BACKGROUND:Peritoneal membrane thickening is a structural feature of chronic peritoneal stress in long-term peritoneal dialysis (PD). Its non-invasive evaluation remains limited. This study explored the associations between ultrasound-based peritoneal membrane thickness assessment, inflammatory markers, and technique outcomes in PD patients. METHODS:In this prospective study, 106 PD patients underwent standardized ultrasonographic measurements of peritoneal membrane thickness across four abdominal quadrants. Serum and dialysate levels of interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) were analyzed as markers of systemic and local inflammation. Relationships between peritoneal membrane thickness and clinical parameters were examined. Patients were followed for 24 months to evaluate technique failure. RESULTS:Median peritoneal membrane thickness was 0.30 mm (Interquartile range [IQR]:0.28-0.37). Peritoneal membrane thickness showed positive correlations with serum and dialysate IL-6 (r = 0.42 and 0.39; P < .01) and dialysate MCP-1 (r = 0.36; P < .05). Thicker membranes were observed in patients with longer PD duration and higher glucose exposure (P < .01). Individuals with prior peritonitis had greater peritoneal membrane thickness (0.45 mm vs 0.29 mm, P < .001). Patients with low transport status tended to have greater peritoneal membrane thickness, largely related to longer PD vintage. In multivariable Cox regression analysis, greater ultrasonographic peritoneal membrane thickness (modeled as a continuous variable) was independently associated with a higher risk of technique failure (Hazard ratio [HR] 31.3, 95% confidence interval [CI] 2.54-385.33). CONCLUSIONS:Ultrasonographic peritoneal membrane thickness appears to reflect both local and systemic inflammation and may indicate cumulative peritoneal stress. Its assessment could provide a feasible, non-invasive approach to monitor peritoneal integrity and identify patients at risk of technique failure.

Familial Mediterranean Fever (FMF) is the most prevalent monogenic autoinflammatory disorder. In the present study, we investigated whether HLA-B polymorphisms contribute to familial Mediterranean fever (FMF) susceptibility and phenotypic variability. We enrolled 50 familial Mediterranean fever (FMF) patients, 40 asymptomatic Mediterranean FeVer (MEFV) mutation carriers, and 50 healthy controls. HLA-B genotypes were determined by the PCR-SSO technique. Allele frequencies were compared using chi-square or Fisher’s exact tests. HLA-B*51 and HLA-B*35 alleles were enriched among FMF patients compared with controls (p = 0.01 and p = 0.03, respectively). HLA-B*27 was moderately increased in patients (p = 0.04), while HLA-B*44 tended to be more common in carriers (p = 0.07). Odds ratio (OR) and confidence interval (CI) analyses indicated an elevated FMF risk for carriers of HLA-B*51 and HLA-B*35. HLA-B variants, particularly B*51 and B*35, may act as immunogenetic modifiers of FMF, supporting the concept of MHC class I linked inflammatory pathways contributing to disease heterogeneity.

BACKGROUND:Vitamin K deficiency impairs the activation of calcification inhibitors such as matrix Gla protein, promoting vascular calcification in CKD. Protein induced by vitamin K absence-II (PIVKA-II) is a filtration-independent marker of vitamin K status validated in hemodialysis, yet no data exist in peritoneal dialysis (PD). METHODS:Sixty prevalent PD patients at a single tertiary center were prospectively followed for 1 year. Serum PIVKA-II, dephosphorylated uncarboxylated matrix Gla protein (dp-ucMGP), and bone morphogenetic protein-2 (BMP-2) were measured at baseline and 12 months. Carotid plaque was assessed by ultrasonography. Independent predictors of plaque were identified by multivariable logistic regression and ROC analysis. RESULTS:Carotid plaque was present in 36 patients (60%). Vitamin K deficiency (PIVKA-II >40 mAU/mL) was identified in 43.3% and was more prevalent in plaque-positive patients (55.5% vs 25.0%; p = 0.019). All three biomarkers were significantly elevated in the plaque group. Age (OR 1.26; 95% CI 1.07-1.42; p = 0.004) and PIVKA-II (OR 1.71; 95% CI 1.09-2.70; p = 0.022) independently predicted plaque. The area under the ROC curve was 0.766 (p = 0.001) with an optimal cutoff of 35.09 mAU/mL (sensitivity 86.1%, specificity 50.0%). Over 12 months, plaque prevalence rose to 70%; baseline BMP-2 was the sole predictor of new plaque development (p = 0.022). CONCLUSION:PIVKA-II-assessed vitamin K deficiency is common in PD and independently associated with carotid plaque. A threshold of 35 mAU/mL may be more sensitive than the conventional 40 mAU/mL cutoff, supporting PIVKA-II screening and targeted supplementation trials in PD.

