glomerulosclerosis
Introduction
Introduction Focal glomeruloscerosis refers to a type of glomerular capillaries in which glomerular capillary loops have focal segmental sclerosis or hyaline degeneration without obvious cell proliferation. Can be used as mesangial hyperplasia, mesangial IgM deposition and focal glomerular sclerosis, but minimally pathological nephropathy is resistant to steroids and the consequences of repeated episodes of chronic progression. Early renal biopsy of primary nephrotic syndrome, which is ineffective against hormones, is focal glomerular sclerosis. Therefore, there is still debate about whether the disease is an independent glomerular disease. However, from a clinical pathological type that is different from other kidney diseases, it can also be regarded as an independent disease, which is more common and has a tendency to increase gradually.
Cause
Cause
(1) The cause of primary focal glomerulosclerosis is unknown.
(B) secondary focal glomerulosclerosis
1. Glomerular disease: heroin-related nephropathy, tumor-associated nephropathy, diabetes, AIDS, hereditary nephritis, IgA nephropathy, pre-eclampsia, and Hodgkin's disease.
2. Renal tubules, interstitial and vascular diseases, reflux nephropathy, radiation nephritis, analgesic nephropathy and sickle cell disease.
3. Others: renal hypoplasia, obesity and senile.
Examine
an examination
Related inspection
Glomerular filtration fraction acute renal failure diagnostic test glomerular filtration fraction (GFF) urinary inclusion body examination tumor contrast angiography
The diagnosis of this disease mainly depends on renal biopsy. Under light microscopy, some segments of some glomeruli are visible as glass-like homogeneous protein substances. The unhardened area is relatively normal. Typical lesions in the sclerotic zone are characterized by a large number of cell-free substrates and transparent materials. PAS staining was positive. Capillary collapse, foam cell formation and local epithelial cell hyperplasia, adhesion of glomeruli to the cystic sac, and the first involvement of the small ball at the junction of the pulp and pulp. In the non-hardened area, glomerular capillary epithelial cells swell and proliferate, and vacuolar degeneration and larger PAS-positive granules are seen in the cytoplasm. Corresponding tubular atrophy and renal interstitial fibrosis were focally distributed. Immunofluorescence: IgM and C3 deposits are often seen in the hardened area. Under electron microscopy: the sclerotic lesion has a large electron dense deposit. Capillary fistula in non-hardened area presents extensive epithelial cell foot process fusion and regression. When the lesion is severe, epithelial cells can be separated and detached from the basement membrane.
Diagnosis
Differential diagnosis
1. Minimal lesion nephropathy (MCD): may be misdiagnosed due to insufficient tissue or lack of access to the paramedullary nephrons. However, MCD rarely shows hypertension and hematuria, and most patients are sensitive to hormone therapy. In addition, the following pathological features contribute to the difference between MCD and FSGS: 1 the glomerular volume of the former is increased, while the glomerular volume of the latter is different; 2 the former is characterized by diffuse foot process fusion, while the latter is segmental 3; the latter can be seen in the vacuolar degeneration of visceral epithelial cells.
2. Secondary FSGS: In addition to the characteristics of the primary disease, the secondary FSGS caused by other diseases include histological features including: glomerular sclerosis, renal tubular wall thickening, and perivascular fibers. The interstitial lesions of the tubules are patchy, and a large amount of inflammatory cells infiltrate. These histological differential diagnosis has great defects. In essence, it is difficult to make a correct differential diagnosis without relying on medical history, clinical manifestations and laboratory tests. In particular, primary and secondary FSGS cannot be distinguished by histomorphological features. Therefore, according to the characteristics of FSGS, the surface markers of visceral epithelial cells such as Cytokeratins can help us distinguish between primary and secondary FSGS.
