The global incidence of chronic kidney disease (CKD) is rising rapidly. Immune cells play a crucial role in the onset and progression of CKD, however, the causal relationships and underlying immunological mechanisms remain incompletely elucidated. This deficiency hinders the development and application of early interventions and immunotherapies for CKD.

In this study, we hypothesize that alterations in immune cell phenotypes (ICPs) in the blood may influence the onset of CKD. We collated Genome Wide Association Studies (GWAS) data for 731 ICPs, alongside summary data for CKD and estimated glomerular filtration rate (eGFR). Utilizing bidirectional mendelian randomization analysis (MR), we identified the impact of ICPs on the onset of CKD.

Preliminary MR analyses revealed three ICPs positively associated with CKD onset: the absolute number of CD45RA+ CD28- CD8+ T cells (p = 1.209 × 10-15, 95% CI: 1.0002-1.0003), the percentage of CD28+ CD45RA+ CD8+ T cells of total T cells (p = 5.831 × 10-6, 95% CI: 1.0028-1.0070), and the percentage of CD45RA- CD28- CD8+ T cells of total T cells (p = 4.292 × 10-5, 95% CI: 1.0005-1.0015). After conducting sensitivity and reverse MR analyses, only the percentage of CD28+ CD45RA+ CD8+ T cells (naïve CD8+ T Cells) was found to have a sufficiently robust causal impact on CKD.

We are the first to demonstrate a significant positive association between the percentage of naïve CD8+ T cells and CKD onset. This finding offers new insights for early prevention and treatment of CKD.

This cross-sectional study aimed to investigate the association between drinking patterns and prevalence of diabetic kidney disease (DKD) among adults in the United States.

Data were analyzed from the NHANES surveys conducted between 1999 and 2016, including 26,473 participants. Drinking patterns were categorized by frequency (weekly, monthly, or yearly) and quantity (light, moderate, or heavy, based on daily consumption). Among participants with diabetes, DKD was defined using the albumin-to-creatinine ratio (ACR ≥30 mg/g) and estimated glomerular filtration rate (eGFR <60 mL/min/1.73 m2). Multivariable logistic regression models were used to evaluate associations, adjusting for potential confounders across the four models. Subgroup analyses were performed to assess the effects of modification by age, sex, race, BMI.

Drinking patterns and DKD were analyzed among 26,473 US adults (mean age, 46.6 years; 53.7% male). After adjusting for multiple confounders, heavy alcohol consumption was associated with a higher risk of DKD than light drinking (OR = 1.23, 95% CI, 1.04-1.46; p = 0.016). Conversely, moderate drinking frequency (3-4 days per week, 2-5 days per month, 3-126 days per year) was associated with a reduced DKD risk (OR = 0.67, 95% CI, 0.49-0.91; OR = 0.75, 95% CI, 0.56-0.99, OR = 0.71, 95% CI, 0.58-0.86, respectively). A nonlinear association was observed between alcohol consumption frequency and DKD in terms of weekly and yearly drinking days.

This study highlights the importance of drinking behavior in the management of diabetic kidney disease. Daily alcohol consumption was associated with an increased risk of DKD, whereas moderate alcohol consumption was associated with a reduced risk. These findings suggest that moderate drinking frequency may not exacerbate renal burden in individuals with diabetes and provide new perspectives for clinical interventions.

Previous studies have reported that renal function is associated brain structure and cognitive dysfunction. However, the association between renal function and memory-related disease was not well characterized.

Altogether, 5,282 individuals were included in this study based on China Longitudinal Study of Health and Retirement. Four estimated glomerular filtration rate indicators (eGFR), including CG, CKD-EPIscr, CKD-EPIscr-cys, and CKD-EPIcys were used to evaluate the association between renal function and memory-related disease.

The multivariable-adjusted HRs (95% CIs) of the memory-related disease in the low eGFR group (eGFR < 90 mL/min/1.73m2) were 1.56 (1.13-2.16) for CG, 1.56 (1.19-2.06) for CKD-EPIscr, 1.45 (1.06-1.99) for CKD-EPIscr-cys and 1.27 (0.91-1.77) for CKD-EPIcys, respectively. Similarly, each SD increase of eGFR was associated with reduced risk of memory-related disease on continuous analyses. Subgroup analyses further confirmed these associations. Moreover, the addition of eGFR to conventional risk factors improved the predictive power for memory-related disease (net reclassification improvement: 13.90% for CG, 19.83% for CKD-EPIscr and 30.65% for CKD-EPIscr-cys).

In conclusion, impaired renal function was associated with the increasing risk of memory-related disease, indicating that renal function may be a potential indicator for memory-related disease. Further studies from other races and populations are needed to replicate our findings and to clarify the potential mechanisms.

Both sleep disorders and chronic kidney disease (CKD) are recognized as significant public health concerns. In the general population, sleep disorders have been shown to be associated with frailty in the elderly. This study aims to evaluate the association between sleep duration and trouble sleeping with frailty in CKD patients, as well as the potential interactive effect between these two factors.

This cross-sectional study analyzed data from the National Health and Nutrition Examination Survey (NHANES) spanning 2005-2018. Sleep duration and trouble sleeping was self-reported. Frailty was assessed using a 49-item frailty index. The associations between sleep duration, trouble sleeping, and frailty were analyzed using weighted multivariate logistic regression and restricted cubic splines. Subgroup analysis was conducted to determine the consistency of the study's conclusions across various subgroups.

A total of 5,211 adult CKD patients were included in this analysis. Regression analysis results indicated that short sleep duration (OR = 1.364, 95% CI: 1.152-1.616), long sleep duration (OR = 1.648, 95% CI: 1.259-2.157), and trouble sleeping (OR = 2.572, 95% CI: 2.102-3.147) were significantly associated with an increased risk of frailty in CKD patients, with an interaction between sleep duration and trouble sleeping. Subgroup analysis revealed that the effects of trouble sleeping and sleep duration on frailty symptoms in CKD patients exhibit significant variation across age groups (p < 0.05 for interaction), with no notable differences observed in other subgroups. RCS results demonstrated a U-shaped relationship between frailty and sleep duration, with the lowest risk of frailty at 7.12 h of sleep.

Our findings indicated that both sleep duration and trouble sleeping were significantly associated with frailty in CKD patients, with a notable interaction between these two factors. Therefore, prevention and intervention strategies for frailty in CKD patients should address multiple aspects of sleep health.

Previous studies have suggested that gut dysbacteriosis may promote the onset of chronic kidney disease (CKD). However, the relationship between consumption of live microorganisms and CKD remains unclear. This study aimed to evaluate the association between dietary consumption of live microorganisms and risk of CKD.

We conducted a cross-sectional analysis using data from the National Health and Nutrition Examination Survey (NHANES) spanning 2001 to 2018. Dietary intake was assessed through self-reported questionnaires, while CKD diagnosis was based on glomerular filtration rate and albumin-creatinine ratio measurements.