HLA-B*38:122 differs from HLA-B*38:01:01:01 by eight nucleotides substutions in Exon 3.

Peritoneal dialysis (PD) is a widely used renal replacement therapy; however, its long-term success is influenced by peritoneal membrane integrity and function. This study aims to investigate the relationship between ultrasonographic peritoneal thickness, inflammatory markers, and clinical outcomes in patients undergoing automated peritoneal dialysis (APD) and continuous ambulatory peritoneal dialysis (CAPD). Demographic data and clinical parameters were recorded. Ultrasonographic peritoneal thickness was measured for all patients from four different quadrants of the abdomen. Inflammatory markers, including intraperitoneal and blood IL-6 and MCP-1 levels, were analyzed. Correlations between peritoneal thickness, inflammatory markers, and clinical outcomes were assessed. Additionally, patient outcomes over a two-year follow-up period, including kidney transplantation, switch to hemodialysis due to peritoneal dialysis failure, and mortality were recorded. A total of 106 adult peritoneal dialysis patients were included in the study, with 53 undergoing APD and 53 undergoing CAPD. The demographic characteristics of the included patients are presented in Table 1. Analyses revealed that the mean ultrasonographic peritoneal thickness was correlated with intraperitoneal IL-6 (r = 0.211, P = 0.031) and peritoneal fluid MCP-1 levels (r = 0.252, P = 0.010), as well as with blood IL-6 levels (r = 0.320, P = 0.001). However, no significant correlation was found between blood MCP-1 levels and peritoneal thickness (r = −0.009, P = 0.930). In patients with a history of peritonitis, ultrasonographic peritoneal thickness (0.45 (0.20–0.77) vs 0.29 (0.22–0.73), P < 0.001), intraperitoneal IL-6 levels (136.61 (16.21–694.40) vs 19.85 (5.80–1781.00), P < 0.001) and blood Il-6 levels (106.65 (20.12–601.70) vs 55.55 (10.20–372.25), P = 0.001) were found to be significantly higher. Additionally, ultrasonographic peritoneal thickness was observed to increase significantly with decreasing peritoneal permeability in PET testing (Fig. 1) (P = 0.046) and correlated with longer duration on peritoneal dialysis (r = 0.469, P < 0.001). During the two-year follow-up period, 5 patients underwent kidney transplantation, 24 transitioned to hemodialysis due to peritoneal dialysis failure, and 7 patients died from cardiac causes. A significant association was observed between ultrasonographic mean peritoneal thickness and switch to hemodialysis due to PD failure (PD group: 0.29 (0.20–0.67), PD failure group: 0.36 (0.25–0.77), P = 0.002). Ultrasonographic peritoneal thickness is significantly associated with intraperitoneal IL-6 and MCP-1 levels, peritoneal permeability, and clinical outcomes in PD patients. The lack of correlation between systemic MCP-1 levels suggests that peritoneal inflammation may be governed by local mechanisms distinct from systemic inflammation. Increased peritoneal thickness correlates with reduced peritoneal permeability, longer PD duration, and history of peritonitis. Furthermore, it is linked to PD failure and adverse patient outcomes. These findings suggest that ultrasonographic peritoneal thickness may serve as a valuable non-invasive marker for monitoring peritoneal membrane integrity and local inflammatory processes and predicting long-term PD outcomes.

