Type 1 diabetes nephropathy

　　Type 1 diabetes nephropathy is common in diabetic patients with a disease duration of more than 10 years. Proteinuria is the earliest manifestation of diabetic nephropathy, and its pathogenesis is very complex and has not been fully elucidated. Research data show that the pathogenesis of diabetic nephropathy is multifactorial, mainly including the following aspects:

　　1. Abnormal renal hemodynamics

　　Abnormal renal hemodynamics plays a key role in the occurrence of diabetic nephropathy, and may even be the initiating factor.

　　(1) During hyperglycemia, the glomerulus is in a hyperperfusion and hyperfiltration state, with increased transcapillary wall pressure, causing mesangial cell expansion, fusion of podocytes, and the formation of dense droplets. Glomerular epithelial cells may be shed from the basement membrane.

　　(2) The increase in type IV collagen messenger RNA in the glomerular basement membrane causes the basement membrane to thicken, eventually forming diffuse and nodular mesangial lesions, leading to glomerulosclerosis.

　　(3) Under increased pressure, protein filtration increases and can also deposit in the mesangial area and glomerular basement membrane, promoting matrix proliferation, forming a vicious cycle, and can cause nodular and diffuse glomerulosclerosis.

　　2. Hyperglycemia

　　The occurrence of diabetic nephropathy is closely related to hyperglycemia. Poor blood glucose control can accelerate the occurrence and development of diabetic nephropathy, while good blood glucose control can significantly delay its progression. The increase in hyperglycemia and the formation of glycated end products cause mesangial cell proliferation, increased extracellular matrix, mesangial expansion, and thickening of the glomerular basement membrane.

　　3. Genetic factors

　　Most diabetic patients will not eventually develop kidney disease, and diabetic nephropathy can also occur in some patients with good long-term blood glucose control. Glucose transporter-1 (GLUT1) is the main glucose transporter on the glomerular mesangial cells. Recent studies have found that the differences in the GLUT1 menu and regulation among mesangial cells of diabetic patients may be one of the factors that make some patients prone to kidney damage. Moreover, the occurrence of diabetic nephropathy also shows a familial aggregation phenomenon, and the incidence of diabetic nephropathy in diabetic patients with a family history of hypertension is also significantly higher than that in patients without a family history of hypertension. In addition, there are differences in the incidence of diabetic nephropathy among different races. All this indicates that the occurrence of diabetic nephropathy is related to genetic factors. 4. There is no direct relationship between hypertension and the occurrence of diabetic nephropathy, but the increase in blood pressure during the pre-existing hypertension or during the stage of microalbuminuria in the course can accelerate the progression of diabetic nephropathy and the deterioration of renal function, and increase the excretion of urinary albumin.

　　Type 1 diabetes nephropathy often complicates with diabetic retinopathy. Patients with diabetic nephropathy syndrome almost always have diabetic retinopathy. Therefore, for patients with diabetic nephropathy syndrome without retinopathy and a course of less than 10 years, consideration should be given to renal biopsy to exclude glomerular diseases of other causes. However, it should be noted that for diabetics undergoing certain diagnostic tests such as intravenous pyelography and angiography, it is particularly easy to cause kidney damage and acute renal failure, especially in those over 50 years old, with a course of more than 10 years, and those with pre-existing renal insufficiency and other diabetic complications, should be particularly cautious. Renal failure generally occurs within 48 to 72 hours after contrast medium or other examination procedures.

　　Common other complications of type 1 diabetic nephropathy include:

　　① There is often skin itching. Some diabetic nephropathy patients may experience dry and desquamating skin, which is very itchy. Female patients are more prone to vaginal itching.

　　② Type 1 diabetic nephropathy often leads to neck hair follicle inflammation. It can appear as pustular inflammation resembling boils on the back of the neck, with tenderness and can develop into boils or cellulitis. After the pus is discharged, it can heal, but it often recurs shortly thereafter.

