Biomarkers Of Chronic Kidney Disease Research Articles

Fibroblast Growth Factors in Cardiovascular Disease.

Despite advancements in managing traditional cardiovascular risk factors, many cardiovascular diseases (CVDs) persist. Fibroblast growth factors (FGFs) have emerged as potential diagnostic markers and therapeutic targets for CVDs. FGF1, FGF2, and FGF4 are primarily used for therapeutic angiogenesis. Clinical applications are being explored based on animal studies using approaches such as recombinant protein administration and adenovirus-mediated gene delivery, targeting patients with coronary artery disease and lower extremity arterial disease. Although promising results have been observed in animal models and early-stage clinical trials, further studies are required to assess their therapeutic potential. The FGF19 subfamily, consisting of FGF19, FGF21, and FGF23, act via endocrine signaling in various organs. FGF19, primarily expressed in the small intestine, plays important roles in glucose, lipid, and bile acid metabolism and has therapeutic potential for metabolic disorders. FGF21, found in various tissues, improves glucose metabolism and insulin sensitivity, suggesting potential for treating obesity and diabetes. FGF23, primarily secreted by osteocytes, regulates vitamin D and phosphate metabolism and serves as an important biomarker for chronic kidney disease and CVDs. Thus, FGFs holds promise for both therapeutic and diagnostic applications in metabolic and cardiovascular diseases. Understanding the mechanisms of FGF may pave the way for novel strategies to prevent and manage CVDs, potentially addressing the limitations of current treatments. This review explores the roles of FGF1, FGF2, FGF4, and the FGF19 subfamily in maintaining cardiovascular health. Further research and clinical trials are crucial to fully understand the therapeutic potential of FGFs in managing cardiovascular health.

Exploring diagnostic biomarkers of type 2 cardio-renal syndrome based on secreted proteins and bioinformatics analysis

Chronic heart failure (CHF) can induce chronic kidney disease (CKD), called type 2 cardio-renal syndrome (CRS2). The mechanism is not completely clear, and there is a lack of early warning biomarkers of CKD in the context of CHF. Two CKD, one CHF-PBMC and four CHF-cardiac tissue expression profile datasets were obtained from GEO database. Differential expression analysis and WGCNA were used to detect CKD key genes and CHF-related secreted proteins. Protein–protein interaction (PPI), functional enrichment, and cMAP analysis reveal potential mechanisms and drugs of CHF-related CKD. Five machine learning algorithms were used to screen candidate biomarkers, construct a diagnostic nomogram for CKD and validate it in two external cohorts. Clinical serum samples were collected in our hospital to evaluate the correlation and diagnostic value of biomarkers and CKD. 225 CKD key genes and 316 CHF-related secreted proteins were identified. Four key subgroups, including 204 genes, were identified as CRS2-related pathogenic genes by PPI analysis. Enrichment analysis revealed that the identified subgroups exhibited significant enrichment in cytokine action, immune responses, and inflammatory processes. The cMAP analysis highlighted metiradone as a drug with greater potential for therapeutic intervention for CRS2. Utilizing five machine learning algorithms, three hub genes (CD48, COL3A1, LOXL1) were pinpointed as potential biomarkers for CKD, and a nomogram model was constructed. Receiver operating characteristic analysis demonstrated that the nomogram’s area under the curve (AUC) exceeded 0.80 in both the CKD combined dataset and two external cohorts. In addition, the three biomarkers were significantly correlated with the glomerular filtration rate, and the AUC of the model predicting disease progression was 0.944. Furthermore, analysis of immune cell infiltration indicated a correlation between the three biomarkers and the infiltration fraction of macrophages, neutrophils, and other immune cells in CKD. Our clinical cohort validated the expression patterns of three biomarkers in serum, and the diagnostic model achieved an AUC of 0.876. CHF has the potential to facilitate the progression of CKD via the release of cardiac and PBMC secreted proteins. Furthermore, CD48, COL3A1, and LOXL1 have been identified as potential biomarkers for the detection of CKD.

