Piyawan Bunpo

Background: Albuminuria is a key biomarker for chronic kidney disease and cardiovascular risk. Point-of-care urine albumin-to-creatinine ratio (UACR) testing may improve access to chronic kidney disease screening. However, limited evidence is available regarding the agreement of the individual albumin and creatinine components of semi-quantitative UACR strip tests with quantitative laboratory measurements. Methods: We evaluated 400 spot urine specimens using the Dirui H13-Cr semi-quantitative UACR strip and compared results with quantitative immunoturbidimetric UACR measurement performed on a Roche Cobas c503 analyzer. Agreement was assessed using Cohen's kappa coefficients, including category-specific agreement according to the KDIGO A1, A2, A3 albuminuria categories, and diagnostic performance was evaluated using sensitivity, specificity, predictive values, likelihood ratios, and diagnostic odds ratio (DOR). Results: Agreement between strip-based and quantitative measurements was substantial for urinary albumin ( κ =0.691; 95% CI, 0.632–0.751) but considerably lower for urinary creatinine ( κ =0.377; 95% CI, 0.331–0.423). Despite this disparity, UACR classification demonstrated substantial agreement ( κ =0.627; 95% CI, 0.541–0.714). The findings suggest that semi-quantitative creatinine estimation is the primary analytical determinant of UACR misclassification. For detection of abnormal albuminuria (UACR ≥30 mg/g), the strip achieved a sensitivity of 83.66% and specificity of 83.22%. The PPV was 89.96% and NPV was 73.91%. Category-specific analysis showed that 131 of 177 A2 specimens (74.0%) were classified as A2 by the strip, whereas 64 of 80 A3 specimens (80.0%) were classified as A2 rather than A3. Conclusion: The Dirui H13-Cr strip demonstrated acceptable performance for albuminuria screening. However, semi-quantitative urinary creatinine estimation represented an important analytical limitation affecting UACR classification accuracy. Future development of strip-based UACR technologies should prioritize improved creatinine measurement to enhance diagnostic performance.

Background: Microalbuminuria, defined as urinary albumin excretion of 30-300 mg/day, is an early marker of renal injury and an established predictor of cardiovascular disease. Its reported prevalence varies widely across populations, and determinants differ by clinical and demographic context. Objectives: To provide a broad synthesis of the available literature rather than a systematic review or meta-analysis, formal risk-of-bias assessment, quality scoring, and quantitative meta-analysis were not performed. Materials and methods: A structured narrative literature review was conducted, synthesizing data from 21 observational studies across diverse geographic regions and adult populations. Studies reporting the prevalence of microalbuminuria and/or associated factors using recognized diagnostic criteria were included. Results: The prevalence of microalbuminuria ranged from 2.8% in normotensive, normoglycemic adults to 61% in diabetic populations. Higher prevalence was frequently associated with diabetes, hypertension, poor glycemic control, older age, obesity, and other cardiometabolic risk factors, although associations varied across populations. Substantial geographic variation was observed, reflecting differences in population characteristics and cardiometabolic risk profiles. Conclusion: Microalbuminuria is common in high-risk cardiometabolic populations and is consistently associated with multiple modifiable risk factors. These findings are consistent with current clinical guidelines supporting screening in high-risk individuals and highlight the importance of early risk assessment and evidence-based management to reduce renal and cardiovascular complications.

Background/Objective: Albuminuria is an early marker of kidney damage and cardiovascular risk. However, data on its prevalence and association with urine dipstick parameters in heterogeneous, hospital-based populations remain limited. The objective of this study was to determine the prevalence of elevated albuminuria measured by the urine albumin-to-creatinine ratio (UACR) in a diverse patient population and evaluate associations with semi-quantitative urine dipstick parameters. Methods: This cross-sectional study included 393 adults recruited from a tertiary-care hospital setting, comprising individuals undergoing clinical evaluation and routine health assessments. Given the hospital-based recruitment and enrichment with chronic conditions, the study population represents a high-risk cohort rather than the general population. Spot urine samples were analyzed for the UACR and dipstick parameters. Elevated albuminuria was defined as a UACR ≥ 30 mg/g. Associations were assessed using chi-square tests and multivariate logistic regression, with adjusted odds ratios (aORs) and 95% confidence intervals (CIs). Results: Elevated albuminuria was observed in 64% of participants. This high prevalence likely reflects the underlying clinical characteristics of the study population, including a substantial burden of chronic kidney disease and other comorbidities, and should not be interpreted as representative of population-level prevalence. Chronic kidney disease was independently associated with elevated albuminuria (aOR 3.14, 95% CI 1.12–8.86, p = 0.030), as was male sex (aOR 1.54, 95% CI 1.01–2.34, p = 0.045). Dipstick-positive blood was significantly associated with elevated albuminuria (85% vs. 60% in those without dipstick blood positivity, p = 0.005). Dipstick albumin strongly correlated with the UACR (p < 0.001), although 22% of individuals with negative dipstick albumin still had an elevated UACR. Other urine dipstick parameters were not significantly associated with elevated albuminuria. Conclusions: In this high-risk, hospital-based cohort, elevated albuminuria was common and associated with kidney disease and male sex. Dipstick blood positivity is significantly associated with albuminuria and may warrant further investigation. However, reliance on dipstick testing alone may underestimate disease burden, supporting the need for broader implementation of UACR-based screening strategies.

