing incidence in low- and middle-income countries, and is associated with high morbidity and mortality, particularly from cardiovascular disease. Protein-restricted diets are one of the most widely used non-pharmacological approaches to slow the progression of CKD and prevent associated metabolic abnormalities. However, some concerns have been raised about the long-term safety of these diets, particularly with regard to patients’ nutritional status and bone and mineral disorders. Therefore, the aim of this article is to review the most recent scientific evidence on the relevance of using protein-restricted diets (with or without keto-analogue supplementation) and, in particular, their relationships with malnutrition and mineral and bone disorders in people with CKD without kidney replacement therapies. Although protein-restricted diets, especially when supplemented with keto-analogues and highly personalized and monitored, do not appear to be associated with malnutrition, research on their effects on bone and mineral disorders is scarce, deserving further investigation. Full article
8 pages, 956 KiB  
Perspective
Diabetic Kidney Disease: Contribution of Phenyl Sulfate Derived from Dietary Tyrosine upon Gut Microbiota Catabolism
by Haoxin Liu, Tram N. Diep, Ying Wang, Yucheng Wang and Liang-Jun Yan
Biomolecules 2024, 14(9), 1153; https://doi.org/10.3390/biom14091153 - 13 Sep 2024
Viewed by 366
Abstract
Deranged gut microbiota can release increased levels of uremic toxins leading to exacerbated kidney injury. In diabetic kidney disease (DKD), phenyl sulfate (PS) derived from tyrosine catabolism by gut microbiota has been demonstrated to be both an early diagnostic marker and a therapeutic [...] Read more.
Deranged gut microbiota can release increased levels of uremic toxins leading to exacerbated kidney injury. In diabetic kidney disease (DKD), phenyl sulfate (PS) derived from tyrosine catabolism by gut microbiota has been demonstrated to be both an early diagnostic marker and a therapeutic target. In this perspective article, we summarize PS generation pathways and recent findings on PS and kidney injury in DKD. Increasing evidence has shown that the underlying mechanisms of PS-induced kidney injury mainly involve oxidative stress, redox imbalance, and mitochondrial dysfunction, which all may be targeted to attenuate PS-induced kidney injury. For future research directions, we think that a deeper understanding of the pathogenic role of PS in kidney injury using a variety of diabetic animal models should be investigated. Moreover, we also suggest beneficial approaches that could be used to mitigate the deleterious effect of PS on the kidney. These approaches include caloric restriction, tyrosine restriction, and administration of ketogenic drugs, ketogenic diets or natural products; all of which should be conducted under obese and diabetic conditions. Full article
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<p>Major pathway of phenyl sulfate formation via gut microbiota catabolism of dietary tyrosine. Tyrosine is converted to phenol by the bacterial enzyme tyrosine phenol lyase followed by further conversion to phenyl sulfate in the liver. Phenyl sulfate is usually eliminated by the kidney but can accumulate in the kidney and cause further kidney damage.</p>
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<p>Major mechanisms underlying PS-induced kidney injury.</p>
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11 pages, 740 KiB  
Article
Health Impacts of Pre-eclampsia: A Comprehensive Analysis of Maternal and Neonatal Outcomes
by Flavius George Socol, Elena Bernad, Marius Craina, Simona-Alina Abu-Awwad, Brenda-Cristiana Bernad, Ioana Denisa Socol, Ahmed Abu-Awwad, Simona Sorina Farcas, Daniel Laurențiu Pop, Daniela Gurgus and Nicoleta Ioana Andreescu
Medicina 2024, 60(9), 1486; https://doi.org/10.3390/medicina60091486 - 12 Sep 2024
Viewed by 382
Abstract
Background and Objectives: Hypertensive disorders, particularly pre-eclampsia, pose significant risks during pregnancy, affecting both maternal and neonatal health. The study aims to analyze short- and long-term health implications for mothers and their children, comparing those with pre-eclampsia to those without, to improve [...] Read more.
Background and Objectives: Hypertensive disorders, particularly pre-eclampsia, pose significant risks during pregnancy, affecting both maternal and neonatal health. The study aims to analyze short- and long-term health implications for mothers and their children, comparing those with pre-eclampsia to those without, to improve understanding of risk factors, diagnostic markers, and outcomes. Materials and Methods: This retrospective observational study involved 235 patients, 98 with pre-eclampsia and 137 without, monitored from 2015 to 2018 at the Obstetrics and Gynecology Department of the “Pius Brînzeu” Emergency County Clinical Hospital in Timișoara, Romania. Results: Women with pre-eclampsia were older, had higher BMIs, and more frequently had a family history of pre-eclampsia, hypertension, and diabetes. They also had lower educational and socioeconomic levels and fewer prenatal visits. Biochemical markers such as higher proteinuria, elevated sFlt-1, and lower PlGF were significant in diagnosing pre-eclampsia. Short-term maternal complications like eclampsia, HELLP syndrome, and acute kidney injury were more prevalent in the pre-eclampsia group. Neonatal outcomes included higher rates of preterm birth, low birth weight, and NICU admissions. Long-term mothers with a history of pre-eclampsia had higher incidences of chronic hypertension, cardiovascular disease, kidney problems, diabetes, and mental health disorders. Their children faced increased risks of neuropsychological delays, chronic respiratory issues, behavioral disorders, learning difficulties, and frequent infections. Conclusions: The study highlights the significant short- and long-term health impacts of pre-eclampsia on both mothers and their children. Early monitoring, intervention, and comprehensive management are crucial in mitigating these risks. These findings underscore the need for personalized care strategies to improve health outcomes for affected individuals. Full article
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<p>Flow diagram of total births and group cases.</p>
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12 pages, 272 KiB  
Article
The Use of Kidney Biomarkers, Nephrin and KIM-1, for the Detection of Early Glomerular and Tubular Damage in Patients with Acromegaly: A Case–Control Pilot Study
by Iulia Stefania Plotuna, Melania Balas, Ioana Golu, Daniela Amzar, Roxana Popescu, Ligia Petrica, Adrian Vlad, Daniel Luches, Daliborca Cristina Vlad and Mihaela Vlad
Diseases 2024, 12(9), 211; https://doi.org/10.3390/diseases12090211 - 11 Sep 2024
Viewed by 262
Abstract
Background: Acromegaly is a rare disorder caused by excessive growth hormone (GH) secreted from a pituitary tumor. High levels of GH and insulin growth factor-1 can lead to renal hypertrophy, as well as to diabetes mellitus and hypertension, which negatively impact kidney function. [...] Read more.
