Rapid progressive glomerulonephritis

　　The following diseases can cause rapid progressive glomerulonephritis:

　　Primary Diffuse Crescentic Glomerulonephritis
　　1. Type I: IgG linear deposition (mediated by anti-glomerular basement membrane antibodies).
　　2. Type II: IgG granular deposition (mediated by immune complexes).
　　3. Type III: little or no Ig deposition (lacking immune response).
　　4. Induced by anti-neutrophil cytoplasmic antibody (ANCA) (vasculitis).

　　Second, secondary to other primary glomerulonephritis membranoproliferative glomerulonephritis (especially type II)
　　1. Accompanied by infectious diseases: poststreptococcal glomerulonephritis, acute or subacute infective endocarditis, chronic sepsis caused by suppurative foci in the viscera, and glomerulonephritis. Other infections: shunt nephritis, hepatitis B virus nephritis, human immunodeficiency virus infection.
　　2. Accompanied by multisystem diseases: systemic lupus erythematosus, pulmonary hemorrhage-glomerulonephritis syndrome, allergic purpura, diffuse vasculitis, allergic vasculitis, and other types, mixed cryoglobulinemia, rheumatoid arthritis with vasculitis, malignant tumors, and recurrent polychondritis, etc.
　　3. Drugs: penicillamine, hydralazine, allopurinol, rifampin, and others.

　　The renal function of patients with rapidly progressive glomerulonephritis deteriorates rapidly, with oliguria or anuria in the early stage. Patients often develop uremia within a few weeks to several months, accompanied by edema, nausea and vomiting, upper gastrointestinal bleeding, and can also develop pulmonary edema, pericarditis, brain edema, acidosis, anemia, and other complications.

　　Rapidly progressive glomerulonephritis has a rapid progression of the disease course, oliguria or anuria, gross hematuria accompanied by a large amount of proteinuria and progressive renal function damage, and typical clinical manifestations. Combined with renal biopsy showing that more than 50% of glomeruli have crescent formation and pathological morphological changes, it is generally not difficult to make a diagnosis.

　　Rapidly progressive glomerulonephritis is usually secondary to acute glomerulonephritis and is further exacerbated by positive and regular treatment, causing a change in clinical and pathological types. Therefore, it is necessary to prevent hyperkalemia and hypokalemia, accurately record the intake and output, and pay attention to the changes in blood potassium levels after diuretic therapy in patients with obvious edema. In addition to paying attention to urine output and the regression of edema, attention should also be paid to the changes in blood potassium levels to prevent the occurrence of hyperkalemia or hypokalemia. Strictly follow the doctor's orders to take antihypertensive drugs, carefully record blood pressure changes, and control blood pressure within a relatively stable range. This can reduce the occurrence of the disease.

　　The diagnosis of rapidly progressive glomerulonephritis relies not only on symptoms and signs but also on relevant laboratory tests, which are indispensable means. The commonly used tests are as follows:
　　1. The prominent manifestation is a persistent increase in blood urea nitrogen and creatinine, a significant decrease in内生肝酐清除率, varying degrees of metabolic acidosis and hyperkalemia. Blood calcium is generally normal, blood phosphorus is also within the normal range, and microscopic hematuria persists throughout.
　　2. Serum complement levels are normal, often accompanied by cryoglobulinemia.
　　3. Blood routine examination mainly shows anemia.
　　4. Immunological examination: Type I patients can detect anti-glomerular basement membrane antibodies; Type II patients may have positive immune complexes, cryoglobulins, and rheumatoid factors; Type III patients show no special changes in the above tests.
　　5. Accurate diagnosis depends on renal biopsy, i.e., when more than 50% of the glomeruli have obstructive crescent formation, it can be diagnosed.

　　Patients with rapidly progressive glomerulonephritis should drink plenty of water, with an intake of more than 2500 milliliters per day to increase urine output and promote the rapid excretion of bacteria, toxins, and inflammatory secretions. The diet of patients should be light and easy to digest. Adequate nutrition should be provided, including sufficient calories, an adequate supply of high-quality protein and vitamins, and so on.

　　The treatment of rapidly progressive glomerulonephritis should be carried out as early as possible. If crescents are present in more than 70% of the glomeruli or the blood creatinine concentration is above 5mg%, although active rescue efforts are made, the chance of renal function recovery is not high, but there are often case reports of severe cases improving after hemodialysis and active treatment. In such patients, there are often high concentrations of anti basement membrane antibodies or immune complexes in the blood. If they are not cleared, they can continue to act on the glomeruli, causing irreversible damage. In addition, coagulation induced by immune reactions is a major condition that stimulates the proliferation of podocyte epithelial cells and the formation of crescents. In animal experiments, the early use of heparin can reduce or prevent crescent formation, so the following measures can be adopted.
　　1. High doses of adrenal cortical hormones and immunosuppressants are used to suppress inflammation and reduce antibody production.
　　2. Anticoagulants such as low molecular weight heparin, urokinase, and warfarin are used in combination with dipyridamole for treatment.
　　3. Due to the continuous progressive course of the disease, the prognosis is poor, and non-dialysis therapy has no definite efficacy. In cases of end-stage renal failure, peritoneal dialysis or hemodialysis should be used, the latter two are safer than long-term use of hormones or immunosuppressants. Peritoneal dialysis is recommended for patients with poor cardiovascular function, bleeding tendency, and older age.
　　4. Plasma exchange is used to reduce the concentration of antibodies or immune complexes in the blood. Plasma is replaced 2 to 4 liters daily or 3 times a week, combined with the use of corticosteroids, cytotoxic drugs, and especially for those with linear Ig deposition in the glomerulus, the recent effect is significant.
　　5. Patients who have undergone kidney transplantation may have a recurrence, but it is difficult to determine the probability of recurrence in each case. Patients with anti basement membrane antibodies in the blood should observe for 3 to 6 months after starting hemodialysis treatment before undergoing kidney transplantation.