Application of a validated prognostic plasma protein biomarker test for renal decline in type 2 diabetes to type 1 diabetes: the Fremantle Diabetes Study Phase II

BackgroundThere are scant data relating to prognostic biomarkers for chronic kidney disease (CKD) complicating type 1 diabetes. The aim of this study was to assess the performance of the plasma protein biomarker-based PromarkerD test developed and validated for predicting renal decline in type 2 diabetes in the context of type 1 diabetes.MethodsThe baseline PromarkerD test score was determined in 91 community-based individuals (mean age 46.2 years, 56.5% males) with confirmed type 1 diabetes recruited to the longitudinal observational Fremantle Diabetes Study Phase II. The performance of the PromarkerD test in predicting the risk of incident CKD (estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73m2 in people without CKD at baseline) or an eGFR decline of ≥ 30% over the next four years was determined. The score can range from 0 to 100%, and is categorized as representing low (< 10%), moderate (10% to < 20%) or high (≥ 20%) risk.ResultsThe area under the receiver operating characteristic curve was 0.93 (95% confidence interval 0.87–0.99) for the composite renal endpoint, indicating strong predictive accuracy. The positive and negative predictive values at moderate (10% to < 20%) and high (≥ 20%) risk PromarkerD cut-offs were 46.7–50.0% and ≥ 92.0%, respectively.ConclusionsThese preliminary data suggest that PromarkerD is at least as good a prognostic test for renal decline in type 1 as type 2 diabetes.

Identification of serum biomarkers for chronic kidney disease using serum metabolomics

This study aimed to identify biomarkers for chronic kidney disease (CKD) by studying serum metabolomics. Serum samples were collected from 194 non-dialysis CKD patients and 317 healthy controls (HC). Using ultra-high-performance liquid chromatography-tandem mass spectrometry (UPLC-MS), untargeted metabolomics analysis was conducted. A random forest model was developed and validated in separate sets of HC and CKD patients. The serum metabolomic profiles of patients with chronic kidney disease (CKD) exhibited significant differences compared to healthy controls (HC). A total of 314 metabolites were identified as significantly different, with 179 being upregulated and 135 being downregulated in CKD patients. KEGG enrichment analysis revealed several key pathways, including arginine biosynthesis, phenylalanine metabolism, linoleic acid metabolism, and purine metabolism. The diagnostic efficacy of the classifier was high, with an area under the curve of 1 in the training and validation sets and 0.9435 in the cross-validation set. This study provides comprehensive insights into serum metabolism in non-dialysis CKD patients, highlighting the potential involvement of abnormal biological metabolism in CKD pathogenesis. Exploring metabolites may offer new possibilities for the management of CKD.

THE IMPORTANCE OF KLOTHO PROTEIN IN THE DIAGNOSIS OF CHRONIC KIDNEY DISEASE

Chronic kidney disease (CKD) is an intrinsically systemic infection that alludes to a long-term misfortune of kidney work. The movement of CKD has repercussions for other organs, driving to numerous sorts of extrarenal complications. Seriously ponders are presently being attempted to uncover the hazard components and pathophysiological component of this malady. Amid the past 20 a long time, expanding prove from clinical and fundamental ponders has shown that klotho, which was at first known as an anti-aging quality and is primarily communicated within the kidney, is altogether connected with the improvement and movement of CKD and its complications. Here, we talk about in detail the part and pathophysiological suggestions of klotho in particle clutters, the aggravation reaction, vascular calcification, mineral bone clutters, and renal fibrosis in CKD. Based on the pathogenic component of klotho insufficiency and klotho decrease in pee early in CKD organize 2 and indeed prior in CKD stage 1, it isn't troublesome to get it that solvent klotho can serve as an early and delicate marker of CKD. Besides, the anticipation of klotho decay by a few components can weaken renal wounds, impede CKD movement, enhance extrarenal complications, and make strides renal work. In this audit, we center on the capacities and pathophysiological suggestions of klotho in CKD and its extrarenal complications as well as its potential applications as a demonstrative and/or prognostic biomarker for CKD and as a novel treatment methodology to progress and diminish the burden of comorbidity in CKD.

