Diabetic nephropathy

Introduction to diabetic nephropathy Diabetic nephropathy is an important complication of diabetic patients, the most characteristic of which is diabetic glomerulosclerosis, the so-called diabetic nephropathy (DN), which is one of the most important chronic complications of microvessels in diabetic patients. In addition, diabetes can cause a significant increase in the chances of renal artery and renal arteriosclerosis and the occurrence of urinary tract infections and contrast-induced nephropathy. basic knowledge The proportion of sickness: 0.102% Susceptible people: no specific population Mode of infection: non-infectious Complications: retinopathy acute renal failure

Causes of diabetic nephropathy

Renal hemodynamic abnormalities (20%):

In the occurrence of diabetic nephropathy, it plays a key role, and may even be the initiating factor.

(1) Hyperglycemia, high perfusion in the glomerulus, high filtration state, increased pressure across the capillary wall, expansion of mesangial cells, epithelial cell foot process fusion and production of dense droplets, glomerular epithelial cells from the base Peel off the membrane. (2) The glomerular basement membrane type IV collagen messenger nucleic acid is increased, the basement membrane is thickened, and finally the diffuse and nodular lesions of the mesangium are formed, and glomerular sclerosis occurs. (3) In the case of increased pressure, increased protein filtration, deposition in the mesangial area and glomerular basement membrane, promote stromal hyperplasia, form a vicious circle, and can cause nodular and diffuse glomerulosclerosis .

High blood sugar (20%):

The occurrence of diabetic nephropathy is closely related to hyperglycemia. Poor blood glucose control can accelerate the development of diabetic nephropathy, and good glycemic control can significantly delay its development. Hyperglycemia and increased production of glycosylation end products cause mesangial cell proliferation, extracellular matrix, mesangial expansion, and thickening of the glomerular basement membrane.

Genetic factors (20%):

Most diabetic patients do not eventually develop kidney disease, and some patients with long-term glycemic control can also develop diabetic nephropathy. Glucose transporter-1 (GLUT1) is the major glucose transporter on mesangial cells. Recent studies have found that differences in the menu and regulation of GLUT1 in mesangial cells of different individuals in diabetic patients may be one of the factors that are susceptible to renal damage in some patients. Moreover, the occurrence of diabetic nephropathy also shows family aggregation. In some diabetic patients with a family history of hypertension, the incidence of diabetic nephropathy is also significantly higher than that of patients without a family history of hypertension. In addition, there are differences in the incidence of diabetic nephropathy among different ethnic groups. All of this indicates that the occurrence of diabetic nephropathy is related to genetic factors.

High blood pressure (25%):

It is not directly related to the occurrence of diabetic nephropathy, but the increase of blood pressure in the original hypertension or the course of microalbuminuria can accelerate the progression of diabetic nephropathy and the deterioration of renal function, and aggravate the discharge of urinary albumin.

Pathogenesis

The basic pathological features of diabetic nephropathy are glomerular basement membrane hypertrophy with increased mesangial cell matrix, glomerular capsule and mesangial cells with nodular hypertrophy and increased permeability. Its pathogenesis includes:

1. High-protein diet exacerbates the deterioration of diabetic nephropathy: Diabetes patients are mainly restricted by high-protein fiber food supply due to strict restriction of carbohydrate intake, which leads to excessive loss and accumulation of protein decomposition products and phosphorus, which in turn exacerbates DN. Pathological damage.

2. The impact of hypertension: Diabetes patients due to lipid metabolism disorders, atherosclerosis and many other reasons, there are many people with hypertension, almost all of these patients can see microalbuminuria, indicating that kidney damage is common.

3. Hyperglycemia: long-term and excessive blood sugar increase, can increase capillary permeability, extravasation of plasma proteins, causing damage to capillary basement membrane, glomerular sclerosis and renal tissue atrophy.

