diabetic nephropathy
Introduction
Introduction to Diabetic Nephropathy Glomerular sclerosis caused by abnormal glucose metabolism in diabetes, accompanied by more than normal urine protein, is called diabetic nephropathy. 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. basic knowledge The proportion of illness: 7%-10% for diabetes less than 5 years, 20-35% for 20-25 years, 37% for more than 25 years of onset Susceptible people: no specific population Mode of infection: non-infectious Complications: Diabetes Nephrotic syndrome
Cause
Causes of diabetic nephropathy
Renal hemodynamic abnormalities (30%):
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 .
Hyperglycemia (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 (10%):
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; diabetic patients due to strict restrictions on carbohydrate intake, and high protein fiber food supply, relying on this, resulting in excessive decomposition and accumulation of protein decomposition products and phosphorus, thereby exacerbating 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, high blood sugar: long-term and excessive blood sugar increased, can cause capillary permeability increased, plasma protein extravasation, causing capillary basement membrane damage, glomerular sclerosis and renal tissue atrophy.
Prevention
Diabetic nephropathy prevention
Early prevention of this disease is very important, and the common preventive measures are as follows:
1, all diabetic patients with more than 5 years of disease, should always check kidney function, urine protein qualitative, 24-hour urine protein quantification, and pay attention to blood pressure, do fundus examination.
2. When conditions permit, urine microprotein determination and 2-microglobulin determination should be performed to detect diabetic nephropathy early. If the microalbuminuria is increased, it should be measured 3 times within 3 to 6 months to determine whether it is continuous. Sexual albuminuria.
3, if it is determined that the increase in microalbumin, and can exclude other factors that cause its increase, such as urinary tract infection, exercise, essential hypertension, should be highly vigilant, and pay attention to efforts to control blood sugar, making it as close to normal as possible If the blood pressure is >18.7/12kPa, the blood pressure should be actively reduced to maintain the blood pressure in the normal range. At the same time, low-salt, low-protein diet should be emphasized, and high-quality protein is preferred.
Complication
Diabetic nephropathy complications Complications Diabetic nephrotic syndrome
Complications such as renal insufficiency and azotemia can often occur.
Symptom
Symptoms of Diabetic Nephropathy Common Symptoms Proteinuria Hematuria Diabetes Islet Cells Destruction Blood Pressure High Ascites Edema Appetite Decreased Glomerulosclerosis
symptom
1, proteinuria early diabetic nephropathy without clinical proteinuria, only by radioimmunoassay can detect microalbuminuria. The only early manifestation of clinical diabetic nephropathy is proteinuria, which gradually evolves from intermittent to persistent.
2, edema clinical diabetic nephropathy generally no edema early, a small number of patients may have mild edema before plasma protein reduction. If a large amount of proteinuria, plasma protein is low, edema is aggravated, and the disease progresses to late stage.
3, hypertension in the type 1 diabetes mellitus patients with diabetes, the prevalence of hypertension is not increased compared with normal people, type 2 diabetes patients with high blood pressure, but if there is proteinuria, the proportion of hypertension is also elevated, in the presence of kidney disease The patient is accompanied by high blood pressure in the syndrome. This hypertension is mostly moderate and a few are severe.
4, renal failure Diabetic nephropathy progress is very different. 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 manifested in 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.
Examine
Examination of diabetic nephropathy
1. Urine sugar qualitative is a simple method for screening diabetes, but there may be false negative or false positive in diabetic nephropathy, so measuring blood glucose is the main basis for diagnosis.
2, urinary albumin excretion rate (UAE) 20 ~ 200g / min, is an important indicator for the diagnosis of early diabetic nephropathy; when UAE continues to be greater than 200g / min or routine test urine protein positive (urinary protein quantification greater than 0.5g / 24h), that is Diagnosed as diabetic nephropathy, urine sediment is generally not obvious change, more white blood cells suggest urinary tract infection; there are a lot of red blood cells, suggesting that there may be other causes of hematuria.
3, advanced diabetic nephropathy, decreased endogenous creatinine clearance and blood urea nitrogen, creatinine increased.
4, the increase in nuclear glomerular filtration rate (GFR) and the increase of renal volume in B-ultrasound, in line with early diabetic nephropathy, GFR decreased significantly in uremia, but the kidney volume is often not significantly reduced.
5, fundus examination, if necessary, for fluorescence fundus angiography, microscopic aneurysm and other diabetic fundus lesions.
Diagnosis
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, clinical diagnosis of diabetic nephropathy: 1 history of diabetes; 2 other intermittent intermittent or persistent clinical proteinuria (urinary protein positive), 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.
Differential diagnosis
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.