N-terminal pro-B-type natriuretic peptide, eGFR, and progression of kidney disease in chronic kidney disease patients without heart failure.

Cardiorenal syndrome highlights the bidirectional relationship between kidney and heart dysfunction. N-terminal pro-B-type natriuretic peptide (NT-proBNP), which is the gold standard biomarker in heart failure (HF), may be an important biomarker for chronic kidney disease (CKD) progression. However, NT-proBNP is negatively related with estimated glomerular filtration rate (eGFR). In this study, we investigated the association of NT-proBNP, eGFR, and progression of kidney disease in CKD patients without HF. This multicentric retrospective cohort study recruited 23 860 CKD patients without HF, who had at least one NT-proBNP record from China Renal Data System database. Linear regression model evaluated the relationship between eGFR and NT-proBNP. Cox regression analysis assessed the association between NT-proBNP and CKD progression. Sensitivity analysis examined the robustness of the main findings. This study involved 23 860 CKD patients without HF, distributed across different CKD stages: 10 526 in stages G1-2, 4665 in G3a, 3702 in G3b, 2704 in G4, and 2263 in G5. NT-proBNP was negatively correlated with eGFR, particularly in stages 4-5 CKD. A 15-unit decrease in eGFR was associated with increases in log (NT-proBNP) levels by 1.04-fold, 1.27-fold, 1.29-fold, 1.80-fold, and 3.50-fold for stages 1-2, 3a, 3b, 4, and 5, respectively. After excluding patients who developed CKD progression within 1 year, the Cox regression analysis revealed that the relationship between NT-proBNP and CKD progression was not significant in stages 4 and 5. However, for stages 1-3, each standard deviation increase in log (NT-proBNP) was associated with a 26%, 36%, and 28% higher risk of CKD progression, with P interaction ≤.001. The hazard ratios were 1.26 (95% confidence intervals (CI), 1.18 to 1.35), 1.36 (95% CI, 1.22 to 1.51), and 1.28 (95% CI, 1.14 to 1.43) for stages 1-2, stage 3a, and stage 3b, respectively. Despite its strong inverse association with eGFR, NT-proBNP was positively associated with the risk of progression of kidney disease in CKD patients with stages 1-3 without HF. Future studies should investigate the effectiveness of NT-proBNP as a predictive biomarker for the progression of kidney disease across diverse racial groups and healthcare settings.

Senescence Biomarkers CKAP4 and PTX3 Stratify Severe Kidney Disease Patients.

Cellular senescence is the irreversible growth arrest subsequent to oncogenic mutations, DNA damage, or metabolic insult. Senescence is associated with ageing and chronic age associated diseases such as cardiovascular disease and diabetes. The involvement of cellular senescence in acute kidney injury (AKI) and chronic kidney disease (CKD) is not fully understood. However, recent studies suggest that such patients have a higher-than-normal level of cellular senescence and accelerated ageing. This study aimed to discover key biomarkers of senescence in AKI and CKD patients compared to other chronic ageing diseases in controls using OLINK proteomics. We show that senescence proteins CKAP4 (p-value < 0.0001) and PTX3 (p-value < 0.0001) are upregulated in AKI and CKD patients compared with controls with chronic diseases, suggesting the proteins may play a role in overall kidney disease development. CKAP4 was found to be differentially expressed in both AKI and CKD when compared to UHCs; hence, this biomarker could be a prognostic senescence biomarker of both AKI and CKD.

