Objective To investigate the level of patient activation and its correlated factors in patients undergoing maintenance peritoneal dialysis (PD). Methods This was a cross-sectional study. Consecutive sampling was used to enroll PD patients who received follow-up at the PD center of the First Affiliated Hospital of Sun Yat-sen University from February 2024 to April 2024. Relevant data were collected. Patient activation level was assessed using the Patient Activation Measure (PAM). Level 1 and 2 were defined as low activation, and level 3 and 4 as high activation. General self-efficacy, social support, insomnia, anxiety, depression, and Charlson comorbidity index were evaluated using the General Self-Efficacy Scale, Perceived Social Support Scale, Athens Insomnia Scale, Hospital Anxiety and Depression Scale, and Charlson Comorbidity Index, respectively. Logistic regression analysis was used to analyze the factors associated with low activation in PD patients. Results A total of 245 PD patients were initially enrolled, of whom 9 did not complete the questionnaire, yielding 236 (96.3%) valid responses. Among the 236 patients, 101 (42.8%) were female. Age was (43.9±11.6) years, and dialysis vintage was 33.0 (11.0, 67.0) months. The PAM score was (63.5±16.2) points, and 41.9% (99/236) of patients were classified as low activation. Significant differences between the high-activation and low-activation groups were observed in sex (χ2=4.139, P=0.042), dialysis vintage (Z=-2.142, P=0.032), education level (χ2=22.980, P0.001), marital status (χ2=6.237, P=0.044), employment status (χ2=4.923, P=0.027), annual household income (χ2=11.921, P=0.008), general self-efficacy score (t=2.505, P=0.013), social support score (t=4.623, P0.001), depression score (t=-2.953, P=0.004), serum phosphorus (t=2.271, P=0.024), and serum triglycerides (Z=-2.334, P=0.020). Multivariate logistic regression analysis showed that education level [reference: high education level, odds ratio (OR)=3.521, 95% confidence interval (CI) 1.777-6.980, P0.001], social support score (OR=0.955, 95% CI 0.925-0.985, P=0.003), serum phosphorus level (OR=0.416, 95% CI 0.197-0.880, P=0.022), and serum triglycerides (OR=1.291, 95% CI 1.027-1.622, P=0.028) were independently associated with low activation in PD patients. Conclusions The prevalence of low activation is relatively high among PD patients. Low education level, low social support score, low serum phosphorus, and high serum triglycerides are the independent correlated factors of low activation in PD patients. Clinicians should pay attention to these factors and implement targeted interventions.

Objective To analyze the characteristics of bone microstructure parameters and their impact on new-onset fracture risk in dialysis patients with refractory secondary hyperparathyroidism (rSHPT). Methods This single?center retrospective study enrolled dialysis patients with rSHPT on regular follow?up at the Department of Nephrology, the Eighth Affiliated Hospital of Southern Medical University between July 1, 2015 and July 4, 2018. Baseline demographic data and clinical biochemical parameters were collected prior to bone biopsy. Areal bone mineral density (aBMD) of the lumbar spine and femur was measured using dual?energy X?ray absorptiometry (DXA), and T?scores were calculated accordingly. Bone microstructure parameters were assessed by high?resolution micro?computed tomography (Micro?CT) using bone biopsy specimens obtained from the right anterior superior iliac spine. Patients were categorized based on dialysis modality (hemodialysis vs. peritoneal dialysis), and by T?score into normal bone mass (T≥-1.0), osteopenia (-2.5T-1.0), and osteoporosis (T≤-2.5) groups. Patients were also divided into new?onset fracture and non?fracture groups according to the occurrence of the endpoint event. The endpoint was new?onset fracture following bone biopsy, with follow?up from completion of bone biopsy to occurrence of new?onset fracture, death, or the end of the study. The C?index was used to evaluate the predictive accuracy of aBMD and bone microstructure parameters for new?onset fractures. Multivariate Cox regression models were applied to assess the impact of bone microstructure parameters on new?onset fracture risk. Results A total of 37 patients were enrolled, with an age of (47.89±11.97) years, a median dialysis vintage of 57 (36, 81) months, and a median follow?up of 67 (55, 77) months. The mean intact parathyroid hormone level was (1 879±780) ng/L. Of the 37 patients, 20 (54.1%) were male; 27 (73.0%) were on hemodialysis and 10 (27.0%) on peritoneal dialysis; 17 (45.9%) had normal bone mass, 10 (27.0%) had osteopenia, and 10 (27.0%) had osteoporosis. During follow?up, 10 patients (27.0%) developed new?onset fractures. No significant differences were observed in volumetric bone mineral density, bone volume/tissue volume, trabecular number (TBN), trabecular thickness, trabecular separation, or structure model index between different dialysis modalities or across different T?score groups (all P0.05). Compared with the non?fracture group, the new?onset fracture group exhibited a significant decrease in aBMD of lumbar vertebrae and TBN (t=-2.440, P=0.022; t=-2.360, P=0.018). C?index analysis showed that TBN had the highest predictive accuracy for new?onset fractures [C?index= 0.731, 95% confidence interval (CI) 0.401-1.062]. Kaplan?Meier survival analysis demonstrated a significantly higher cumulative incidence of new?onset fractures in patients with TBN0.85/mm compared with those with TBN≥0.85/mm (Log?rank χ2=3.282, P=0.046). Multivariate Cox regression analysis, after adjusting for age and dialysis vintage, identified TBN0.85/mm as an independent factor associated with new?onset fractures in rSHPT dialysis patients [hazard ratio (HR)=0.307, 95% CI 0.098-0.961, P=0.043]. Conclusion In dialysis patients with rSHPT, decreased TBN is an independent risk factor for new-onset fractures.