Background: Acromegaly is a rare disorder caused by excessive growth hormone (GH) secreted from a pituitary tumor. High levels of GH and insulin growth factor-1 can lead to renal hypertrophy, as well as to diabetes mellitus and hypertension, which negatively impact kidney function. It is believed that high GH may also be involved in the onset of diabetic nephropathy, the main cause of end-stage kidney disease in developed countries. Material and methods: This case–control study was conducted on 23 acromegalic patients and on a control group represented by 21 healthy subjects. The following parameters were determined for all the subjects: serum creatinine, serum urea, estimated glomerular filtration rate (eGFR), urinary albumin/creatinine ratio (UACR), nephrin and kidney injury molecule 1 (KIM-1). Results: Patients with acromegaly showed higher levels of UACR and lower levels of eGFR as compared to healthy subjects. No significant correlations were found between clinical or biochemical parameters associated with acromegaly and nephrin or KIM-1. Conclusions: There was no glomerular or proximal tubular damage at the time of the study, as proven by the normal levels of the biomarkers nephrin and KIM-1. Studies including more patients with uncontrolled disease are needed to clarify the utility of nephrin and KIM-1 for the detection of early kidney involvement in acromegalic patients. Full article
13 pages, 1190 KiB  
Systematic Review
Prevalence and Risk Factors of Renal Artery Stenosis in Patients Undergoing Simultaneous Coronary and Renal Artery Angiography: A Systematic Review and Meta-Analysis of 31,689 Patients from 31 Studies
by Konstantin Schwarz, Ida Straume Bah, Maximilian Will, Chun Shing Kwok, Julia Mascherbauer, Marko Kumric, Josko Bozic and Josip A. Borovac
Diseases 2024, 12(9), 208; https://doi.org/10.3390/diseases12090208 - 11 Sep 2024
Viewed by 214
Abstract
Background/Objectives: Renal artery stenosis (RAS) is associated with coronary artery disease (CAD), exacerbation of arterial hypertension, and progression to heart failure, but remains frequently unrecognized in clinical practice. Methods: We conducted a systematic review and meta-analysis of studies by pooling data [...] Read more.
Background/Objectives: Renal artery stenosis (RAS) is associated with coronary artery disease (CAD), exacerbation of arterial hypertension, and progression to heart failure, but remains frequently unrecognized in clinical practice. Methods: We conducted a systematic review and meta-analysis of studies by pooling data of patients undergoing CAG due to suspected or stable CAD that received a bilateral renal artery angiography. Results: A total of 31 studies with 31,689 patients were included (mean age 63.2 ± 8.7 years, 20.9% were female). Overall, 13.4% (95%CI 10.5–16.7%) of patients undergoing coronary angiography had significant RAS, with 6.5% (95% CI 4.5–8.9%) and 3.7% (95%CI 2.5–5.2%) having severe and bilateral RAS. The mean weighted proportion of patients with three-vessel coronary disease (3VD) was 25.1 (95%CI 19.6–30.9%) while 4.2% (95%CI 2.6–6.2%) had left main (LM) coronary disease. Patients with RAS compared to those without RAS were significantly older (mean difference, MD 4.2 years (95%CI 3.8–4.6)). The relative risk of RAS was greater for the female sex (risk ratio, 95%CI; RR 1.3, 1.03–1.57), presence of diabetes (RR 1.2, 1.10–1.36), arterial hypertension (RR 1.3, 1.21–1.46), dyslipidemia (RR 1.1, 1.06–1.14), peripheral artery disease (PAD) (RR 2.1, 1.40–3.16), chronic kidney disease (CKD) (RR 2.6, 2.04–3.37), 3VD (RR 1.6, 1.30–1.87), and LM disease (RR 1.8, 1.28–2.47). Smoking had a neutral effect on the risk of RAS occurrence (RR 1.0, 0.94–1.06). Conclusions: RAS is common in patients undergoing coronary angiography. CKD, PAD, older age, and severe CAD were among the strongest predictors for the presence of significant RAS. Full article
(This article belongs to the Section Cardiology)
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<p>PRISMA flowchart depicting selection and inclusion process of potential studies.</p>
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<p>The pooled weighted proportions of significant, severe, and bilateral renal artery stenosis (RAS). Panel (<b>A</b>), proportion of significant RAS; Panel (<b>B</b>), proportion of severe RAS; Panel (<b>C</b>), proportion of bilateral RAS in patients undergoing simultaneous coronary artery and renal artery angiography. <b>Abbreviations</b>: RAS—renal artery stenosis.</p>
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<p>The pooled weighted proportions of three-vessel disease: Panel (<b>A</b>), based on available data from 14,771 patients and left main disease; Panel (<b>B</b>), based on available data from 10,670 patients with CAD undergoing cardiac catheterization.</p>
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16 pages, 1965 KiB  
Article
Proteinuria Assessment and Therapeutic Implementation in Chronic Kidney Disease Patients—A Clinical Audit on KDIGO (“Kidney Disease: Improving Global Outcomes”) Guidelines
by Gabriela Adelakun, Maria Boesing, Munachimso Kizito Mbata, Zahra Pasha, Giorgia Lüthi-Corridori, Fabienne Jaun, Felix Burkhalter and Jörg D. Leuppi
J. Clin. Med. 2024, 13(17), 5335; https://doi.org/10.3390/jcm13175335 - 9 Sep 2024
Viewed by 440
Abstract
Background/Objectives: Chronic kidney disease (CKD) is a major health problem with a rising prevalence due to comorbidities like diabetes and hypertension. The aim of this research was to audit the assessment and therapeutic management of proteinuria in CKD patients at the Cantonal [...] Read more.
Background/Objectives: Chronic kidney disease (CKD) is a major health problem with a rising prevalence due to comorbidities like diabetes and hypertension. The aim of this research was to audit the assessment and therapeutic management of proteinuria in CKD patients at the Cantonal Hospital Baselland (KSBL) in Switzerland and determine associations between patient comorbidities, rehospitalisation, death, and the quality of therapeutic management. Methods: We analysed data from 427 adults with CKD (eGFR < 45 mL/min/1.73 m2) hospitalised on the internal medicine ward in 2022. Results: The mean age was 85 years (range: 79–89), 45.9% were female, and the median eGFR was 32.8 mL/min/1.73 m2 (range: 25–40). Proteinuria assessment was performed in 120 (28.1%) patients (the ProtU group), and a corresponding treatment was prescribed in 59%. The ProtU group had a higher quota of patients with diabetes (44.1% vs. 33%, p = 0.048) and obesity (21.2% vs. 12.5%, p = 0.039) when compared to the group without proteinuria assessment (the Ustix group). Twelve-month survival was not significantly different between the groups (HR: 0.75; 95% CI: 0.488–1.154; p-value = 0.191). However, survival was significantly better in patients who received an antiproteinuric treatment compared to those who did not (HR: 0.30; 95% CI: 0.121–0.0761; p = 0.011). Conclusions: Improvements need to be made in managing CKD at the KSBL in accordance with the guidelines. Full article
(This article belongs to the Section Nephrology & Urology)
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<p>Flowchart diagram.</p>
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<p>Assessment availability.</p>
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<p>Frequency of monitoring by GFR value and albuminuria category (Inker, Astor et al., 2014 [<a href="#B1-jcm-13-05335" class="html-bibr">1</a>]—reprinted with permission).</p>
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<p>Patients with main risk factors in CKD. Abbreviations: ACR = albumin-to-creatinine ratio, HT = hypertension, PCR = protein-to-creatinine ratio, RASi = renin angiotensin system inhibitor.</p>
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<p>Kaplan–Meier curves for (<b>a</b>) 6-month rehospitalisation by group (log-rank <span class="html-italic">p</span>-value = 0.037) and (<b>b</b>) 12-month overall survival by diagnostic group (log-rank <span class="html-italic">p</span>-value = 0.191). Abbreviations: ProtU = UACR or UPCR testing available, Ustix = no assessment available, CI = confidence interval, eGFR = estimated glomerular filtration rate, HR = hazard ratio.</p>
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<p>Kaplan–Meier curves for (<b>a</b>) 6-month rehospitalisation by treatment group (log-rank <span class="html-italic">p</span>-value = 0.672) and (<b>b</b>) 12-month overall survival by treatment group (log-rank <span class="html-italic">p</span>-value = 0.267). Abbreviations: CI = confidence interval, eGFR = estimated glomerular filtration rate, HR = hazard ratio, RASi = renin angiotensin system inhibitor.</p>
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<p>Kaplan–Meier curves for (<b>a</b>) 6-month rehospitalisation by treatment group (log-rank <span class="html-italic">p</span>-value = 0.921) and (<b>b</b>) 12-month overall survival by treatment group (log-rank <span class="html-italic">p</span>-value = 0.011). Abbreviations: CI = confidence interval; eGFR = estimated glomerular filtration rate; HR = hazard ratio; RASi = renin angiotensin system inhibitor.</p>
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16 pages, 3522 KiB  
Article
Repurposing Niclosamide to Modulate Renal RNA-Binding Protein HuR for the Treatment of Diabetic Nephropathy in db/db Mice
by Lili Zhuang, Wenjin Liu, Xiao-Qing Tsai, Connor Outtrim, Anna Tang, Zhou Wang and Yufeng Huang
Int. J. Mol. Sci. 2024, 25(17), 9651; https://doi.org/10.3390/ijms25179651 - 6 Sep 2024
Viewed by 278
Abstract
Hu antigen R (HuR) plays a key role in regulating genes critical to the pathogenesis of diabetic nephropathy (DN). This study investigates the therapeutic potential of niclosamide (NCS) as an HuR inhibitor in DN. Uninephrectomized mice were assigned to four groups: normal control; [...] Read more.