Analysis of neutrophil-to-lymphocyte and platelet-to-lymphocyte ratios as inflammatory biomarkers in chronic kidney disease: impact of parathyroidectomy

Resumo Introdução: O hiperparatireoidismo secundário (HPTS) é uma das causas de inflamação na DRC. Avaliamos o impacto da paratireoidectomia (PTX) nas relações neutrófilo/linfócito (N/L) e plaqueta/linfócito (P/L) em pacientes com HPTS. Métodos: Foram analisados 118 pacientes [hemodiálise (HD, n = 81) e transplantados (TX, n = 37)] submetidos à PTX entre 2015 e 2021. Resultados: Houve redução significativa de cálcio e PTH nos dois grupos, além de elevação de vitamina D. No grupo HD, a PTX não mudou as relações N/L e P/L. Já no grupo TX, houve redução nas relações N/L e P/L acompanhadas de elevação significativa do número de linfócitos totais. Conclusão: As relações N/L e P/L não são marcadores fidedignos de inflamação em pacientes com HPTS submetidos à PTX. A uremia, que induz um estado de inflamação crônica em pacientes dialíticos, e o uso de imunossupressão em pacientes transplantados renais são alguns dos fatores de confusão que impedem o uso dessa ferramenta na prática clínica.

Analysis of neutrophil-to-lymphocyte and platelet-to-lymphocyte ratios as inflammatory biomarkers in chronic kidney disease: impact of parathyroidectomy.

Secondary hyperparathyroidism (SHPT) is one of the causes for inflammation in CKD. We assessed the impact of parathyroidectomy (PTX) on neutrophil-to-lymphocyte (N/L) and platelet-to-lymphocyte (P/L) ratios in SHPT patients. A total of 118 patients [hemodialysis (HD, n = 81), and transplant recipients (TX, n = 37)] undergoing PTX between 2015 and 2021 were analyzed. There was a significant reduction in calcium and PTH levels in both groups, in addition to an increase in vitamin D. In the HD group, PTX did not alter N/L and P/L ratios. In the TX group, there was a reduction in N/L and P/L ratios followed by a significant increase in total lymphocyte count. N/L and P/L ratios are not reliable biomarkers of inflammation in SHPT patients undergoing PTX. Uremia, which induces a state of chronic inflammation in dialysis patients, and the use of immunosuppression in kidney transplant recipients are some of the confounding factors that prevent the use of this tool in clinical practice.

A Comprehensive Review of Advanced Biomarkers for Chronic Kidney Disease in Older Adults: Current Insights and Future Directions.

Chronic kidney disease (CKD) is a growing health concern, particularly in older adults, due to its high prevalence and association with increased morbidity and mortality. Early detection and effective management are crucial to slowing disease progression and reducing complications such as cardiovascular events and end-stage renal disease (ESRD). Traditional biomarkers, including serum creatinine and estimated glomerular filtration rate (eGFR), often have limitations in older populations, where age-related physiological changes can obscure early signs of kidney dysfunction. Advanced biomarkers offer a more precise and comprehensive understanding of kidney health, providing insights into pathological processes such as inflammation, fibrosis, oxidative stress, and tubular injury. These biomarkers have the potential to enhance early diagnosis, predict disease progression, and inform personalized treatment approaches, particularly in the elderly. This review explores the current landscape of advanced biomarkers for CKD in older adults, highlighting their clinical utility and limitations. Key biomarkers, including those related to inflammation (C-reactive protein, interleukin-6), fibrosis (transforming growth factor-beta, collagen degradation products), oxidative stress (F2-isoprostanes, malondialdehyde), and tubular injury (kidney injury molecule-1, neutrophil gelatinase-associated lipocalin), are examined in the context of CKD. Emerging technologies, such as multi-omics and machine learning, are also discussed as they offer new opportunities for biomarker discovery and integration into clinical practice. While challenges remain, including the need for longitudinal studies and better standardization, advanced biomarkers hold promise for transforming CKD management in older adults, paving the way for earlier detection, better risk stratification, and more targeted therapeutic interventions.

A Comprehensive Review of Biomarkers for Chronic Kidney Disease in Older Individuals: Current Perspectives and Future Directions.