Objective To investigate whether disulfiram (DSF) can alleviate vascular calcification (VC) in chronic kidney disease (CKD), and explore its possible mechanism for providing new options for the prevention and treatment of VC. Methods RNA sequencing dataset from aortic tissue in uremic rat from the GEO database was downloaded. Thresholds of absolute log₂ (fold changes) ≥1 and adjusted P0.05 were used to identify differentially expressed genes. The results of differentially expressed genes were visualized in Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis through the DAVID database. Forty male C57BL/6 mice, aged 8 weeks and weighing approximately 25 g, were randomly divided into 5 groups by random number table: normal control group, normal diet+gavage administration of dimethyl sulfoxide (DMSO); uremia group, 0.2% adenine diet+gavage administration of DMSO; low, medium, and high-dose DSF groups, 0.2% adenine diet+ gavage administration of different doses of DSF (25, 50, 75 mg·kg^-1·d^-1), with 8 mice in each group. After 8 weeks, all mice were sacrificed, and the kidneys, aorta and serum were collected for subsequent experiments. HE staining was used to detect the pathological changes of kidney, and the kits were used to detect the serum creatinine, calcium and phosphorus. Alizarin Red S staining and aortic calcium content measurement were used to detect the calcium deposition of aorta. Western blotting was used to detect the aortic calcification indicator α-smooth muscle actin (α?SMA) and the osteoblast marker Runt-related transcription factor 2 (Runx2). Finally, high-dose DSF was used as the intervention to explore potential signaling pathways involved in its anti-VC effect. Western blotting was performed to detect the protein expression levels of tumor necrosis factor-α (TNF-α)/nuclear factor κB (NF-κB) signaling pathway in the aorta. Results Bioinformatics analysis identified 713 differentially expressed genes. GO analysis results showed that the differentially expressed genes were mainly enriched in ossification, inflammatory response, and signal transduction in biological process; extracellular space, collagen-containing extracellular matrix, and extracellular region in cellular component; and protein binding, extracellular matrix structural constituent, and integrin binding in molecular function. KEGG analysis results showed that the differentially expressed genes were mainly enriched in signaling pathways such as fluid shear stress and atherosclerosis, osteoclast differentiation, alcoholic liver disease, malaria, TNF signaling pathway, and mitogen-activated protein kinase signaling pathway. Compared with the normal control group, the uremia group exhibited renal pathological changes such as necrosis and shedding of renal tubular epithelial cells, dilation of renal tubules and deposition of yellow brown crystals in the lumen, had higher serum creatinine and serum phosphorus levels (both P0.05), and no significant difference was observed in serum calcium (P0.05). Compared with the normal control group, the uremia group had significantly increased calcium salt deposition and higher aortic calcium content (P0.05). The low, medium and high-dose DSF groups could dose-dependently reduce the deposition of calcium salt and aorta calcium content (all P0.05). Compared with the normal control group, the uremia group had lower expression level of α-SMA and higher expression level of Runx2 (both P0.05). Compared with the uremia group, the low-dose DSF group had higher protein expression level of α-SMA, but the difference was not statistically significant (P0.05); medium and high-dose DSF groups had significantly higher expression protein levels of α-SMA (both P0.05). Compared with the uremia group, Runx2 protein expression levels in the low and medium-dose DSF groups were lower, but the differences were not statistically significant (both P0.05); Runx2 protein expression level in the high-dose DSF group was significantly lower (P0.05). Compared with the normal control group, the protein expression levels of TNF-α and phosphorylated (p)-NF?κB/NF-κ B ratio in the aorta in the uremia group were significantly higher, while the protein expression levels of TNF-α and p-NF?κB/NF?κB ratio in the aorta in the high-dose DSF intervention group were significantly lower compared to the uremia group (all P0.05). Conclusions DSF can effectively attenuate VC in uremia mice. The anti-VC mechanism of DSF may be related to inhibition of TNF-α/NF?κB signaling pathway.

