Tubular atrophic lesion, or focal segmental glomerulosclerosis (FSGS), is a common primary glomerular disease in children and adults with nephrotic syndrome (NS). It is characterized histopathologically by segmental glomerular scarring with or without intra-glomerular capillary foam cell formation and adhesions. Focal means that only part of the glomerulus is involved (50% of the glomerulus is involved); segmental means that part of the glomerular lobules are involved; and glomerulosclerosis means staged glassy changes or scarring of the entire glomerulus. Pathological features are mostly associated with tubular atrophic lesions and interstitial fibrosis. Differential diagnosis of tubular atrophic lesions: 1. Non-collapsed focal segmental glomerulosclerosis There is still controversy about the relationship between CG and FSGS. Some scholars believe that CG is an independent disease, and most scholars believe that CG is a severe type of non-collapsing focal segmental glomerulosclerosis (NC-FSGS). The difference between them is that clinically significantly more patients with CG have urine protein >10g/d than NC-FSGS; a high proportion of renal insufficiency at onset and rapid deterioration of renal function. The pathological differences are: ① CG is a collapse of glomerular capillaries with marked expansion of the stromal material, and the lesioned segment rarely adheres to the glomerular capsule, while NC-FSGS is the opposite. (ii) CG had obvious epithelial cell hypertrophy and intraepithelial cell granules. ③The lesioned segment of CG was rarely located at the glomerular vascular pole, while this change was common in NC-FSGS. ④Tubular interstitial inflammation, atrophy and fibrosis were more pronounced in CG than in NC-FSGS. Despite this, CG is still classified as idiopathic focal segmental glomerulosclerosis because of the focal distribution of the lesions, but as a special subtype, its clinical manifestations and morphological changes are different from those of idiopathic FSGS. 2. Focal and segmental proliferative glomerulonephritis The late stage lesions may also resemble the pathological changes of this disease, which are also seen in IgA nephropathy, focal proliferative lupus nephritis, purpura nephritis, and small vessel vasculitis. The pathological changes are focal segmental endothelial cell and thylakoid cell hyperplasia with focal and segmental crescent formation. According to their corresponding clinical manifestations and characteristic immunofluorescence, they can be differentiated. 3. Focal glomerular fibrosis is a different concept from this disease in terms of pathology and is less common. The lesioned glomeruli are wrinkled with collagen fiber staining, and negative for silverophilic and PAS staining. In the early stage of FSGS, the lesion is mostly limited to the corticomedullary junction area, so the kidney biopsy is often confused with MCD because it cannot penetrate this area. Therefore, attention should be paid to the differentiation of the two, such as glucocorticoid insensitive individuals and older individuals, who may have early FSGS, and repeat renal biopsy if necessary. Serial sections may improve the diagnostic yield. glomeruli in MCD rarely have morphologic changes under light microscopy. Bifollicular fat droplets are seen within the renal tubular epithelium, and vacuole-like changes are seen in the proximal tubular epithelium. Electron microscopy showed swelling of epithelial cells, fusion of pedicles into sheets, and filter pore occlusion with vacuolar degeneration of epithelial cells, microvilli morphology, increased protein uptake droplets and lysosomes. Immunofluorescence examination was mostly negative, with occasional IgG and/or IgM, IgA, and C3 deposition.