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Diabetic nephropathy2017-01-12 16:28
The basic pathological features of the disease are glomerular basement membrane hypertrophy and glomerular mesangial cell matrix, glomerular and glomerular mesangial cells with nodular hypertrophy and increased permeability. Its pathogenesis includes:The deterioration of the high protein diet increased in diabetic nephropathy: Patients with diabetes due to ingestion of restricted carbohydrate, high protein fiber in food supply, resulting in protein decomposition products of care for this and lose that load, and the excessive accumulation of phosphorus and aggravate the pathological damage, DN damage.Influence of hypertension: Patients with diabetes due to disorders of lipid metabolism, atherosclerosis and many other reasons, many with hypertension, these patients can almost see trace protein in urine, renal damage generally show.High blood sugar: long-term and excessive hyperglycemia, can lead to a significant increase in capillary permeability, plasma protein extravasation caused by capillary basement membrane damage, glomerular sclerosis and renal atrophy.Urinary tract disease is divided into 5 stages of kidney damage.Glomerular filtration stage expired. The glomerular filtration rate (GFR) increased and renal volume characteristics of newly diagnosed insulin-dependent diabetic patients had the change, at the same time, renal blood flow and glomerular capillary perfusion and internal pressure were increased. The early stage of renal involvement in this disease is consistent with high blood glucose levels and is reversible and can be restored by insulin treatment, but not necessarily fully restored. This period has no histopathological damage.Stage of normal albuminuria. The urinary albumin excretion rate (UAE) was normal (20 g/min or < 30mg/24h), and the UAE increased after exercise. In this period, there has been glomerular structural changes, glomerular basement membrane (GBM) thickening and mesangial matrix increased, GFR much higher than normal and consistent with the level of blood glucose, glycosylated hemoglobin in patients with 150mL/min GFR > > 9.5% often. GFR > 150mL/min and UAE > 30 g/min patients are more likely to develop clinical diabetic nephropathy. The blood pressure of diabetic patients with renal damage. Phase I and II patients with GFR increased, UAE normal, so the two phase can not be called diabetic nephropathy.Stage of early diabetic nephropathy. The main performance of UAE is higher than 20 ~ 200 g/min (equivalent to 30 ~ 300mg/24h), the initial UAE20 ~ 70 g/min GFR began to decline to close to normal (130mL/min). High filtration may be one of the causes of persistent microalbuminuria in patients, and, of course, factors associated with poor long-term metabolic control. This period of patients with mild blood pressure, blood pressure can be reduced by reducing the excretion of urine microalbumin. GBM thickening and mesangial matrix were increased more significantly, the glomerular zone type and diffuse type lesions and hyaline arteriolosclerosis, and has begun to appear glomerular obsolescence. According to the results of a long-term follow-up, the incidence of this period was 16%, which occurred in the course of the disease for more than 5 years of diabetes, and increased with the course of disease.Clinical stage of diabetic nephropathy or diabetic nephropathy. This period is characterized by a large number of albuminuria, UAE > 200 g/min or continuous urinary protein daily 0.5g, non selective proteinuria. Increased blood pressure. The patient's GBM was significantly thickened, the mesangial matrix widened, and the abandoned glomeruli increased (mean 36%). Diffuse damage the patient's urine protein and glomerular pathological damage, severe daily volume of urine protein, 2.0g, often accompanied by mild hematuria and a small amount of tube type, and Never mind between patients with nodular type proteinuria and pathological damage. The characteristics of urinary protein in clinical diabetic nephropathy, unlike those of other kidney diseases, do not decrease with the decrease of GFR. With a large number of urinary protein loss can appear hypoproteinemia and edema of diabetic nephropathy, but "the typical triad" - proteinuria (> 3.0g/24h), edema and hypertension, and in approximately 30% of patients with diabetic nephropathy. Diabetic nephropathy edema is more serious, poor response to diuretics, in addition to low plasma protein, at least in part because of diabetic nephropathy, sodium retention than other causes of severe nephrotic syndrome. This is because insulin changed the expression of Na+, K+ operation, whether hyperinsulinemia or insulin injection in type I patients with stage II patients, long-term high insulin levels can change the metabolism of Na+, the diabetes patient retention Na+, especially in the case of high Na+ diet. In this period, patients with GFR decreased, with an average monthly decline of about 1mL/min, but most patients had a low level of serum creatinine.V stage: the stage of renal failure. Diabetic patients once appear persistent proteinuria development for clinical diabetic nephropathy, glomerular basement membrane due to extensive thickening of the glomerular capillary lumen stenosis and more glomerular waste, glomerular filtration function were decreased, resulting in renal failure patients, finally GFR < 10mL/min, serum creatinine and blood urea nitrogen levels, with serious hypertension, hypoproteinemia and edema. Patients generally have azotemia caused by gastrointestinal reactions, such as anorexia, nausea and vomiting, and secondary anemia and severe hyperkalemia, metabolic acidosis and low calcium tetany, can also be secondary to uremic neuropathy and myocardial lesions. These serious complications are often the cause of death in patients with diabetic nephropathy.