What are the symptoms of nephritis in women

In the early stages of nephritis, there are no obvious symptoms, except for occasional tonsillitis. The onset is usually sudden, and patients will feel pain in the throat, but will not associate it with nephritis. Therefore, many patients will misdiagnose their disease and miss the best time for treatment. Therefore, you should go to the hospital for examination as soon as these symptoms occur.

1. Early symptoms Most patients have a history of precursor infection one month before the onset of the disease, such as purulent tonsillitis, with sudden onset and high fever, but the disease may also be latent and slow in onset.

2. The onset of the disease often begins with oliguria, or gradually becomes oliguria, or even anuria. It may be accompanied by gross hematuria of varying duration, but microscopic hematuria persists and the changes in urine routine are basically the same as those in acute glomerulonephritis.

3. Edema: About half of the patients develop edema when they begin to have oliguria, especially in the face and lower limbs. Once edema occurs, it is difficult to subside.

4. Some patients have hypertension at the onset of hypertension, while others develop hypertension after the onset of the disease. Once blood pressure rises, it becomes persistent and is not easy to drop on its own.

5. The characteristic of this disease is that renal function damage continues to worsen. A significant decrease in glomerular filtration rate and renal tubular dysfunction coexist.

The pathological changes of acute glomerulonephritis are that the kidney volume may increase compared to normal, and the lesions mainly affect the glomeruli. The pathological type is endocapillary proliferative glomerulonephritis. Under light microscopy, it is usually a diffuse glomerular lesion, with endothelial cell and mesangial cell proliferation as the main manifestation, and may be accompanied by neutrophil and monocyte infiltration in the acute phase. When the lesion is severe, the proliferating and infiltrating cells can compress the capillary loops, causing the capillary lumen to narrow or even occlude, and damage the glomerular filtration membrane, resulting in hematuria, proteinuria, and tubular urine.

It also decreases the glomerular filtration rate, thereby reducing the excretion of water and various solutes (including nitrogen-containing metabolites and inorganic salts), resulting in water and sodium retention, which in turn causes an increase in the extracellular fluid volume. Therefore, clinically there are edema, oliguria, and systemic circulatory congestion such as dyspnea, hepatomegaly, and increased venous pressure. Renal tubular lesions are usually not obvious, but there may be edema and focal inflammatory cell infiltration in the renal interstitium.