　　③ Diabetic nephropathy often leads to skin erythema, which resembles burn blisters. The wall is very thin, containing translucent serum inside, with no red halo around the blister. Typically, erythema appears on the back or bottom edge of the fingers, toes, hands, and feet, and can be single or multiple, healing within a few weeks but often recurring.

　　④ Diabetic nephropathy often leads to abnormal sweating. There is often profuse sweating for no apparent reason, and it is more common in the upper limbs or trunk. Some patients may even experience excessive sweating.

　　⑤ Diabetic nephropathy often leads to xanthomas. On the flexor side of the limbs, buttocks, neck, knees, and other skin areas, there are often clusters of eruptive yellowish orange small nodules or papules, surrounded by a red halo, and accompanied by itching.

　　⑥ Diabetic nephropathy often leads to foot gangrene. Patients may often experience foot pain, loss of thermal sensation, dryness and cracking, prone to ulcers, abscesses, necrosis, and difficult to heal, even leading to foot perforation.

　　The basic pathological feature of type 1 diabetic nephropathy is the uniform thickening of the glomerular basement membrane, accompanied by increased glomerular mesangial cell matrix, nodular hypertrophy of the glomerular capsule and mesangial cells, and increased permeability. Due to the non-specific symptoms of early diabetic nephropathy, diabetic patients are often unaware of whether they have diabetic nephropathy. Generally, the symptoms of diabetic nephropathy are mainly proteinuria, edema, hypertension, or azotemia, accompanied by increased fasting blood glucose or diabetic symptoms.

　　1. Proteinuria

　　In the early stages of diabetic nephropathy, there is no clinical proteinuria, and only radioimmunoassay can detect微量proteinuria. The only manifestation of early clinical diabetic nephropathy is proteinuria, which gradually develops from intermittent to persistent.

　　2. Edema

　　In the early stages of clinical diabetic nephropathy, edema is generally not present. Some patients may have mild edema before the decrease in plasma protein. If there is a large amount of proteinuria and low plasma protein, edema can worsen, which is often a manifestation of the disease progressing to the late stage.

　　3. Hypertension

　　In type 1 diabetic patients without kidney disease, the prevalence of hypertension is not increased compared to normal people. In type 2 diabetes patients, there are more cases of hypertension, but if proteinuria occurs, the proportion of hypertension also increases. In patients with nephrotic syndrome, hypertension is often present, most of which are moderate, with a few being severe.

　　4. Renal failure

　　There is a significant difference in the progression speed of diabetic nephropathy. Some patients may have mild proteinuria for many years, but their renal function remains normal. In some patients, even with little proteinuria, kidney disease can develop rapidly, leading to nephrotic syndrome, progressive deterioration of renal function, and eventually uremia.

　　5. Anemia

　　Patients with obvious azotemia may have mild anemia.

　　Other organ complications include cardiovascular diseases such as heart failure and myocardial infarction. Nerve diseases such as peripheral neuropathy. When autonomous nerves are involved, neurogenic bladder may occur. Retinopathy, when diabetic nephropathy is severe, almost 100% is complicated with retinopathy, but those with severe retinopathy may not have obvious kidney damage. As diabetic nephropathy progresses, retinopathy often accelerates deterioration.

　　The early prevention of type 1 diabetic nephropathy is very important, and the common preventive measures are as follows:

　　(1) All diabetic patients with a disease course of more than 5 years should regularly check renal function, urine protein qualitative, 24-hour urine protein quantitative, and pay attention to measuring blood pressure and fundus examination.

　　(2) When possible, urine microalbumin and β2-microglobulin should be measured to detect diabetic nephropathy early. If the urinary microalbumin increases, it should be measured for 3-6 months for 3 times in a row to determine whether it is persistent microalbuminuria.

　　(3) If it is confirmed that there is an increase in microalbumin and other factors causing its increase, such as urinary tract infection, primary hypertension, etc., it should be highly alert and try to control blood sugar to make it as close to normal as possible. If blood pressure is > 18.7/12 kPa, it should be actively reduced to maintain blood pressure within the normal range. At the same time, it should be emphasized that low-salt and low-protein diets are preferred with high-quality protein.