Hu antigen R (HuR) plays a key role in regulating genes critical to the pathogenesis of diabetic nephropathy (DN). This study investigates the therapeutic potential of niclosamide (NCS) as an HuR inhibitor in DN. Uninephrectomized mice were assigned to four groups: normal control; untreated db/db mice terminated at 14 and 22 weeks, respectively; and db/db mice treated with NCS (20 mg/kg daily via i.p.) from weeks 18 to 22. Increased HuR expression was observed in diabetic kidneys from db/db mice, which was mitigated by NCS treatment. Untreated db/db mice exhibited obesity, progressive hyperglycemia, albuminuria, kidney hypertrophy and glomerular mesangial matrix expansion, increased renal production of fibronectin and a-smooth muscle actin, and decreased glomerular WT-1+-podocytes and nephrin expression. NCS treatment did not affect mouse body weight, but reduced blood glucose and HbA1c levels and halted the DN progression observed in untreated db/db mice. Renal production of inflammatory and oxidative stress markers (NF-κBp65, TNF-a, MCP-1) and urine MDA levels increased during disease progression in db/db mice but were halted by NCS treatment. Additionally, the Wnt1-signaling-pathway downstream factor, Wisp1, was identified as a key downstream mediator of HuR-dependent action and found to be markedly increased in db/db mouse kidneys, which was normalized by NCS treatment. These findings suggest that inhibition of HuR with NCS is therapeutic for DN by improving hyperglycemia, renal inflammation, and oxidative stress. The reduction in renal Wisp1 expression also contributes to its renoprotective effects. This study supports the potential of repurposing HuR inhibitors as a novel therapy for DN. Full article
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<p>Increased renal HuR staining, and protein production were observed in the diabetic db/db mouse kidney. (<b>A</b>) Representative photomicrographs of renal immunofluorescent staining for HuR (red) at 400× magnification are shown from normal mice (NC), diabetic db/db mice at 14 weeks (db/db–14wk), diabetic db/db mice at 22 weeks (db/db–22wk) and diabetic db/db mice treated with NCS at 22 weeks (db/db + NCS–22wk). A few cells with cytoplasmic staining for HuR are indicated by arrows in the diabetic kidneys. (<b>B</b>) Representative Western blots illustrate the total cellular protein expression of HuR and ß-actin in the renal cortex tissue. (<b>C</b>) Quantification of the Western blot band density. Protein values are expressed as fold-changes relative to the normal control, which was set to unity. * <span class="html-italic">p</span> &lt; 0.05, vs. NC; # <span class="html-italic">p</span> &lt; 0.05, vs. db/db–14wk; £ <span class="html-italic">p</span> &lt; 0.05, vs. db/db–22wk.</p>
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<p>Treatment with NCS arrests the progression of albuminuria in diabetic db/db mice. Urine and urinary albumin excretion levels over 24 h (UAE/24 h) were collected and determined at the ages of 14, 18, and 22 weeks, as described in the <a href="#sec4-ijms-25-09651" class="html-sec">Section 4</a>. * <span class="html-italic">p</span> &lt; 0.05, vs. NC; # <span class="html-italic">p</span> &lt; 0.05, vs. db/db–14wk; £ <span class="html-italic">p</span> &lt; 0.05, vs. db/db–22wk.</p>
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<p>Treatment with NCS reduces glomerular hypertrophy, glomerulosclerosis, glomerular matrix protein deposition and expression in diabetic db/db mice. (<b>A</b>) The representative microscopic images illustrate PAS staining of kidney sections, which was used to detect glomerular size and extracellular matrix (ECM) deposition (stained pink). Magnification, ×400. (<b>B</b>) Representative photomicrographs of glomerular immunofluorescent staining for type IV collagen (Col-IV). Magnification, ×400. (<b>C</b>–<b>E</b>) The graphs summarize the results of average glomerular size (<b>C</b>), glomerular ECM deposition (<b>D</b>) and glomerular Col-IV staining score (<b>E</b>), quantified using image-J. (<b>F</b>) Western blots of FN, a-SMA, and ß-actin from normal mouse kidneys and diabetic kidneys of untreated and treated mice. Molecular weight is labelled on the right. (<b>G</b>,<b>H</b>) The graphs present the results of band density measurements for FN (<b>G</b>) and a-SMA (<b>H</b>) in the kidneys. The protein values are expressed relative to normal control, which was set to unity. (<b>I</b>–<b>K</b>) The graphs show the relative mRNA levels of FN (<b>I</b>), Collagen I-a1 (Col-I) (<b>J</b>), and Collagen IV-a1 (Col-IV) (<b>K</b>) in the kidneys, as determined by the real-time RT–PCR assay. * <span class="html-italic">p</span> &lt; 0.05, vs. NC; # <span class="html-italic">p</span> &lt; 0.05, vs. db/db–14wk; £ <span class="html-italic">p</span> &lt; 0.05, vs. db/db–22wk.</p>
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<p>Treatment with NCS reverses the glomerular podocyte number and nephrin expression in diabetic db/db mice. (<b>A</b>) Kidney sections from normal mice (NC), diabetic db/db mice at 14 weeks (db/db–14wk), diabetic db/db mice at 22 weeks (db/db–22wk) and diabetic db/db mice treated with NCS at 22 weeks (db/db + NCS–22wk) were stained with nephrin and WT-1-postive podocytes. Magnification, 400×. (<b>B</b>,<b>C</b>) The graphs summarize the results of glomerular nephrin staining (<b>B</b>) and WT-1<sup>+</sup> cells (<b>C</b>), quantified using image-J. * <span class="html-italic">p</span> &lt; 0.05, vs. NC; # <span class="html-italic">p</span> &lt; 0.05, vs. db/db–14wk; £ <span class="html-italic">p</span> &lt; 0.05, vs. db/db–22wk.</p>
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<p>Treatment with NCS reduces renal NF-kBp65 and Nox2 protein production in diabetic db/db mice. (<b>A</b>) Representative Western blots illustrate the protein expression of NF-kBp65, Nox2 and ß-actin in the kidney tissue from normal mice and diabetic untreated and treated mice. Molecular weight is labelled on the right. (<b>B</b>,<b>C</b>) The graphs present the results of band density measurements for NF-kBp65 (<b>B</b>) and Nox2 (<b>C</b>) in the kidneys. Protein values are expressed relative to normal control, which was set to unity. * <span class="html-italic">p</span> &lt; 0.05, vs. NC; # <span class="html-italic">p</span> &lt; 0.05, vs. db/db–14wk; £ <span class="html-italic">p</span> &lt; 0.05, vs. db/db–22wk.</p>