Objective The exact effects of MEFV variants on inflammation are still under investigation, and reports on variants of unknown significance, particularly the E148Q variant, have been conflicting. Therefore, this study aims to investigate patients exhibiting E148Q heterozygosity, focusing on diagnoses and disease courses to assist physicians in interpreting the variant. Methods Data of pediatric patients presenting to the Pediatric Rheumatology clinic between November 2016 and September 2023, exhibiting only E148Q heterozygosity in MEFV gene analysis, were extracted. Patients who were lost before 9 months of follow-up have been excluded to ensure the completion of initial diagnostic tests and evaluations. Results Among the 119 patients with E148Q variant, the diagnoses were as follows: healthy, 51.3%; IgA vasculitis, 10.1%; Familial Mediterranean Fever (FMF), 7.6%; Periodic fever, Aphtous stomatitis, Pharyngitis, Adenitis (PFAPA), 6.7%; and other diagnoses, 19.3%. IgA vasculitis patients experienced articular, gastrointestinal, and renal involvement at rates of 91.7%, 58.3%, and 16.7%, respectively. Complete response, partial response, and no response to colchicine were 37.5%, 12.5%, and 50%, respectively, in PFAPA patients. All FMF patients responded to colchicine treatment resulting in reduced mean FMF episode counts in 6 months from 3.22 ± 0.92 to 0.56 ± 0.52. Conclusions The E148Q variant may amplify inflammation and modify disease courses. Patients with the E148Q variant experiencing typical FMF episodes should receive colchicine, but clinicians should exercise caution regarding alternative diagnoses. Additionally, the E148Q variant may increase acute phase reactants and disease severity in IgA vasculitis. However, to reach definitive conclusions on its treatment-modifying role in PFAPA, universal diagnosis and treatment response criteria should be adopted.

At position 778 (C→T) in exon 3, the new allele C*05:01:81 is distinct from C*05:01:01.

At position 778 (C -> T) in exon 3, the new allele C*05:01:81 is distinct from C*05:01:01.

At position 778 (C→T) in exon 3, the new allele C*05:01:81 is distinct from C*05:01:01.

At position 778 (C→T) in exon 3, the new allele C*05:01:81 is distinct from C*05:01:01.

ObjectiveThe exact effects of MEFV variants on inflammation are still under investigation, and reports on variants of unknown significance, particularly the E148Q variant, have been conflicting. Therefore, this study aims to investigate patients exhibiting E148Q heterozygosity, focusing on diagnoses and disease courses to assist physicians in interpreting the variant. MethodsData of pediatric patients presenting to the Pediatric Rheumatology clinic between November 2016 and September 2023, exhibiting only E148Q heterozygosity in MEFV gene analysis, were extracted. Patients who were lost before 9 months of follow-up have been excluded to ensure the completion of initial diagnostic tests and evaluations. ResultsAmong the 119 patients with E148Q variant, the diagnoses were as follows: healthy, 51.3%; IgA vasculitis, 10.1%; Familial Mediterranean Fever (FMF), 7.6%; Periodic fever, Aphtous stomatitis, Pharyngitis, Adenitis (PFAPA), 6.7%; and other diagnoses, 19.3%. IgA vasculitis patients experienced articular, gastrointestinal, and renal involvement at rates of 91.7%, 58.3%, and 16.7%, respectively. Complete response, partial response, and no response to colchicine were 37.5%, 12.5%, and 50%, respectively, in PFAPA patients. All FMF patients responded to colchicine treatment resulting in reduced mean FMF episode counts in 6 months from 3.22 +/- 0.92 to 0.56 +/- 0.52. ConclusionsThe E148Q variant may amplify inflammation and modify disease courses. Patients with the E148Q variant experiencing typical FMF episodes should receive colchicine, but clinicians should exercise caution regarding alternative diagnoses. Additionally, the E148Q variant may increase acute phase reactants and disease severity in IgA vasculitis. However, to reach definitive conclusions on its treatment-modifying role in PFAPA, universal diagnosis and treatment response criteria should be adopted.

Drug reaction with eosinophilia and systemic symptoms (DRESS) is a rare but life-threatening drug hypersensitivity reaction. It has recently been shown that those carrying some human leukocyte antigen (HLA) haplotypes are at high risk for the development of DRESS syndrome with some drugs. There is a strong association with HLA-A*32:01 positivity and vancomycin-induced DRESS syndrome. Here, we present two pediatric cases, one Turkish and the other Syrian, both of whom developed DRESS syndrome during the use of multiple antibiotics included vancomycin, and were shown to have HLA-A*32:01 positivity. To determine the causative drug in patients with DRESS syndrome, patch testing can be administered at least six months after the reaction while the lymphocyte transformation test can only be performed in reference centers. Therefore, delays may occur in identifying the causative drug, especially in patients using multiple drugs. As in our patients, it is important to note that screening for HLA-A*32:01 may enable earlier detection of the responsible drug, which is vancomycin.