　　(4) Salt intake in diet should be limited. To protect the kidneys and reduce their workload, diabetic patients' dishes should be as tasteless as possible, and the salt intake should be within 7 grams per day. In severe renal failure, water intake should also be restricted. Properly limit the intake of potassium and protein. Restrict the intake of potassium-containing beverages and fruits. Protein should be controlled at 0.6-0.8 grams per kilogram of body weight per day, and easily digestible fish and lean meat are preferred, because plant protein is not easily absorbed and will increase the kidney burden. In addition, protein contains a high amount of potassium, and controlling protein intake to some extent also helps to limit potassium intake. Intake sufficient vitamins and trace elements. Especially vitamin B, vitamin C, and zinc, calcium, iron, etc., can have a protective effect on the kidneys.

　　In type 1 diabetic nephropathy, the main basis for laboratory tests is the determination of urinary microalbumin levels by modern biochemical and immunological detection techniques. This is currently the main means to detect early diabetic nephropathy. Detailed examination is as follows:

　　1. Provocation test

　　In the early stage of diabetic nephropathy, the 24-hour urine protein level is generally

　　2. Renal function and other laboratory tests

　　The functional changes and structural changes in diabetic nephropathy are parallel. In the early stage, the renal plasma flow increases and the glomerular filtration rate increases. In recent years, it has been found that the excretion of N-acetyl-β-D-glucosaminidase (NAG) in the urine of diabetic patients has increased, and it is positively correlated with urinary protein excretion and retinopathy, increasing with the progression of the disease.

　　3. Urinalysis and renal function tests

　　(1) Renal histopathology examination: Renal histopathology examination is an important means of diagnosing diabetic nephropathy. Specific changes account for 50%, mainly nodular glomerulosclerosis, glomerular and efferent arteriole hyaline change, and exudative changes on the renal capsule surface. Non-specific changes include thickening of the glomerular and renal tubular basement membranes. Immunofluorescence examination shows the deposition of albumin and IgG on the glomerular and renal tubular basement membranes and the surface of the renal capsule.

　　(2) Fundus examination: Diabetic retinopathy is part of diabetic microvascular complications and often coexists with diabetic nephropathy, so once retinopathy is detected, it is necessary to be vigilant about the existence of kidney microvascular lesions.

　　(3) Renal morphology examination: In the early stage of diabetic nephropathy, the kidney volume increases and weight increases. The size of the kidneys is measured, and their weight is calculated according to intravenous pyelography or B-ultrasound. The length of the kidney is the maximum distance between the upper and lower poles, and the width is the maximum distance from the middle inner side to the outer side of the kidney.

　　Type 1 diabetes nephropathy is one of the serious complications of diabetes control failure. Therefore, diabetics need to be highly vigilant about diabetes nephropathy and should strengthen self-care and self-protection from the beginning, especially starting with diet to reduce the burden on the kidneys.

　　1. Blood sugar control is crucial.

　　The key to controlling blood sugar: first, strictly limit calorie intake; second, consistently take hypoglycemic drugs; third, avoid factors that can cause blood sugar fluctuations, such as emotional excitement and infection.

　　2. Limit salt intake.

　　To protect the kidneys and reduce their workload, the diet of diabetics should be as tasteless as possible, with salt intake limited to 7 grams per day, and water intake should also be limited in severe renal failure.

　　3. Appropriately limit the intake of potassium and protein.

　　Limit the intake of potassium-containing beverages and potassium-rich fruits. Protein intake should be controlled at 0.6-0.8 grams per kilogram of body weight per day, and it is best to choose easily digestible fish and lean meat, as plant protein is not easily absorbed and can increase the kidney burden. Additionally, protein contains a high amount of potassium, and controlling protein intake can also help limit potassium intake to some extent.