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<p>Treatment with NCS ameliorates renal angiopoietin (Angpt) 1 and 2 expression in diabetic db/db mice. (<b>A</b>) Representative Western blots illustrate the protein expression of Angpt1, Angpt2 and ß-actin in the kidney tissue from normal mice and diabetic untreated and treated mice. Molecular weight is labelled on the right. (<b>B</b>–<b>D</b>) The graphs present the results of band density measurements for Angpt1 (<b>B</b>), Angpt2 (<b>C</b>) and the ratio of Angpt1 to Angpt2 (<b>D</b>) in the kidneys. Protein values are expressed relative to normal control, which was set to unity. * <span class="html-italic">p</span> &lt; 0.05, vs. NC; # <span class="html-italic">p</span> &lt; 0.05, vs. db/db–14wk; £ <span class="html-italic">p</span> &lt; 0.05, vs. db/db–22wk.</p>
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<p>Treatment with NCS reduces renal mRNA and protein expression of Wisp1 in diabetic db/db mice. (<b>A</b>) The graph shows the relative mRNA levels of Wisp1 in the kidneys, as determined by the real-time RT–PCR assay. (<b>B</b>) Representative Western blots illustrate the protein expression of Wisp1 and GAPDH in the kidney tissue from normal mice and diabetic untreated and treated mice. Molecular weight is labelled on the right. (<b>C</b>) The graph summarizes the results of band density measurements for Wisp1 and GAPDH in the kidneys. Protein values are expressed relative to normal control, which was set to unity. * <span class="html-italic">p</span> &lt; 0.05, vs. NC; # <span class="html-italic">p</span> &lt; 0.05, vs. db/db–14wk; £ <span class="html-italic">p</span> &lt; 0.05, vs. db/db–22wk.</p>
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13 pages, 1382 KiB  
Article
Prevalence, Clinical Characteristics, and Treatment of Patients with Resistant Hypertension: A Single-Center Study
by Stefan Naydenov, Emil Manov and Nikolay Runev
J. Cardiovasc. Dev. Dis. 2024, 11(9), 279; https://doi.org/10.3390/jcdd11090279 - 5 Sep 2024
Viewed by 337
Abstract
Background: Resistant hypertension (HTN) is associated with a high risk of cardiovascular complications. Our study aimed to assess the prevalence, characteristics, and treatment of patients with resistant HTN. Methods: We screened 4340 consecutive cardiovascular patients hospitalized in our clinic and identified 3762 with [...] Read more.
Background: Resistant hypertension (HTN) is associated with a high risk of cardiovascular complications. Our study aimed to assess the prevalence, characteristics, and treatment of patients with resistant HTN. Methods: We screened 4340 consecutive cardiovascular patients hospitalized in our clinic and identified 3762 with HTN. Of them, 128 fulfilled criteria for resistant HTN and were included in our study. We matched these patients to 128 hospitalized patients with controlled HTN. Results: Resistant HTN patients comprised 3.4% of all hypertensive individuals. Most of these patients (67.2%) were at high or very high cardiovascular risk compared to controlled HTN patients (40.6%); p < 0001. Resistant HTN patients more commonly had concomitant chronic kidney disease (CKD) (60.9%), overweight/obesity (52.3%), dyslipidemias (35.2%), smoking (27.3%), and diabetes (21.9%) compared to controlled HTN patients (37.5%, 29.7%, 28.1%, 14.1%, and 7.8%, respectively); p < 0.001. Regression analysis showed the strongest association of resistant HTN with CKD (OR 6.64), stage III HTN (OR 3.07), and obesity/overweight (OR 2.60). In contrast, single-pill combinations (SPCs) were associated with a lower likelihood of uncontrolled HTN (OR 0.58). Conclusions: Resistant HTN represented a small proportion of all hypertensives in our study, but it was characterized by high/very high cardiovascular risk. Optimized therapy including increased use of SPCs could improve blood pressure control and long-term prognosis for these patients. Full article
(This article belongs to the Section Cardiovascular Clinical Research)
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<p>Screening and selection of participants for our study. HTN—arterial hypertension.</p>
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<p>CKD stage of patients with resistant and controlled HTN according to the equation recommended by the 2021 Guidelines of CKD Epidemiology Collaboration Group [<a href="#B25-jcdd-11-00279" class="html-bibr">25</a>]; <span class="html-italic">p</span> — <span class="html-italic">p</span>-value for statistical significance.</p>
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<p>Dipping state of patients with resistant and controlled HTN. Normal dipping state—10–20% decrease in the nighttime SBP and DBP to the daytime values; non-dipping—1–9% decrease in nighttime SBP and/or DBP compared to the daytime values; reverse dipping—nighttime SBP and/or DBP increase compared to the daytime values; <span class="html-italic">p</span>—<span class="html-italic">p</span>-value for statistical significance.</p>
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<p>Cardiovascular risk of the study population. HTN—arterial hypertension; <span class="html-italic">p</span> — <span class="html-italic">p</span>-value for statistical significance.</p>
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<p>Treatment with double and triple single-pill combinations. HTN—arterial hypertension; SPC—single-pill combination; <span class="html-italic">p</span>—<span class="html-italic">p</span>-value for statistical significance.</p>
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28 pages, 5829 KiB  
Opinion
Slot Blot- and Electrospray Ionization–Mass Spectrometry/Matrix-Assisted Laser Desorption/Ionization–Mass Spectrometry-Based Novel Analysis Methods for the Identification and Quantification of Advanced Glycation End-Products in the Urine
by Takanobu Takata, Shinya Inoue, Kenshiro Kunii, Togen Masauji and Katsuhito Miyazawa
Int. J. Mol. Sci. 2024, 25(17), 9632; https://doi.org/10.3390/ijms25179632 - 5 Sep 2024
Viewed by 486
Abstract
Proteins, saccharides, and low molecular organic compounds in the blood, urine, and saliva could potentially serve as biomarkers for diseases related to diet, lifestyle, and the use of illegal drugs. Lifestyle-related diseases (LSRDs) such as diabetes mellitus (DM), non-alcoholic steatohepatitis, cardiovascular disease, hypertension, [...] Read more.
