Objective To explore the correlation between serum creatinine/cystatin C ratio (Scr/CysC) and muscle mass and muscle strength, and evaluate the predictive value of Scr/CysC for all-cause mortality in peritoneal dialysis patients. Methods It was a prospective cohort study. The patients who received regular peritoneal dialysis treatment for more than 3 months and had stable conditions in the Renal Division of Peking University First Hospital from April 1, 2011 to August 1, 2012 were included, and the clinical data were collected. The patients were divided into the male group and the female group, and the differences of clinical data between the two groups were compared. The lean body mass (LBM) directly measured by the dual-energy X-ray absorptiometry (LBM-DEXA) was used as the reference gold standard and compared with the LBM estimated by the creatinine method (LBM-CK) and the anthropometric method (LBM-A). Muscle strength was measured by a grip strength meter for the dominant hand grip strength. Pearson correlation and multiple linear regression analysis method were used to analyze the correlations between Scr/CysC and LBM as well as grip strength, and subgroup analyses were conducted according to gender groups. Cox regression model was used to analyze the value of Scr/CysC in predicting all-cause mortality in peritoneal dialysis patients. Results A total of 213 peritoneal dialysis patients were included in this study, including 95 males (44.6%) and 118 females (55.4%). The age was (56.46±12.42) years old. The dialysis age was 24.0 (9.0, 52.5) months. The baseline Scr/CysC was (1.77±0.73). LBM-DEXA (t=-17.764, P<0.001), LBM-CK (t=-7.702, P<0.001), LBM-A (t=-16.813, P<0.001), grip strength (t=-11.083, P<0.001) and Scr/CysC (t=-2.965, P=0.003) in the male group were all significantly higher than those in the female group. Pearson correlation analysis showed that Scr/CysC was positively correlated with LBM-DEXA (r=0.204, P=0.003), LBM-CK (r=0.279, P<0.001), LBM-A (r=0.198, P=0.004), and grip strength (r=0.341, P<0.001). Multiple linear regression analysis showed that Scr/CysC wasn't independently correlated with LBM-DEXA, but was independently correlated with grip strength (β=0.134, P=0.006). Cox regression analysis showed that baseline Scr/CysC was not an independent influencing factor of all-cause mortality in peritoneal dialysis patients (HR=1.005, 95% CI 0.751-1.346, P=0.972). Conclusion Scr/CysC is associated with muscle mass and muscle strength in peritoneal dialysis patients, but has no value in predicting all-cause mortality in peritoneal dialysis patients.

Objective To investigate the relationship between thoracic aortic calcification (TAC) and autonomic nervous system (ANS) function in patients receiving continuous ambulatory peritoneal dialysis (CAPD). Methods It was a cross-sectional study. The CAPD patients with dialysis duration >6 months between January and December 2022 were retrospectively enrolled. The baseline clinical data, heart rate variability (HRV) data such as standard deviation of all normal to normal intervals (SDNN), root mean square of successive differences between adjacent normal?to?normal intervals (RMSSD), high frequency (HF), very low frequency (VLF), low frequency (LF), LF/HF, acceleration capacity (AC) and deceleration capacity (DC), and skin sympathetic nerve activity (SKNA) were collected. TAC was defined as TAC score (TACS) >100 AU. The patients were divided into TACS >100 AU group and TACS≤100 AU group based on whether the thoracic aorta was calcified. The differences of those data between the two groups were compared. Logistic regression model was used to analyze the related factors of TAC. Spearman correlation analysis method was used to analyze the correlation between peripheral blood neuropeptide Y, ANS parameters, average amplitude SKNA (aSKNA) and TACS.　