Of the most remarkable molecules associated with atherosclerosis and the cardiovascular outcome are S100A12 (10,379.5 Da) and soluble receptor for advanced glycation end products (sRAGE‐42,803 Da) in the hemodialysis (HD) population. We designed a study investigating the effects of the medium cut‐off (MCO) dialyzers focusing on S100A12 and sRAGE in HD patients compared with low‐flux and high‐flux dialyzers.

Introduction: This study aims to determine the relationship between vascular calcification, carotid artery intima-media thickness (CIMT) and malnutrition with inflammatory parameters in dialysis patients. Materials and Methods: 140 CKD patients and 44 healthy controls were included in the study. CIMT was measured by ultrasonography. Valvular calcification was assessed by echocardiography and vascular calcification scores (VCS) were done based on the radiograms. Biochemical parameters were assessed using routine laboratory methods. Subjective global assessment (SGA) was used to evaluate malnutrition. Results: In the study, VCS showed no differences between hemodialysis (HD) and peritoneal dialysis (PD) patients (1.84±2.35 for HD, 1.77±1.64 for PD; p:0.83). CIMT, Osteopontin (OPN), interleukin-6 (IL-6) and homocysteine were significantly different in both dialysis groups compared to healthy controls. The Mean carotid intima-media thickness (m-CIMT) was higher in HD patients compared to PD group. CIMT, vascular calcification and SGA scores showed positive correlation with age, dialysis duration and valvular calcification grades, and negative correlation with albumin levels. A positive correlation between SGA scores and high-sensitive C-reactive protein (hs-CRP) levels was also noted. On multiple regression analysis, m-CIMT was independently associated with age, VCS and albumin levels. VCS was found to be independently associated with only albumin levels. Conclusion: Vascular and valvular calcification, an indicator of cardiovascular mortality and morbidity in dialysis patients, was found to be significantly associated with malnutrition. We found higher rates of valvular calcification in patients with vascular calcification. Malnutrition was more prominent in these patients.

OBJECTIVES:Incidence of new-onset diabetes after transplant negatively affects graft and patient survival. Obesity, impaired fasting glucose before transplant, and a history of diabetes in first-degree relatives are well-defined risk factors. TCF7L2 and CDKAL1 gene polymorphisms have been implicated in the pathogenesis.We investigated the effect of single gene polymorphisms of TCF7L2 (rs7903146) and CDKAL1 (rs7754840) on new-onset diabetes in renal transplant recipients.MATERIALS AND METHODS:We evaluated 239 renal transplant recipients. TCF7L2 and CDKAL1 gene polymorphisms were assessed by polymerase chain reaction.RESULTS:Mean patient age was 43 ± 13 years. There were 148 male patients (61.9%), and 91 were female (38.1%). New-onset diabetes was detected in 55 patients (23%). In 20 cases (36%), the glycemic disorder was transient; 61% of patients required insulin therapy. In terms of CDKAL1, 108 patients had the wild-type allele, 112 had a single-allele mutation, and 19 had a 2-allele mutation (45.2%, 46.9%, and 7.9%, respectively). In terms of TCF7L2, 163 of the patients had the wild-type allele, 49 had a single-allele mutation, and 27 had a 2-allele mutation (68%, 20%, and 11%, respectively). New-onset diabetes-related factors were age at transplant, body mass index after transplant (calculated as weight in kilograms divided by height in meters squared), tacrolimus, mycophenolate, andTCF7L2 polymorphism but not CDKAL1 polymorphism. After multiple regression analysis, the effect of TCF7L2 polymorphism persisted. A single allelic change resulted in a risk factor 1.4 times higher for new-onset diabetes after transplant (P = .043; 95% CI, 1.142-1.874) and a double allelic change was 2.7 times higher (P < .01; 95% CI, 1.310-4.073).CONCLUSIONS:TCF7L2 (rs7903146) gene polymorphism is an independent risk factor for new-onset diabetes in Turkish renal transplant patients. This study is the first in Turkey to show the distribution and effect of these genes in kidney transplant patients.