Proteins, saccharides, and low molecular organic compounds in the blood, urine, and saliva could potentially serve as biomarkers for diseases related to diet, lifestyle, and the use of illegal drugs. Lifestyle-related diseases (LSRDs) such as diabetes mellitus (DM), non-alcoholic steatohepatitis, cardiovascular disease, hypertension, kidney disease, and osteoporosis could develop into life-threatening conditions. Therefore, there is an urgent need to develop biomarkers for their early diagnosis. Advanced glycation end-products (AGEs) are associated with LSRDs and may induce/promote LSRDs. The presence of AGEs in body fluids could represent a biomarker of LSRDs. Urine samples could potentially be used for detecting AGEs, as urine collection is convenient and non-invasive. However, the detection and identification of AGE-modified proteins in the urine could be challenging, as their concentrations in the urine might be extremely low. To address this issue, we propose a new analytical approach. This strategy employs a method previously introduced by us, which combines slot blotting, our unique lysis buffer named Takata’s lysis buffer, and a polyvinylidene difluoride membrane, in conjunction with electrospray ionization-mass spectrometry (ESI)/matrix-assisted laser desorption/ionization-mass spectrometry (MALDI-MS). This novel strategy could be used to detect AGE-modified proteins, AGE-modified peptides, and free-type AGEs in urine samples. Full article
(This article belongs to the Section Biochemistry)
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<p>Precursor molecules of advanced glycation end products (AGEs) [<a href="#B38-ijms-25-09632" class="html-bibr">38</a>,<a href="#B81-ijms-25-09632" class="html-bibr">81</a>]. Glucose and fructose are classified as saccharides. Other compounds are produced from glucose and/or fructose. Glucose, glyceraldehyde, glycolaldehyde, methylglyoxal, glyoxal, and 3-deoxyglucosone are precursors of AGE-1, -2, -3, -4, -5, and -6, respectively.</p>
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<p>Free-type AGEs containing one amino acid residue. Lys, lysine; Arg, arginine. CML, <span class="html-italic">N</span><sup>ε</sup>-carboxymethyl-lysine [<a href="#B34-ijms-25-09632" class="html-bibr">34</a>,<a href="#B48-ijms-25-09632" class="html-bibr">48</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>]; CEL, <span class="html-italic">N</span><sup>ε</sup>-carboxyethyl-lysine [<a href="#B35-ijms-25-09632" class="html-bibr">35</a>,<a href="#B42-ijms-25-09632" class="html-bibr">42</a>,<a href="#B43-ijms-25-09632" class="html-bibr">43</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>]; pyrraline [<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B94-ijms-25-09632" class="html-bibr">94</a>,<a href="#B95-ijms-25-09632" class="html-bibr">95</a>,<a href="#B96-ijms-25-09632" class="html-bibr">96</a>], GLAP, 3-hydroxy-5-hydroxymethyl-pyridinium [<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B77-ijms-25-09632" class="html-bibr">77</a>,<a href="#B97-ijms-25-09632" class="html-bibr">97</a>]; CMA, <span class="html-italic">N</span><sup>ω</sup>-carboxymethylarginine [<a href="#B48-ijms-25-09632" class="html-bibr">48</a>,<a href="#B98-ijms-25-09632" class="html-bibr">98</a>,<a href="#B99-ijms-25-09632" class="html-bibr">99</a>]; MG-H1, <span class="html-italic">N</span><sup>δ</sup>-(5-hydro-5-methyl-4-imidazolone-2-yl)-ornithine (methylglyoxal-derived hydroimidazolone) [<a href="#B45-ijms-25-09632" class="html-bibr">45</a>,<a href="#B46-ijms-25-09632" class="html-bibr">46</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B74-ijms-25-09632" class="html-bibr">74</a>,<a href="#B77-ijms-25-09632" class="html-bibr">77</a>]; G-H1, glyoxal-derived hydroimidazolone [<a href="#B45-ijms-25-09632" class="html-bibr">45</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B100-ijms-25-09632" class="html-bibr">100</a>,<a href="#B101-ijms-25-09632" class="html-bibr">101</a>]; argpyrimidine [<a href="#B46-ijms-25-09632" class="html-bibr">46</a>,<a href="#B48-ijms-25-09632" class="html-bibr">48</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B77-ijms-25-09632" class="html-bibr">77</a>].</p>
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<p>Free-type AGEs containing two amino acid residues. Lys, lysine; Arg, arginine. Pentosidine [<a href="#B34-ijms-25-09632" class="html-bibr">34</a>,<a href="#B35-ijms-25-09632" class="html-bibr">35</a>,<a href="#B36-ijms-25-09632" class="html-bibr">36</a>,<a href="#B37-ijms-25-09632" class="html-bibr">37</a>]; glucosepane [<a href="#B107-ijms-25-09632" class="html-bibr">107</a>,<a href="#B108-ijms-25-09632" class="html-bibr">108</a>,<a href="#B109-ijms-25-09632" class="html-bibr">109</a>]; <span class="html-italic">N</span><sup>ε</sup>-{2-[(5-amino-5-carboxypentyl)-amino]-2-oxoethyl}-lysine (GOLA) [<a href="#B110-ijms-25-09632" class="html-bibr">110</a>]; glyoxal-derived imidazolium cross-link (GODIC) [<a href="#B111-ijms-25-09632" class="html-bibr">111</a>]; methylglyoxal-derived imidazolium cross-link (MODIC) [<a href="#B111-ijms-25-09632" class="html-bibr">111</a>]; 3-doxyglucosone-derived imidazolium cross-link (DODIC) [<a href="#B111-ijms-25-09632" class="html-bibr">111</a>].</p>
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<p>Crude advanced glycation end-product (AGE) pattern [<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B51-ijms-25-09632" class="html-bibr">51</a>]. GLAP, MG-H1, and argpyrimidine structures were generated from glyceraldehyde, and the proteins were modified to generate each AGE in PANC-1 cells [<a href="#B77-ijms-25-09632" class="html-bibr">77</a>]. GLAP, 3-hydroxy-5-hydroxymethyl-pyridinium [<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B77-ijms-25-09632" class="html-bibr">77</a>,<a href="#B97-ijms-25-09632" class="html-bibr">97</a>]; MG-H1, <span class="html-italic">N</span><sup>δ</sup>-(5-hydro-5-methyl-4-imidazolone-2-yl)-ornithine (methylglyoxal-derived hydroimidazolone) [<a href="#B45-ijms-25-09632" class="html-bibr">45</a>,<a href="#B46-ijms-25-09632" class="html-bibr">46</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B74-ijms-25-09632" class="html-bibr">74</a>,<a href="#B77-ijms-25-09632" class="html-bibr">77</a>]; argpyrimidine [<a href="#B46-ijms-25-09632" class="html-bibr">46</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B77-ijms-25-09632" class="html-bibr">77</a>].</p>
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<p>Type 1 (1A, 1B, 1C) and 2 diverse advanced glycation end-product (AGE) patterns [<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B51-ijms-25-09632" class="html-bibr">51</a>]. Closed blue circles indicate the amino acids. The black numbers represent the residue number in proteins A, B, C, and D; CEL, <span class="html-italic">N</span><sup>ε</sup>-carboxyethyl-lysine [<a href="#B35-ijms-25-09632" class="html-bibr">35</a>,<a href="#B42-ijms-25-09632" class="html-bibr">42</a>,<a href="#B43-ijms-25-09632" class="html-bibr">43</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>]. (<b>a</b>) MG-H1, <span class="html-italic">N</span><sup>δ</sup>-(5-hydro-5-methyl-4-imidazolone-2-yl)-ornithine (methylglyoxal-derived hydroimidazolone) [<a href="#B45-ijms-25-09632" class="html-bibr">45</a>,<a href="#B46-ijms-25-09632" class="html-bibr">46</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B74-ijms-25-09632" class="html-bibr">74</a>,<a href="#B77-ijms-25-09632" class="html-bibr">77</a>]; CMA, <span class="html-italic">N</span><sup>ω</sup>-carboxyethyl-arginine [<a href="#B48-ijms-25-09632" class="html-bibr">48</a>,<a href="#B98-ijms-25-09632" class="html-bibr">98</a>,<a href="#B99-ijms-25-09632" class="html-bibr">99</a>]. Type 1 diverse AGE pattern. Each protein A is modified by a certain AGE at same or different amino acid, respectively. The left and middle glycated protein A are classified as Type 1A diverse AGE pattern (Protein A is modified by MG-H1 or CMA at the fourth amino acid residue). The middle and right glycated protein A are classified as Type 1B diverse AGE pattern (Protein A is modified by CMA at the fourth and second amino acid residues). The left and right glycated protein A are classified as Type 1C diverse AGE pattern (Protein A is modified by MG-H1 and CMA at the fourth and second amino acid residues, respectively). (<b>b</b>) Type 2 diverse AGE pattern. (CEL is bound to proteins B, C, and D).</p>