Chronic kidney disease (CKD) is a progressive condition characterized by a gradual loss of kidney function, leading to significant health complications and an increased risk of cardiovascular events. Early detection and effective management are crucial for slowing disease progression and improving patient outcomes. Biomarkers are valuable tools in CKD diagnosis, prognosis, and treatment. Traditional biomarkers, such as serum creatinine and urine protein, are widely used, but emerging biomarkers like cystatin C, kidney injury molecule-1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL) offer enhanced diagnostic precision and insights into disease severity. These advanced biomarkers are particularly important in older adults, who may present with age-related physiological changes and comorbid conditions that complicate CKD management. This review explores the current state of biomarker research in CKD, focusing on their application in older populations. It highlights the role of traditional and emerging biomarkers, discusses their relevance for early detection and prognosis, and examines future directions in biomarker research, including technological innovations and personalized medicine approaches. By integrating biomarkers into clinical practice, healthcare providers can achieve more accurate diagnoses, tailor treatments to individual patient needs, and potentially improve the overall management of CKD. Continued research and development in this field are essential for addressing the complexities of CKD and advancing patient care.

Extent of Equivalence of Results for Urine Albumin among 3 Candidate Mass Spectrometry Reference Measurement Procedures.

Urine albumin (UA) is an important biomarker of chronic kidney disease. Current in vitro diagnostic medical devices (IVD-MDs) for measuring UA are not standardized, and median results among IVD-MDs differ by approximately 45%. Since fixed decision values are used to interpret UA, higher-order reference measurement procedures (RMPs) are needed for metrological traceability. Three candidate liquid chromatography-tandem mass spectrometry RMPs have been developed for UA. Eight single-donation human urine samples were measured by 3 candidate RMPs. Results were compared using t-test and variance component analysis. The mean results for each urine sample from each RMP laboratory were not statistically different from the overall mean value by t-test. The median total CV including contributions from bias and imprecision among the 3 RMP laboratories was 6.23% using variance component analysis for each sample. The allowable bias to the RMP for an end-user IVD-MD was ≦9.0% or ≦3.0% based on the desirable or optimal total allowable error of 30% or 24%, respectively. A maximum allowable standard uncertainty for an RMP result was determined to be 4.3% or 3.3% for desirable or optimal performance, respectively. The standard uncertainties for all of the RMP laboratories meet the desirable and optimal standard uncertainty specifications. The candidate RMPs for UA in these 3 laboratories have suitable agreement of results and uncertainties for use as higher-order RMPs in the metrological traceability of end-user IVD-MDs for measuring UA.

The Relationship between Circulating Kidney Injury Molecule-1 and Cardiovascular Morbidity and Mortality in Hemodialysis Patients.

The importance of identifying mortality biomarkers in chronic kidney disease (CKD), and especially in patients treated with hemodialysis (HD), has become evident. In addition to being a marker of tubulointerstitial injury, plasma kidney injury molecule-1 (KIM-1) has been mentioned in regard to HD patients as a risk marker for cardiovascular (CV) mortality and coronary artery calcification. The aim of this study was to assess the level of plasma KIM-1 as a marker of cardiovascular disease (CVD) and mortality in CKD5-HD patients (patients with CKD stage G5D treated with hemodialysis). We conducted a prospective case-control study that included 63 CKD5-HD patients (HD for 1-5 years) followed up for 48 months and a control group consisting of 52 non-dialysis patients diagnosed with CKD stages G1-G5 (ND-CKD). All patients had a CVD baseline assessment including medical history, echocardiography, and electrocardiography (ECG). Circulating plasma KIM-1 levels were determined with single-molecule counting immunoassay technology using an enzyme-linked immunosorbent assay. We obtained the following parameters: serum creatinine and urea; the inflammation markers CRP (C-reactive protein) and IL-6 (interleukin-6); and the anemia markers complete blood count, serum ferritin, and transferrin saturation (TSAT). The mean plasma KIM-1 level was 403.8 ± 546.8 pg/mL, showing a statistically significant correlation with inflammation (CRP, R = 0.28, p = 0.02; IL-6, R = 0.36, p = 0.005) and with anemia (hematocrit, R = -0.5, p = -0.0316; hemoglobin (Hb), R = -0.5, p = 0.02). We found that patients with left ventricular hypertrophy (LVH) on echocardiography (59.7%) had significantly lower mean levels of plasma KIM-1 than patients from the control group (155.51 vs. 432.12 pg/mL; p = 0.026). Regarding the patients' follow-up, we assessed all-cause mortality as an endpoint. After 24 months of follow-up, we found a mortality rate of 22.23%, while after 48 months, the mortality rate was 50.73%. A plasma KIM-1 level < 82.98 pg/mL was significantly associated with decreased survival in hemodialysis patients (p < 0.001). In patients treated with hemodialysis, low levels of plasma KIM-1 were associated with cardiovascular changes and an increased risk of mortality. Plasma KIM-1 levels were significantly higher in HD patients compared to ND-CKD patients.

