Microscopic glomerular nephritis

　　What causes microscopic glomerular nephritis:

　　The pathogenesis of microscopic glomerular nephritis is unknown, characterized by the loss of negative charge on the glomerular capillary wall. The disease can also occur in transplanted kidneys, thus supporting the view that there may be a humoral factor in the circulating blood that consumes the negative charge of glomeruli. This factor damages the charge barrier of glomeruli, causing selective proteinuria. In addition, in cases of microscopic glomerular nephritis associated with Hodgkin's disease, steroids and alkylating agents are effective, and the nephritis can be rapidly relieved after the affected lymph nodes are removed. Some patients also have concurrent viral infections such as measles, and the disease also relieves, all of which suggest abnormal T lymphocyte function, and certain lymphokines produced by them increase the permeability of the glomerular capillary wall. However, this substance has not been confirmed yet.

　　What diseases can be complicated with microscopic glomerular nephritis:

　　Microscopic glomerular nephritis generally has a good prognosis, with a 10-year survival rate reported by Cameron of over 95%, and most of the deceased are adults (especially the elderly). The main causes of death are cardiovascular diseases and infections, the latter often being side effects of improperly used hormones and cytotoxic drugs. Long-term follow-up has found that it is rare for it to develop into chronic renal failure, with about 3% of adults developing chronic renal failure, and it is even rarer in children. Chronic renal failure often occurs in patients with resistance to hormones, accompanied by focal glomerulosclerosis.

　　The peak age of children is between 2 and 6 years old, and adults are more common between 30 and 40 years old. In the nephrotic syndrome of patients over 60 years old, the incidence of minimal change nephrotic syndrome is also very high. In children, the male-to-female ratio is twice as high as that of females, and the male-to-female ratio in adults is basically similar. About 1/3 of patients may have upper respiratory tract or other infections before the disease. The onset is usually acute, and the typical initial symptom of the disease is usually a marked nephrotic syndrome, accounting for 90% of pediatric nephrotic syndrome and 20% of adult nephrotic syndrome. Blood pressure is normal.

　　20% of patients may have varying degrees of microscopic hematuria. With the increase in age, the incidence of microscopic hematuria also increases, especially in patients over 60 years old, due to interstitial inflammation, fibrosis, and vascular lesions, the incidence of microscopic hematuria is higher. However, gross hematuria is rare. Due to hypovolemia and decreased renal perfusion, about 1/3 of patients may have decreased glomerular filtration rate during their first visit, and urine sediment examination shows no cells or casts. In severe cases, 24-hour urine protein can exceed 40g.

　　Urinary protein in children is a typical high-selective proteinuria, mainly including albumin and a small amount of high-molecular-weight proteins such as IgG, α2-macroglobulin, C3. In adults, the manifestations are varied. In elderly patients over 60 years old, the nephrotic syndrome caused by minimal change disease can manifest as non-selective proteinuria, and it is often accompanied by hypertension and decreased glomerular filtration rate. In recent years, it has been found that the transferrin with a molecular weight of 88000, due to its spherical structural characteristics, also leaks into the tubular fluid. In urine with a pH of 4.5 to 5.5, the iron in transferrin is released into the tubular fluid, and Fe3+ can produce many oxygen free radicals that damage the renal interstitium and tubules. Fe3+ can also directly damage the tubules and interstitium. There are no fibrin degradation products or C3 in the urine, the complement components in the blood are normal, but there may be a slight decrease in C1q. The IgG concentration is generally low during the attack, while IgM is slightly increased during both the attack and remission. The tissue compatibility antigen HLA-B12 is significantly more common in minimal change nephrotic syndrome, suggesting that the disease may be related to heredity, and the titer of anti-O antibody is often significantly decreased.

　　Microscopic glomerular nephritis should be differentiated from Hodgkin's disease. In addition, in nephrotic syndrome caused by non-steroidal anti-inflammatory drug allergy, the histology can be similar to that of microscopic glomerular nephritis, but it is usually accompanied by interstitial nephritis and decreased renal function.