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<p>Type I and II multiple AGE patterns [<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B51-ijms-25-09632" class="html-bibr">51</a>]. Black and red numbers indicate amino acid residue numbers. Closed blue circles represent amino acids (<b>a</b>) Type I multiple AGE pattern. CEL-, Arg-P-, and MG-H1-modified protein X, but not protein X alone (one molecule, but not one type of protein). CEL, <span class="html-italic">N</span><sup>ε</sup>-carboxyethyl-lysine [<a href="#B35-ijms-25-09632" class="html-bibr">35</a>,<a href="#B42-ijms-25-09632" class="html-bibr">42</a>,<a href="#B43-ijms-25-09632" class="html-bibr">43</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>]. Arg-P: argpyrimidine [<a href="#B46-ijms-25-09632" class="html-bibr">46</a>,<a href="#B48-ijms-25-09632" class="html-bibr">48</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B77-ijms-25-09632" class="html-bibr">77</a>]; MG-H1, <span class="html-italic">N</span><sup>δ</sup>-(5-hydro-5-methyl-4-imidazolone-2-yl)-ornithine (methylglyoxal-derived hydroimidazolone) [<a href="#B45-ijms-25-09632" class="html-bibr">45</a>,<a href="#B46-ijms-25-09632" class="html-bibr">46</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B74-ijms-25-09632" class="html-bibr">74</a>,<a href="#B77-ijms-25-09632" class="html-bibr">77</a>]. (<b>b</b>) Type II multiple AGE pattern showing an intermolecular covalent bond. D1: AGE structure that binds to the second amino acid residue in protein Y and the fifth amino acid residue in protein Z.</p>
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<p>Flowchart showing the steps in the novel analysis method for AGEs in urine.</p>
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<p>Schematic describing membrane chromatography. The open white box is the membrane. The black arrows indicate the flow path of the samples. (<b>a</b>) The sample flows perpendicular to the membrane. Closed yellow circles indicate high molecular weight compounds. Closed red circles indicate low molecular compounds. (<b>b</b>) Samples flow horizontally in the membrane. Closed pink circles indicate compounds with high affinity for the membrane. Closed blue stars indicate compounds that do not have affinity to the membrane.</p>
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<p>Schematic showing the application of the sample solution using a vacuum aspirator. Closed black apparatus indicates the slot blot apparatus. Closed white box indicates the PVDF membrane. Closed boxes square indicate the filter paper.</p>
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<p>Spaces on the PVDF membrane that contain the sample solution. The closed gray boxes indicate the lanes with the sample solution. The general slot blot apparatus (e.g., Bio-dot SF microfiltration apparatus (Bio-Rad, Hercules, CA, USA)) has 48 lanes on the membrane (9 cm × 12 cm) [<a href="#B50-ijms-25-09632" class="html-bibr">50</a>,<a href="#B117-ijms-25-09632" class="html-bibr">117</a>].</p>
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<p>Mechanism underlying the formation of carbamylated protein with urea [<a href="#B150-ijms-25-09632" class="html-bibr">150</a>,<a href="#B151-ijms-25-09632" class="html-bibr">151</a>]. (<b>a</b>) The reaction path of ammonium and isocyanate from urea. Two-way arrow indicates the reversible reaction. (<b>b</b>) Isocyanic acid attack on N-terminal lysine, arginine, and cysteine residues in protein. Closed blue circles indicate the amino acids. The black numbers represent the residue number in protein. Arrow indicates the reaction of carbamylation.</p>
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<p>Schematic showing the ESI- or MALDI-MS analysis of free-type AGEs. CEL, <span class="html-italic">N</span><sup>ε</sup>-carboxyethyl-lysine [<a href="#B35-ijms-25-09632" class="html-bibr">35</a>,<a href="#B42-ijms-25-09632" class="html-bibr">42</a>,<a href="#B43-ijms-25-09632" class="html-bibr">43</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>]; CMA, <span class="html-italic">N</span><sup>ω</sup>-carboxyethyl-arginine [<a href="#B48-ijms-25-09632" class="html-bibr">48</a>,<a href="#B98-ijms-25-09632" class="html-bibr">98</a>,<a href="#B99-ijms-25-09632" class="html-bibr">99</a>]; Arg-P, argpyrimidine [<a href="#B46-ijms-25-09632" class="html-bibr">46</a>,<a href="#B48-ijms-25-09632" class="html-bibr">48</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B77-ijms-25-09632" class="html-bibr">77</a>]. Closed blue circles indicate the amino acids. The black numbers represent the residue number in proteins A, B, and C.</p>
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<p>Schematic showing ESI- or MALDI-MS analysis of AGE-modified peptides. MG-H1, <span class="html-italic">N</span><sup>δ</sup>-(5-hydro-5-methyl-4-imidazolone-2-yl)-ornithine (methylglyoxal-derived hydroimidazolone) [<a href="#B45-ijms-25-09632" class="html-bibr">45</a>,<a href="#B46-ijms-25-09632" class="html-bibr">46</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B74-ijms-25-09632" class="html-bibr">74</a>,<a href="#B77-ijms-25-09632" class="html-bibr">77</a>]; CEL, <span class="html-italic">N</span><sup>ε</sup>-carboxyethyl-lysine [<a href="#B35-ijms-25-09632" class="html-bibr">35</a>,<a href="#B42-ijms-25-09632" class="html-bibr">42</a>,<a href="#B43-ijms-25-09632" class="html-bibr">43</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>]; Arg-P, argpyrimidine [<a href="#B46-ijms-25-09632" class="html-bibr">46</a>,<a href="#B48-ijms-25-09632" class="html-bibr">48</a>,<a href="#B49-ijms-25-09632" class="html-bibr">49</a>,<a href="#B77-ijms-25-09632" class="html-bibr">77</a>]. Closed blue circles indicate the amino acids. The black numbers represent the residue number in protein.</p>
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11 pages, 628 KiB  
Article
Association of Renal Hyperfiltration with Incidence of New-Onset Diabetes Mellitus: A Nationwide Cohort Study
by Min-Ju Kim, Min Kyoung Kang, Ye-Seon Hong, Gwang Hyun Leem and Tae-Jin Song
J. Clin. Med. 2024, 13(17), 5267; https://doi.org/10.3390/jcm13175267 - 5 Sep 2024
Viewed by 424
Abstract
Background and Objectives: While the connection between decreased kidney function and diabetes mellitus (DM) is commonly acknowledged, there is insufficient research examining the relationship between higher-than-normal estimated glomerular filtration rate (eGFR) and the incidence risk of new-onset DM. Our research aimed to explore [...] Read more.
