2017年 · 第33卷第10期

Proteinuria is the most common clinical manifestation of kidney disease and one of the diagnostic criteria for nephrotic syndrome. The formation of proteinuria is mainly related to impaired glomerular filtration barrier, renal tubular reabsorption disorder, renal and urinary secretion. The cleft membrane between the glomerular podocyte and the foot process is the last filtration barrier, and Nephrin molecule is its important structural basis. The doxorubicin nephropathy model mainly leads to proteinuria production by interfering with the synthesis of molecules such as Nephrin in podocytes. Tripterygium wilfordii can reduce the formation of proteinuria by protecting and repairing the glomerular charge barrier, improving the damage of the glomerular mechanical barrier, inhibiting immune response, inducing apoptosis, and non-specific scavenging of oxygen free radicals, and exerting renal protective effects. However, there are few studies on the protective effect of tacrolimus on doxorubicin nephropathy, and its relationship with Notch pathway has not been reported. In this study, we compared the effects of triptolide and tacrolimus on adriamycin nephropathy, and explored the mechanism of renal protection of tacrolimus.

Any hemodialysis access relies on an unobstructed return to heart pathway. In recent years, the number of cases of central venous depletion caused by improper use of hemodialysis catheters has been increasing. How to establish follow-up access for these patients and extend their dialysis life has become a challenge for us. This paper reports a case of central venous depletion, an arteriovenous fistula was established on the same side of the occlusive lesion, and the internal fistula was kept unobstructed through the open collateral branch to maintain dialysis, which provides a new option for maintaining hemodialysis in the case of central venous depletion.

Antigen presentation is a key link in the occurrence of autoimmune response. dendritic cells (DC), macrophages and some B cells and other full-time antigen presenting cells simultaneously express MHC class II molecules (MHC-Ⅱ) and costimulatory molecules B7 family proteins, such as B7-1 (also known as CD80), B7-2 (also known as CD86), etc., which can bind to Th cell receptor CD28 family molecules and activate CD4⁺Helper T cells (Th cells), which in turn initiate an immune response by secreting cytokines, recruiting, and activating other immune cells^[1]。 At present, it has been found that non-immune cells, such as certain epithelial cells, can also be used as non-professional antigen presenting cells to mediate antigen presentation. For example, in patients with primary Sjogren's syndrome, their salivary gland epithelial cells not only express MHC-Ⅱ^[2]It can also upregulate the expression of B7-1 and B7-2 under inflammation, and has the antigen presentation property of activating T cells. It can be used before and after inflammation^[3,4]All of them showed immune activation characteristics, and continued to secrete autoantigens such as Ro/SSA and La/SSB^[5]It is believed to be a possible initiator of autoimmune response. Many recent studies suggest that glomerular and tubular epithelial cells can also be used as non-professional antigen presenting cells, which play an important role in the occurrence and development of glomerular diseases and tubulointerstitial diseases.