Focal segmental glomerulosclerosis should do what?

A urine routine examination, microscopic hematuria, proteinuria, and often aseptic white blood cells in urine, grape diabetes. Impaired renal tubular function, urinary amino acids and phosphate in urine, its high incidence of other types of NS.
Blood tests have significantly lower serum albumin, serum albumin is usually less than 25g / L, and a few up to 10g / L below. Decline in glomerular filtration rate (GFR). BUN, creatinine increase. The majority of patients with hyperlipidemia. Serum C3 is usually normal IgG level decreased, C1q is mostly normal. 10% ~ 30% of patients positive for circulating immune complexes. Hypovolemia can cause the increase in hematocrit.Normal white blood cells and classification. Platelets slightly elevated. Water retention will result in lower sodium concentration, the long period of sodium or acquired adrenal insufficiency, can lead to lower sodium concentration. Hyperlipidemia can cause pseudo-hyponatremia, and platelets in vitro release of potassium ions, thrombocytosis can also cause pseudo hyperkalemia.
A renal biopsy light microscopy typical FSGS lesions characteristic focal segmental glomerular damage, lesions involving a small number of glomeruli and glomerular some segments of hyaline sclerosis. The lesions are often deep from the cortex or nearly medullary parts of the glomerulus began, and gradually extended to the renal cortex.Glomerular lesions showed segmental glomerular sclerosis, uninvolved normal of glomerular mesangial matrix increase. Hyaline material deposited in the damaged capillary loop endothelial cells, hardened area with occasional foam cell formation, proliferation of epithelial cells of the common limitations. Early lesions may only local epithelial cells and basement membrane from the epithelial cell swelling, vacuolar degeneration, basophilic cytoplasm. Hardening of the capillary loop wall adhesions with Bowman. Each segmental glomerular damage of a different range of disease progression may contribute to global sclerosis. Fully developed cases of lesions, easily mistaken for the "non-specific chronic sclerosing glomerulonephritis, and through immunofluorescence differential diagnosis. Renal tubular damage often appears as a focal thickening of the basement membrane and atrophy. Coexist, such as focal tubular damage and mild glomerular changes should be suspected of FSGS. Renal tissues of focal, global glomerulosclerosis FSGS often late performance, associated with severe tubulointerstitial lesions in pediatric patients up to 30%. The typical adult hormone-sensitive minimal change can be seen a small number of global sclerosis of glomeruli, with FSGS phase difference. In addition to primary FSGS, many diseases of the kidney tissue can be seen the similar FSGS change. FSGS may also overlap with primary glomerular diseases.
Electron microscopy a large number of proteinuria cases most or all of the glomerulus shows diffuse or segmental foot process change. Early visible in the capillary wall and (or) mesangial foam cells, mesangial matrix increase and part of the capillary collapse.Endothelial cells and mesangial area corresponding to the electron dense deposits, mesangial cell proliferation, large electron-dense material under the light microscope hyalinization and immunofluorescence IgM and C3 deposition. Ball collateral membrane area and endothelial cells can also be found fine granular electron dense deposits.
3 immunofluorescence sclerosis or necrosis can be found in the C3 or IgM and C1q was irregular, granular or nodular distribution. Glomerular lesions were negative. Occasionally mesangial have IgM and C3 distribution and IgG, IgA, rare.