2018年 · 第34卷第05期

membranous nephropathy (MN) is a class of glomerular diseases characterized by the deposition of immune complexes under the glomerular epithelium. Some patients have definite secondary factors, such as autoimmune diseases (more common in systemic lupus erythematosus), viral infections, tumors and special medication history, which are called secondary membranous nephropathy^[1]。 Most patients have unknown cause, which is called idiopathic membranous nephropathy (IMN). In 2009, Salant^[2]And his team discovered that phospholipase A2 receptor (PLA2R) is the main target antigen of IMN. The results of follow-up studies suggest that PLA2R antibody levels are correlated with disease activity, prognosis and response to treatment; In addition to serum PLA2R antibodies, glomerular PLA2R antigen deposit (GAg) is also an important feature of IMN. Several studies have confirmed^[3,4,5,6]Patients with positive serum PLA2R antibodies are often accompanied by glomerular PLA2R antigen deposition. In addition, glomerular antigen deposition can also be detected in patients who are partially negative for serum antibodies. Detection of PLA2R antigen deposition can increase the sensitivity of IMN diagnosis, and has unique clinical value in predicting the therapeutic response and the risk of relapse of IMN^[6,7]。 However, at present, some literatures describe simple methods for the detection of PLA2R in kidney tissue, and the methods are different, resulting in extremely different positive rates of PLA2R in kidney tissue in IMN (50% ~93%), which will inevitably lead to differences in the research results of membranous nephropathy. This study aims to establish a reproducible method for the detection of PLA2R antigen in renal tissue by evaluating the efficacy of immunofluorescence staining and immunohistochemical staining in the detection of PLA2R in renal tissue.

The prevalence of hyperuricemia in Chinese adults reached 8.4%^[1]。 The kidney is the most vulnerable target organ in hyperuricemia. Gouty nephropathy is a disease in which hyperuricemia leads to the deposition of urate microcrystals in the kidney, resulting in interstitial inflammatory reaction, tubular obstruction and loss of nephron^[2]。 The mechanisms of hyperuricemia causing gouty nephropathy include the activation of renin-angiotensin system and cyclooxygenase 2 system, endothelial cell dysfunction and inflammatory reaction^[3]。 Inflammatory response is closely related to the activation of innate immune system, which induces inflammatory response. NOD-like receptor thermal protein domain 3 (NLRP3) inflammasome is a protein complex located in cells, consisting of NLRP3 scaffold, apoptosis-associated speckle-like protein (ASC) and aspartate-specific protease 1 (caspase-1), which releases a large number of inflammatory factors under the action of urate to undergo inflammatory response^[4]。 In this study, the expression of NLRP3 inflammasome in the NLRP3 inflammasome signaling pathway in peripheral blood mononuclear cells of patients with gouty nephropathy was investigated, and its mechanism in renal damage caused by hyperuricemia was investigated.

A 53-year-old female was diagnosed with "polycystic kidney and polycystic liver" in Guangdong Provincial People's Hospital in 1997. Previous history of glucose-6-phosphate dehydrogenase deficiency and hysterectomy, denied history of viral hepatitis. Because of "repeated abdominal distension", he was hospitalized for diagnosis and treatment many times. Abdominal color ultrasound showed peritoneal effusion, polycystic kidney and polycystic liver. In 1997 and 2005, he performed liver cyst puncture and aspiration twice, and the postoperative symptoms could be relieved. In 2011, refractory ascites began to appear, and abdominal puncture and drainage were performed many times, and the symptoms were relieved. Hemodialysis was started in November 2012 for end-stage kidney disease, but ascites remained recurrent. In January 2015, he was hospitalized in the interventional department of our hospital due to "refractory ascites". The auxiliary examination showed that the serum transaminase was normal, the viral hepatitis indicators were negative, and the serum albumin was 27.05 g/L. Abdominal enhanced CT showed that the compression of the hepatic segment of the inferior vena cava was linear, the compression of the middle and right hepatic veins was linear, partially interrupted, and a large amount of fluid accumulated in the abdominal cavity, seeFigure 1。 Upper abdominal enhanced MR showed local stenosis of the hepatic segment of the inferior vena cava, slight stenosis of the middle and right hepatic veins, and a large amount of fluid accumulation in the abdominal cavity; Inferior vena cava and hepatic venography through the right femoral vein showed that the hepatic segment of inferior vena cava was not developed (considering complete occlusion), and its collateral branches were increased, thickened and tortuous. The measured vena cava pressure was about 22 cm H₂O; Because the hepatic vein could not be reached, the superior vena cava and hepatic venography were performed through the left internal jugular vein. The results showed that the left hepatic vein and superior vena cava were visualized, but the hepatic segment of the vena cava was not visualized (considering complete occlusion). The pressure of the left hepatic vein was measured to be about 17cm H₂O, seeFigure 2。 Due to complete occlusion of the hepatic segment of the vena cava, stent implantation and balloon dilatation cannot be performed, and liver transplantation is recommended. The patient was unable to undergo liver transplantation due to financial reasons. At present, blood purification (3 times a week), human albumin transfusion during hemodialysis and abdominal puncture and drainage (once a week, about 3000~4000 ml/time) are still used to relieve the symptoms of intractable ascites.

Autologous arteriovenous fistula (AVF) is known as "the lifeline of hemodialysis patients". Whether its function is good or not directly related to the adequacy of dialysis and the prognosis of patients. However, to date, AVF failure remains one of the important factors of death in maintenance hemodialysis (MHD) patients. Among the factors associated with AVF failure, vascular calcification has been increasingly concerned. Vascular calcification is a pathophysiological process that progresses gradually with age. In patients with chronic kidney disease (CKD), especially MHD, the incidence of vascular calcification is as high as 40%, and the degree of disease is more severe^[1]。 MHD causes the occurrence of AVF calcification, and severe vascular calcification affects the maturation and use of AVF in MHD patients. This article will review the latest research progress around the occurrence of AVF calcification in MHD patients and its relationship with the prognosis of MHD patients.

chronic kidney disease (CKD) has become one of the important public health issues of global concern. It is of great practical significance to explore the pathophysiological mechanism of CKD in depth and find new targets to delay the progression of CKD. The etiology of CKD is varied, but the pathological changes eventually enter into peritubular capillary loss^[1]Common pathways of renal tubular atrophy and interstitial fibrosis^[2]。 In a variety of animal models of kidney disease^[3,4]CKD patients^[5,6]Peritubular capillary injury was observed in the study of rejection of kidney transplantation and transplantation. Inflammation, hypoxia, oxidative stress, and decreased endothelial stability can all lead to a decrease in microvessel density^[7]Among them, vascular pericytes are the core of maintaining the stability of vascular endothelium, and they are also one of the hot spots in recent years^[8]。 This article will review the origin of capillary pericytes and their relationship with vascular injury, and briefly describe the mechanism of their involvement in maintaining vascular stability and their significance in the progression of CKD.