2017年 · 第33卷第04期

The ankle-brachial index (ABI) is a non-invasive, simple and reproducible vascular screening method^[1]。 Abnormal ABI as an independent predictor of all-cause mortality in hemodialysis (HD) patients^[2]。 More and more dialysis centers are starting to use ABI as a routine examination. In many studies, ABI measurement of dialysis patients is generally carried out on non-dialysis days or 5~30 min before dialysis, and there is no uniform standard for the start time of measurement in each study^[3]。 We know that blood pressure, fluid load and other indicators of HD patients change greatly with time due to the existence of dialysis factors, especially with ultrafiltration, blood pressure fluctuates. The majority of dialysis patients are in outpatient clinics, due to time constraints. If non-dialysis day or pre-dialysis measurement is taken, it may cause low compliance and inconvenience to patients. Then, whether it can be measured during dialysis and whether the measurement results are different from those before dialysis, no similar articles have been found in the literature. Therefore, in this study, ABI was measured at two time points before and during dialysis in maintenance hemodialysis (MHD) patients, to evaluate the effect of dialysis on ABI, and to explore the feasibility of measuring ABI during dialysis.

The main causes of poor maturation and loss of function in autologous endovascular fistula (AVF) are stenosis and thrombosis, which in turn is the main cause of thrombosis^[1]。 There are many causes of internal fistula stenosis, including hemodynamic changes in arteriovenous or artificial vascular-venous anastomosis, surgical injury of internal fistula surgery, polytetrafluoroethylene (PTFE) artificial blood vessels (which can attract macrophages to release cytokines), hemodialysis needle injury, uremic toxin stimulation, oxidative stress response, etc^[2]In which the inflammatory response plays an important role^[3]。 neutrophil/lymphocyte ratio (NLR) is similar to white blood cells and C-reactive protein, which are indicators reflecting the state of inflammatory response and can be obtained by routine blood tests^[4]。 In addition to the arteriovenous diameter, whether there is a correlation between the patient's preoperative condition, inflammatory response and postoperative AVF stenosis is a question worth investigating. This study investigated whether there was an association between AVF stenosis and preoperative basic indexes and inflammatory response indexes.

A 31-year-old female was admitted for "abnormal urine test with increased creatinine for half a month". Half a month ago, I was hospitalized in a local hospital for "uterine fibroids". During this period, routine urine examination showed occult blood 3+, protein 3+, and red blood cell count 1.0891×10⁹Piece/L, 24-h urine protein content 4.0 g; Renal function showed creatinine 114 μ mol/L and nephrocentesis was performed on 14 Jul 2016. The creatinine was increased progressively after multiple postoperative reexaminations. On July 19, the creatinine was 226 μ mol/L. For further diagnosis and treatment, he was transferred to Zhejiang Provincial People's Hospital. Physical examination: blood pressure (BP) 117/79 mmHg, no special heart, lung and abdomen, no depressed edema in both lower limbs. Auxiliary tests: positive anti-nuclear antibody (1:100), positive anti-mitochondrial antibody; Neutrophil cytoplasmic antibody (ANCA) was negative, and anti-glomerular basement membrane (GBM) antibody was negative (19.7 RU/ml) (normal value 0-20 RU/ml); Urinary routine showed protein 3+, occult blood 3+, red blood cell count 7.728×10⁸pieces/L; Blood routine showed white blood cells 3.94×10⁹/L, hemoglobin 110.0 g/L, platelets 184×10⁹/L, immunoglobulin +; IgG 11.5 g/L (normal range 8.0-14.5 g/L), IgA 2.05 g/L (normal range 1.14-2.26 g/L), IgM 1.63 g/L (normal range 0.77-1.93 g/L), C₃0.87 g/L (normal range 0.8~1.5), C₄0.17 g/L (normal range 0.2~0.6 g/L); Albumin 32.1 g/L (normal range 35-55 g/L), urea 8.14 mmol/L, creatinine 247.9 μ mol/L, uric acid 373 μ mol/L; erythrocyte sedimentation rate 17.0 mm/h (normal range 0-20 mm/h); B-ultrasound of both kidneys: 101 mm ×42 mm (right), 115 mm ×45 mm (left). Renal histopathological examination: Light microscopy: 33 glomeruli, 2 glomerular sclerosis, 8 cellular, 1 cellular fibrous, 4 segmental cellular crescent formation, 5 glomerular vessel wall rupture, 4 glomerular vascular loop segment fibrous necrosis, 8 glomerular vascular loops ischemic shrinkage, 13 glomerular peripheral loops adhesion to cyst wall, focal cyst wall thickening and delamination; Interstitial chronic lesions were mild (about 15%). Immunofluorescence: IgA (4+), IgM (3+), C₃(3+) granular deposition in diffuse spherical mesangial region; IgG (4+), IgG₁(3+), IgG₄(2+) diffuse bulbous vascular loop linear deposition; Type IV collagen a1, a3 and a5 were all continuously positive; Kappa light chain (4+), lambda light chain (3+), diffuse spherical mesangial region, vascular loop granular, linear deposition. Electron microscopy: The foot process was partially fused, and a small amount of electron density deposition was seen in the mesangial region. SeeFigure 1。 Diagnosis: atypical anti-GBM with IgA nephropathy with crescent formation (41.9%). The patient had 5 plasma exchanges, methylprednisolone 500 mg shock for 3 days and then changed to 40 mg/d, combined with cyclophosphamide 1.0 g shock once (July 25) and intravenous gamma globulin 20 g ×5 days (August 2 to August 6). During this period, anti-GBM antibody gradually decreased (anti-GBM antibody 2.4 RU/ml on August 11), but renal function was progressively impaired (creatinine was 376.0 μ mol/L on August 14), and hemoglobin decreased to 80.0 g/L (August 11); On August 2, urine protein 2+, red blood cell count 5.8664×10⁹Piece/L. After discussion, the patient and his family asked to be transferred to Nanjing Military Region General Hospital. After telephone follow-up, it was learned that the patient's creatinine decreased (details are unknown), and he is currently lost to follow-up.