This article reports a case of left-sided pleuroperitoneal communication in a peritoneal dialysis (PD) patient, who was successfully treated with uniportal video-assisted thoracoscopic surgery (VATS) using indocyanine green (ICG) fluorescence imaging and subsequently resumed PD. A 33-year-old female patient developed reduced ultrafiltration five months after initiating regular PD. Chest CT revealed left-sided pleural effusion. Thoracentesis yielded a transudate, and the pleural fluid-to-serum glucose gradient was 5.98 mmol/L, confirming the diagnosis of PD-related pleuroperitoneal communication. Intraoperatively, after intraperitoneal injection of ICG, fluorescence thoracoscopy identified two tiny defects in the central tendon of the diaphragm, which were barely visible under white light. A triple-mechanical repair was performed: the main defect was sutured, followed by reinforcement with a "sandwich" structure using non-absorbable polyester cardiovascular patches, and both defects were covered with absorbable polyglycolic acid felt. PD was resumed on postoperative day 20 using an incremental strategy, starting with a low dialysate volume and gradually increasing to the pre-operative prescription. No recurrence of hydrothorax was observed during five months of follow-up. This case demonstrates that fluorescence thoracoscopy combined with ICG facilitates accurate identification of occult diaphragmatic defects and assists in effective repair of pleuroperitoneal communication, thereby offering a safe and effective approach to preserve PD viability.

This article reports the efficacy and safety of budesonide enteric-coated capsules in two IgA nephropathy patients with normal or mildly impaired renal function. Case 1 was a 44-year-old woman with baseline 24-hour urine protein of 0.491 g, estimated glomerular filtration rate (eGFR) 99.8 ml·min^-1·(1.73 m²)^-1, and microscopic hematuria (red blood cells 38.27/high-power field). Renal biopsy showed Lee gradeⅢ(Oxford classification M0E0S1T0-C0). Initial treatment consisted of leflunomide combined with hydroxychloroquine sulfate and losartan potassium. After one month, urine protein rose to 0.700 g/d, and the regimen was switched to budesonide enteric-coated capsules (16 mg/d). Case 2 was a 32-year-old male with baseline 24-hour urine protein of 0.740 g/d, eGFR 73.4 ml·min^-1·(1.73 m²)^-1, and hematuria (red blood cells 74.71/high- power field). Renal biopsy showed Lee gradeⅢ(Oxford classification M0E1S1T0-C1). Initial treatment consisted of glucocorticoid therapy. After one month, although proteinuria improved (0.652 g/d), eGFR declined to 65.2 ml·min^-1·(1.73 m²)^-1. Therefore, the regimen was switched to budesonide enteric-coated capsules (16 mg/d). Both patients received budesonide enteric-coated capsules in combination with supportive therapy. After treatment of nine months, urinary protein decreased to approximately 0.1 g/d in both patients with stable renal function, and no serious adverse events occurred. This case report aims to accumulate real-world experience with the use of budesonide enteric-coated capsules and provide a case-based reference for clinical decision-making.

This article reports two young male patients with biopsy-confirmed IgA nephropathy (IgAN) (Oxford pathological classification: case 1, M0E0S0T0C1; case 2, M1E0S0T0C0), both of whom were positive for hepatitis B surface antigen and negative for hepatitis B virus (HBV) DNA, indicating inactive HBV infection. Both patients presented with nephrotic-range proteinuria (24 h urinary protein excretion of 2.9 g and 3.7 g, respectively), microscopic hematuria, and hypertension, and case 2 had mild renal impairment [serum creatinine, 118.0 μmol/L; estimated glomerular filtration rate, 80.1 ml·min?1·(1.73 m2)?1]. The treatment regimen included: (1) supportive therapy with renin-angiotensin system inhibitors combined with sodium-glucose cotransporter 2 inhibitors, including irbesartan, 0.15 g once daily in case 1, sacubitril/valsartan 200 mg once daily in case 2, and dapagliflozin 10 mg once daily in both patients;(2) enteric budesonide capsules 16 mg/d to reduce galactose-deficient IgA1 and IgA immune complex formation; (3) oral hydroxychloroquine 200 mg twice daily to attenuate glomerular inflammatory responses; and (4) antiviral therapy, with case 1 receiving telbivudine 0.6 g once daily followed by entecavir 0.5 mg once daily, and case 2 receiving entecavir 0.5 mg once daily. After 12 and 13 months of follow-up, respectively, 24 h urinary protein excretion decreased compared with pretreatment levels (case 1, from 1.2 g to 0.3 g, a 75.0% reduction; case 2, from 3.7 g to 0.3 g, a 91.9% reduction), and microscopic hematuria achieved complete remission. Renal function remained stable. Safety monitoring showed that all HBV reactivation warning indicators remained continuously below the lower limit of detection, and no infectious events occurred during treatment. This article preliminarily suggests that, under strict monitoring of HBV markers, enteric budesonide capsules combined with intensive supportive and antiviral therapy may provide a therapeutic option for patients with IgAN complicated by HBV infection that provides both renal protection and viral safety; however, its efficacy and safety require further validation in future studies.

