2016年 · 第32卷第10期

Parathyroidectomy (PTX) is currently the preferred treatment for severe secondary hyperparathyroidism (SHPT)^[1]However, some patients cannot undergo traditional surgery due to severe cardiopulmonary dysfunction, difficulty in tolerating general anesthesia, and repeated neck surgery. Therefore, ultrasound-guided percutaneous thermal parathyroid ablation becomes another option^[2,3]。 Recently, a patient with severe SHPT with grade IV cardiac function was admitted to our department, and the report is as follows.

Podocytes are terminally differentiated glomerular visceral epithelial cells, and membrane proteins, cytoskeleton and other cellular components are the basis of their structure and function. The changes of these components can lead to podocyte damage, and the early changes of membrane surface proteins can lead to the fusion and shedding of podocyte foot processes and the disappearance of subcellular structures in the later stage^[1]。 At present, molecular pathological studies suggest that the mechanisms of podocyte injury are mainly divided into four categories: abnormal expression of hiatus septum (SD) molecules, abnormal actin (actin) in cytoskeleton, impaired normal adhesion between podocyte and glomerular basement membrane, and destruction of negative charge barrier on podocyte surface^[2]。 Endocytosis, as the main means of cell transport of macromolecular proteins, is involved in the renewal of membrane proteins and the transduction of cell signals, and its abnormality can lead to podocyte damage^[3]。

Podocytes, namely glomerular visceral epithelial cells, belong to terminally differentiated cells and are located in the outermost layer of glomerular filtration membrane. In recent ten years, with the rapid development of research technology, the establishment of immortalized podocyte lines, and the successive discovery of important molecules such as Nephrin and Podocin in the foot process, the research of podocyte has made breakthrough progress. The structural maintenance and morphological changes of eukaryotic cells are often closely related to the intracellular skeleton system. In recent years, some studies have shown that podocytes may be important local antigen presenting cells in the glomerulus, so the cytoskeleton and its related proteins in podocytes may also participate in the antigen presenting function of podocytes, but the specific mechanism is far from being elucidated. This review will describe the research progress of intrapodocyte cytoskeleton and its related protein type I myosin, focusing on its relationship with podocyte antigen presentation, and provide directions for further research on targeted therapy of autoimmune glomerulonephritis.

1968 Berger et al.^[1]IgA nephropathy (IgA) was proposed for the first time, which is characterized by an abnormally increased proportion of galactose-deficient IgA1 in the circulation, and IgA immune complex is deposited in the glomerular mesangium, resulting in mesangial cell proliferation. IgAN is the most common primary glomerular disease in China. Studies have shown that abnormally increased IgA in patients is an important factor in the occurrence and development of IgAN^[2]。 However, the origin of these abnormal IgA is still unclear, and understanding the mechanism of IgA increase is an important bottleneck to solve IgAN treatment. In recent years, it has been found that patients with IgAN are often accompanied by tonsil infection symptoms. At the same time, tonsillectomy has positive significance for IgAN treatment. The role of tonsil in IgAN has become a research hotspot^[3]。 Recent studies suggest that IgA1 polymer deposited in IgAN mesangium may be derived from tonsil-sensitized plasma cells, suggesting an association between tonsil and IgAN.