Cox regression model was used to analyze the risk factors of all-cause mortality in patients with CAPD. Results The study included 106 CAPD patients with 50 males (47.2%), age of (46.04±11.10) years and dialysis duration of (41.55±30.52) months. TACS>100 AU group exhibited significantly lower heart rate (t=2.015, P=0.046), DC (t=2.131, P=0.035), LF/HF (Z=3.332, P<0.001) and ln(LF/HF) (t=3.326, P=0.001), and higher AC (t=-2.392, P=0.019) than TACS≤100 AU group. Multivariate logistic regression analysis results showed that after adjusting for age and eosinophil count, lnVLF (OR=0.66, 95% CI 0.45-0.98, P=0.038), lnLF (OR=0.69, 95% CI 0.49-0.97, P=0.032), DC (OR=0.79, 95% CI 0.64-0.99, P=0.039) and AC (OR=1.32, 95% CI 1.04-1.68,P=0.021) were independently correlated with the risk of TAC. Spearman correlation analysis showed that neuropeptide Y level in peripheral blood was correlated with aSKNA (r=0.23, P=0.017), lnSDNN (r=-0.20, P=0.036) and TACS (r=0.19, P=0.048). During the follow-up period of (25.8±4.2) months, 5 patients (4.72%) died, including 1 patient in the TACS≤100 AU group and 4 patients in the TACS>100 AU group. Compared with the survival group, the death group had higher TACS (Z=-2.262, P=0.024) and lower LF/HF (Z=-2.750, P=0.006). Cox regression analysis results showed that increased ln(LF/HF) was an independent influencing factor for all-cause mortality in CAPD patients (HR=0.22, 95% CI 0.05-0.83, P=0.026). Conclusions HRV parameters (lnVLF, lnLF, AC and DC) of CAPD patients are independently associated with TAC. The dysfunction of ANS in CAPD patients (especially the decreased vagus nerve activity) may promote TAC.

Objective To explore the predictive value of baseline complete blood count derivative marker levels for the occurrence of the first peritonitis in patients undergoing peritoneal dialysis (PD). Methods This study was a retrospective cohort study. The data of inpatients who underwent PD catheterization in Tongji Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology from April 1, 2005 to February 29, 2024 were collected and followed up until June 1, 2024. According to the 2022 International Society for Peritoneal Dialysis guidelines for peritonitis prevention and treatment, the patients were divided into the peritonitis group and the non-peritonitis group. Basic demographic data and laboratory parameters of the patients were collected, and inflammatory markers derived from complete blood count were calculated, including the comprehensive index of systemic inflammation, the systemic inflammation response index (SIRI), the ratio of hemoglobin to platelets (HPR), and the ratio of monocytes to lymphocytes (MLR). Cox regression analysis was conducted to identify factors associated with the occurrence of peritonitis. Results A total of 824 PD patients aged ≥18 years were included in this study. Among them, there were 398 males (48.30%), with an age of 42.06 (33.04, 52.01) years, and the follow-up time was 595.00 (173.50, 1 158.00) d. The proportion of conversion to hemodialysis or death in the peritonitis group was higher than that in the non-peritonitis group (40.91% vs. 13.58%, χ² =56.173, P<0.001). The age of the peritonitis group was greater than that of the non-peritonitis group [45.05(34.92, 52.99) year old vs. 41.11(32.89, 51.46) year old, Z=-1.978, P=0.048], and the follow-up time was lower than that in the non-peritonitis group [529.50(146.25, 861.00) d vs. 627.00(177.00, 1 222.50)d, Z=-2.260, P=0.024]. A multivariate Cox analysis model was constructed based on the univariate Cox analysis. After adjusting for covariates, the results showed the comprehensive index of systemic inflammation (HR=0.997, 95% CI 0.995-0.998, P<0.001), HPR (HR=0.520, 95% CI 0.271-0.995, P=0.048), MLR (HR=7.027, 95% CI 1.468-33.636, P=0.015) and SIRI (HR=2.673, 95% CI 1.302-5.488, P=0.007) were the related factors for the first occurrence of peritonitis. Conclusion The levels of inflammatory markers derived from baseline complete blood count, especially MLR, SIRI and HPR, are the independent influencing factors for the occurrence of the first peritonitis in patients with PD.