Copper-loaded ZIF-8-based immunosensor for early diagnosis of chronic kidney disease by detecting neutrophil gelatinase-associated lipocalin (NGAL) biomarker

Metal-organic frameworks (MOFs) is a promising contender among the nanomaterials for biosensors due to their special properties, including high surface area, tunable porosity, and adaptable functionalization competences. Zeolitic imidazolate frameworks (ZIFs), a subclass of MOFs, have drawn precise attention for their excellent chemical stability and ease of synthesis. This study, for the first time, concentrates on the preparation and characterization of a Cu-loaded ZIF-8-based immunosensor for the detection of neutrophil gelatinase-associated lipocalin (NGAL), a crucial biomarker for chronic kidney disease (CKD). Loading copper (Cu) into the ZIF-8 framework improves its electrochemical properties, conductivity, and surface area, leading it an ideal platform for antibody immobilization and NGAL detection. The immunosensor utilized Staphylococcal Protein A (SPA) IgG binding protein for antibody immobilization, providing an alternative to traditional crosslinking chemistry, enhancing biosensor functionality. Structural analysis, morphological assessment, elemental mapping, and stoichiometric analysis confirmed the successful synthesis of Cu-loaded ZIF-8 nanocomposite. Assessment of the electrochemical performance of the immunosensor demonstrated sufficiently low limit of detection (80 pg mL−1) over a wide range of 0.1 ng mL−1 to 1000 ng mL−1 of NGAL along with superior selectivity, reproducibility, stability, and clinical feasibility. This advancement contributes to the rising knowledge on MOF-based biosensors and holds promise for future applications in disease diagnosis and healthcare monitoring.

Determination of the reference interval for urinary klotho to creatinine ratio of healthy dogs.

For several years, alpha klotho has been considered as a candidate biomarker in chronic kidney disease (CKD), progression of CKD and CKD mineral bone disorders (CKD-MBD). The evidence on the relationship between klotho and kidney function is controversial in some areas. The aim of the study was to identify the influence of age, sex and breed on urinary alpha klotho, values in the early stages of CKD within the studied population and determine a reference interval in a group of healthy dogs. Significantly higher values were measured in older dogs over 6 years old (p = 0.026, p = 0.0007) and in the breed German Shepherd than Belgian Shepherd (p = 0.0401). On the basis of sex and in small breed dogs, no significant differences were noted. In dogs with CKD stage 2, alpha klotho values were significantly lower (p = 0.0135) than in healthy dogs. Within the studied population, a reference interval for urinary klotho to creatinine ratio (UrKl/Cr) was determined in the range of 3.94-23.55 pg/gCr. Since our findings show that alpha klotho is associated with older age, we assume that this may have influenced the results in the group of dogs with CKD stage 1 due to the presence of predominantly old dogs in this group. Future studies would be needed to consider age as a factor affecting urinary alpha klotho in dogs with CKD.

Identification of GTF2I Polymorphisms as Potential Biomarkers for CKD in the Han Chinese Population : Multicentric Collaborative Cross-Sectional Cohort Study.

