Acute renal小球肾炎

　　Acute renal小球肾炎 has various etiologies, generally those with extrarenal manifestations or with clear primary disease are called secondary acute renal小球肾炎, such as secondary to allergic purpura, systemic lupus erythematosus, etc., occasionally secondary to certain primary glomerular diseases, such as mesangiocapillary glomerulonephritis and membranous nephropathy patients, those with unknown etiology are called primary acute renal小球肾炎, these diseases are the focus of this description. Primary acute renal小球肾炎 more than half of the patients have a history of upper respiratory tract prodromal infection, among whom a few present with typical streptococcal infection, other patients present with viral respiratory tract infection, patients with this disease have serological evidence of Coxsackievirus B5 infection, but the serum titers of influenza and other common respiratory viruses are not significantly elevated, so the relationship between this disease and viral infection is still waiting for further observation. In addition, a few patients with acute renal小球肾炎 have a history of sensitization to tuberculosis bacilli antigens (history of tuberculosis infection), and this disease occurs during the treatment with rifampin, individual intestinal inflammatory diseases can also be accompanied by this disease, and the classification of various etiologies is as follows:

　　1. Primary glomerular disease

　　2. Idiopathic crescentic glomerulonephritis (the disease)

　　(1) Type I: Antiglomerular basement membrane antibody type (without pulmonary hemorrhage).

　　(2) Type II: Immune complex type.

　　(3) Type III: Minimal immunoglobulin deposition type (70% to 80% of which are small vessel vasculitis nephritis or ANCA-positive nephritis).

　　3. Membranoproliferative glomerulonephritis

　　(1) Membranous nephropathy.

　　(2) IgA nephropathy.

　　(3) Secondary glomerulonephritis.

　　4. Goodpasture syndrome (pulmonary hemorrhage-nephritis syndrome)

　　5. Post-infection nephritis

　　(1) Nephritis following streptococcal infection.

　　(2) Nephritis following endocarditis.

　　(3) Nephritis following sepsis and other infections.

　　6. Secondary to other systemic diseases

　　(1) Purpura nephritis.

　　(2) Lupus nephritis.

　　(3) Polymyalgia rheumatica.

　　(4) Wegener's granulomatosis.

　　(5) Scleroderma.

　　(6) Cryoglobulinemia.

　　(7) Other: Certain chemical toxins may also be the cause of acute proliferative nephritis (anti-basement membrane antibody type), among which the contamination of various hydrocarbons is closely related to the occurrence of the disease. The disease can occur after the administration of penicillamine-D, which may be related to the activation of polyclonal B cells leading to the formation of autoantibodies. There are also reports of cases induced by antihypertensive drugs such as hydralazine. The immune genetic susceptibility may be related to the disease, with HLA-DR2 seen in more than 85% of type I patients; while type II DR2, MT3, and BfF frequencies are increased.

　　Acute proliferative glomerulonephritis (rapidly progressive glomerulonephritis, RPGN) refers to a group of clinical syndromes that appear oliguria, anuria, and acute renal failure within a short period of time based on the nephritic syndrome. The complications of acute proliferative glomerulonephritis are common, including renal failure, hypertension, heart failure, pleural effusion, ascites, anemia, etc.

　　Patients with acute proliferative glomerulonephritis can occur at any age, but there are two peaks of onset in young and middle-aged and elderly people, with a male to female ratio of 2:1. The disease can present acutely, and most patients develop acute nephritis syndrome after fever or upper respiratory tract infection, such as edema, oliguria, hematuria, proteinuria, hypertension, etc. At the time of onset, the patient's systemic symptoms are relatively severe, such as fatigue, weakness, listlessness, weight loss, and can be accompanied by fever and abdominal pain. The condition develops rapidly, and oliguria and progressive renal function failure will appear within a few days of onset. Some patients have a relatively subtle and slow onset, and the condition gradually worsens.

　　Acute proliferative glomerulonephritis is a group of clinical syndromes characterized by acute nephritis syndrome, with rapid progression of renal function damage. It is often accompanied by oliguria or anuria. The pathological manifestations of renal biopsy show extensive crescent formation in glomeruli (more than 50% of glomeruli have crescent formation), so it is also called crescentic glomerulonephritis. Prevention is better than treatment, so what are the preventive measures for acute proliferative glomerulonephritis? The following experts introduce the preventive measures for acute proliferative glomerulonephritis.