　　4. Ensure adequate intake of vitamins and trace elements.

　　Especially vitamin B, vitamin C, and zinc, calcium, iron, etc., can play a protective role for the kidneys. The multi-element in Jinkang is abundant in variety and appropriate in proportion, easy to take, and only one tablet per day is needed. Vitamin E can be up to 11 international units per day, and vitamin C 0.3 grams per day, and it is not a problem if the dosage is slightly higher.

　　Diabetes nephropathy, as a complication of diabetes, has different dietary requirements because the dietary principle of diabetes nephropathy requires a high-quality low-protein diet. The term 'high-quality' refers to milk protein, followed by egg, poultry egg protein, then fish protein and lean meat protein. Plant protein is considered inferior protein, such as in soy products, daily bread, and rice, which should be limited to avoid increasing the kidney burden. Pay special attention not to eat foods that stimulate the kidneys, such as horseradish and chili, as this may worsen kidney disease.

　　Patients with diabetic nephropathy should keep the total amount of staple food per day between 250~300 grams, and vegetables can be eaten in large quantities. Although there is proteinuria, for those with normal kidney function, the daily protein intake should be appropriately relaxed, with 80~100 grams as preferred.

　　In addition, diet should also pay attention to high calcium and low phosphorus, as high-calcium foods often also have high phosphorus, such as animal internal organs, pork ribs, shrimp skin, and bone-building powder, which are definitely high in phosphorus and should not be eaten in large quantities.

　　Traditional Chinese medicine believes that diabetic nephropathy is caused by long-term injury of Yin and Qi in diabetes, Yin damage leading to Yang, deficiency of both Qi and Yin, deficiency of both Yin and Yang, long-term illness entering the meridians, phlegm turbidity, pathogenic heat, blood stasis, and Qi depression mutually adhering, forming 'microscopic masses', causing damage to the kidney body and loss of kidney function. In the clinical stage of diabetic nephropathy, due to kidney injury, Qi transformation fails, endogenous turbidity and toxicity, turbidity and toxicity can further injure the kidney source, consume Qi and blood, block the rise and fall of Qi, and eventually manifest as the critical condition of uremia 'Guange'. Treatment should focus on purging turbidity and detoxifying, with the protection of kidney function as the main task.

　　In the early stage, the key to treatment should be to strengthen the spleen and invigorate the Qi, tonify the kidney and nourish the liver, and nourish Yin and activate blood circulation, using modified Qijuhuang Decoction and Taohong Siwu Decoction.

　　In the middle stage, the key to treatment is to strengthen the spleen and tonify the kidney, activate blood circulation and promote diuresis, using Jinkui Shenqi Pill, Shengshi Shenqi Pill, and modified Shizhi Decoction; in the later stage, dynamic辨证, select according to symptoms, such as Linggui Zhugan Decoction, Zhenwu Decoction, Taohu Shengqi Decoction, Dahuang Fuzi Decoction, etc.

　　Medication experience: Invigorate the body, use raw Astragalus 30-60g. Nourish yin, use Fructus Corni, Fructus Lycii, Dioscorea opposita, Schisandra chinensis, raw Rehmannia, etc. Activate blood circulation, use 3g of Hirudo. For disease prevention, it is advisable to add tonifying kidney products in time, one to warm the yang to invigorate the body, and the other to 'seek yin in yang' with drugs such as Epimedii Herba, Morinda officinalis, and Cistanche deserticola. Promote bowel movement and activate blood circulation, take 3-9g of Rhei Preparata and Cinnamon, using both cold and hot properties to complement and invigorate. Sweet and bland diuretics do not harm the body, drugs such as raw Astragalus, Poria, raw Coix Seed, Poria cocos,冬瓜皮, winter melon seed, and strong drugs should not be used arbitrarily.

　　Acupuncture treatment for diabetes emphasizes the combination of dialectical acupoint selection and symptomatic acupoint matching. The treatment generally adopts a comprehensive treatment method that combines various treatment methods, and its efficacy is relatively reliable. However, the operation technique of acupuncture is not something that all patients can master correctly, so acupuncture treatment is not suitable as a self-care technique for patients. It should be performed by doctors in the hospital.