Chronic kidney disease (CKD) poses a global health challenge, but its molecular mechanisms are poorly understood. Genetic factors play a critical role, and phenome-wide association studies (PheWAS) and genome-wide association studies (GWAS) shed light on CKD's genetic architecture, shared variants, and biological pathways. Using data from the multicenter collaborative precision medicine cohort, we conducted a retrospective prospectively maintained cross-sectional study. Participants with comprehensive information and genotyping data were selected, and GWAS and PheWAS analyses were performed using the curated Taiwan Biobank version 2 array to identify CKD-associated genetic variants and explore their phenotypic associations. Among 58,091 volunteers, 8,420 participants were enrolled. Individuals with CKD exhibited higher prevalence of metabolic, cardiovascular, autoimmune, and nephritic disorders. Genetic analysis unveiled two closely linked SNPs, rs117026326 and rs73366469, both associated with GTF2I and CKD (r2=0.64). Further examination revealed significant associations between these SNPs and various kidney-related diseases. The CKD group showed a higher proportion of individuals with specific genotypes (CT/TT for rs117026326 and CT/CC for rs73366469), suggesting potential associations with CKD susceptibility(p<0.001). Furthermore, individuals with these genotypes developed CKD at an earlier age. Multiple logistic regression confirmed the independent association of these genetic variants with CKD. Subgroup analysis based on estimated glomerular filtration rate (eGFR) demonstrated an increased risk of CKD among carriers of the rs117026326 CT/TT genotypes (OR=1.15, 95% CI: 1.07-1.24, p<0.001; OR=1.32; 95% CI: 1.04-1.66, p=0.02, respectively) and carriers of the rs73366469 CT/CC genotypes (OR=1.13, 95% CI=1.05-1.21, p<0.001; OR=1.31, 95% CI: 1.08-1.58, p=0.0049, respectively). Additionally, men had a higher CKD risk than women at lower eGFR levels (OR=1.35, 95%: 1.13-1.61, p<0.001). Our study reveals important links between genetic variants GTF2I and susceptibility to CKD, advancing our understanding of CKD development in the Taiwanese population and suggesting potential for personalized prevention and management strategies. More research is needed to validate and explore these variants in diverse populations.

A case of chronic kidney disease with refractory periodic vomiting and hypertension in a pediatric patient.

Patients with chronic kidney disease (CKD) sometimes experience gastrointestinal symptoms, such as nausea and vomiting. In addition, hypertension and CKD are closely linked, and sustained hypertension in children is associated with the progression of CKD, leading to early cardiomyopathy and premature atherosclerosis. These symptoms substantially affect the quality of daily life of CKD patients, and particularly in children with CKD, they may cause growth retardation. Therefore, establishing effective management methods to alleviate these symptoms is very important. Here, we report a case of a male patient who was born at 34weeks of gestation weighing 1400g. At birth, abdominal ultrasonography displayed left multicystic dysplastic kidney. From 6months after birth, he was frequently hospitalized owing to refractory periodic vomiting. At 9 months old, he was diagnosed as having stage 3a CKD, and at 20 months old, he presented with stage 2 high blood pressure. In Japan, the uremic toxin adsorbent AST-120 and angiotensin-converting enzyme inhibitor-I (ACE-I) are not strongly recommended for CKD patients. However, after the patient underwent combination therapy of AST-120 and ACE-I, his frequent hospitalizations for refractory periodic vomiting ceased, and his blood pressure decreased. These results indicate that AST-120 and ACE-I are effective for refractory periodic vomiting and hypertension associated with CKD. The patient's height, weight, and mental development are catching up smoothly. The cause of the patient's refractory periodic vomiting remains unclear. However, his impaired kidney function owing to congenital anomalies of the kidney and urinary tract may have caused the refractory periodic vomiting and dehydration. The production of uremic toxins in CKD patients is thought to lead to the secretion of proinflammatory cytokines into the circulation. However, our patient had low serum levels of proinflammatory cytokines, and his serum levels of the chemokines CX3CL1 and CCL2 decreased with age, together with improvement in his clinical course. Therefore, some specific chemokines might be diagnostic and/or prognostic biomarkers of CKD.

