2015年 · 第31卷第03期

With the increasing number of elderly hemodialysis and diabetic patients, the life span of dialysis population is prolonged, and it is more difficult to establish autologous arteriovenous fistula (AVF), and the early power loss rate of AVF also increases. It has been reported that the 1-year efficacy rate of AVF is only 50%^[1]The stenosis rate reached 5.2% ~10.63% at 1 year after operation^[2,3]。 The study showed that more than 55% to 80% of the strictures occurred within 5 cm of the anastomosis and its vicinity^[3,4]Venous intimal hyperplasia is the main cause. How to improve the success rate and long-term open rate of AVF reconstruction is a clinical concern. Although the use of balloon dilation can improve the stenosis and secondary thrombosis caused by vascular collapse at the puncture point and other sites, the effect on stenosis caused by anastomosis and nearby intimal hyperplasia is not satisfactory, and the cost of balloon exceeds the cost of operation itself, resulting in an increase in the overall cost of operation. In recent years, aiming at AVF failure caused by stenosis in the anastomosis and its vicinity, we reconstructed the anastomosis at the proximal end by ipsilaterally crossing the stenotic vessel, and used the biliary tract bougie to locally dilate the proximal venous vessel during the operation, and achieved satisfactory results, which are reported as follows.

Macrophages first differentiate from myeloid progenitor cells in bone marrow to monocytes, and then migrate and infiltrate into tissue interstitium to differentiate from monocytes under inflammatory reaction, trauma and other environments. Macrophages play an important role in maintaining tissue homeostasis, remodeling tissues, removing cellular debris, and regulating immune response. During the development of acute and chronic kidney diseases, monocytes/macrophages have both pathogenic and protective effects, depending on the type and state of their activation. In kidney diseases, classically activated macrophages mainly play a pro-inflammatory and pro-fibrotic role; alternatively activated macrophages mainly play an anti-inflammatory role and promote repair and reconstruction of damaged tissues. In recent years, more and more scientific research teams have focused on replacing activated macrophages, hoping to apply their role in promoting the repair of damaged tissues to clinical practice. This article reviews the role of macrophages in some acute and chronic kidney diseases, aiming to provide a reference for opening up new therapeutic strategies.

A 40-year-old male was admitted to the hospital on 3 March 2014 due to "facial edema for 1 month and edema of both lower limbs for 15 days". Facial edema appeared without inducement 1 month ago, and edema of both lower limbs appeared 15 days ago. The treatment effect of the local hospital was poor, so I was transferred to our hospital. Physical examination: BP 173/104 mmHg, anemic appearance, depressed edema of both lower limbs. Auxiliary examination: Hb 92 g/L, urine protein (2+), urine protein amount 13.73 g/24 h, blood Scr 122~213.8 μ mol/L, albumin 28.4 g/L, C3 0.62 g/L, C4 0.17 g/L; ANA, ANCA, anti-GBM negative, IgG 1.74 g/L, IgM 1.72 g/L, IgA 0.49 g/L, blood immunofixation electrophoresis IgM/κ type, urine peripheral protein (-), β 2 microglobulin 6.60 mg/L, cryoglobulin test, rheumatoid factor, infectious disease examination (-), skull and pelvis plain film no abnormalities, bone marrow puncture showed plasma cells accounting for 14.2%, lymphoma-like plasma cells can be seen. Flow cytometry showed that 6.31% plasma cells in bone marrow cells showed loss of CD19 and/or expression of CD56. Kappa light chain in plasma cells was expressed monoclonally, and the phenotype was consistent with multiple myeloma cells. Renal pathology: Immunofluorescence IgM (+ ~2+), C3 (2+), κ (2+), capillary wall with granular deposition in mesangial region. Under light microscope, moderate to severe diffuse hyperplasia and insertion of mesangial cells and stroma, diffuse proliferation of endothelial cells, diffuse double-track and multi-track formation of basement membrane, and microthrombotic substances can be seen in capillary loop cavity; Vacuolar and granular degeneration of renal tubular epithelial cells, diffuse edema of renal interstitium; Congo red staining and oxidation were negative. Under electron microscope, moderate to severe proliferation and extensive insertion of mesangial cells and stroma of glomerulus, deposition of electron density in subendothelial and mesangial areas, segmental widening of loose layer in basement membrane, extensive fusion of epithelial foot processes, and vacuolar degeneration of renal tubular epithelium. Pathological diagnosis: membranoproliferative glomerulonephritis (MPGN) with monoclonal immunoglobulin deposition. SeeFigure 1。 Final diagnosis: Multiple myeloma (IgM type) kidney damage; MPGN with monoclonal immunoglobulin deposition. Treatment: Bortezomib combined with dexamethasone regimen was treated 4 times, supplemented by symptomatic treatment such as blood pressure control. Efficacy: After 4 months of follow-up, the edema disappeared, urine protein turned negative, albumin 34.8 g/L, renal function recovered, and Scr 77 μ mol/L.

A 57-year-old male developed persistent periumbilical pain for 17 h without trigger. He had been treated with anisodamine hydrochloride without relief. B-ultrasound showed urinary retention, accompanied by aversion to cold and low fever. He was given urinary catheterization and anti-infective treatment. Abdominal CT examination considered left renal infarction, seeFigure 1。 On admission, the patient had periumbilical pain, poor urination, and sometimes headache. Since the onset of the disease, there was no low back pain, chest tightness and melena, and no history of hypertension, diabetes and cardiovascular and cerebrovascular diseases. Physical examination: blood pressure 135/70 mmHg, painful appearance, soft abdomen, periumbilical tenderness, no rebound pain, no percussion pain in the kidney area, and no vascular murmur in the abdomen. Blood test WBC 11.4×10⁹/L, N 94.91%, urine protein negative, occult blood +, blood BUN 4.60 mmol/L, Scr 110.00 μ mol/L, AST 119.00 U/L, creatine kinase (CK-MB) 28.00 U/L, lactate dehydrogenase (LDH) 2250 U/L, blood lipids, electrolyte, D-dimer normal, anti-neutrophil cytoplasmic antibody (ANCA) negative. Electrocardiogram and chest CT were normal, and cranial CT angiography showed bilateral basal ganglia infarction, but there was no abnormality. Clinical diagnosis: left renal infarction.