After adjusting for potential confounders, participants with high live microbial intake had a significantly lower risk of CKD compared to those with low intake [odds ratio (OR): 0.79, 95% confidence interval (CI): 0.68-0.91, p = 0.001]. Similarly, those with moderate/high live microbial intake exhibited a reduced CKD risk compared to the low intake group (OR: 0.87, 95% CI: 0.78-0.97, p = 0.009). Subgroup analyses revealed a significant interaction between live microbial intake and CKD risk among participants with less than a high school education, as well as among Mexican Americans and other racial groups (including multiracial) (all P values for interaction < 0.05). A U-shaped dose-response relationship was identified between microbial intake and CKD risk, with significant non-linear associations observed for high consumption levels (P for non-linearity = 0.013).

High dietary intake of live microorganisms is associated with a lower risk of CKD, highlighting the potential role of gut microbiota modulation in CKD prevention.

The chronic kidney disease (CKD) poses a serious threat to human health. Long-term monitoring of urine is important in the management of CKD. Currently, the accuracy and stability of smartphone-based colorimetric analysis of urine indicators are limited due to the impact of different image-taking conditions on captured digital images of urine test strips. Herein, an attachment-free colorimetric correction analysis system (CCAS for short), consisting of a self-designed urine test strip array and an Android application integrated with an image calibration algorithm, were proposed for quantitative analysis of nine urine indicators. With this system the impact of image-taking conditions on captured digital image were largely corrected, and thus the accuracy and stability for digital image colorimetric analysis of urine test strip were improved. The limits of detection of creatinine, nitrite, urinary calcium, microalbumin, bilirubin, protein, pH, haemoglobin, and glucose were 1.607 mmol/L, 1.232 μmol/L, 0.297 mmol/L, 11.116 mg/L, 1.155 μmol/L, 0.042 g/L, 0.044, 0.058 mg/L, and 0.122 mmol/L, respectively. The accuracy of CCAS was validated by analyzing artificial urine samples and 143 clinical urine samples. As an accurate, low-cost and reliable system, CCAS addresses specific needs for patients to monitor their urine whenever and wherever possible with only their own smartphone.

Anthropogenic vanadium (V) emissions and exposure in the general population have recently increased. Experimental studies have shown that V is a nephrotoxic agent, but little is known about its effects on human kidney health. This work evaluated the association between urinary V concentrations with early kidney damage biomarkers and function in a pediatric population without any disease diagnosed.

A cross-sectional study was carried out and included 914 healthy subjects and determined urinary V concentrations, glomerular filtration rate (eGFR), albumin-creatinine ratio (ACR), and the presence of kidney injury molecule 1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) in urine. We evaluated the V effect using linear and logistic regression models adjusted by confounders.

Subjects found in the second and third tertiles of V showed an increase in urinary log-NGAL levels (βT2 vs. T1 = 0.39; 95% CI 0.14, 0.64, and βT3 vs. T1 = 1.04; 95% CI 0.75, 1.34) and log-KIM-1(βT2 vs. T1 = 0.25; 95% CI 0.04, 0.45 and βT3 vs. T1 = 0.39; 95% CI 0.15, 0.63); in addition, subjects in the third tertile had a positive and significant association with ACR (ORT3 vs. T1 = 1.96; 95% CI 1.29, 2.97) and increased in eGFR (βT3 vs. T1 = 3.98, 95% CI 0.39, 7.58), compared with subjects in the first tertile.

Our study reports the effect of V on kidney markers in a healthy pediatric population. It could be related to tubulointerstitial lesions and function abnormalities.

Platinum-based chemotherapies are essential in the treatment of several malignancies. However, such medications can damage the kidneys, frequently leading to both acute and chronic kidney disease. Treatment becomes more difficult for such problems. Physicians may alter chemotherapy regimens and utilize kidney-protecting medications to lessen renal damage. New imaging techniques and biomarkers also aid in the early detection of renal issues. To effectively handle the mentioned situation, oncologists, nephrologists, and pharmacists must collaborate. However, additional study is still required to develop customized therapies, discover strategies to minimize kidney injury and produce new platinum medicines. Hereupon, the present review's authors are being sought to address the causes, prospective treatments, and management of nephrotoxicity caused by platinum-based chemotherapy.

Recent studies have demonstrated that the transcription factor hepatocyte nuclear factor 4α (HNF4A) drives epithelial differentiation in the renal proximal tubules (PTs) and is critical for maintaining a mature PT phenotype. Furthermore, HNF4A down-regulation has been observed following kidney injury in mouse models. The aim of the present work was to investigate the role of HNF4A during acute and chronic human kidney disease and the loss of the mature PT phenotype in cultured PT cells. Loss of HNF4A expression and gain of vimentin expression were reciprocal and gradual during both acute and chronic kidney disease, as indicated by immunohistochemistry. Healthy human kidneys demonstrated partial or total loss of HNF4A expression in vimentin-positive scattered tubular cells. Primary cell isolation and subculture of PT cells recapitulated HNF4A-associated loss of the PT phenotype. Re-expression of HNF4A in cultured PT cells by adenoviral transduction increased transcripts related to brush border formation as well as absorptive and transport processes, as shown by RNA sequencing and gene set enrichment analyses. Thus, the reduction of HNF4A and increase of vimentin expression were connected to both acute and chronic kidney disease and represented a stereotypic injury response of the PT, resulting in dedifferentiation. HNF4A re-expression in cultured primary PT cells could provide a more reliable and predictive in vitro model to study PT function and injury.

With the increasing demand for dialysis, there is a growing emphasis on patient-centered care. This study investigated patients' satisfaction levels with peritoneal dialysis (PD) and hemodialysis (HD) care in Iran.

A cross-sectional multicenter study was conducted among 346 patients with chronic kidney disease (CKD) covered by the Iran Health Insurance Organization who received dialysis services from October to December 2022 across the country. Data were gathered using a self-made questionnaire through telephone interviews. Data analysis included descriptive statistics, t tests, ANOVA, and linear logistic regression using R software.

Patients reported high satisfaction with doctors and nurses, health care facilities, and costs. PD patients had higher overall satisfaction (P < 0.001) and were more satisfied with costs (P < 0.001), while HD patients reported greater satisfaction with doctor and nurse behavior (P = 0.012). Significant factors associated with satisfaction included marital status (P = 0.012), insurance coverage duration (P = 0.027), dialysis type (P < 0.001), and time to dialysis initiation (P = 0.027). Doctor and nurse behavior had the greatest impact on satisfaction (P < 0.001).

While patients were generally satisfied with the care provided, the findings revealed areas for improvement, particularly regarding the availability of medical centers and costs among dialysis patients. Focusing on patient education, communication, and supportive insurance policies has the potential to significantly enhance patient satisfaction and improve quality of life for dialysis patients.