Background: The urinary albumin–to–creatinine ratio (UACR) is a key marker for early kidney dysfunction. This study assessed UACR levels and their associations with demographic and clinical factors in a Thai university population. Materials and methods: A cohort of 158 participants (53 males, 105 females) was recruited from Chiang Mai University between January and May 2024. Urinary albumin and creatinine were measured by turbidimetric immunoassay and creatininase method, respectively, and expressed as UACR (mg/gm creatinine). UACR was categorized as normoalbuminuria (0.05), whereas obesity class II, elevated fasting blood glucose (≥126 mg/dL) and systemic lupus erythematosus (SLE) were significantly associated with increased urinary albumin excretion (Chi-square, p<0.05). Conclusion: Elevated blood glucose, obesity, and SLE were significantly linked to increased UACR, emphasizing the importance of early identification and management of these risk factors to prevent kidney disease progression.

Glucosidase II (GluII) is a heterodimeric enzyme localized in the endoplasmic reticulum (ER), essential for the sequential trimming of glucose residues during N-linked glycosylation. This critical function facilitates glycoprotein folding via the calnexin/calreticulin chaperone system, maintaining ER homeostasis. Dysregulation or inhibition of GluII has been implicated in various pathological processes, including cancer, viral infections, and glycoprotein misfolding disorders. This review summarizes the current knowledge of GluII’s structure and function, highlights a wide range of natural and synthetic GluII inhibitors—including iminosugar derivatives (e.g., deoxynojirimycin (DNJ), castanospermine (CAST)), non-iminosugar compounds (e.g., bromoconduritol, catechins), and mechanism-based cyclophellitol analogues—and evaluates their biological effects and therapeutic potential. The cellular impact of GluII inhibition is explored in the context of ER stress, unfolded protein response (UPR), tumor cell apoptosis, and viral replication. Key challenges in developing selective GluII inhibitors are discussed, with a focus on strategies to minimize off-target effects, including prodrug design, allosteric modulation, and emerging genetic approaches such as microRNA (miRNA)-mediated downregulation of GluII subunits. Taken together, these insights underscore the therapeutic relevance of GluII as a druggable target and pave the way for the rational design of next-generation inhibitors in oncology, infectious diseases, and metabolic disorders.

Introduction: the benefits of consuming extra Ascorbic Acid (AA) while exercising are not well understood. Aim: This study aims to explore the effects of AA supplementation on oxidative stress, the immunological response, and inflammation in healthy women after a single bout of high-intensity exercise. Materials and Methods: In a crossover design, 20 sedentary women (aged 18-22) underwent 30 minutes of vigorous cycling. They were divided into two groups: one receiving daily 1,000 mg ascorbic acid supplementation (1,000AA) and the other without supplementation (0AA). This regimen was maintained for one week. Blood samples obtained pre-exercise, immediately post-exercise, and 24 hours post-exercise underwent analysis for oxidative stress, inflammatory markers, CD4+ and CD8+ lymphocytes, and neutrophil phagocytic activity. Results: An AA supplement significantly increased plasma concentrations of AA (p<0.05) and reduced post-exercise plasma MDA levels (p<0.05) but did not affect creatine kinase activity. White blood cells, CD8+ T cells, and IL-6 increased significantly after exercise but remained unchanged in the 1,000AA group compared to the 0AA group, while the neutrophil count increased (p<0.05) after exercise with no change in phagocytic function. A slight drop in phagocytic function was observed 24 hours after exercise in the 1,000AA group. Exercise and AA supplements had no effect on CD4+ T cells. Conclusion: a single session of high-intensity exercise caused oxidative stress, muscle injury, and inflammation, as well as a transient increase in CD8+ T cells. A short administration of AA attenuated the exercise-induced oxidative stress and reduced inflammation by limiting the increase in IL-6 and CD8+ T cells.