　　In extremely rare cases, acute renal failure can occur without obvious hypovolemia, due to hypoalbuminemia leading to a decrease in blood colloid osmotic pressure, and renal pre-renal azotemia caused by severe hypovolemia is seen in 7% to 38% of patients. If there are no typical clinical manifestations of hypovolemia, such as decreased urine concentration, increased sodium excretion, and especially if urine output does not increase after administration of plasma products or albumin, then renal acute renal failure should be considered. At this time, in addition to considering drug-induced acute tubular necrosis (nephrotoxic drugs such as gentamicin, etc.) or acute interstitial nephritis (antibiotics, non-steroidal anti-inflammatory drugs, etc.), another special form of acute renal failure should also be recognized.

　　6. The underlying glomerular disease of nephrotic syndrome with idiopathic oliguric acute renal failure is often minimal change nephropathy (minimal changedisease) or mild mesangial proliferative glomerulonephritis (mesangialproliferativeGN), which is more common in older patients with severe nephrotic syndrome, high blood pressure, especially systolic pressure, and vascular sclerosis. The pathological changes, in addition to the manifestations of minimal change nephropathy, include flattened proximal tubular epithelial cells, shedding of brush borders, and (or) interstitial edema, but without typical tubular necrosis or interstitial nephritis. Since the pathological changes of minimal change nephropathy in conjunction with acute renal failure are mild and often reversible, it is a condition mainly characterized by hemodynamic changes. Although blood volume and renal blood flow are generally normal, the glomerular filtration rate shows a transient decrease, resulting in a decrease in the filtration index (FF). The two components of the glomerular filtration rate per single kidney unit show significant changes: the ultrafiltration coefficient decreases by more than 50%; due to the decrease in intravascular colloidal osmotic pressure, the net ultrafiltration pressure (netdrivingforce, i.e., the hydrostatic pressure difference ΔP across the capillary membrane minus the difference in colloidal pressure Δπ between the inside and outside of the blood vessels) increases, and the interstitial edema becomes more severe.

　　How to prevent nephrotic kidney disease:

　　If you不幸 suffer from kidney disease, please go to a specialized kidney hospital and consult a kidney specialist for the most appropriate treatment. Otherwise, seeking out quacks and taking herbal remedies may miss the treatment opportunity, leading to more complications and even developing uremia in a short period of time.

　　1. Drink adequate (sufficient) water and do not hold urine. Urine that stays in the bladder for too long is prone to bacterial growth, and bacteria may likely infect the kidneys through the ureters, leading to kidney infection. Drinking plenty of water and urinating regularly can also prevent kidney stones.

　　2. Control hypertension. If you have hypertension, please consult a doctor immediately and take medication to control your blood pressure within a safe range. Long-term hypertension will continuously damage the small blood vessels of the kidneys, as the kidneys are composed of two million glomeruli (microvessels).

　　3. Control diabetes, as the blood vessels of diabetic patients slowly harden, especially in the small vessels. The kidneys are composed of millions of tiny blood vessels, and in severe diabetes, kidney function may also be damaged. Statistics show that one quarter to one fifth of 'dialysis' patients are caused by end-stage diabetes.

　　4. Regular renal function tests require urine screening and blood pressure checks every six months. Half of the kidney disease patients have their kidney damage process occur without their knowledge, so it is likely that by the time they feel discomfort, they may already be at the end stage of kidney disease - the time when dialysis is necessary for survival.

　　There are many items to check for kidney disease, in addition to general examinations, there are some other items to be checked. Here are some examples:

　　1. UrinalysisThe best time to collect urine is the first morning's midstream urine, and it should be tested within one hour. Women during their menstrual period generally do not take urine tests. The purpose of the urine test is mainly to understand whether there are proteins, red blood cells, casts, specific gravity, and acidity or alkalinity in the urine.