Mass Spectrometric Identification of Urinary Biomarkers of Chronic Kidney Disease: A Proteomic-related Preliminary Report

Background Chronic kidney disease (CKD) is a gradual loss of kidney function and has an increased prevalence rate worldwide. Our study was intended to identify potential biomarkers of progression using urine proteomics. Materials and Methods This preliminary study consisted of 32 patients with stage V CKD. Urine samples were subjected to liquid chromatography–mass spectrometry (LCMS), and the network of protein interaction was analyzed using STRING. Results A total of 135 proteins were identified, of which 35 were listed as candidates based on their clinical significance. Protein– protein interaction study provides novel insights into the functional constitution of the proteome, selecting urine as a source of biomarkers. Conclusion The present study observed that the potential markers such as EndoG, HPX, APN, AnxA1, Mic60, LONP1, and HYOU1 correlate with renal damage and its progression to CKD stage V.

Changes in Alzheimer's disease blood biomarkers in kidney failure before and after kidney transplant.

Alzheimer's disease (AD) blood biomarkers show promise for clinical diagnosis but their reliability in chronic kidney disease (CKD) is debated. This study investigates the impact of kidney transplant (KT) on AD biomarkers in CKD. We assessed AD biomarkers in 46 CKD patients pre-KT, at 12weeks and 12 months post-KT, with baseline measures from 13 non-CKD controls. Using linear mixed models, we examined associations with participant groups, estimated glomerular filtration rate (eGFR) and cognition. CKD patients showed elevated levels of neurofilament light (117±72vs. 11±5 pg/mL), phosphorylated tau 181 (75±42vs. 13±8 pg/mL), glial fibrillary acidic protein (193±127vs. 94±39 pg/mL), amyloid β 42 (17±5vs. 5±1 pg/mL), and amyloid β 40 (259±96vs. 72±17 pg/mL) compared to controls. Post-KT, biomarker levels approached normal with improved eGFR, paralleled by enhanced cognitive function. AD blood biomarker elevations in CKD are reversible with improved kidney function through KT. AD biomarker levels are extremely high in severe CKD.AD biomarker levels are higher in patients with kidney failure on dialysis when compared to CKD patients not on dialysis.These elevations in AD biomarker levels in kidney failure are reversable and decrease dramatically after kidney transplantation.The change in biomarker levels after transplantation align with changes in kidney function.The change in biomarker levels after transplantation align with changes in cognitive function.

Indole Lactic Acid in Plasma and Urine: A Potential Biomarker for Chronic Kidney Disease and Inflammatory.

We aimed to explore changes in plasma and urine indole lactic acid (ILA) levels and the relationship between inflammation and ILA in chronic kidney disease (CKD) patients and healthy people. Forty-seven CKD patients and 30 healthy individuals were included in this study. One-way ANOVA was used for variables with normal distribution and homogeneous variance. A rank-sum test was performed for non-normally distributed variables. Correlation analyses were performed using Pearson's or Spearman correlation analyses. Independent relationship between patients and CKD was analyzed using ordinal and binary logistic regressions. Receiver operating characteristic (ROC) curve was used. Plasma and urine ILA levels were positively correlated (r = 0.51, P < 0.01). Plasma ILA was positively correlated with BMI, age, creatinine, BUN, triglycerides, and uric acid and negatively correlated with hemoglobin levels. Urine ILA levels were positively correlated with age, creatinine, BUN, and uric acid and negatively correlated with hemoglobin and albumin levels. Ordered logistic regression analysis showed that CKD was significantly correlated with plasma ILA (OR=4.49, P < 0.01), urinary ILA (OR=2.14,P < 0.01), urea levels (OR=1.43, P < 0.01) and hemoglobin levels (OR=0.95, P < 0.01) were significantly related. ROC curves indicated that plasma and urinary ILA were reliable predictors of CKD. CKD was correlated with plasma, urine ILA (OR=5.92, P < 0.01; OR=2.79, P < 0.01) and Hs-CRP (OR=2.45, P < 0.01). Plasma and urine ILA can potentially be used as biomarkers of CKD and inflammatory status.