Mitochondrial autophagy, mitochondrial biogenesis, and proteolytic systems in mitochondria work together to maintain a balanced state of intracellular mitochondrial quantity and quality, namely mitochondrial homeostasis^[1]Among them, mitophagy is the main pathway to eliminate mitochondria. 2005 Lemasters et al.^[2]The concept of "mitophagy" is proposed, that is, damaged mitochondria are degraded and cleared by specific, selective cellular autophagy. This concept was proposed to explain the 1962 Ashford et al.^[3]Encapsulation of mitochondria by lysosomes observed under electron microscope. Mitochondrial autophagy is both a macroautophagy and a selective autophagy. The phosphatase and tensin homologue (PTEN) -induced putative kinase 1 [PINK1] /Parkin pathway is a signaling pathway that specifically regulates mitochondrial autophagy. The process of mitochondrial autophagy is roughly as follows: under starvation, oxidative stress, etc., mitochondrial DNA mutation, increased production of reactive oxygen species (ROS), decreased membrane potential and other mitochondrial dysfunctions appear, and mitochondrial autophagy-related proteins activate and activate mitochondrial autophagy, thus promoting the isolated membrane to wrap mitochondria to form mitochondrial autophagosomes. Subsequently, mitochondrial autophagosomes fuse with lysosomes to form mature mitochondrial autophagy lysosomes, so that mitochondria are degraded in lysosomes with intact organelles, and their degradation products are recycled^[4]。 There are three main methods for detecting mitochondrial autophagy and its activity: (1) Direct method: observe mitochondrial autophagosome by electron or fluorescence microscope; (2) Indirect method: flow cytometry to detect mitochondrial membrane potential and total mitochondria; The expression of mitochondrial autophagy-related proteins was detected by immunoblotting; (3) Human-made experimental intervention of mitochondrial autophagy pathway to explore the effect of mitochondrial autophagy on cell or body homeostasis. The proposal of mitophagy not only further clarifies the mechanism of maintaining the quality and quantity of healthy mitochondria, but also enriches the content of autophagy, and provides a new perspective for people to study the pathogenesis of diseases.

The v-Src gene is the first proto-oncogene to be named, and the group of non-receptor tyrosine kinases encoded by it is collectively referred to as Src family kinases (SFKs). The activation of SFKs can cause a series of cell biological effects such as cell proliferation, differentiation, migration and adhesion, which is closely related to the progression and prognosis of tumors. In recent years, it has also been found that it is involved in many disease processes in the body. In this paper, the role of Src kinase in the progression of chronic kidney disease and its related mechanisms were reviewed by literature review and combined with our previous research basis.

Vascular access is the lifeline of maintenance hemodialysis patients. Autologous arteriovenous fistula (AVF) or grafted arteriovenous fistula (AVG) has the advantages of lower infection rate and fewer complications than other vascular access such as tunnel dialysis catheter, and most guidelines recommend it as the first choice. However, AVF and AVG also have shortcomings such as maturity difficulties and low long-term patency rate. Studies have shown that the exclusion of immature internal fistulas (referring to postoperative inability to use for dialysis or loss of function within 3 months^[1]), with a patency rate of 60% at 12 months after AVF^[2]； The use rate of AVF was 40% in 1140 Canadian patients with internal fistula (including those with immature internal fistula) at 4 to 5 months after surgery^[3]； Patency rate as low as 23% for 1 year of first AVG^[4]。 In recent years, fruitful achievements have been made in the pathology and pathogenesis of internal fistula dysfunction, and it provides potential targets and intervention means for the treatment of internal fistula dysfunction, so as to improve the maturity rate of internal fistula and prolong the service life.