Patients with chronic kidney disease may concurrently present with metabolic syndrome and protein-energy wasting. To assess energy balance, identify high-risk populations, and guide nutritional interventions, accurate estimation of total energy expenditure is important. Total energy expenditure comprises resting energy expenditure, physical activity energy expenditure, and the thermic effect of food. The gold-standard methods for measuring total energy expenditure are direct calorimetry and the doubly labeled water method, but these methods are costly and operationally complex. Clinicians commonly estimate total energy expenditure by multiplying resting energy expenditure by the physical activity level. The gold standard for measuring resting energy expenditure is indirect calorimetry. Prediction equations developed for the general population show poor applicability in chronic kidney disease patients. Although chronic kidney disease-specific predictive formulas have been established, they require further validation in large and multi-ethnic cohorts. Physical activity level can be objectively measured using accelerometers, with the average daily metabolic equivalent of task being relatively reliable. General-population questionnaires have limited applicability in chronic kidney disease patients, and the validity of chronic kidney disease-specific questionnaires still requires further validation. This review summarizes methods for estimating total energy expenditure and the current research advances in patients with chronic kidney disease, with the aim of providing a reference for optimizing energy assessment and nutritional management in this population.

Chronic kidney disease (CKD) is a severe public health issue that affects global health. Traditional clinical diagnostic markers for CKD often only show abnormalities in the middle and late stages of the disease, which delay the optimal timing for treatment and quality of life for patients. Metabolomics, a novel omics technology that identifies and quantitatively analyzes small- molecule metabolites, can reflect the dynamic pathophysiological state of a biological organism. Blood and urine samples, due to their minimally invasive and non-invasive characteristics, are commonly used as testing samples. This review summarizes the latest progress of blood and urine metabolomics in the exploration of novel biomarkers for CKD, research on pathogenesis, prognosis assessment, and therapeutic drug applications. It may provide important evidence for understanding the metabolic imbalance mechanisms of CKD and for optimizing strategies for assessment and management.

Lysine acetylation, dynamically regulated by histone acetyltransferases (writers), deacetylases (erasers), and interpreted by bromodomain-containing proteins (readers), plays a critical role in kidney diseases. This review summarizes the role of protein acetylation in the pathogenesis of kidney diseases, including acute kidney injury (AKI), chronic kidney disease (CKD), the AKI-to-CKD transition, as well as tissue repair after AKI, and diabetic kidney disease (DKD). In AKI, dynamic changes in acetylation levels can protect the kidney and promote repair, whereas dysregulation of this process may drive the transition from AKI to CKD. In CKD and associated fibrosis, acetylation modifications accelerate disease progression by regulating pro-fibrotic signals. In DKD, different histone deacetylase (HDAC) and sirtuin subtypes exert either pathogenic or protective effects. Small-molecule inhibitors or activators targeting the acetylation machinery have shown therapeutic potential in animal models. Future high-quality clinical trials are needed to validate their translational value.

This article provides an interpretation of the 2025 consensus on chronic kidney disease–mineral and bone disorder (CKD-MBD) issued by the Kidney Disease: Improving Global Outcomes (KDIGO). CKD-MBD is a common complication of chronic kidney disease (CKD), involving disturbances in mineral metabolism, bone abnormalities, and vascular calcification. In 2025, KDIGO released the consensus derived from the KDIGO 2023 CKD-MBD Controversies Conference, introducing a new damage-oriented framework that redefines CKD-MBD as two major syndromes: CKD-related osteoporosis and CKD-related cardiovascular disease. This framework emphasizes the importance of multifactorial interactions and comprehensive assessment. This article interprets the major updates of the consensus, outlines the latest advances in pathogenesis, diagnostic evaluation, and management strategies, and aims to promote precise stratification and individualized intervention in CKD-MBD.