Common clinical hereditary or/and genetic glomerular diseases are: 1. Hereditary nephritis or Alprt syndrome Clinical manifestations: may have a family history, more common in males. Microscopic hematuria and proteinuria; late renal impairment with eye or/and ear disease. Light microscopy: no obvious lesions in early stages, sometimes interstitial vesicle i cell infiltration is seen; glomerulosclerosis and interstitial fibrosis in later stages. Immunopathology: mostly negative. Electron microscopy: thin and thick glomerular basement membrane with longitudinal splitting and stratification of the thickened basement membrane. 2, thin basement membrane nephropathy or benign familial hematuria Clinical manifestations: microscopic hematuria, may have family history. Electron microscopy: diffuse thinning of the glomerular basement membrane (equivalent to 1/2-1/4 of the normal basement membrane). 3, nail-patellar syndrome Clinical manifestations: nail softening, bone dysplasia, hematuria and proteinuria, gradually progressing to renal insufficiency. Photomicroscopy: no obvious lesions in the early stage and progression to nephrosclerosis in the later stage. Immunopathology: negative. Electron microscopy: thickening of glomerular basement membrane and proliferation of collagen fibers. 4. Collagen type III glomerulopathy Clinical manifestations: proteinuria, microscopic hematuria, or NS, often accompanied by hypertension and renal function impairment. Light microscopy: diffuse irregular thickening of the glomerular basement membrane, formation of multi-track and double-track signs, and thylakoid hyperplasia. Immunopathology: negative; or granular deposition of IgM and C3 along the capillary wall and thylakoid region, and type III collagen deposition along the basement membrane. Electron microscopy: a large number of collagen fibers are seen in bundle-like deposition in the mesenteric region within GBM, similar to nail-patellar syndrome. 5. Congenital NS Clinical presentation: NS appears after birth or in infants of several months Light microscopy: cystic dilatation of the proximal and distal tubules and immature glomeruli (Finnish type); diffuse cytosclerosis of the glomerular tract (French type). Immunopathology and electron microscopy: no specific findings. 6. Fabry disease Clinical manifestations: proteinuria and hematuria, progressive progression to renal insufficiency. Angiokeratoma is common. Light microscopy: severe vacuolar degeneration of epithelial cells in the dirty glomerular layer, also seen in tubular epithelial cells and vascular endothelial cells. Immunopathology: negative. Electron microscopy: numerous myeloid vesicles were seen in the glomerular epithelial cells. The diagnosis of these nephropathies is mainly confirmed by renal biopsy pathology combined with their genetic features. Then the treatment after diagnosis will be different. A combination of Chinese and Western medicine treatment options may be chosen through their clinical manifestations. The genetic diagnosis and treatment are still in the exploratory stage.