Ozone (O3) is an important environmental pollutant that has garnered growing public concern. Epidemiological studies indicate that exposure to O3 is associated with an elevated risk of kidney disease, a common complication of diabetes. However, the harmful effects of O3 on the kidneys remain unconfirmed. Herein, we established models of non-diabetic and diabetic mice exposed to 0.5 ppm O3 for 28 days (4 h/day). We evaluated O3-induced renal injury and potential mechanisms through analyzing biochemical markers related to renal function, along with histopathology and transcriptomic sequencing of the kidneys. The results showed that O3 exposure caused glomerular hypertrophy in both non-diabetic and diabetic mice, with mesangial hypercellularity and kidney function impairment specifically in diabetic mice. Furthermore, renal levels of free fatty acids and cholesterol were significantly elevated in O3-exposed diabetic mice. The important roles of lipid and water-electrolyte metabolism related pathways in O3-induced kidney damage were found by transcriptome sequencing analysis. The mRNA and/or protein expressions of some genes involved in β-ENaC and AQP2 pathways, which are related to renal water and sodium retention, were changed in diabetic mice following O3 exposure by real-time quantitative PCR, immunofluorescence staining, and Western blotting. Overall, diabetic mice exhibited a higher vulnerability to adverse effects in the kidney after O3 exposure than non-diabetic mice. Dysregulation of lipid metabolism and imbalance in water-electrolyte homeostasis have been discovered as key contributing mechanisms. This study offers valuable insights into mechanisms through which ambient O3 poses renal health risks to both the general subjects and susceptible individuals.

Renal fibrosis, resulting from myofibroblast-mediated excessive extracellular matrix (ECM) deposition, lacks effective treatments. Novel peptide DR3penA developed by our group showed therapeutic potential for fibrotic diseases; however, its application was hindered by poor stability and bioavailability. To address this unmet need, we implemented stepwise optimization of DR3penA. The conformationally restricted analogs designed via structural predictions enhanced both activity and stability. Through structure-activity relationship analysis and cleavage site mapping, introducing unnatural amino acids improved stability. Fatty acid modifications conferred fibroblast-selective cytotoxicity and improved pharmacokinetics. After several rounds of progressive modification, peptide 27 exhibited remarkable stability, with a 5.68-fold extended half-life compared to DR3penA. Following profibrotic stimuli, peptide 27 effectively inhibited myofibroblast activation, epithelial-mesenchymal transition, and ECM synthesis. It also attenuated renal fibrosis in a unilateral ureteral obstruction model. Our study leverages multiple modifications that integrate cell and animal models to identify peptide 27 as a promising candidate for renal fibrosis therapy.

Renal tubular injury and activation of peripheral fibroblasts are hallmarks of chronic kidney disease (CKD), suggesting a close connection between the two cell types. Exosomes transport miRNAs and other substances to recipient cells. The involvement of exosome-mediated intercellular communication has been suggested in various diseases, including renal fibrosis. However, the underlying mechanisms remain to be determined.

Rab 27a-knockout mice were constructed to confirm the role of exosomes in mice with adenine-induced renal fibrosis. Exosome secretion from the kidneys of mice with adenine-induced renal fibrosis and UA-stimulated NRK-52E cells were investigated. Exosomes released from NRK-52E cells were harvested and incubated with NRK-49 F fibroblasts or injected intravenously into the mice via the tail vein. High-throughput miRNA sequencing was used to evaluate the miRNA profiles of UA-Exo. The roles of candidate miRNAs and their target genes and related pathways were predicted and evaluated in vitro and in vivo using specific miRNA mimics, miRNA inhibitors, siRNAs, and adeno-associated viruses (AAV).

Inhibition of exosome secretion by Rab27a knockout or siRNA Rab27a treatment inhibited fibroblast activation and ameliorated renal fibrosis. Significantly increased renal fibrosis was seen in mice treated with adenine, and exosome release was increased after UA treatment of NRK-52E cells. Exosomes released from NRK-52E cells after UA stimulation activated fibroblasts and exacerbated renal fibrosis. The expression of miR-330-3p in exosomes was significantly increased in the UA-Exo group compared with the control group, suggesting the potential use of miR-330-3p as a marker of renal fibrosis. CREBBP was found to be a specific target of miR-330-3p. The stimulation or inhibition of exosomal miR-330-3p release from renal tubular epithelial cells thus promoted or blocked fibroblast activation in vitro, while miR-330-3p-deficient exosomes attenuated renal fibrosis by modulating CREBBP in vivo.

The findings suggest that exosomes play an important role in promoting renal fibrosis by mediating the communication between renal tubular epithelial cells and fibroblasts. This role is associated with inhibition of CREBBP activity by exosomal miR-330-3p in fibroblasts. Thus, the miR-330-3p/CREBBP axis is a promising target for the treatment and management of renal fibrosis.

Chronic kidney disease (CKD) is creating an ever heavier global health burden with population ageing. This study aimed to examine the longitudinal associations of remnant cholesterol (RC) with CKD morbidity in a large high-risk population (type 2 diabetes and hypertension).

A total of 11,881 participants who participated in annual health examinations from 2021 to 2023 were included in our analysis. The Cox proportional hazards model was performed to analyze the associations of baseline RC, cumulative RC, and variability of RC with CKD morbidity. The cross-lagged panel analysis was used to examine the temporal relationship between RC and renal function.

The results of the multivariable-adjusted models showed that higher baseline, cumulative RC, and variability of RC were related to higher risks of developing CKD, the adjusted HR (95% CI) comparing tertile 3 with tertile 1 were 1.26 (95% CI 1.10-1.45), 1.33 (95% CI 1.16-1.52), 1.36 (95% CI 1.20-1.55), respectively. Stratified analysis found that gender did not change these associations. Compared with individuals in the low cumulative and variability RC group, those in the high cumulative and variability RC group had a 1.62 times higher risk of CKD (95% CI: 1.34-1.96). The cross-lagged panel analysis showed that the increase in RC levels may precede the decrease in eGFR.

High baseline level, cumulative exposure to RC, and variability of RC are associated with increased CKD risk. Therefore, monitoring RC-related parameters is crucial to delay the occurrence and development of CKD in high-risk populations.

Kidney disease is a global health issue that affects over 850 million people, and early detection is key to preventing severe disease and complications. Kidney diseases are associated with complex and dysregulation of lipid metabolism. Spatial metabolomics through mass spectrometry imaging (MSI) enables spatial mapping of the lipids in tissue and includes a variety of techniques that can be used to image lipids. In the kidney, MSI studies often seek to resolve individual functional tissue units such as glomeruli and proximal tubules. Several different MSI techniques, such as matrix-assisted laser desorption/ionization (MALDI) and desorption electrospray ionization (DESI), have been used to characterize lipids and small molecules in chronic kidney disease, acute kidney injury, genetic kidney disease, and cancer. In this review we provide several examples of how spatial metabolomics data can provide critical information concerning the localization of changes in various disease states. Additionally, when combined with pathology, transcriptomics, or proteomics, the metabolomic changes can illuminate underlying mechanisms and provide new clinical insights into disease mechanisms. Semin Nephrol 36:x-xx © 20xx Elsevier Inc. All rights reserved.