Diabetic nephropathy is a systemic disease characterized by chronic hyperglycemia as the main clinical manifestation of insulin and fat metabolism in the body due to different etiology and pathogenesis. Diabetes can damage the kidney by different ways. These damages can affect all the structures of the kidney, but only glomerulosclerosis is directly related to diabetes, also known as diabetic nephropathy, which is one of the systemic microvascular complications of diabetes. In patients with diabetes, if there is persistent proteinuria in the presence of kidney damage, the condition is irreversible and often progresses to end-stage renal failure. Diabetic nephropathy has become the leading cause of death in diabetic patients.

Diabetic nephropathy prevention

The prevention and treatment of diabetic nephropathy follows the general principles of prevention and treatment of diabetes and chronic renal insufficiency. It is important to prevent and treat diseases, including publicity and patient education. Comprehensive measures are taken for diabetic patients after diagnosis, including controlling diet, limiting protein intake, and avoiding Various risk factors, strengthen blood sugar control, correct metabolic disorders, and require blood sugar to achieve ideal control. At the same time, there are plans to regularly and regularly predict predictors of diabetic nephropathy such as blood pressure, GFR, etc., if necessary, renal biopsy.

Diabetic nephropathy complications Complications retinopathy acute renal failure

Clinical diabetic nephropathy is associated with diabetic retinopathy, and diabetic nephrotic syndrome is almost always associated with diabetic retinopathy. Therefore, renal biopsy should be considered for patients with diabetic nephrotic syndrome who have no retinopathy and have a disease course shorter than 10 years. In addition to other reasons for glomerular disease, but should pay attention to some diagnostic tests for diabetics such as intravenous pyelography and angiography, especially prone to kidney damage and acute renal failure, especially older (> 50 Years), patients with longer course (>10 years) and prior renal dysfunction and other diabetic complications should be particularly careful. Renal failure usually occurs within 48-72 hours after contrast or other examination procedures.

Diabetic nephropathy symptoms common symptoms glomerular sclerosis loss of appetite, diabetes, isotonic, hematuria, hypertension, ascites, proteinuria

symptom

1. Proteinuria: Early diabetic nephropathy has no clinical proteinuria, and only micro-proteinuria can be detected by radioimmunoassay. The only early manifestation of clinical diabetic nephropathy is proteinuria, which gradually evolves from intermittent to persistent.

2. Edema: There is generally no edema in the early stage of clinical diabetic nephropathy, and a small number of patients may have mild edema before plasma protein is reduced. If a large amount of proteinuria, plasma protein is low, edema is aggravated, and the disease progresses to late stage.

3. Hypertension: The prevalence of hypertension in type 1 diabetic patients without kidney disease is not increased compared with normal people. Type 2 diabetes patients have more hypertension, but if there is proteinuria, the proportion of hypertension increases. Patients with nephrotic syndrome are associated with hypertension, which is mostly moderate and few are severe.

4. Renal failure: There is a big difference in the progress of diabetic nephropathy. Some patients with mild proteinuria can last for many years, but the kidney function is normal, some patients have few urinary protein, can rapidly develop nephrotic syndrome, kidney function gradually deteriorates, and finally uremia.

5. Anemia: Patients with significant azotemia may have mild anemia.

6. Other organ complications: cardiovascular disease such as heart failure, myocardial infarction. Neuropathy such as peripheral neuropathy. A neurogenic bladder can occur when the autonomic nerve is involved. Retinopathy, almost 100% of diabetic nephropathy with retinopathy, but severe retinopathy does not necessarily have significant renal lesions. When diabetic nephropathy progresses, retinopathy often accelerates to worsen.

Staging

Stage I: characterized by increased glomerular filtration rate and increased renal volume. This initial lesion is consistent with high blood glucose levels, but reversible, can be restored by insulin treatment, but not necessarily fully restored to normal.

Stage II: The urinary albumin excretion rate is normal but the glomerular structure has changed. This period of urinary albumin excretion rate (UAE) was normal (<20g/min or <30mg/24h), and the UAE increased group could recover after rest after exercise. This stage of glomerular glomerular structure has changed, glomerular capillary basement membrane (GBM) thickening and mesangial matrix increased, GFR is higher than normal and consistent with blood glucose levels, GFR>150mL / min patients with glycated hemoglobin often >9.5%. Patients with GFR >150 mL/min and UAE >30 g/min are more likely to develop clinical diabetic nephropathy. The blood pressure of patients with stage I and II diabetes mellitus is normal. Stage I and II patients have elevated GFR and normal UAE, so the second phase cannot be called diabetic nephropathy.