　　2. Urinary protein quantification:They can accurately reflect the amount of urinary protein excretion in the body. The method is to collect 24 hours of urine (record the total amount), take a part for inspection. If the protein in each 100 milliliters of urine exceeds 0.5 grams, the protein定性 in the urine routine examination is often (4+).

　　3. Serum immunoglobulins (IgG, IgA, IgM, IgD, IgE):The increase or decrease of these values has a significant impact on the differentiation of various kidney diseases and the estimation of the prognosis.

　　4. Serum complement (total complement, C3, C4, C19):The changes in these values help to differentiate between different types of nephritis, and regular checks can estimate the prognosis of nephritis.

　　5. The main checks for understanding the severity of kidney disease and estimating the prognosis include:The main tests for understanding the severity of kidney disease and estimating the prognosis include: blood creatinine clearance rate (Ccr), blood creatinine (Scr), blood urea nitrogen (BUN), urinary creatinine, phenol red excretion test (PSP), urinary sugar, 'B' ultrasound scan, renal pelvis imaging, renal biopsy, etc. It is not necessary to perform all these tests; they should be conducted only to achieve the diagnostic purpose. The main purpose is to reduce the patient's suffering and alleviate the economic burden on the family. Additionally, the kidneys have a strong compensatory capacity. Once renal function, such as Ccr, Scr, BUN, etc., shows abnormalities, it indicates that the kidney disease has become relatively severe.

　　1. Attention should be paid to friends with nephrotic syndrome who have negative proteinuria and no edema.

　　1. Sodium Salt Intake:

　　During edema, a low-salt diet should be adopted to avoid exacerbating edema. It is generally advisable to consume no more than 2g of salt per day, and to avoid preserved foods, reduce the use of monosodium glutamate and alkali, and return to a normal diet when the edema subsides and plasma protein approaches normal levels.

　　2. Protein Intake:

　　Nephrotic syndrome is characterized by the excretion of a large amount of plasma protein in the urine, leading to a decrease in body protein and a state of protein malnutrition. Hypoproteinemia causes a decrease in plasma colloid osmotic pressure, resulting in persistent edema that is difficult to resolve and a decrease in the body's resistance. Therefore, in the early and acute stages, when there is no renal failure, it is recommended to provide a high-quality, high-protein diet (1~1.5g/kg*d), such as fish and meat, etc. This helps alleviate hypoproteinemia and some associated complications. However, a high-protein diet can increase renal blood flow and glomerular filtration rate, putting glomerular capillaries under high pressure, and consuming a large amount of protein also increases urinary protein, which can accelerate the hardening of the glomeruli. Therefore, for patients with chronic, non-acute nephrotic syndrome, it is recommended to consume a smaller amount of high-quality protein (0.7~1g/kg*d). When chronic renal dysfunction occurs, a low-protein diet (0.65g/kg*d) should be adopted.

　　3. Fat intake:

　　Patients with nephrotic syndrome often have hyperlipidemia, which can cause atherosclerosis and glomerular injury, sclerosis, etc., therefore, the intake of foods rich in cholesterol and fat such as animal organs, fatty meat, and certain seafood should be restricted.

　　4. Supplementation of trace elements:

　　Due to the increased permeability of the glomerular basement membrane in patients with nephrotic syndrome, in addition to losing a large amount of protein in the urine, certain trace elements and hormones bound to protein are also lost, leading to a deficiency of calcium, magnesium, zinc, iron, and other elements in the human body. Appropriate supplementation should be given. Generally, it is advisable to consume vegetables, fruits, and coarse grains rich in vitamins and trace elements for supplementation.

　　Second, dietary habits for friends with nephrotic syndrome whose proteinuria has turned negative and there is no edema

　　1. Staple food intake:

　　The normal dietary intake of foods such as steamed buns and rice.

　　2. Sodium intake:

　　According to normal taste or light diet.

　　3. Quality protein intake:

　　According to 1.0~1.2g/(kg body weight, per day), about 1 egg white/1 two of lean meat/half a cup of milk is needed per day.