Chronic kidney disease (CKD) is a progressive, irreversible impairment of kidney function due to various etiologies. Numerous studies have shown that sodium-glucose cotransporter-2 inhibitors (SGLT2i) slow the progression of CKD, due to their pleiotropic effects. Therefore, there has been an increase in interest in their effects not only on kidney function but also on other parameters in patients with CKD. The aim of the study was to examine the effects of SGLT2i on serum lipid values and kidney function in patients with CKD undergoing SGLT2i treatment.

This study was a retrospective data analysis of 75 patients with CKD on SGLT2i treatment. We compared the values of biochemical parameters, renal function outcomes, and blood pressure at two time points: baseline and 24 months after.

Total cholesterol (Chol) significantly decreased in all patients, while triglyceride (Tg) and low-density lipoprotein cholesterol (LDLc) levels also decreased in all patients. High-density lipoprotein cholesterol (HDLc) levels increased, but this increase was not significant. Creatinine clearance (Ccr) significantly decreased, and serum urea (Sur) significantly increased in all patients. The proteinuria (Prt) levels did not change significantly. The results showed that the diastolic blood pressure (DBP) significantly decreased in all patients.

This study showed that the use of SGLT2i reduced total Chol in all patients with CKD during the 24-month follow-up, regardless of diabetes mellitus (DM) status. No significant differences were observed for the Tg, LDLc, and HDLc values.

Chronic kidney disease induces alterations in the heterogeneity of iron deposition within the basal ganglia. Quantitative analysis of the heterogeneity of iron deposition within the basal ganglia may be valuable for diagnosing chronic kidney disease-related cognitive impairment.

In this prospective observational cohort study, quantitative susceptibility mapping (QSM) was performed in chronic kidney disease patients. Susceptibility values of each nucleus within the basal ganglia were measured. Radiomic features were extracted from habitats of the basal ganglia on QSM images. Habitat-based models for diagnosing cognitive impairment were constructed using the random forest algorithm. Logistic regression was employed to build the clinical model and the combined model. The performance of each model was evaluated by the receiver operating characteristic (ROC) analysis.

A total of 146 patients (mean age, 51 ± 13 years; 92 male) were included, of which 79 had cognitive impairment. The two habitats-based model achieved an area under the curve of 0.926 (95% CI 0.842-1.000) on the test set, the highest among all prediction models. The two-habitat maps indicated that chronic kidney disease had two distinct patterns of impact on iron deposition in the basal ganglia region. The capability of the two habitats-based model to identify chronic kidney disease-related cognitive impairment was significantly superior to that of the susceptibility values measured in various nuclei (all p < 0.05).

This study innovatively applied a habitat-based quantitative analysis technique to QSM, successfully constructing a model that accurately diagnoses chronic kidney disease-related cognitive impairment.

This study was approved by the Beijing Friendship Hospital Ethics Board (ClinicalTrials.gov Identifier: NCTO5137470) and conducted in accordance with the Declaration of Helsinki ethical standards.

Chronic kidney disease (CKD) is projected to rank among the top five causes of mortality by 2050. In addition to established risk factors, adverse childhood experiences (ACEs) have recently emerged as significant contributors to health risks, including CKD and depressive syndrome (DS). However, the mechanisms linking ACEs, DS, and CKD remain unclear. This study aims to explore the role of ACEs in CKD development, with a focus on the mediating effects of DS.

This retrospective cohort study analyzed data from 10,247 participants in the China Health and Retirement Longitudinal Study (CHARLS). Logistic regression models were applied to assess the associations between ACEs, DS, and incident CKD, adjusting for demographic and lifestyle factors. Mediation analysis was conducted to evaluate the role of DS in the relationship between ACEs and CKD.

Logistic regression analysis indicated that participants with a history of ACEs were at higher risk for both DS and CKD. Mediation analysis demonstrated that DS partially mediated the associations between CKD and seven specific ACEs: physical abuse, household substance abuse, household mental illness, domestic violence, unsafe neighborhood, peer bullying, and parental disability. Notably, DS fully mediated the relationship between CKD and unsafe neighborhood.

ACEs significantly influence CKD risk in middle-aged and older adults, with DS serving as a key mediator. These findings underscore the importance of early mental health interventions and ACE-focused preventive strategies to reduce the burden of CKD.

Hypertensive nephropathy is increasingly prevalent and a leading cause of end-stage renal disease. Current treatment strategies for hypertensive nephropathy focus on blood pressure control and reducing urinary albumin. However, the use of angiotensin-converting enzyme inhibitor (ACEI)/angiotensin receptor blocker (ARB) medications carries risks, including a potential decrease in glomerular filtration rate (GFR). This report aims to assess the clinical effectiveness of Quanduzhong capsules (QDZCs) in early-stage hypertensive kidney damage, contributing to the evidence base for their use in traditional Chinese medicine for hypertension treatment.

The patients, two middle-aged gentlemen with over a decade of hypertension in their medical history, were currently in the early phase of grade 1 hypertension. Notably, their blood pressure readings consistently exceeded the normal parameters. Furthermore, they exhibited signs of microalbuminuria and proteinuria in their clinical presentations. Based on these symptoms, they received a diagnosis of hypertensive kidney damage, specifically at the microalbuminuria stage.

After admission, the two patients took QDZCs for treatment. The medication method was: 2 times a day, 3 capsules each time. The results showed that the microalbuminuria of case 1 and the proteinuria of case 2 were reduced within 12 weeks after taking the medicine, and the average 24-h blood pressure was also reduced. Case 2 experienced a slight decrease in creatinine clearance and glomerular filtration rate after treatment, but the difference was not significant. During the 12-week follow-up period, there were no significant abnormalities in serum creatinine, blood urea nitrogen, creatinine clearance, and estimated glomerular filtration rate.

This case report shows that Quanduzhong capsule can lower blood pressure and improve symptoms of microalbuminuria and proteinuria in patients with early hypertensive renal damage, and may provide a promising treatment option for the management of early hypertensive renal damage. However, the evidence is preliminary and larger, controlled studies are needed to determine its efficacy and potential advantages.

The transcription factor brain and muscle Arnt-like protein-1 (BMAL1) is a clock protein involved in various diseases, including atherosclerosis and cancer. However, BMAL1's involvement in kidney fibrosis and the underlying mechanisms remain largely unknown, a gap addressed in this study. Analysis through Masson's trichrome and Sirius red staining revealed that all groups exposed to unilateral ureteral obstruction showed increased BMAL1 protein expression accompanied by increased TGF-β1 expression and elevated key fibrosis markers, including α-SMA, compared with sham groups. Although TGF-β1 induced BMAL1 protein expression accompanied by increased α-SMA expression in NRK-49F cells, the REV-ERBα agonist GSK4112, a transcriptional repressor of BMAL1, or siRNA targeting BMAL1 significantly inhibited TGF-β1-induced α-SMA expression. Furthermore, BMAL1 knockdown significantly suppressed TGF-β1-induced NOX4/ROS/p38 pathways in NRK-49F cells. Thus, BMAL1 positively regulates TGF-β1-induced signaling associated with fibrotic responses via the NOX4/ROS/p38 pathway. Overall, this study uncovers BMAL1 as a promising therapeutic target for preventing and treating kidney fibrosis, potentially preventing renal failure.

