1. Urine examination:24-hour urine volume is basically normal, and the 24-hour urine protein excretion (normal value ≤0.4g/24h) is significantly increased. There may be a large amount of protein in the urine, and in some cases, it may reach dozens of grams per day; the urine sediment red blood cell count is increased, showing polymorphism, and there may be leukocyte urine. Urinary complement C3 is increased (normal value ≤2.76mg/L), urinary α2-macroglobulin is increased, urinary N-acetyl-β-glucosaminidase is elevated (normal value ≤16.5U/g creatinine), urine osmolality decreases after 13 hours of water deprivation, and urine sugar is negative.
2. Blood examination:White blood cells, hemoglobin, platelets, peripheral blood lymphocytes are basically normal or elevated, blood albumin is decreased, blood lipids are elevated, blood creatinine and blood urea nitrogen are progressively increased.
3. Immunological examination:Abnormal changes may occur in IgG, IgA, IgM, C3, C4, and C-reactive protein (CRP). Increased levels of anti-streptolysin O, negative for antinuclear antibodies, double-stranded DNA antibodies, and extractable nuclear antigen peptide antibody. Some patients may have a positive HBsAg in the five-item hepatitis B test.
The morphological changes in the kidney of diacetylmorphine nephropathy are diverse, including FSGS, membranous proliferative glomerulonephritis. In patients who are often given subcutaneous injections of diacetylmorphine, kidney amyloidosis may also occur. In addition to glomerular lesions, patients may also have marked interstitial inflammation.
4. Renal tissue biopsy:The type of glomerular damage in this syndrome is focal and can also be diffuse. The type of glomerular damage determines the clinical manifestations and the degree of renal function failure. The common type of renal damage in patients is acute staphylococcal post-infectious glomerulonephritis, with diffuse lesions.
(1) Microscopic examination: Light microscopy shows globular atrophy of renal glomeruli, with纤维素ous exudates still present in the atrophic cysts. Some glomeruli exhibit capsular lesions with twisted and shrunken segmental loops, adjacent to which there are paired endothelial cells and foamy cells, solitary nucleated cells, and swollen, proliferative parietal epithelial cells with large vacuoles in the cytoplasm. Other glomerular parietal epithelial cells are also swollen, with widened segmental mesangial areas, mesangial cell proliferation, slightly thickened Bowman's capsule walls, negative PASM-Masson staining, mild acute tubulointerstitial lesions, tubular epithelial edema and变性, with many small vacuoles, focal loss of brush border of tubular epithelial cells, protein casts in the lumen, no tubular cystic dilation, reduced tubular number in the medulla, focal tubular atrophy, thickened basement membranes, slightly widened interstitial area of the medulla, fibrosis, focal cellular infiltration, and渗出 in small arteries; crescent formation may also occur, which is difficult to distinguish from other types of post-infectious glomerulonephritis.
(1) Electron microscopy examination: Under the electron microscope, deposits can be seen under the epithelium and within the basement membrane, usually with granular deposits of immunoglobulins and complements, supporting the pathogenesis related to immune complexes. In addition, electron microscopy also shows glomerulosclerosis, extensive podocyte lesions, obvious microvilli in the cytoplasm, formation of a large number of vacuoles in the cytoplasm, some cytoplasm becomes pale, organelles decrease, foot processes widely fuse, flatten, the gaps between unfused foot processes become narrow, and occasionally foot processes are shed from the glomerular basement membrane.
(2) Electron microscopy: Under the electron microscope, deposits can be seen under the epithelium and within the basement membrane, usually with granular deposits of immunoglobulins and complements, supporting the pathogenesis related to immune complexes. In addition, electron microscopy also shows glomerulosclerosis, extensive podocyte lesions, obvious microvilli in the cytoplasm, formation of a large number of vacuoles in the cytoplasm, some cytoplasm becomes pale, organelles decrease, foot processes widely fuse, flatten, the gaps between unfused foot processes become narrow, and occasionally foot processes are shed from the glomerular basement membrane.
(4) The damage caused by hepatitis B virus-related membranous glomerulonephritis in patients with this syndrome is similar to that of idiopathic membranous nephropathy. Electron microscopy and immunohistochemistry show deposits in the membrane and mesangium. Some researchers have found various hepatitis B antigens and antibodies in kidney tissue or its filtrate.
(5) The pathological changes of HIV-AN kidney disease often show collapse of glomerular capillary plexus, proliferative microcyst formation in renal tubules, and severe tubular degeneration. Under the electron microscope, a large number of reticular structures appear in the glomerular endothelial cells.
5. Ultrasound examination:Late B-ultrasound can show shrinkage of both kidneys.