2018年 · 第34卷第04期

Chronic kidney disease (CKD) has become a public health problem that seriously affects human health^[1]。 Hemodialysis (HD) is a major renal replacement therapy for patients with end-stage kidney disease (ESRD). This study conducted an epidemiological investigation on the incidence rate, year-end incidence rate, primary disease, dialysis age, first dialysis vascular access, dialysis frequency, etc. of maintenance hemodialysis patients in our province from 2013 to 2015, so as to preliminarily understand the current situation of hemodialysis patients in Shanxi Province, provide data basis for studying risk factors, prognosis analysis, etc., and also provide data support for the quality control of blood purification.

radio-cephalic arteriovenous fistula (RCAVF) can provide more puncture sites, and it is easier to revise after the fistula loses its function (failure), so it has become the first choice for vascular access in hemodialysis patients. Originating from the dorsal venous network of the hand between the thumb and index finger, the dorsal hand branch of the cephalic vein of the wrist, 4 to 5 cm proximal to the wrist stria, merges into the main trunk^[1]。 Different dialysis centers have different practices on whether to ligate the dorsal branch of the hand. The party advocating ligation believes that there are inevitable hemodynamic abnormalities at the bifurcation of the dorsal branch of the hand, which can easily increase the incidence of stenosis there, and preventive ligation can improve the patency rate of internal fistula^[2]。 The other side believes that the dorsal branch of the hand can be used as a backup pathway, and when the main trunk is occluded, the patency rate can be increased by compensating the collateral branch circulation^[3]。 We used a randomized, non-blind method to compare the effects of ligation of the head vein in the dorsal branch of the hand on the initial patency rate and the secondary patency rate of the internal fistula at one year.

The TB infection rate of the uremic dialysis population is 6~25 times that of the general population due to cellular immune impairment, anemia, malnutrition, etc^[1,2,3,4]。 tuberculous peritonitis (TBP) is the most common form of tuberculosis infection in patients on peritoneal dialysis^[5]。 Due to the long diagnosis cycle and high misdiagnosis rate of TBP, the treatment opportunity is often delayed, resulting in impaired peritoneal function and failure of peritoneal dialysis technology. Therefore, early and rapid diagnosis of TBP has been a challenge for nephrologists.

Fever is a common complication of maintenance hemodialysis (MHD) patients. The causes of fever include infection, pyrogen reaction, transfusion reaction, hyperthermia dialysis and unknown cause^[1]。 Respiratory tract infection was the most common infection site, followed by vascular access, and the infection rate of autologous arteriovenous fistula (AVF) was about 2% ~3%^[2]。 A case of hemodialysis-related fever is reported as follows.

Vascular access-related complications are the leading cause of hospitalization in chronic hemodialysis (hemodialysis) patients. In recent years, although many clinical strategies have been developed to address this important problem, methods to date to reduce complications associated with arteriovenous fistula (AVF) have not significantly improved AVF patency. The underlying pathophysiological mechanism of loss of function (failure) of AVF remains to be elucidated by further studies. Various stimulating factors, including local blood gas factors, repeated puncture, congenital vascular variation, endothelial dysfunction, inflammation and platelet activation, can lead to intimal hyperplasia (IH) and thrombosis of AVF and graft fistula (AVG)^[1]While the degree of influence of the above factors in AVF failure is still controversial. In order to reveal the underlying mechanism of AVF failure, it is particularly necessary to adopt animal models similar to human AVF pathophysiological changes as the study object. It is difficult to study the complex factors of AVF pathway from the molecular and cellular levels in clinic. Using suitable animal models has the advantages of cheap, readily available and short modeling time. Moreover, the pathophysiological mechanism of AVF failure can be deeply studied from the cellular and molecular levels. In determining a suitable animal model, not only the species of animal, but also the site of anastomosis, the choice of anticoagulant therapy and the implementation of postoperative follow-up should be considered. Although cost, availability, ease of handling, postoperative mortality, and vessel size are often used to guide animal selection, it is most important to select an animal model that can correctly simulate human pathophysiological-related processes^[2]。 This paper reviews a variety of AVF models that have been applied in the past 10 years, and discusses the advantages and limitations of these models in combination with the authors' research results^[3]。

restless leg syndrome (RLS), also known as restless leg syndrome, refers to the indescribable physical discomfort that occurs at rest, thus forcing involuntary movements of the limbs. The incidence rate is low in healthy people. The disease was first reported by English physician Thomas Willis in 1685. In 1945, Swedish scholar Ekbom first used the term RLS and described the clinical manifestations of this disease in detail. Therefore, RLS is also called Willis-Ekbom disease (WED) internationally. The International Restless Legs Syndrome Study Group (IRLSSG) has revised the diagnostic criteria several times, and the latest diagnostic criteria is the 2014 edition^[1]。 The incidence of RLS in patients with chronic kidney disease (CKD) is as high as 20%, much higher than that in healthy people, and the risk of disease gradually increases with the decline of renal function^[2]。 RLS secondary to CKD mostly appears in the middle and late stages of the disease. Besides iron deficiency and dopamine dysfunction, the etiology may be related to the decline of renal function and toxin accumulation caused by inadequate dialysis. Multiple drug and non-drug treatments are available for primary RLS, but are not fully applicable due to complications and changes in pharmacokinetics in patients with CKD. At present, there are few research data on CKD patients with RLS. This article will review the pathogenesis, diagnosis and treatment measures of CKD patients with RLS.

interleukin-18 (IL-18) is a newly discovered cytokine in recent years. It was developed by Okamura et al. in 1995^[1]Purified from a mouse liver extract co-treated with heat-inactivated P. reacutans and lipopolysaccharide, initially designated gamma interferon inducible factor (IGIF). In 1996 Ushio et al.^[2]The cDNA of human IGIF was cloned using murine IGIF as a probe and expressed in E. coli, and then designated IL-18. It is a member of the IL-1 superfactor family and is present as an inactive precursor in almost all cells of healthy humans and animals, requiring conversion to active cytokines by cysteine-containing aspartate proteolytic enzyme 1 (caspase-1) treatment^[3]。 IL-18 can enhance the cytotoxic effects of natural killer cells (NK) and T lymphocytes, induce the production of gamma interferon (IFN-γ), and enhance the cytotoxic effects of Th1 cells and NK cells mediated by Fas/FasL, thus exerting strong defense function, anti-infection, anti-hypersensitivity and other biological activities, and is closely related to the occurrence and development of autoimmune diseases, inflammatory diseases, metabolic diseases and other diseases. The expression of IL-18 in normal kidney tissue is very weak, only a very small amount is expressed in glomerulus, but the expression of IL-18 is significantly enhanced in renal inflammation state, and the positive expression is distributed in glomerular endothelial cells, parietal epithelial cells, mesangial cells, podocytes, renal tubular epithelial cells and renal interstitial cells. IL-18 is a sensitive and early marker of renal tubular injury. At present, IL-18 has been shown to be involved in renal injury in renal disease models such as ischemia-reperfusion injury, lupus nephritis, chronic kidney disease (CKD), and glomerular nephritis. The mechanism of renal injury is mainly through the activation of inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), IFN-γ and monocyte chemotactic protein-1 (MCP-1), which leads to macrophage and neutrophil infiltration. IL-18 expression was upregulated in podocytes, interstitial myofibroblasts, infiltrating interstitial macrophages, and renal tubular epithelial cells in different nephropathy models^[4]。 In this paper, the main biological characteristics of IL-18 and the current research progress in the correlation of renal diseases are reviewed.