Objective To evaluate the impact of roxadustat on thyroid function and to identify the associated factors in patients undergoing maintenance peritoneal dialysis (PD). Methods This study was a single-center retrospective study. PD patients who received roxadustat or recombinant human erythropoietin (rHuEPO) treatment at Nanjing Drum Tower Hospital between January 2020 and June 2024 were included. The general and clinical information as well as laboratory indexes were collected. Serum free triiodothyronine (FT3), free thyroxine (FT4) and thyroid?stimulating hormone (TSH) were compared before and after treatment initiation. Hemoglobin (Hb) responses were also observed between the two groups. Logistic regression analysis was performed to explore the factors associated with thyroid function changes. Results A total of 120 patients were enrolled, with an age of (55.17±16.42) years, including 66 males (55.0%). There were 81 patients received roxadustat (roxadustat group) and 39 patiens received rHuEPO (rHuEPO group). Compared to the rHuEPO group, the roxadustat group had a higher proportion of patients with diabetes (χ²=4.172, P=0.041), a shorter PD vintage (Z=-3.406, P=0.002), a lower serum level of total cholesterol (Z=-2.082, P=0.037) and a lower level of fasting blood glucose (Z=-2.589, P=0.010). Following treatment with roxadustat, the levels of FT4 (Z=-5.349, P<0.01) and TSH (Z=-3.720, P<0.01) decreased significantly. In contrast, no significant changes in FT4 or TSH levels were observed in the rHuEPO group (both P>0.05). For both roxadustat and rHuEPO groups, there were no significant changes in FT3 levels after treatment (both P>0.05). Multivariate analysis identified that higher baseline TSH (TSH≥2.27 μIU/ml, OR=1.581, 95% CI 1.196-2.089, P=0.001) and roxadustat exposure (OR=3.432, 95% CI 1.410-8.355, P=0.007) as independent associated factors of subsequent TSH decline, and identified that higher baseline FT4 (FT4≥14.9 pmol/L, OR=1.390, 95% CI 1.162-1.662, P=0.001) and roxadustat exposure (OR=5.798, 95% CI 2.225-15.113, P=0.001) as independent associated factors of subsequent FT4 decline. The degrees of hemoglobin changes after roxadustat or rHuEPO treatment did not differ significantly between roxadustat group and rHuEPO group (t=-1.062, P=0.290). Of the 31 patients who underwent a second thyroid function test during roxadustat treatment, 24 continued with the original regimen, while 7 discontinued roxadustat. Among 24 patients who maintained roxadustat treatment, TSH (Z=-0.400, P=0.689) and FT4 (t=0.143, P=0.888) remained stable between the second and third tests. All 7 patients who discontinued roxadustat treatment showed TSH rebound and the changes of TSH levels were more significant than that in continuers (Z=-2.505, P=0.012). FT4 recovery occurred in only 3 of them, with no significant difference in FT4 change between discontinuers and continuers (Z=-0.685, P=0.493). Conclusions Roxadustat commonly suppresses TSH and FT4, but not FT3, in PD patients. Baseline levels of TSH and FT4 are key associated factors of the inhibitory effect of roxadustat on thyroid function. This suppression does not intensify with prolonged exposure and is reversible after discontinuation, with TSH levels normalizing more quickly than FT4. Roxadustat‐induced thyroid suppression does not compromise its efficacy in treating renal anemia.