IgA nephropathy (IgAN), the world's most common primary glomerular disease, carries a significant lifetime risk for kidney failure as well as an enormous socioeconomic burden. In the past, studies in patients with IgAN largely focused on optimizing so-called supportive care, that is, blockade of the renin-angiotensin system, blood pressure control, and lifestyle modifications. The effectiveness of immunosuppressive measures, particularly high-dose corticosteroid therapy, has been reported variably, but there is considerable evidence for an increase in serious adverse effects with such therapies. This disappointing situation has changed dramatically with a better understanding of the pathogenesis of IgAN, and with regulatory agencies accepting changes in proteinuria and the estimated glomerular filtration rate loss or slope over 2 to 3 years as surrogate outcome markers. A multitude of new therapies are now being evaluated in IgAN, and several drugs, such as sodium-glucose transporter-2 inhibitors, sparsentan (a dual endothelin-1 and angiotensin II receptor blocker), nefecon (a targeted release formulation of budesonide), and iptacopan (a complement factor B inhibitor), have been approved, with more to come in the next few years. In this review, we propose a new treatment paradigm that combines therapies with different mechanisms of action to target the immune components and the chronic kidney disease components of IgAN in parallel to preserve long-term kidney survival.

Chronic Kidney Disease (CKD) has become one of the major life-threatening conditions. Moringa seeds have been reported to exhibit renoprotective effects, with Niazimicin as its characteristic component.

To investigate the anti-renal injury effects of Niazimicin and its mixed micelles (N-M) that composed of monomethyl ether poly (ethylene glycol)-polycaprolactone (mPEG-PCL) and polyethylene glycolated chitosan (PEG-CS) on adenine-induced CKD mice.

PEG-CS was prepared via formaldehyde linkage method. The thin film dispersion method was employed for the preparation of N-M before it was characterized in vivo and in vitro. The anti-renal injury effects were evaluated by analyzing the serum levels of creatinine (Cr), p-Cresol sulphate (pCs), indole sulphate (IS) and hematoxylin-eosin (HE)-stained sections of hepatic and renal pathological tissues in CKD mice.

The N-M were spherical micelles of uniform size and highly dispersed with particle size of 42.94 ± 0.58 nm, encapsulation efficiency (EE) of 97.73 ± 2.33% and drug loading (DL) of 16.17 ± 0.28%, as well as good stability, and a very low critical micelle concentration (CMC) value of 0.00731 mg/mL. The N-M had a delayed-release effect and higher oral bioavailability compared to Niazimicin.

In CKD mice, Niazimicin exhibited an anti-renal injury effect, while the renoprotective effect of N-M was superior to that of Niazimicin.

It is unclear whether trimethylamine N-oxide (TMAO) and its precursors are bidirectionally associated with kidney dysfunction.

This study aims to investigate whether increased TMAO and its precursors are linked to decreased estimated glomerular filtration rate (eGFR) and whether reduced eGFR is associated with elevated TMAO and its precursors.

Our study consists of participants with creatinine, TMAO, and its precursors (choline, carnitine, and betaine) repeatedly measured from the Fuxin rural cohort. We utilized cross-lagged panel models to assess the potential bidirectional associations of TMAO and its precursors with eGFR. Age (≥60 and <60 y) and sex-specified associations and interaction effects were examined using multi-group cross-lagged panel models. The Bonferroni method was applied for multiple comparisons.

Of 1746 participants [mean age 59.4 ± 9.3 y, 584 (33%) male], TMAO was inversely related to eGFR after 2 years [cross-lagged coefficient, 95% confidence interval: -0.030, -0.058, -0.002, P = 0.035], and eGFR was negatively associated with carnitine after 2 years (-0.138, -0.198, -0.078, P < 0.001). Subgroup analysis showed significant associations between baseline TMAO and eGFR after 2 years in individuals aged 60 and older (-0.061, -0.107, -0.014, P = 0.011) and between baseline eGFR and carnitine after 2 years in individuals aged 60 and older (-0.093, -0.164, -0.022, P = 0.010), in those under 60 (-0.153, -0.226, -0.079, P < 0.001), and in females (-0.154, -0.229, -0.079, P < 0.001). Additionally, baseline eGFR is nominally associated with choline after 2 years in those aged under 60 (0.092, 0.017, 0.167, P = 0.017) and in males (0.114, 0.015, 0.213, P = 0.025).

Deceased eGFR is related to elevated serum carnitine concentrations and may be linked to choline. Conversely, elevated TMAO may be linked to reduced kidney function. This provides novel evidence that managing healthy kidney function helps keep TMAO and its precursors at optimal levels, whereas maintaining low TMAO concentrations reduces risk of kidney disease.

The open conformation of the enzyme transglutaminase 2 (TG2) contributes to kidney fibrosis through transamidase activity by cross-linking extracellular matrix fibres and releasing transforming growth factor β1 (TGFβ1), a key driver of fibrogenesis. We investigated the antifibrotic potential of TG2 inhibition downstream of TGFβ1 using two TG2 inhibitors, LDN27219 and Z-DON, which modulate TG2 into the closed and open state, respectively.

The TG2 inhibitors were studied in human precision-cut kidney slices (PCKS) and in cell cultures of primary renal cell types: endothelial and epithelial cells, and fibroblasts. PCKS and cell cultures were stimulated with TGFβ1 (10 ng/ml) for 48 h with or without LDN27219 (10 μmol/l) or Z-DON (40 μmol/l). We evaluated mRNA and protein expression of TG2 and fibrosis markers (fibronectin, α-smooth muscle actin and collagens), and TG2 transamidase activity.

In PCKS, TG2 was unaffected by TGFβ1, but mRNA levels of fibrosis markers increased with the stimulation and decreased in most LDN27219-treated PCKS compared to the control. No changes in protein expression of fibrosis markers were achieved with TGFβ1. In endothelial and epithelial cells, but not fibroblasts, fibronectin expression was increased with TG2 inhibition. Conversely, collagen 3α1 decreased by TG2 inhibition, further amplified by the closed conformation.

The antifibrotic effects of TG2 inhibition extend beyond the release of TGFβ1, specifically in the closed conformation, although this varies among cell types. Our results indicate that the closed conformation of TG2 has an active antifibrotic potential in humans, in addition to blocking transamidase activity.

Self-care and self-efficacy are crucial in managing kidney failure requiring hemodialysis. However, traditional education methods have not effectively improved self-care and self-efficacy. Therefore, utilizing more effective models, such as the partnership care model, is essential. This study aimed to determine the impact of the partnership care model on self-care and self-efficacy in hemodialysis patients.

This quasi-experimental study was conducted with 74 hemodialysis patients at Shahid Beheshti Hospital in Hamadan. Patients were divided into control and intervention groups. The control group received only routine care, while the intervention group received nursing care based on the partnership care model in addition to routine care. This included eight educational sessions over one month, with two sessions per week. Data were collected using self-care and Sherer self-efficacy questionnaires before and two months after the intervention. Data were analyzed using SPSS version 16.