　　1. Pay attention to rest, avoid fatigue, prevent infection, and have a diet low in protein. Pay attention to supplementing vitamins. Avoid using drugs that damage the kidneys.

　　During the medication period, visit the outpatient department every 1 to 2 weeks to observe the urine routine, liver and kidney function, and growth and development to guide the completion of the course.

　　After the control of active lesions and the completion of the course, repeat renal biopsy should be performed to evaluate the pathological changes of renal tissue, observe the presence of chronicization tendency, so as to take timely measures.

　　In summary, it is important not to ignore the following important links in the prevention: protecting the residual renal function, correcting various factors that reduce renal blood flow (such as hypoproteinemia, dehydration, hypotension, etc.), and preventing infection.

　　Rapidly progressive glomerulonephritis is a clinical syndrome characterized by hematuria, proteinuria, and progressive renal function decline, which is the most serious type of glomerulonephritis. Renal biopsy pathology usually shows crescentic glomerulonephritis. So, what kind of laboratory tests are needed for the diagnosis of rapidly progressive glomerulonephritis? The following experts introduce the laboratory tests needed for rapidly progressive glomerulonephritis.

　　1. Urine laboratory examination

　　Common hematuria, atypical red blood cell urine, and red blood cell casts, often accompanied by proteinuria; the amount of urinary protein varies, and it can excrete a large amount of proteinuria like nephrotic syndrome, but the obvious manifestations of nephrotic syndrome are not common.

　　2. Other

　　Enzyme-linked immunosorbent assay for soluble human glomerular basement membrane antigen to check for anti-glomerular basement membrane antibodies, the most common type is IgG type.

　　Acute nephritis is the most easily treated type of kidney disease. Generally, patients with acute nephritis do not need to be hospitalized for treatment. During the illness, if patients with acute nephritis adopt appropriate treatment and辅以科学的饮食，the condition can be controlled quickly. The following introduces the most suitable diet for early acute nephritis patients:

　　One: Salt intake

　　During the period when edema is obvious, patients should especially avoid the intake of salt, and the taste can be adjusted with unsalted soy sauce in the diet; after the blood pressure returns to normal and the edema completely subsides, 2 to 3 grams of salt can be consumed daily.

　　Two: Diet principles

　　The general principle of diet for early acute nephritis patients is to focus on palatable and light food.

　　1. Daily protein intake: for patients with mild illness, 0.8 grams per kilogram of body weight is appropriate, and for patients with moderate illness, 0.5 grams per kilogram is appropriate. If the patient loses too much protein, appropriate protein supplements can be taken, and more milk, soy milk, chicken, duck, fish, and other protein-rich foods should be eaten.

　　2. Daily salt and potassium intake: should be less than 500mg, and high-salt foods such as pickled vegetables, bean curd, and ham should be avoided, and the intake of high-potassium foods (such as fruits, potatoes, chives, and rapeseed) should be limited.

　　6. Adhere to the principle of high sugar and low-fat diet: high sugar does not increase the burden on the kidneys, glucose, honey, fruit juice, sugar, and grains can be consumed; fat should not be consumed in excess; oils should mainly be plant oils (because most plant oils are unsaturated fatty acids); appropriate alkaline substances should be supplemented, and more orange juice, lemon water, and vegetable juice should be drunk to regulate the acid-base balance in the body; sufficient amounts of various vitamins, especially B-group vitamins and trace elements, such as multiple vitamins and 21st-century vitamins, should be supplemented.

　　4. Acute nephritis generally does not strictly limit fat intake, and it is better to eat less fat.

　　5. Suitable food types: water chestnuts, green beans, winter melon, lotus leaves, mung beans, soybeans, corn silk, crucian carp, dried tangerine peel, and mulberry bark. The above foods have the effects of clearing heat and promoting diuresis, and detoxifying and reducing swelling. Patients with conditions can be given water chestnut and green bean soup, winter melon and lotus leaf soup, mung bean and winter melon soup, crucian carp and red bean soup, winter melon and crucian carp soup, etc., for diuresis and reducing swelling, and clearing heat and promoting diuresis. Some dried tangerine peel, mulberry bark, and corn silk can be added to the food.

