Acute progressive glomerulonephritis in children

　　The disease has various etiologies. Generally, those with extrarenal manifestations or with a clear primary disease are called secondary rapidly progressive glomerulonephritis, such as those secondary to allergic purpura, systemic lupus erythematosus, and occasionally secondary to certain primary glomerular diseases, such as mesangiocapillary glomerulonephritis and membranous nephropathy. Those with unknown etiology are called primary rapidly progressive glomerulonephritis. More than half of the patients with primary rapidly progressive glomerulonephritis have a history of upper respiratory tract preceding infection. A few patients present with typical streptococcal infection, while other patients present with viral respiratory tract infection. In addition, a few patients with rapidly progressive glomerulonephritis have a history of tuberculous bacillus sensitization (tuberculosis infection), and the disease occurs during the treatment with rifampin.

　　In addition to clinical manifestations, pediatric rapidly progressive glomerulonephritis can also lead to renal failure, hypertension, cardiac insufficiency, pleural effusion, ascites, anemia, and others, which should be highly regarded by both clinicians and patients.

　　The disease can present acutely. Most patients develop acute glomerulonephritis syndrome, including edema, oliguria, hematuria, proteinuria, hypertension, and others, after fever or upper respiratory tract infection. At the onset of the disease, the patient's systemic symptoms are severe, such as fatigue, weakness, depression, weight loss, and may be accompanied by fever and abdominal pain. The disease progresses rapidly, with oliguria and progressive renal failure occurring within a few days of onset. Some patients have a relatively insidious and slow onset, with the condition gradually worsening.

　　To prevent this disease, it is important to rest and avoid fatigue. The diet should be low in protein and vitamin supplementation should be noted. Avoid drugs that damage the kidneys. Correct factors that reduce renal blood flow (such as hypoproteinemia, dehydration, hypotension, etc.) and prevent infection are important aspects of prevention.

　　The main examination methods for this disease are as follows.

　　1. UrinalysisThe urine sediment shows red blood cells, white blood cells, hyaline casts, and granular casts, especially red blood cell casts.

　　2. Routine blood testThe examination shows that hemoglobin levels are often below 90g/L, indicating normochromic, normocytic anemia. There is usually mild to moderate thrombocytopenia.

　　3. Renal functionThe renal function is significantly reduced. The renal function is often low to below 50% of normal, hence the increased blood urea nitrogen and creatinine levels

　　4. Immunological examinationThe examination shows increased levels of IgG and IgM.

　　5. Pathology and biopsy examination of rapidly progressive glomerulonephritisThe light microscopy shows diffuse lesions. More than 50% of the glomeruli have large crescentic masses occupying more than 50% of the glomerular capsule area. Renal tubules present with turbid swelling, granular degeneration, and vacuolar degeneration in the early stage of the disease. In the later stage, renal tubular atrophy and interstitial fibrosis occur.

　　6. Imaging Examination: Radionuclide renal scan shows reduced renal perfusion and filtration.

　　7. Renal Ultrasound Examination: The examination can find the kidney to be increased or normal in size with a regular contour, but the junction between the cortex and medulla is unclear.

　　Children should rest in bed, pay attention to low-salt diet. After renal failure, a low-protein diet should also be consumed. The daily calorie intake is 55-60kcal/kg to maintain basic metabolism and nitrogen balance. The daily intake should not be too much to reduce the kidney burden.

　　The main treatment methods for this disease are as follows:

　　1. General Treatment

　　Children should rest in bed, pay attention to low-salt diet. After renal failure, a low-protein diet should also be consumed. The daily calorie intake is 55-60kcal/kg to maintain basic metabolism and nitrogen balance. The daily intake should not be too much to reduce the kidney burden.

　　2. Adrenal Cortex Hormone Pulse Therapy

　　Methylprednisolone intravenous infusion, completed within 1-2 hours, once a day, for a continuous period of 3 times as a course. After 3 days, the second course can be started, with a pulse every other day for a total of 3 pulses, and then changed to prednisone (Prednisone) oral treatment.

　　3. Plasma Exchange or Immune Adsorption Therapy

　　The main purpose of plasma exchange is to clear pathogenic antibodies such as anti-glomerular basement membrane antibodies, immune complexes, inflammatory factors, etc. 50ml/kg is exchanged each time, once every other day, for a continuous period of 2 weeks or until the anti-basement membrane antibodies in the blood disappear. Immune adsorption is mainly to selectively remove various IgG antibodies, which can be adsorbed continuously for several times until the antibodies in the blood disappear.

　　4. Anticoagulation Therapy

　　This disease can be treated with heparin and other drugs.

　　5. Quadruple Therapy

　　The quadruple therapy refers to the combined oral treatment with prednisone, cyclophosphamide or azathioprine, heparin or warfarin, and dipyridamole (Persantin). Now it is mostly improved to use methylprednisolone (methylprednisone) and cyclophosphamide pulse therapy followed by prednisone (Prednisone), dipyridamole (Persantin), heparin or warfarin for continuous oral administration, and intermittent cyclophosphamide pulse therapy.

　　6. Dialysis Therapy

　　Peritoneal dialysis or hemodialysis can be used for severe circulatory congestion.

　　7. Renal Transplantation

　　After renal transplantation, the anti-glomerular basement membrane antibodies in the blood of children can act on the transplanted kidney to cause recurrence. Therefore, dialysis for half a year is required before renal transplantation until the antibodies in the blood turn negative before the operation can be performed.