Controllable Fabrication of Molecularly Imprinted Microspheres with Nanoporous and Multilayered Structure for Dialysate Regeneration.

Adsorption of urea from dialysate is essential for wearable artificial kidneys (WRK). Molecularly imprinted microspheres with nanoporous and multilayered structures are prepared based on liquid-liquid phase separation (LLPS), which can selectively adsorb urea. In addition, we combine the microspheres with a designed polydimethylsiloxane (PDMS) chip to propose an efficient urea adsorption platform. In this work, we propose a formulation of LLPS including Tripropylene glycol diacrylate (TPGDA), ethanol, and acrylic acid (30% v/v), to prepare urea molecularly imprinted microspheres in a simple and highly controllable method. These microspheres have urea molecular imprinting sites on the surface and inside, allowing selective adsorption of urea and preservation of other essential constituents. Previous static studies on urea adsorption have not considered the combination between urea adsorbent and WRK. Therefore, we design the platform embedded with urea molecular imprinted microspheres, which can disturb the fluid motion and improve the efficiency of urea adsorption. These advantages enable the urea absorption platform to be highly promising for dialysate regeneration in WRK.

Relationship between hypoalbuminemia, hyperlipidemia and renal severity in patients with lupus nephritis: a prospective study.

AIM OF THE STUDY: The purpose is to evaluate the relationship between hypoalbuminemia, hyperlipidemia, nephrotic and renal severity in patients with lupus nephritis. MATERIAL AND METHODS: Autoantibodies and serological parameters were measured and analyzed in 429 patients with lupus nephritis in a single centre. RESULTS: The prevalence for anti-dsDNA, anti-nucleosome and anti-histone was higher in the nephrotic syndrome (NS) patients than that in non-NS patients (p < 0.0001 for all comparisons). The NS patients had a higher proportion of diffuse proliferative renal lesions (69.05%) and membranous lesions (68.00%). Serum total cholesterol and albumin levels were associated with activity and severity of renal disease. The levels of proteinuria and serum albumin were positively correlated with activity and chronicity index (p < 0.001 for all correlations). The incidence of a poor renal outcome (p = 0.0461) in the NS patients was significantly increased. On the other hand, the remission rate (p = 0.0002) was significantly reduced and recurrence rate (p = 0.0027) was significantly increased in NS patients. CONCLUSIONS: This paper highlights that nephrotic-range proteinuria, elevated total cholesterol level and decreased serum albumin levels may reflect the activity and severity of renal damage in SLE patients.

The sphingosine-1-phosphate receptor agonist FTY720 prevents the development of anti-glomerular basement membrane glomerulonephritis.

The sphingosine-1-phosphate (S1P) agonist FTY720 prolongs the survival of organ allograft and attenuates autoimmune-mediated injury in experimental models. Most cases of glomerulonephritis (GN) in human appear to be immunologically initiated. In this study, we evaluated the potential therapeutic role of FTY720 in GN via a mouse anti-glomerular basement membrane (GBM) model. Mice were immunized with rabbit IgG in complete Freund's adjuvant (CFA) followed by an intravenous injection of a rabbit anti-mouse GBM serum. Disease and immune responses were assessed on day 14. Mice were treated with FTY720 (0.3 or 3 mg/kg) and prednisone (10 mg/kg) from days 0 to 14. The S1P modulator reduced proteinuria, serum creatinine, crescent formation and serum IgG level. The expressions of splenic S1P receptor and renal Th-1 cytokine were also inhibited at the transcription stage. Treatment with FTY720 increased splenocyte production of protective Th2 cytokine IL-4 and promoted the apoptosis of splenic CD4+ T cells in the animal models, which suggests that FTY720 played a protective role at the induction stage of GN by inhibiting mRNA expressions of splenic S1P receptor 1, S1P receptor 2, and S1P receptor 5.

[The research on the relationship between the polymorphism of 1082A/G, anti-inflammatory interleukin-10 gene promoter with its effect of preventing ESRD patients from microinflammation and arteriosclerosis].

OBJECTIVE: We do this investigation in order to reveal the relationship between the polymorphism of 1082A/G, anti-inflammatory interleukin-10 gene promoter, and end stage renal disease (ESRD) patients microinflammatory state and arteriosclerosis (AS). METHODS: We used PCR-RFLP to measure the various kinds of distribution of IL-10 gene-1082A/G genotype and relevant indexes of microinflammatory state and AS of 870 ESRD patients and 1000 healthy persons of control group and to analyze the mechanism of its protection effect keeping ESRD patients away from microinflammation and arteriosclerosis. RESULTS: Compared with the control group, CRP, TNF-alpha, CH50, C3, IL-10 and Alb of ESRD group were in the normal range, but still significantly higher than those of the control group, while IL-10, Alb were significant lower (P < 0.05). The genotype distribution and allele frequency of IL-10A/G gene had no significant differences between the healthy group and the control group (P > 0.05). Levels of CRP, TNF-alpha, CH50 and C3 of ESRD patients with IL-10A/A genotype were significantly higher than those of ESRD patients with G/G and G/A genotype (P < 0.05), while IL-10 and Alb were significantly lower (P < 0.01). The production of IL-10 in serum from patients with IL-10A/A genotype was significantly lower than that of patients with G/G and G/A genotype (P < 0.01). The incidence rate of AS of patients with IL-10-1082A/A genotype was significantly higher than that of patients with G/G and G/A genotype (P < 0.01). The raise of AS incidence rate was correspondent with the decline of serum IL-10 and raise of serum CRP and Fib. CONCLUSION: The IL-10A/A genotype is a predictable factor of microinflammatory state and high AS incidence rate in ESRD patients. We use IL-10G/G genotype to modulate the high production of serum IL-10, to decline inflammatory reaction and to keep away from microinflammation and AS in ESRD patients. We should work hard on improving the dialysis membrane to reduce the anti-inflammatory factors in uremia for chronic renal failure patients with high arteriosclerosis risk.