　　Three: Distribution of three meals a day

　　A three-meal diet plan is provided for early acute nephritis patients as follows:

　　Breakfast: 0.5 to 1 jin of milk, 1 boiled egg, half a cake or steamed bun.

　　Lunch: For patients with mild illness, 2～3 two of rice, 1 fruit, 1 two of lean meat, 1 jin of vegetables.

　　For patients with severe illness, 2～3 two of rice, 1～2 jin of vegetables, 1～2 fruits.

　　Dinner: 1 two of congee or noodle soup, 2 two of rice or bread, 1 jin of vegetables, 1～2 fruits.

　　4. Water intake

　　Patients without significant edema, hypertension, oliguria, cardiac enlargement, and congestive heart failure do not need to limit the intake of water excessively. For those with edema, the intake of water should generally ensure the daily requirement, usually within 800～1500 milliliters in total.

　　Rapidly progressive glomerulonephritis has an acute onset, rapid progression, and rapid deterioration, with a very high mortality rate. The principle is to make an early diagnosis, receive adequate treatment, and perform targeted combined treatment. It is necessary to differentiate between acute and chronic glomerular injury. The formation of a large number of crescents and纤维素样坏死 suggests that the lesion is in an active phase, and active treatment should be given. Fibrotic crescents and interstitial fibrosis suggest that the lesion has entered the chronic phase, and attention should be paid to protecting renal function; for those with systemic symptoms, cyclophosphamide and methylprednisolone (methylprednisone) should be used as soon as possible to control symptoms.

　　1. Acute phase treatment

　　The key to treatment during the acute phase is to make an early diagnosis and provide timely intensive suppressive measures against immune reactions and inflammatory processes, which can effectively control disease progression and reduce mortality. According to reports, 73% of 339 cases of rapidly progressive glomerulonephritis died or experienced renal death (surviving on dialysis) before treatment with immunoinflammatory intensive inhibitors. The 5-year survival rate (not dependent on dialysis) after treatment reached 60%～80%, among which 32 of 42 cases (76%) improved after treatment, indicating that modern treatment measures are effective. The specific treatment methods are as follows:

　　(1)Pulse therapy:

　　①Corticosteroids and immunosuppressants: On the basis of conventional treatment with steroid hormones and cytotoxic drugs, methylprednisolone pulse therapy is added, i.e., 1g or (15～30mg/kg) of methylprednisolone dissolved in 150～250ml of 5% glucose solution is administered intravenously within 1～2h, once a day, 3 times as a course, and then repeat 1～2 courses with an interval of 3～4 days. Maintenance therapy is maintained during and after treatment with prednisone (prednisone) 1～2mg/(kg·d) taken every other day. This therapy is applied when blood creatinine is below 707mol/L (8mg/dl), otherwise it will affect the efficacy if it is too late. Methylprednisolone pulse therapy is more effective than simple oral prednisone (prednisone) and cytotoxic drugs, especially effective for type II and III, among which 70% of patients can discontinue dialysis and maintain normal renal function for more than two years, but it is not effective for type I. The combined use of cyclophosphamide (CTX) high-dose pulse therapy can enhance efficacy, improve renal function, reduce proteinuria, and decrease the number of cellular crescents. The dosage of cyclophosphamide (CTX) is 0.5～1g/m2 of body surface area, once a month, for a total of 6～12 times. Methylprednisolone 500～1000mg/d for 3 days, followed by oral prednisone (prednisone) 60～100mg/d, gradually reduced to 30mg/d after 3 months, and then gradually withdrawn.

