内科学英文课件Humanglomerulardiseases.ppt
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1、Human glomerular diseasesObjectivesUnderstand the basic knowledge on the epidemiology,pathology,pathogenesis,clinical manifestations,diagnosis,and treatment for major primary and secondary glomerular diseases.Understand the relationship between basic science findings and clinical features(Bench vers
2、us Bedside).Update the recent findings and clinical trials in the field.Meet the standard of the core curriculum at Shanghai Jiao Tong University School of Medicine.OutlineGlomerulus:structure and functionPathophysiology:Nephrotic syndrome versus nephritic syndromePrimary glomerular diseasesSecondar
3、y glomerular diseasesCase discussion with questions for practiceGlomerular StructureVideo of podocyte EM structure6Podocyte Foot Process3D reconstitution of podocytes from EMPicture of a podocyte from 3D printer using prototyping technology 9Glomerular Filtration BarrierSlit Diaphragm of PodocytesSl
4、it diaphragm580nm40nmGagliardini et al.2010Slit Diaphragm has porespore size 20nm diameterSlit Diaphragm pores are smaller than albuminFoot process of podocytes have negative chargepodocalyxin:Tx-Mb glycoprotein,negatively charged.important for stability of FP to prevent it from collapsingNegative c
5、hargeFaul et al.TRENDS in Cell Biology 2007Highly motileSD is motile and regulated by actinSD is regulated by mechanic forceHydrostatic and oncotic pressuresShear stress from blood circulation in the capillary loop(horizontal).Shear stress from glomerular filtration(vertical)Stretching of podocytes
6、from GBMResistance of GBMHighly motileBloodUrineSD at molecular levelsFiltration barriersize barriercharge barrierMaintenance of the capillary loop shapecounteract intraglomerular pressureSynthesis and maintenance of the GBMMaintenance of the endothelium(VEGF)by crosstalk among cellsPodocyte Functio
7、nHighly differentiated and quiescent cellsPodocyte injury is a major cause of glomerular diseaseMutation of podocyte proteinsStructural changes:EffacementPodocyte loss:Detachment/apoptosisPodocyte ProliferationEffacementreduction of filtration areaimpairment of filtration barrier function:proteinuri
8、aKriz W.et al.1998.Podocyte loss Podocyte Depletion Denuded GBM Protein Leakage Tufts Adhesion GSPodocyte loss causes glomerulosclerosis and podocyte number correlates with the progression of glomerular diseaseGlomerular basement membrane(GBM)1.Composition of GBM:type IV collagen(alpha 3,4,5 chains)
9、laminin,proteoglycans(haparan sulfate),and nidogen2.Mutations of type IV collagen cause hereditary kidney disease(Alport Syndrome).3.Both thicken or thin GBM are associated with glomerular disease(Diabetic nephropathy vs thin basement membranous nephropathy).4.Deposition of immune complex in GBM ca
10、uses glomerular disease(Membranous Nephropathy).Glomerular endothelial cells1.Glomerular endothelial cells have fenestration in their peripheral cytoplasm(60-80nm)and regulate filtration rate.2.Glomerular endothelial cells synthesize matrix for GBM.3.Fenestrations are coated with negative charged gl
11、ycocalyx.4.Glomerular endothelial cells maintain capillary loops5.Glomerular endothelial cell injury causes the rupture of capillary leading to hematuria.6.Glomerular endothelial cells undergo proliferation in the disease condition.Reduction of endothelial fenestration is seen in diabetic nephropath
12、yMesangial cells1.Mesangial cells provide structural support.2.Mesangial cells regulate blood flow of the glomerular capillaries by their contractile activity.2.Mesangial cells phagocytize glomerular basal lamina components and immunoglobulins.4.Mesangial cells are major contributors to the extracel
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