Background: This study was designed to determine the effects of ascorbic acid (AA) supplementation on immune status following a single bout of exercise. Materials/Methods: In a crossover design with a 1 week wash-out period, 20 healthy sedentary women performed 30 minutes moderate-intensity cycling with (1,000AA) or without (0AA) ingesting 1,000 mg of AA daily for 1 week. Blood samples were taken immediately before, immediately after and 24 hours post-exercise to determine the oxidative stress markers, hematological parameters, immunophenotyping of peripheral blood lymphocytes and neutrophil phagocytic function with Candida albicans. Results: Moderate-intensity exercise in subjects ranged in age from 21 to 23 years, showed no significant changes in oxidative stress markers in both cohorts. Plasma total creatine kinase was increased immediately after exercise and returned to baseline at 24 h post-exercise in both cohorts. Subjects ingesting 1,000 mg AA demonstrated significant higher level of plasma AA at pre-exercise and post-exercise as compared with the same time point in 0AA group. White blood cell and absolute neutrophil counts were increased immediately after exercise and returned to baseline at 24 h post-exercise in both cohorts. Exercise resulted in increased lymphocyte count, CD4+ T cells, CD8+ T cells, CD45+/CD3-/CD4- cells, CD45+/CD3+/CD4- cells, CD45+/CD3-/CD8- cells, CD45+/CD3+/CD8- cells and CD45+/CD3-/CD8+ cells immediately after exercise (p C. albicans in both cohorts. Conclusion: A single bout of exercise induced muscle damage and transient changes in neutrophil count as well as lymphocyte subpopulations in sedentary women. Ascorbic supplementation does not show beneficial effect to the moderate-intensity exercise.

Ascorbic acid is a water-soluble chain breaking antioxidant. It scavenges free radicals and reactive oxygen species (ROS), which are produced during metabolic pathways. Exercise can produce an imbalance between ROS and antioxidants, leading to oxidative stress-related tissue damages. This study was designed to determine the effects of ascorbic acid supplementation on circulating biomarkers of oxidative stress and muscle damage following a single bout of exercise. In a crossover design with a 1 wk. wash-out period, 19 healthy women performed 30 min moderate-intensity cycling after ingesting 1000 mg of ascorbic acid (AA) or placebo. Blood samples were taken immediately before, immediately after and 30 min post-exercise to determine plasma albumin, total protein, glucose, oxidative stress and muscle damage markers. Plasma albumin and total protein levels increased immediately after exercise in placebo alongside slight reductions in glucose (p = 0.001). These effects were absent in AA cohort. Ferric reducing ability of plasma and vitamin C levels in AA cohort significantly increased after exercise (p < 0.05). Superoxide dismutase activity was significantly elevated after exercise (p = 0.002) in placebo but not AA. Plasma malondialdehyde did not change after exercise in placebo but was significantly decreased in AA (p < 0.05). The exercise protocol promoted slight muscle damage, reflected in significant increases in total creatine kinase in all subjects after exercise. On the other hand, plasma C-reactive protein and lactate dehydrogenase remained unchanged. Supplementation with ascorbic acid prior exercise improves antioxidant power but does not prevent muscle damage.

The purpose of this study was to investigate the impact of ascorbic acid (AA) consumption on the oxidative stress status of untrained volunteers participating in a supervised exercise program. The study included 46 young adults (average age, 23.5 ± 0.59 years; 37 females, 9 males) who remained sedentary (n = 16) or participated in 30 min of outdoor aerobic running (n = 30) at an intensity corresponding to 65%–75% of maximum heart rate for 3 times per week for 12 weeks. Exercised subjects were randomly assigned to an exercise group without AA supplementation (control; n = 10) or received either 250 mg (n = 10) or 500 mg (n = 10) of AA supplementation previous to each exercise session. Blood samples were taken on day 0 and day 84 to evaluate metabolic profiles and antioxidant status. Sedentary subjects underwent in a single bout of aerobic running to determine total antioxidant status (TAS) and malondiadehyde (MDA) at pre- and postexercise with or without AA supplementation. No significant change in TAS was observed. Plasma MDA significantly increased at postexercise (P < 0.05), and AA supplementation decreased MDA level significantly (P < 0.05). After 3 months of exercise, there was no significant change in blood glucose, lipid profile, MDA, TAS, superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase activities amongst groups. Supplementation of AA was associated with minor and inconsistent reductions in SOD, GPx, and catalase activities (P < 0.05). These findings indicate that pre-exercise supplementation of ascorbic acid does not alter oxidative stress markers in the plasma and erythrocytes of young adults engaged in a supervised exercise program.