Background and Objectives: While the connection between decreased kidney function and diabetes mellitus (DM) is commonly acknowledged, there is insufficient research examining the relationship between higher-than-normal estimated glomerular filtration rate (eGFR) and the incidence risk of new-onset DM. Our research aimed to explore the relationship between an eGFR and the incidence risk of new-onset DM in the Korean general population through a nationwide longitudinal study. Methods: This research employed the cohort records of the National Health Insurance Service in Korea, analyzing records from 2,294,358 individuals between the ages of 20 and 79 who underwent health check-ups between 2010 and 2011. The eGFR levels from the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation were used to assess the renal function. New-onset DM was defined as two or more claims with the International Classification of Diseases-10 classification codes E10 to E14, being prescribed any medication for lowering blood glucose, or having a record of fasting plasma glucose levels of ≥126 mg/dL from a health examination after the index date. Results: The mean age of subjects was 47.34 ± 13.76 years. The 150,813 (6.57%) new-onset DM cases were identified over a median follow-up of 9.63 years. In the multivariable Cox regression analysis, in comparison with the 5th decile, the 10th (≥114.12 mL/min/1.73 m2) (hazard ratio (HR): 0.52, 95% confidence interval (CI) (0.50–0.54), p < 0.001) eGFR decile was significantly associated with a decreased incidence of new-onset DM. Moreover, eGFR >120 mL/min/1.73 m2 was associated with a reduced risk of new-onset DM (HR: 0.40, 95% CI (0.39–0.42), p < 0.001). These results were consistent regardless of the presence of impaired glucose tolerance, age, or obesity. Conclusion: Our study showed higher-than-normal eGFR levels were associated with a lower risk of incidence for new-onset DM regardless of the presence of impaired glucose tolerance, age, or obesity. In general population, higher-than-normal eGFR may be associated with a lower risk of incidence of new-onset DM. Full article
(This article belongs to the Section Nephrology & Urology)
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<p>Diagram illustrating the process of selecting participants for the study.</p>
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<p>Hazard ratios for new-onset DM determined by estimated glomerular filtration rate ((<b>A</b>): deciles; (<b>B</b>): ranges). The hazard ratios, depicting the correlation between renal function and the incidence of new-onset DM, are presented either by (<b>A</b>) decile groups or (<b>B</b>) eGFR ranges. The solid blue line illustrates the multivariate-adjusted hazard ratios with corresponding 95% confidence intervals for each group, while the dashed lines denote a hazard ratio of 1. The red line signifies restricted cubic spline curves. The hazard ratios were calculated using the multivariable Cox model outlined in <a href="#jcm-13-05267-t002" class="html-table">Table 2</a>.</p>
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14 pages, 304 KiB  
Article
The Evaluation of Selected Trace Elements in Blood, Serum and Blood Cells of Type 2 Diabetes Patients with and without Renal Disorder
by Marcin Kosmalski, Rafał Frankowski, Joanna Leszczyńska, Monika Różycka-Kosmalska, Tadeusz Pietras and Iwona Majak
Nutrients 2024, 16(17), 2989; https://doi.org/10.3390/nu16172989 - 4 Sep 2024
Viewed by 606
Abstract
Background: An appropriate diet is the basis for the treatment of type 2 diabetes (T2DM). However, there are no strict recommendations regarding the content of micronutrients and their modifications in the presence of chronic kidney disease (CKD). Therefore, we decided to investigate whether [...] Read more.
Background: An appropriate diet is the basis for the treatment of type 2 diabetes (T2DM). However, there are no strict recommendations regarding the content of micronutrients and their modifications in the presence of chronic kidney disease (CKD). Therefore, we decided to investigate whether T2DM patients, including those with CKD, have different levels of chromium, nickel, cobalt, magnesium, and zinc in various blood elements compared to healthy individuals. Methods: We divided our subjects into three groups: the control group (individuals without T2DM and proper renal function), those with T2DM and proper renal function, and those with T2DM and GFR < 60 mL/min/1.73 m2. Results: We observed higher levels of chromium in all materials examined in patients with T2DM and impaired renal function. Both study groups found higher levels of nickel in samples of whole blood and red blood cells. Patients with T2DM and proper renal function had higher levels of serum manganese. Both study groups had lower levels of serum zinc. We observed higher levels of chromium in all materials examined in patients with T2DM and impaired renal function. Both study groups found higher levels of nickel in samples of whole blood and red blood cells. Patients with T2DM and proper renal function had higher levels of serum manganese. Both study groups had lower levels of serum zinc. Conclusions: In order to ensure effective care for patients with T2DM, it is necessary to improve the standard diet, including the content of micronutrients and their modification in patients with concomitant CKD. Full article
(This article belongs to the Special Issue Nutrition Intervention in Glycaemic Control and Diabetes)
6 pages, 383 KiB  
Communication
Factors Contributing to In-Hospital Mortality in Dengue: Insights from National Surveillance Data in Mexico (2020–2024)
by Eder Fernando Ríos-Bracamontes, Oliver Mendoza-Cano, Agustin Lugo-Radillo, Ana Daniela Ortega-Ramírez and Efrén Murillo-Zamora
Trop. Med. Infect. Dis. 2024, 9(9), 202; https://doi.org/10.3390/tropicalmed9090202 - 3 Sep 2024
Viewed by 689
Abstract
This study aimed to identify the factors associated with all-cause in-hospital mortality in laboratory-confirmed dengue cases from 2020 to mid-2024. A nationwide retrospective cohort study was conducted in Mexico and data from 18,436 participants were analyzed. Risk ratios (RRs) and 95% confidence intervals [...] Read more.