The study demonstrated significant improvements in self-care and self-efficacy among hemodialysis patients following the collaborative care intervention. Post-intervention, the experimental group showed substantial benefits with an effect size of 1.41 for self-care (95 % CI: 0.87-1.95, p < 0.001) and an effect size of 1.55 for self-efficacy (95 % CI: 0.99-2.10, p < 0.001), highlighting the effectiveness of the intervention.

The study demonstrated that the partnership care model, through comprehensive education and social and motivational support, significantly improved self-care and self-efficacy in hemodialysis patients. Therefore, it is recommended that hospitals and nurses adopt this model to enhance the health and quality of life of patients.

Periodontitis is a ubiquitous chronic inflammatory disease affecting the supporting tissues of the teeth and is a major cause of multiple tooth loss. Despite being preventable, periodontitis and dental caries are responsible for more years lost to disability than any other human condition. The most severe form of periodontitis affects 1 billion individuals, and its prevalence is increasing globally. Periodontitis arises from a dysregulated and hyperactive inflammatory response to dysbiosis in the periodontal microbiome. This response has systemic effects associated with premature mortality and elevated risk of several systemic non-communicable diseases (NCDs), including atheromatous cardiovascular disease, type 2 diabetes and chronic kidney disease (CKD). This risk association between periodontitis and NCDs is independent of their shared common risk factors, suggesting that periodontitis is a non-traditional risk factor for NCDs such as CKD. As periodontitis progresses, the immune cells and mediators underpinning its pathophysiology leak into the systemic circulation through the ulcerated oral mucosal lining, inducing in a systemic inflammatory profile that closely mirrors that observed in patients with CKD. The relationship between periodontitis and CKD seems to be bi-directional, but large-scale intervention studies are required to clarify causality and could lead to new care pathways for managing each condition as an exposure for the other.

Afamin is a vitamin E-binding glycoprotein primarily expressed in the liver and kidney. This study investigated whether serum afamin concentrations are associated with kidney function and incident kidney failure.

Prospective cohort study with 6.5 years follow-up.

5,041 White patients enrolled in the German Chronic Kidney Disease (GCKD) study with measured afamin concentrations and either an estimated glomerular filtration rate (eGFR) of 30-60mL/min/1.73m2 or an eGFR>60mL/min/1.73m2 with a urinary albumin-creatinine ratio (UACR) of≥300mg/g at study entry.

Serum afamin concentrations (mg/L).

Incident kidney failure (initiation of kidney replacement therapy or kidney-related death).

Generalized linear regression and quantile regression models fit to investigate the association of afamin concentrations with eGFR and UACR. Adjusted Cox regression analysis to examine the association of afamin concentrations with incident kidney failure.

The mean±SD afamin concentration at study entry was 73.2±17.6mg/L. Higher afamin concentrations were associated with better kidney function with a 2.60mL/min/1.73m2 higher eGFR (95% CI, 2.30-2.89) and a 5.97mg/g lower UACR (95% CI, 3.04-8.90) for each 10mg/L higher level of afamin concentration in adjusted analysis. During the follow-up period, each 10mg/L higher level of afamin concentration was associated with a 14% lower risk of kidney failure (HR, 0.86 [95%CI, 0.81-0.92], P<0.001).

Residual confounding, and potential limited generalizability to non-White populations and people with mild stages of chronic kidney disease (CKD) or no CKD.

Higher serum afamin concentrations appear to be associated with a higher eGFR, less albuminuria, and a lower risk for future kidney failure in patients with CKD.

Although previous studies showed toxicity of brominated flame retardants (BFRs) in human kidney cells in vitro, less is known about actual effects of BFRs exposure on kidney impairment. This study aims to examine associations of joint exposure to multiple BFRs with kidney impairment risk among adults, and with all-cause mortality risk among kidney impairment adults. Information on study participants and their serum concentrations of eleven BFRs (ten PBDEs and one PBB) were obtained from NHANES 2003-2004 and National Death Index. Factor analysis was applied to identify BFR exposure patterns. Data were analyzed using weighted multivariate logistic and Cox proportional regressions to examine the associations of BFR exposure patterns with kidney impairment risk and with all-cause mortality risk, respectively. Results showed concentrations of PBDE-28, PBDE-47, PBDE-85, PBDE-100, PBDE-154 and PBDE-66 among participants with kidney impairment were significantly higher than those without kidney impairment (all p < 0.050). Three exposure patterns were identified under an eigenvalue of ≥ 1.0 (p of Bartlett's test: <0.001; KMO value: 0.787), and one pattern of them, which was characterized by high exposure to PBDE-28, PBDE-47, PBDE-85, PBDE-99, PBDE-154 and PBDE-66, was positively associated with kidney impairment risk (weighted covariates-adjusted OR: 1.317; 95 % CI: 1.031-1.683). The median of follow-up period was 190.0 months. All patterns were not significantly associated with all-cause mortality risk during the follow-up period (all p > 0.050). In conclusion, this study found for the first time that high exposure to some PBDEs may increase kidney impairment risk, but not directly affect prognosis of kidney impairment among adult population.

Chronic kidney disease (CKD) is an incapacitating illness associated with distressing symptoms (DS) that have negative impact on patients' health-related quality of life (HRQOL).

To assess the severity of DS and their relationships with HRQOL among patients with CKD in Jordan.

A descriptive cross-sectional design was used. A convenience sampling approach was used to recruit the participants. Patients with CKD (n = 140) who visited the outpatient clinics in four hospitals in Amman between November 2021 and December 2021 were included.

The Edmonton Symptom Assessment System was used to measure the severity of the DS while the Short Form-36 tool was used to measure the HRQOL. Participants' mean age was 50.9 (SD = 15.14). Most of them were males (n = 92, 65.7%), married (n = 95, 67.9%), and unemployed (n = 93, 66.4%). The highest DS were tiredness (mean = 4.68, SD = 2.98) and worse well-being (mean = 3.69, SD = 2.43). The highest HRQOL mean score was for the bodily pain scale with a mean score of 68.50 out of 100 (SD = 32.02) followed by the emotional well-being scale with mean score of 67.60 (SD = 18.57).

Patients with CKD had suboptimal HRQOL, physically and mentally. They suffer from multiple DS that have a strong association with diminished HRQOL such as tiredness and depression. Therefore, healthcare providers should be equipped with the essential knowledge and skills to promote individualized strategies that focusing on symptom management.

Chronic kidney disease (CKD), which represents a significant global health concern, is characterized by a gradual decline in kidney function, leading to complications such as electrolyte imbalance, cardiovascular disease, and immune dysfunction. Standard CKD management includes dietary modifications, ketoanalogues supplementation, blood pressure and blood glucose control, hydration maintenance, and treatment of the underlying causes. Emerging evidence has indicated a significant role of the gut microbiota in CKD, and that dysbiosis of the gut microbiota contributes to the progression of CKD towards end-stage renal disease. Probiotics and prebiotics have recently garnered attention owing to their potential to enhance gastrointestinal health and well-being by restoring the balance of the gut microbiota. Specific probiotic strains, including Lactobacillus and Bifidobacterium, promote beneficial bacterial growth, suppress harmful bacteria, and exert anti-inflammatory, antihypertensive, and antidiabetic effects. The combination of Streptococcus thermophilus, Lactobacillus acidophilus, Bifidobacterium longum, and Bacillus coagulans has demonstrated potential as a therapeutic formulation for CKD management in various studies, highlighting its promise in treating CKD; however, supporting evidence remains limited, making it crucial to conduct further investigations to determine the specific effects of different probiotic formulations on outcomes in patients with CKD.

