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Background : The objective of this study was to compare the impact of citrate dialysate (CD) and standard acetate dialysate (AD) in hemodialysis by central delivery system (CDS) on heparin demand, and clinical parameters. Methods : We retrospectively evaluated 75 patients on maintenance hemodialysis with CDS. Patients underwent hemodialysis with AD over a six-month period (AD period), followed by another six-month period using CD (CD period). Various parameters including mean heparin dosage, high sensitivity C-reactive protein (hsCRP), calcium-phosphate product (CaxP), intact parathyroid hormone (iPTH), and urea reduction ratio (URR) were collated at the end of each period. Results : Patients were 60.5 ± 14.7 years old, of whom 62.7% were male. Patients required less heparin when receiving CD (AD period: 1,129 ± 1,033 IU/session vs. CD period: 787 ± 755 IU/session, P < 0.001). After the CD period (ΔCD), pre-dialysis total CO2 increased to 1.21 ± 2.80 mmol/L, compared to −2.44 ± 2.96 mmol/L (P < 0.001) after the AD period (ΔAD). After the CD period, concentrations of iPTH (ΔAD: 73.04 ± 216.34 pg/mL vs. ΔCD: −106.66 ± 251.79 pg/mL, P < 0.001) and CaxP (ΔAD: 4.32 ± 16.63 mg2/dL2 vs. ΔCD: −4.67 ± 15.27 mg2/dL2, P = 0.015) decreased. While hsCRP levels decreased after the CD period (ΔAD: 0.07 ± 4.09 mg/L vs. ΔCD: −0.75 ± 4.56 mg/L, P = 0.705), the change was statistically insignificant. URR remained above clinical guideline of 65% after both periods (ΔAD: 72.33 ± 6.92% vs. ΔCD period: 69.20 ± 4.49%, P = 0.046). Conclusion : Our study confirmed that the use of CD in CDS required lower heparin doses compared to the use of AD. The use of CD also provided a more stable acid-base status.

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a potential cause of hyponatremia of the central nervous system (CNS). Although SIADH has been reported to be associated with many other central nervous disorders, its association with neuromyelitis optica (NMO) or NMO spectrum disorders are rare. NMO is a demyelinating disorder characterized by optic neuritis and transverse myelitis. Aquaporin-4 (AQP4), which is the target antigen for a NMO autoantibody, is the predominant CNS water channel. However, some NMO patients show seronegative AQP4 antibody results. The spectrum of NMO has been changed, and new findings about the disease have been reported. Here, we report a case of seronegative NMO spectrum disorder associated with SIADH.

Background: Immunoglobulin E (IgE) has traditionally been associated with anaphylaxis and atopic disease. Previous studies reported that serum IgE levels are elevated in nephrotic syndrome and suggested IgE levels as a prognostic indicator in glomerular diseases. The aim of this study was to explore the association between serum IgE levels and renal outcome in patients with immunoglobulin A nephropathy (IgAN). Methods: We included 117 patients with biopsy-proven IgAN. Renal progression was defined if a patient meets one of these criteria: (1) a negative value of delta estimated glomerular filtration rate (mL/min/1.73 m2/mo) or (2) a rise in serum creatinine to an absolute level of ≥ 1.3 mg/dL (male) or 1.2 mg/dL (female). We defined delta changes in serum creatinine, estimated glomerular filtration rate, and proteinuria as a difference of values during the follow-up period. Results: A total of 117 patients with IgAN were included. The serum IgE level was significantly high in the renal progressive group compared with the nonprogressive group. Sex and history of gross hematuria were significantly different between the high-IgE group and the low-IgE group. Regression analysis showed that a male sex, initial proteinuria, and change of proteinuria were significantly associated with serum IgE levels. Conclusion: The serum IgE level is potentially associated with disease progression and pathogenesis of IgAN.

Background: Transforming growth factor-beta (TGF-β) is a multifunctional cytokine involved in immune disorders, cancer, asthma, lung fibrosis, and chronic kidney disease, and its signal pathways are considered crucial mediators of a variety of cellular processes. In addition, several recent studies have reported that TGF-β receptor (TGF-βR) gene polymorphism is associated with chronic kidney disease. However, the association between end-stage renal disease (ESRD) and the TGF-β gene polymorphism has not been sufficiently investigated. In this study, we hypothesized that polymorphisms of the TGF-β ligands or their receptors may be related to ESRD. Methods: We assessed the relationship between four single-nucleotide polymorphisms (SNPs) in the TGF-βR2 and TGF-β2 genes and ESRD, in 312 patients with ESRD and 258 controls. Results: Compared with the control participants, the frequencies of the TGF-βR2 (rs764522⁎C) and TGF-βR2 (rs3087465⁎G) alleles were significantly higher in the patients with ESRD. Genotyping analysis demonstrated that two SNPs in TGF-βR2 of the four SNPs included in the study were significantly associated with ESRD in the codominant 1 [rs764522, odds ratio (OR)=1.65; rs3087465, OR=1.63], dominant (rs764522, OR=1.63; rs3087465, OR=1.57), and log-additive (rs764522, OR=1.54; rs3087465, OR=1.39) models after adjusting for age and sex. Conclusion: We suggest that TGF-βR2 polymorphisms (rs764522 and rs3087465) increase the risk of development of ESRD.