2015年 · 第31卷第10期

peptidyl-prolyl cis-trans isomerase 1 (Pin1) belongs to the Pin1 subfamily of peptidyl-prolyl isomerase family, which is highly conserved and specific, and can specifically catalyze the isomerization of phosphorylated silk/threo-pro amino acid motifs, so that the conformation of substrate proteins changes and their functions are regulated^[1,2]。 Studies have shown that Pin1 is involved in the regulation of multiple signaling pathways^[3,4,5,6], is highly expressed in many types of tumors^[7,8], is a predictor of tumor prognosis^[9]。 While Nechama et al.^[10]Studies have found reduced Pin1 activity in low-calcium diet-induced secondary hyperparathyroidism (SHPT) mouse models or adenine-induced chronic kidney disease (CKD) mouse models. Previous studies showed that the single nucleotide polymorphism in the promoter region of Pin1 gene was associated with CKD secondary hyperparathyroidism (CKD-SHPT)^[11]。 However, the level of serum Pin1 in CKD-SHPT population and its relationship with relevant clinical indexes in CKD-SHPT patients have not been reported in domestic and foreign literatures. This paper aims to detect the serum Pin1 level and explore the correlation between serum Pin1 and various clinical indexes of CKD-SHPT.

Diabetic nephropathy (DN) is one of the most common and serious microvascular complications of diabetes mellitus (DM). Its incidence is increasing year by year, accounting for about 30% ~40% of end-stage renal diseases. Proteinuria is the most common clinical manifestation in patients with DN, but the mechanism of proteinuria is still not fully understood. In recent years, podocytic lesions have been recognized as a central link in the pathogenesis of DN^[1]。 Recent studies have shown that the immunosuppressive tacrolimus (FK506) reduces urine protein in DM rats^[2]However, there are few reports on whether it is related to reducing apoptosis of podocyte. This study aims to construct a rat model of type 2 diabetes mellitus (T2DM) to investigate whether tacrolimus reduces urine protein and delays the progression of DN in T2DM rats by reducing apoptosis of podocytes.

antineutrophil cytoplasmic antibody (ANCA) is a kind of autoantibody targeting neutrophil and monocyte cytoplasmic components. It has become a specific serological diagnostic marker for some primary small vessel vasculitis^[1]。 Detection methods for ANCA include indirect immunofluorescence (IIF) and enzyme-linked immunosorbent assay (ELISA). Cytoplasmic ANCA (cANCA) combined with anti-proteinase 3 (PR3) antibody positive and perinuclear ANCA (pANCA) combined with anti-myeloperoxidase (MPO) antibody positive for the diagnosis of ANCA associated vasculitis (AAV) specificity can reach 99%. Immunofluorescence staining of AAV was "oligoimmune". A case of AAV patient with renal pathological immunofluorescence accompanied by massive IgA deposition was found in our department, which is reported as follows, and the relevant literature was reviewed to summarize its clinicopathological characteristics.

A 51-year-old female was treated with maintenance hemodialysis through a long-term dialysis catheter with right internal jugular vein with tunnel and polyester sleeve 5 years ago due to "hypertensive nephropathy, chronic kidney disease stage 5". The patient had previously undergone autologous arteriovenous fistula surgery on both forearms separately, which was unsuccessful. In May 2015, I underwent left forearm U-shaped artificial vascular arteriovenous fistula in our hospital, and started regular dialysis through artificial vascular fistula 4 weeks later. When I planned to remove the right internal jugular vein dialysis catheter, it was found that the catheter could not be removed. The patient was immediately transferred to our hospital after clamping the stump of the dialysis catheter with hemostatic forceps.

lecithin-cholesterol acyltransferase (LCAT) deficiency nephropathy is a rare clinical disease, with clinical manifestations of proteinuria and renal dysfunction, which is easily misdiagnosed as primary glomerulonephritis. A case of nephropathy related to lecithin-cholesterol acyltransferase deficiency is reported as follows. Through literature review, the aim is to improve the understanding of this disease.