This study aimed to identify the factors associated with all-cause in-hospital mortality in laboratory-confirmed dengue cases from 2020 to mid-2024. A nationwide retrospective cohort study was conducted in Mexico and data from 18,436 participants were analyzed. Risk ratios (RRs) and 95% confidence intervals (CIs), estimated using generalized linear regression models, were used to evaluate the factors associated with all-cause in-hospital mortality risk. The overall case–fatality rate was 17.5 per 1000. In the multiple model, compared to dengue virus (DENV) 1 infections, DENV-2 (RR = 1.81, 95% CI 1.15–2.86) and DENV-3 (RR = 1.87, 95% CI 1.19–2.92) were associated with increased mortality risk. Patient characteristics, such as increasing age (RR = 1.02, 95% CI 1.01–1.03), type 2 diabetes mellitus (RR = 2.07, 95% CI 1.45–2.96), and chronic kidney disease (RR = 3.35, 95% CI 2.03–5.51), were also associated with an increased risk of a fatal outcome. We documented the influence of both the virus and individual susceptibility on mortality risk, underscoring the need for a comprehensive public health strategy for dengue. Full article
(This article belongs to the Special Issue Beyond Borders—Tackling Neglected Tropical Viral Diseases)
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<p>Date of symptom onset of the analyzed inpatients by identified dengue virus (DENV) serotype, Mexico 2020–2024. Note: The total number of patients by serotype was as follows: DENV-1, 2286 (12.4%); DENV-2, 7111 (38.6%); DENV-3, 8806 (47.8%); and DENV-4, 233 (1.3%).</p>
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15 pages, 279 KiB  
Article
Relationship of Non-Invasive Arterial Stiffness Parameters with 10-Year Atherosclerotic Cardiovascular Disease Risk Score in Post-COVID-19 Patients—The Results of a Cross-Sectional Study
by Danuta Loboda, Beata Sarecka-Hujar, Marta Nowacka-Chmielewska, Izabela Szoltysek-Boldys, Wioleta Zielinska-Danch, Michal Gibinski, Jacek Wilczek, Rafal Gardas, Mateusz Grabowski, Mateusz Lejawa, Andrzej Malecki and Krzysztof S. Golba
Life 2024, 14(9), 1105; https://doi.org/10.3390/life14091105 - 2 Sep 2024
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Abstract
This study evaluated the relationship of non-invasive arterial stiffness parameters with an individual 10-year risk of fatal and non-fatal atherosclerotic cardiovascular disease (ASCVD) events in the cohort post-coronavirus disease 2019 (COVID-19). The study group included 203 convalescents aged 60.0 (55.0–63.0) and 115 (56.7%) [...] Read more.
This study evaluated the relationship of non-invasive arterial stiffness parameters with an individual 10-year risk of fatal and non-fatal atherosclerotic cardiovascular disease (ASCVD) events in the cohort post-coronavirus disease 2019 (COVID-19). The study group included 203 convalescents aged 60.0 (55.0–63.0) and 115 (56.7%) women. The ASCVD risk was assessed as low to moderate to very high based on medical history (for 62 participants with pre-existing ASCVD/diabetes/chronic kidney disease in the entire cohort) or calculated in percentages using the Systemic Coronary Risk Evaluation 2 (SCORE2) algorithm based on age, sex, smoking status, systolic blood pressure (BP), and non-high-density lipoprotein cholesterol (for 141 healthy participants). The stiffness index (SI) and reflection index (RI) measured by photoplethysmography, as well as pulse pressure (PP), calculated as the difference between systolic and diastolic BP, were markers of arterial stiffness. Stiffness parameters increased significantly with the increase in ASCVD risk in the entire cohort. In 30 (14.8%) patients in the low- to moderate-risk group, the median SI was 8.07 m/s (7.10–8.73), RI 51.40% (39.40–65.60), and PP 45.50 mmHg (40.00–57.00); in 111 (54.7%) patients in the high-risk group, the median SI was 8.70 m/s (7.40–10.03), RI 57.20% (43.65–68.40), and PP 54.00 mmHg (46.00–60.75); and in 62 (30.5%) patients in the very-high-risk group, the median was SI 9.27 m/s (7.57–10.44), RI 59.00% (50.40–72.40), and PP 60.00 mmHg (51.00–67.00). In healthy participants, the SI ≤ 9.0 m/s (sensitivity of 92.31%, area under the curve [AUC] 0.686, p < 0.001) based on the receiver operating characteristics was the most sensitive variable for discriminating low to moderate risk, and PP > 56.0 mmHg (sensitivity of 74.36%, AUC 0.736, p < 0.001) was used for discriminating very high risk. In multivariate logistic regression, younger age, female sex, PP ≤ 50 mmHg, SI ≤ 9.0 m/s, and triglycerides < 150 mg/dL had the best relationship with low to moderate SCORE2 risk. In turn, older age, currently smoking, PP > 56.0 mmHg, RI > 68.6%, and diastolic BP ≥ 90 mmHg were related to very high SCORE2 risk. In conclusion, arterial stiffness is significantly related to ASCVD risk in post-COVID-19 patients and can be helpful as a single risk marker in everyday practice. Cut-off points for arterial stiffness parameters determined based on SCORE2 may help make individual decisions about implementing lifestyle changes or pharmacological treatment of ASCVD risk factors Full article
(This article belongs to the Special Issue Human Health before, during, and after COVID-19)
17 pages, 1293 KiB  
Review
Proteinuric and Non-Proteinuric Diabetic Kidney Disease: Different Presentations of the Same Disease?
by Larissa Fabre, Juliana Figueredo Pedregosa-Miguel and Érika Bevilaqua Rangel
Diabetology 2024, 5(4), 389-405; https://doi.org/10.3390/diabetology5040030 - 2 Sep 2024
Viewed by 303
Abstract
Background: Diabetic kidney disease (DKD) is a leading cause of end-stage kidney disease (ESKD) worldwide. This review examines the potential differences in clinical presentation, outcomes, and management between individuals with proteinuric DKD (P-DKD) and non-proteinuric DKD (NP-DKD). Methods: We analyzed articles published globally [...] Read more.
Background: Diabetic kidney disease (DKD) is a leading cause of end-stage kidney disease (ESKD) worldwide. This review examines the potential differences in clinical presentation, outcomes, and management between individuals with proteinuric DKD (P-DKD) and non-proteinuric DKD (NP-DKD). Methods: We analyzed articles published globally from 2000 and 2024. Results: Individuals with NP-DKD generally have lower blood pressure levels and a more favorable lipid profile. In contrast, histological studies show that P-DKD is associated with more severe glomerulosclerosis, mesangial expansion, arteriolar hyalinosis, interstitial-fibrosis/tubular atrophy, and immune complex deposits. Additionally, those with P-DKD are more likely to develop diabetic retinopathy and have a higher risk of all-cause mortality and progression to ESKD. Strategies to slow DKD progression, applicable to both NP-DKD and P-DKD, include non-pharmacologic and pharmacologic interventions such as renin–angiotensin system blockers, sodium-glucose co-transporter-2 inhibitors, finerenone, and glucagon-like protein receptor agonists. Conclusions: NP-DKD and P-DKD represent different presentations of the same underlying disease. Full article
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Figure 1

Figure 1
<p>(<b>A</b>). Risk of chronic kidney disease progression, frequency of visits and referral to nephrology, as indicated by the kidney icon, are stratified based on eGFR and albuminuria. Adapted from [<a href="#B13-diabetology-05-00030" class="html-bibr">13</a>]. The eGFR and albuminuria grid illustrates the risk through color coding, ranging from favorable to unfavorable (green, yellow, orange, red, deep red). (<b>B</b>). Trajectories of kidney function in DKD. Adapted from [<a href="#B8-diabetology-05-00030" class="html-bibr">8</a>].</p>
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<p>Laboratory, clinical, histological and prognostic differences between NP-DKD and P-DKD.</p>
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