Patients with heart failure (HF) and chronic kidney disease (CKD) are often suboptimally treated due to concerns of hyperkalaemia, declining kidney function, and hypotension. They commonly suffer from fluid overload which can lead to frequent hospitalisations and death. This research aims to determine the characteristics associated with hospital admissions and death in patients with CKD and HF.

Consecutive patients with CKD stage 3-5 and HF (regardless of ejection fraction) attending a large, specialised CKD-HF clinic between 12/Sept/2019 and 11/Nov/2021 were identified and data were collected on demographic factors, renal and heart function, medications, hospitalisations, and death. Multinomial and Cox regressions determined the characteristics of patients requiring hospitalisation and their risk of death, respectively.

A total of 667 admissions were attributable to 318 patients, 201 admissions were for HF. Men were less likely than women to have been admitted to hospital for HF (risk ratio [RR] 0.43, 95% CI 0.20, 0.94) and non-HF causes (RR 0.21, 95% CI 0.10, 0.47). A serum haemoglobin level greater than 100 g/L was associated with fewer HF and non-HF admissions compared to a serum haemoglobin less than 100 g/L (RR 0.26, 95% CI 0.09, 0.74; RR 0.17, 95% CI 0.06, 0.47). Compared to CKD stage 3, CKD stage 4 was associated with an increased risk of HF and non-HF admissions (RR 4.01, 95% CI 1.04, 15.5; RR 4.33, 95% CI 1.13, 16.5). Having a HF admission (HR 2.41, 95% CI 1.27, 4.60), HFrEF (HR 2.18, 95% CI 1.30, 3.63), CKD stage 4 (HR 1.91, 95% CI 1.16, 3.16), and loop diuretic use (HR 2.24, 95% CI 1.14, 4.40) were associated with a significantly increased risk of death compared to people with no admissions, with HF with reduced preserved ejection fraction, CKD stage 3, and no diuretic use, respectively. The use of RAAS inhibitors halved the risk of death compared to non-prescribed patients (HR 0.44, 95% CI 0.27, 0.72).

Hospital admissions among CKD-HF patients were common, particularly in those with lower serum haemoglobin levels and advanced CKD stage. The risk of death was higher in those with HF admissions, the presence of HFrEF, advanced CKD stage, loop diuretic use, and those not prescribed RAAS inhibitors.

Peritoneal dialysis (PD) is a vital treatment for end-stage renal disease patients, but its efficacy is often compromised by complications such as infections and peritoneal fibrosis. Biological field-effect transistors (BioFETs) present a promising solution for rapid, sensitive, and non-invasive detection of indicators and biomarkers associated with these complications, potentially enabling early intervention. However, BioFETs are yet to be adopted for PD monitoring. This review presents a forward-looking analysis of the capacity and potential integration of BioFETs into PD management systems, highlighting their capacity to monitor both routine indicators of dialysis efficiency and metabolic status, as well as specific biomarkers for complications such as inflammation and fibrosis. We examine the challenges in adapting BioFETs for PD applications, focusing on key areas for improvement, including sensitivity, specificity, stability, reusability, and clinical integration. Furthermore, we discuss various approaches to address these challenges, which are crucial for developing point-of-care (PoC) and multiplexed wearable devices. These advancements could facilitate continuous, precise, and user-friendly monitoring, potentially revolutionizing PD complication management and enhancing patient care.

Psychological determinants underlying the dietary management intention (DMI) of Chinese patients with chronic kidney disease (CKD) are not well understood. This hinders the development of theory-informed dietary interventions targeting this population. The aim of this study was to identify factors influencing DMI of Chinese patients with CKD through the lens of Protection Motivation Theory (PMT).

500 patients with CKD from a nephrology ward of a large teaching hospital in China completed a survey including measures of PMT constructs (i.e., perceived vulnerability, perceived severity, intrinsic and extrinsic rewards, self-efficacy, response efficacy, and response cost) using validated scales adapted from previous studies. Data were analyzed using confirmatory factor analysis and multiple linear regression.

Three PMT constructs, namely perceived severity [B = 0.198, P < 0.001], response efficacy [B = 0.331, P  < 0.001], and self-efficacy [B = 0.325, P  < 0.001], two demographic variables, namely single status [B = -0.180, P = 0.028] and education level [B = 0.080, P = 0.007], and a disease-related variable, namely CKD stage [B = .056, P = 0.001], predicted 39.3% of the variance of the CKD DMI. No significant effect on CKD DMI was observed for other predictor variables (P > 0.05).

Applying the PMT, significant predictors of DMI in Chinese patients with CKD were identified, which should be targeted in behavior change initiatives aimed at promoting dietary management.

An observational study suggested sodium-glucose cotransporter 2 (SGLT2) inhibitors might promote healthy aging. However, whether brain-related phenotypes mediate this association is still a question. We applied Mendelian randomization (MR) to investigate the effect of SGLT2 inhibition on chronological age, biological age, and cognition and explore the mediation effects of brain imaging-derived phenotypes (IDPs).

We selected genetic variants associated with both expression levels of SLC5A2 (Genotype-Tissue Expression and eQTLGen data; n = 129 to 31 684) and hemoglobin A1c (HbA1c) levels (UK Biobank; n = 344 182) and used them to proxy the effect of SGLT2 inhibition. Aging-related outcomes, including parental longevity (n = 389 166) and epigenetic clocks (n = 34 710), and cognitive phenotypes, including cognitive function (n = 300 486) and intelligence (n = 269 867) were derived from genome-wide association studies. Two-step MR was conducted to explore the associations between SGLT2 inhibition, IDPs, and aging outcomes and cognition.

SGLT2 inhibition was associated with longer father's attained age [years of life increase per SD (6.75 mmol/mol) reduction in HbA1c levels = 6.21, 95% confidence interval (CI) 1.27-11.15], better cognitive function (beta = .17, 95% CI 0.03-0.31), and higher intelligence (beta = .47, 95% CI 0.19-0.75). Two-step MR identified 2 IDPs as mediators linking SGLT2 inhibition with chronological age (total proportion of mediation = 22.6%), where 4 and 5 IDPs were mediators for SGLT2 inhibition on cognitive function and intelligence, respectively (total proportion of mediation = 61.6% and 68.6%, respectively).

Our study supported that SGLT2 inhibition increases father's attained age, cognitive function, and intelligence, which was mediated through brain images of different brain regions. Future studies are needed to investigate whether a similar effect could be observed for users of SGLT2 inhibitors.