Stage III: Also known as early diabetic nephropathy. The urinary albumin excretion rate was 20-200 g/min, and the patient's blood pressure was slightly elevated, and glomerular ruin began to appear.

Stage IV: clinical diabetic nephropathy or dominant diabetic nephropathy. This phase is characterized by large amounts of albuminuria (more than 3.5 grams per day), edema and high blood pressure. Diabetic nephropathy is more serious and has a poor response to diuretics.

Stage V: End-stage renal failure. Diabetic patients develop persistent urinary protein into clinical diabetic nephropathy, due to extensive thickening of the glomerular basement membrane, progressive glomerular capillary stenosis and more glomerular ruin, renal filtration function progressively declines, Causes kidney failure.

Examination of diabetic nephropathy

1. Provocation test: In the early stage of diabetic nephropathy, 24h urine protein is generally <150mg, and it is intermittent. Strict control of blood glucose can make urinary protein disappear, and urine protein can be increased after exercise. Mogensen believes that exercise test is an early diagnosis of diabetic nephropathy. Sensitive test.

2. Renal function and other laboratory tests: functional changes and structural changes of diabetic nephropathy are parallel, early renal plasma flow increases, glomerular filtration rate increases, and in recent years, urine N-acetyl-BD glucosamine was found in diabetic patients. Enzyme (NAG) excretion increased, and was positively correlated with urinary protein excretion and retinopathy, and increased with prolonged disease duration.

3. Urine examination and renal function test.

4. Renal histological examination: Renal histological examination is an important means of diagnosing diabetic nephropathy, in which specific changes account for 50%, mainly nodular glomerular sclerosis, goo- and afferent arterioles, kidney The exudative changes on the surface of the vesicles, non-specific changes in the glomerular and tubular basement membrane thickening, immunofluorescence showed glomerular and tubular basement membrane and renal capsule surface albumin and IgG deposition.

5. Fundus examination: Diabetic retinopathy is a part of diabetic microangiopathy, often accompanied by diabetic nephropathy, so once the retinopathy is found, it is necessary to be alert to the presence of renal microangiopathy.

6. Examination of kidney morphology: Diabetic nephropathy early kidney volume increases, weight increases, the size of the kidney is measured according to intravenous pyelography or B-ultrasound, and the weight is measured, the length of the kidney is the maximum distance between the upper and lower poles, and the width The maximum distance from the medial side to the lateral side of the kidney.

Diagnosis and diagnosis of diabetic nephropathy

Diagnose based on

1. Diagnosis of early diabetic nephropathy: mainly based on the increase of urinary albumin excretion rate (normal <20g/min, <30mg/24h). The diagnosis requires that the continuous urine test has a two-fold albumin excretion rate of >20 g/min within 6 months, but <200 g/min (ie between 30 and 300 mg/24 h), and other causes that may cause an increase should be excluded. Such as urinary tract infections, exercise, essential hypertension, heart failure and increased water load. When the control of diabetes is poor, it can also cause microalbuminuria. The discharge of urinary albumin can be >20g/min. Such urinary albumin excretion cannot be diagnosed as early diabetic nephropathy. However, if diabetes is effectively controlled, the amount of urinary albumin excreted is still 20 to 200 g/min, and it can be considered that there is early diabetic nephropathy.

2. Diagnostic basis for clinical stage diabetic nephropathy: 1 history of diabetes; 2 intermittent or persistent clinical proteinuria (urinary protein positive) for other reasons, which is the key to clinical DN diagnosis; 3 may be associated with renal insufficiency 4 with retinopathy, this is a strong evidence; 5 kidney biopsy confirmed, generally only when the diagnosis is doubtful.

Other causes of urinary protein must be ruled out. When hematuria is obvious, renal nipple necrosis, kidney tumor, calculus, pyelonephritis, cystitis or nephritis must be carefully excluded. If necessary, renal biopsy should be considered for diagnosis.

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