Objective To explore the role of curcumin (Cur) in improving IgA nephropathy (IgAN) and its related mechanisms. Methods Fifty 7-month-old miR-23b knockout (miR-23b^-/-) mice weighing (25±5) g were used to establish an IgAN disease model, and were randomly divided into IgAN group, IgAN+Cur (150 mg/kg) group and IgAN+Cur (300 mg/kg) group using simple randomisation. Sixteen healthy 7-month-old weighing (25±3) g C57BL/6J wild-type mice served as the normal control group. IgAN+Cur (150 mg/kg) and IgAN+Cur (300 mg/kg) groups were respectively gavaged continuously with 150 mg/kg Cur and 300 mg/kg Cur for 8 weeks, and the normal control and IgAN groups were gavaged continuously with an equal dose of 0.9% sodium chloride solution for 8 weeks. The samples of urine, serum, intestinal fluid, intestinal tissues, kidney tissues and liver tissues were collected from each group. In vitro experiments, human cloned colon adenocarcinoma (Caco-2) cells were divided into blank control (Ctrl), Ctrl+Cur (10 μmol/L), Ctrl+ Cur (60 μmol/L), tumor necrosis factor?α （TNF‐α), TNF‐α+Cur (10 μmol/L) and TNF‐α+Cur (60 μmol/L) groups. Enzyme-linked immunosorbent assay was used to detect serum alanine transaminase, aspartate transaminase, secretory IgA (sIgA), creatinine, blood urea nitrogen, 24 h urine microalbumin, as well as sIgA, TNF-α, interleukin （IL)-6 and IL-1β in the intestinal fluids. HE staining was used to observe the effect of Cur on liver tissues, the hyperplasia of glomerular mesangial zone in kidney tissues and the morphological and structural changes of intestinal epithelial barrier, and the histopathological damage scores were performed respectively. PAS staining was used to observe the changes of glomerular basement membrane and mesangial matrix. Immunofluorescence was used to observe the deposition of immune complexes in the glomerular mesangial zone. Real-time quantitative PCR was used to detect the mRNA expression levels of B?cell activating factor (BAFF)and a proliferation inducing ligand (APRIL). Western blotting was used to detect the protein expression levels of tight junction proteins zonula occluden?1 (ZO-1) and occludin in the mouse intestinal tissues. The potential targets of Cur in IgAN were predicted. Western blotting was used to detect the protein expression levels of tight junction proteins, as well as Toll?like receptor 9 (TLR9), myeloid differentiation primary response protein (MyD88), nuclear factor?κB p65 (NF-κB p65) and p-NF-κB p65. Results Genetic identification results revealed that all IgAN model mice exhibited the miR-23b^-/- genotype, confirming successful model establishment. Seven-month-old mice were subsequently selected for Cur treatment. Histopathological analysis demonstrated no significant differences in hepatic tissue morphology across groups, with comparable liver histopathological injury scores and unaltered liver function parameters, thereby validating the safety of Cur administration. Compared with the normal control group, IgAN mice displayed elevated levels of serum sIgA, serum creatinine, blood urea nitrogen and 24 h urine microalbumin (all P<0.05). Renal pathological results revealed severe mesangial hypercellularity in glomeruli, higher glomerular injury scores, and notable glomerular mesangial deposits of IgA, IgG and complement C3 in IgAN mice (all P<0.05). Additionally, intestinal pathological alterations were observed, including structural changes in intestinal epithelium and Peyer's patches, accompanied by significantly higher intestinal histopathological injury scores in IgAN mice (P<0.05). Intestinal epithelial expression levels of ZO-1 and occludin were significantly reduced, while sIgA, TNF-α, IL-1β and IL-6 in intestinal fluid were elevated (all P<0.05). Serum FITC fluorescence intensity was markedly increased, and intestinal tissue exhibited upregulated mRNA expression of BAFF and APRIL (all P<0.05). Following Cur treatment, serum sIgA level and renal function indices in mice showed partial recovery (all P<0.05). Renal pathological improvements included alleviated mesangial hypercellularity, reduced glomerular injury scores, and diminished glomerular immune complex deposition (all P<0.05). Intestinal pathologies, including epithelial and Peyer's patch lesions, were mitigated, with decreased intestinal histopathological injury scores (P<0.05). Additionally, intestinal tight junction protein expression levels were upregulated, intestinal fluid sIgA level was reduced, inflammatory markers were attenuated, serum FITC fluorescence intensity was declined, and intestinal BAFF and APRIL mRNA expression levels were downregulated (all P<0.05). In vitro experiments demonstrated that TNF-α exposure reduced tight junction protein expression in Caco-2 cells, whereas Cur treatment reversed the effect (all P<0.05). Target prediction analysis revealed that Cur effectively bound to TLR9 structural domain in IgAN. Experimental validation confirmed that Cur treatment suppressed the upregulated protein expression levels of TLR9, MyD88, NF-κB p65 and p-NF-κB p65 in intestinal tissues of IgAN mice (all P<0.05). Conclusion Cur has a significant effect in the treatment of IgAN and can regulate intestinal mucosal immunity by inhibiting the TLR9/MyD88/NF-κB signaling pathway, thereby reducing renal injury and protecting the kidneys.