　　4. Common edible vegetables:

　　Tofu, cabbage, scallions (for seasoning), kale, bracken, elm money, pumpkin, winter melon, mung bean sprouts, red sweet potato, kidney beans, luffa, green beans, eggplant, cabbage, onion, winter melon, pumpkin, zucchini, cucumber, Chinese cabbage, radish, bitter vegetables, green beans, chili (for seasoning), taro, lima beans, carrots, chive, lettuce, cauliflower, tomatoes, sweet bell peppers, bean sprouts, lettuce, rapeseed, yam, lotus root, sauerkraut, garlic (for seasoning), ginger, clover, bitter melon, spinach, preserved vegetables, dried mushrooms, silver ear, cilantro, potatoes.

　　5. Avoid:

　　Spicy and pungent foods, fried foods, seafood such as sea fish, sea crab, chili, garlic, green onions, coriander, dog meat.

　　Precautions before the treatment of minimal change nephrotic syndrome

　　Before the application of hormones and modern antibiotics, spontaneous remission was estimated to be between 25% to 40%. Due to infection and embolic complications, the 5-year mortality rate of pediatric patients at that time was over 50%, which is currently around 7% to 12%; for children with hormone-sensitive cases, it is less than 2%. The conventional dose of prednisone for children is 60mg/m2 per day, for adults 40 to 60mg per day, and then gradually reduced over a period of 4 to 6 months. 90% of children are effective within 4 weeks, and 90% of adults within 8 weeks. If there is still a large amount of proteinuria after treatment, immunosuppressants should be added.

　　For patients sensitive to hormones, about 50% can maintain negative urinary protein or relapse after reducing or discontinuing medication, but most patients can be relieved in the end. Another 50% of patients often relapse or present with hormone dependence (indicating that a larger dose of hormones is needed to control proteinuria), and this is often accompanied by side effects of hormones, which are more obvious in pediatric patients. The addition of cyclophosphamide 2 to 3mg/kg (children 75mg/m2 per day) for 8 to 12 weeks can extend the remission period of hormone-sensitive patients. Due to the toxic effects on the gonads, teratogenic effects, and other toxic reactions of cytotoxic drugs, they are only used when both kidney disease and hormone side effects are severe. When hormone therapy is effective, but there are recurrent episodes or dependence on hormones, and there is no indication for adding cytotoxic agent cyclophosphamide, cyclosporine A can be chosen, 3.5 to 4mg/(kg·d), taken orally. After 4 months, the nephrotic syndrome in most patients with minimal change nephropathy can be completely relieved, and the dose of hormones can be significantly reduced.

　　When the nephrotic syndrome caused by minimal change nephropathy cannot be relieved by the above active treatment, it is necessary to pay attention to the following situations:

　　1. Control or remove internal infection foci, especially in search of hidden infection foci.

　　2. For the formation of renal vein thrombosis, a CT scan should be performed in a timely manner. When diagnosed with renal vein thrombosis, systemic urokinase 40,000 to 80,000 units per day can be administered, added to 40ml of 0.9% sodium chloride, and administered intravenously 1 to 2 times a day. It is also possible to perform a femoral artery puncture and catheterization on the renal artery on the side of renal vein thrombosis, and administer urokinase in a fractional manner within 1 hour, with a total dose of 200,000 units. After that, oral dipyridamole 25mg, three times a day, and warfarin 2.5mg, once a day, can be taken. One month later, a CT re-examination showed an efficacy of 100%, and after 5 years of long-term follow-up, the treatment method was found to be effective. We believe that early diagnosis of renal vein thrombosis and active anticoagulant treatment can improve the prognosis of primary glomerulonephritis and various primary glomerulonephritis, and maintain normal renal function.

　　3. Most patients insensitive to hormones have focal glomerulosclerosis.

　　4. To reduce the recurrence rate after hormone discontinuation, it is necessary to measure the blood cortisol concentration before discontinuing hormones. For those with normal blood cortisol concentration, it is less likely to recur after hormone discontinuation.