　　② Plasma Exchange Therapy: This therapy involves removing a large amount of anticoagulated whole blood from the patient, separating the plasma and blood cells by centrifugation or using a large-pore fiber membrane ultrafiltration, removing the plasma, and then supplementing an equal amount of healthy fresh plasma or other substitutes. This method can remove antigens, antibodies, immune complexes, and inflammatory mediators from the circulation, enhance the phagocytic function of the reticuloendothelial system, improve the stability of the internal environment of the body, and is conducive to the recovery of the condition. Plasma exchange therapy is effective in Type I, especially in the early stage of Type I disease, before it develops into oliguria renal failure, blood creatinine

　　③ Quadruple Therapy: The combined use of glucocorticoids, cytotoxic drugs, anticoagulants, and platelet aggregation inhibitors. Specific methods: A, heparin is added to 250-500ml of 5% glucose solution and infused, with a doubling of the prothrombin time as the index for adjusting the dosage, with a total daily dose of 5000-20000U. After 5-10 days, oral anticoagulants such as warfarin can be substituted. B, antiplatelet aggregation drugs such as dipyridamole (Persantin), aspirin, and sulfinpyrazone. C, cyclophosphamide (CTX) or azathioprine, cyclophosphamide (CTX) can be used in pulse therapy or azathioprine 2mg/(kg·d). D. Prednisone (Prednisone) 60mg, once daily, or methylprednisolone pulse therapy. There are reports that the aforementioned therapy is effective in diuresis, protecting renal function, and improving prognosis. Since in the process of the disease, the cleaved fibrinogen is converted into fibrinopeptides, which act as chemoattractants for monocytes and play an important role in the formation of crescents, the application of quadruple therapy, also known as the cocktail therapy, has a certain theoretical basis.

　　④ Renal Transplantation: Recurrence after transplantation is a matter of attention for this disease (especially Type I). The recurrence rate after transplantation in Type I can reach 10% to 30%. Therefore, renal transplantation should be performed after half a year of stable condition. Children with Type I disease should monitor the blood anti-GBM antibody titer, and continue the aforementioned medication for several months after it drops to normal, which can reduce the recurrence rate to below 10%. Similarly, for Type III, blood ANCA levels should be monitored to determine the timing of drug discontinuation and transplantation.

　　2. Treatment for Recurrence and Worsening

　　In this disease, type 1 and type 3 often have relapses after clinical remission, which can occur in a few months or several years. Repeated treatment as mentioned above can still lead to remission after recurrence. The worsening of the condition during the treatment process is often related to infection, and it is necessary to actively remove the focus of infection and control the infection.

　　3. Chronic Phase Treatment

　　The lesions in the active phase of the disease can be controlled, but they cannot prevent the disease from progressing to chronicity (glomerular sclerosis, tubular atrophy, interstitial fibrosis). For the judgment of the chronic phase of the disease, it cannot be solely based on the duration of the disease course, nor can it depend on whether oliguria and renal failure appear clinically, because some patients may develop end-stage renal failure within a few weeks, and their clinical manifestations are not consistent with pathological changes. Therefore, whether the disease enters the chronic phase of the disease course depends on whether chronic changes dominate in the pathological changes. The specific method of treatment in the chronic phase is:

　　(1) Stop the suppression of immune inflammation: The long-term and large-scale use of immunosuppressive drugs in chronic phase patients has serious side effects. At this time, it is generally necessary to reduce glomerular filtration pressure and protect residual renal function as much as possible. However, in type 3 patients who have developed partial chronic lesions, the continuation of intensive treatment may still achieve certain efficacy.

　　(2) Hemodialysis: Hemodialysis treatment should be implemented as soon as possible. When blood creatinine is greater than 530μmol/L (≥6mg/dl) during the acute phase, it should be performed simultaneously with immunosuppressive therapy. Hemodialysis not only guarantees immunosuppressive therapy but also creates conditions for diagnosis and treatment. If the condition enters the chronic phase and renal function cannot be restored, then long-term dependence on hemodialysis treatment is necessary.

　　(3) Kidney Transplantation: Patients with chronic kidney disease who have been long-term dependent on hemodialysis treatment should consider kidney transplantation.

　　Kidney transplantation should be performed half a year after the condition is stable. The disease is prone to recurrence after kidney transplantation, especially in type 1, the recurrence rate reaches 10% to 30%. Type 1 patients should monitor the titer of blood anti-GBM antibody and continue to take medication for several months after it drops to normal, and the recurrence rate can be reduced to below 10%. For type 3, ANCA levels should be monitored to determine the timing of discontinuation of medication and transplantation.