The study, which was based on NHANES data (1999-2018), included 21,234 nondiabetic individuals aged 20 years and older to investigate the associations between the estimated glucose disposal rate (eGDR) and the risk of chronic kidney disease (CKD) and proteinuria. CKD was defined as an estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73 m2, and proteinuria was defined as a urinary albumin-to-creatinine ratio (UACR) exceeding 30 mg/g. The results demonstrated a significant inverse association between eGDR levels and the risks of CKD and proteinuria. After adjusting for potential confounders, the association between eGDR and CKD showed that, compared with those for Q1, the adjusted odds ratios (ORs) for Q2, Q3, and Q4 were 0.82 (95% CI: 0.61-1.11), 0.62 (95% CI: 0.39-0.98), and 0.55 (95% CI: 0.28-1.05), respectively. For the relationship between eGDR and proteinuria, the adjusted ORs for Q2, Q3, and Q4 were 0.54 (95% CI: 0.42-0.69), 0.41 (95% CI: 0.27-0.62), and 0.65 (95% CI: 0.43-0.98), respectively. Moreover, each standard deviation increase in eGDR was associated with a 9% reduction in CKD risk (OR: 0.91, 95% CI: 0.85-0.98) and a 13% reduction in proteinuria risk (OR: 0.87, 95% CI: 0.82-0.93). Further adjustments via restricted cubic spline (RCS) regression analysis revealed a significant nonlinear relationship between eGDR and CKD and a U-shaped relationship between eGDR and proteinuria. A lower risk of proteinuria was observed when eGDR levels were between 8.70 and 9.91. These findings, combined with those of previous studies, suggest that eGDR may serve as a potential alternative metric for insulin resistance (IR). In nondiabetic individuals, the eGDR was significantly associated with the risk of CKD and proteinuria, with a notable nonlinear pattern in these relationships.

Chronic kidney disease (CKD) is commonly accompanied by cognitive dysfunction and dementia, which, in turn, increase the risk of hospitalization, cardiovascular events and death. Over the last 30 years, only four studies focused on genetic markers of cognitive impairment in CKD and kidney failure (KF), indicating a significant gap in research. These studies suggest potential genetic predispositions to cognitive decline in CKD patients but also underscore the necessity for more comprehensive studies. Seventeen reports have established connections between cognitive function and kidney disease markers such as estimated glomerular filtration rate (eGFR), Cystatin C and albuminuria. A rapid eGFR decline has been associated with cognitive deterioration and vascular dementia, and mild to moderate eGFR reductions with diminished executive function in elderly men. Various biomarkers have been associated to Alzheimer's disease or dementia in CKD and KF. These include amyloid beta and phosphorylated tau proteins, uremic toxins, gut microbiota, metabolic indicators, hypertension, endothelial dysfunction, vitamins and inflammation. However, the causal relevance of these associations remains unclear. Overall, the available evidence points to a complex interplay between the different biomarkers and cognitive health in CKD patients, underscoring the need for more research to elucidate these relationships.

The Atherogenic Index of Plasma (AIP) has been reported as a strong predictor of all-cause mortality in the overall population. However, the lipid profile changes in individuals with end-stage kidney disease (ESKD) undergoing peritoneal dialysis (PD) may affect the prognostic utility of AIP for all-cause mortality. The connection between them remains unclear.

This study included patients receiving PD at five hospitals in China from January 1, 2013, to December 31, 2019, with follow-up until June 30, 2020. The primary exposure variable in this investigation was the logarithm of the triglycerides (TG)/high-density lipoprotein cholesterol (HDL-C) ratio, which was used to compute the AIP, and the outcome variable was all-cause mortality. A Cox proportional hazards regression model was employed to analyze the association between AIP and all-cause mortality. Moreover, stratified analyses were performed to investigate this association further. Kaplan-Meier curves were employed for survival analysis, assessing the prognostic implications of varying AIP levels. Nonlinear associations were examined using smooth curve fitting techniques.

A total of 869 patients were included in this study, of whom 153 died during the follow-up period. An inverse association was observed between AIP and all-cause mortality risk in the highest tertile compared to the lowest tertile (HR: 0.56, 95% CI: 0.37-0.84) after correcting for potential confounding variables. Moreover, a nonlinear association was observed between the rates of all-cause mortality and AIP. A segmented Cox regression model identified an inflection point at an AIP value of 0.63 (P = 0.014 for the log-likelihood ratio test). More specifically, it was negatively associated with the all-cause mortality risk (HR: 0.42, 95% CI: 0.25-0.73, P = 0.002) when AIP was ≤ 0.63. On the other hand, AIP showed a positive association with the risk of all-cause mortality when it was more than 0.63 (HR: 8.94, 95% CI: 1.66-48.10, P = 0.011).

The present study identified a non-linear association between AIP and all-cause mortality in patients receiving peritoneal dialysis.

 This cross-sectional study aimed to investigate the oral health-related quality of life (OHRQoL), its associated factors, and the prevalence of possible sarcopenia in Thai well-maintained patients with end-stage renal disease (ESRD) undergoing peritoneal dialysis (PD).

 Data were collected from 63 participants undergoing PD at Banphaeo-Charoenkrung Hemodialysis Center. Dry mouth was evaluated through unstimulated salivary flow rate measurement and self-reported xerostomia questionnaires. OHRQoL was assessed using the Thai version of Oral Health Impact Profile (OHIP-14).

 Statistical analyses were conducted using IBM SPSS Statistics version 21.0. Descriptive statistics summarized participant characteristics, and normality was tested with the Kolmogorov-Smirnov test. Continuous variables were expressed as medians and interquartile ranges, while categorical variables were presented as frequencies and percentages. The Mann-Whitney U test and Fisher's exact test were used to assess differences between OHRQoL groups. Partial Spearman's rank correlation examined variable relationships, and logistic regression identified factors linked to a higher negative impact on OHRQoL, adjusting for age, sex, body mass index, chair stand test, and salivary flow rate. A p-value of < 0.05 was considered significant.

 The median age was 59 years (range 27-79), with a possible sarcopenia prevalence of 52.4%. OHIP-14 scores ranged from 0 to 32, with medians of 4 and 13 in a lower (n = 31) and higher (n = 32) negative impact on OHRQoL, respectively. Those with a higher negative impact on OHRQoL exhibited a significantly higher proportion of self-reported xerostomia (p = 0.01), lower salivary flow rate (p = 0.01), and longer 5-time chair stand test (p = 0.04) compared to individuals with the lower negative impact on OHRQoL. Correlation between the time of the chair stand test and the handgrip strength adjusting for age (r = -0.439, p < 0.001) and sex (r = -0.351, p = 0.006) was revealed. Multivariate logistic regression showed a significant association between salivary flow rate and a higher negative impact on OHRQoL (odds ratio 0.018; 95% confidence interval: 0.001, 0.545; p = 0.02).

 This finding suggests that reduced salivary flow affected OHRQoL in well-maintained ESRD patients with PD, highlighting the importance of managing dry mouth to alleviate their OHRQoL.