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Knowledge of diabetic nephropathy


Due to abnormal diabetic glucse metabolism, it is mainly caused by glomerular hardening, and the content of urine protein exceeding normal is called diabetic nephropathy.


1. History and symptoms

There is a history of diabetes, and the clinical manifestations of kidney damage are positively correlated with the degree of glomuel sclerosis. When trace proteinuria occurs, the history of diabetic disease has been 5 to 6 years. Clinical diagnosis is early diabetic nephropathy, without any clinical manifestations; about 80%of patients have developed into clinical diabetic nephropathy within 10 years, that is, the quantity of urine protein is greater than 0.5g/24h 24h. There are usually no obvious hematuria, and the clinical manifestations are edema and hypertension. Once persistent proteinuria occurs, it is accompanied by loss of appetite, nausea and vomiting, and anemia, indicating that chronic renal insufficiency has occurred.

Second, physical examination discovery

Hypertension and edema at different degrees, ascites and chest water can occur in severe extent. Multiple diabetic retinopathy.

3. Auxiliary inspection

(1) The qualitative of urine glucose is a simple way to screen diabetes, but pseudo -negative or false positives can occur in diabetic nephropathy. Therefore, measurement of blood glucose is the main basis for diagnosis.

(2) Urine leukoprotein excretion rate (UAE) 20 ~ 200 μg/min is an important indicator of early diabetic nephropathy; when UAE continues to be greater than 200 μg/min or routinely checks the positive urine protein (urine protein quantity is greater than 0.5g/24h), The diagnosis is diabetic nephropathy. Urinary sediment is generally not obvious. When more white blood cells, urinary tract infections are prompted; there are a large number of red blood cells, indicating that there may be hematuria caused by other causes.

(3) In the late stage of diabetic and nephropathy, endogenous creatinine clearance decreased and hematocarbon nitrogen and creatinine were increased.

(4) The increase in nucleo renal dynamic glomerular filtration rate (GFR) and B -ultrasound measure the increase in renal volume, which is in line with early diabetic nephropathy. GFR decreases significantly during uremia, but the kidney volume often does not significantly shrink.

(5) Fundamental examination. If necessary, a fluorescent eye shaping is performed, and diabetic eye lesions such as microorphosis can be seen.

Fourth, differential diagnosis

It is necessary to exclude other causes of urine protein. When hematuria is obvious, it is necessary to carefully remove renal nipple necrosis, kidney tumors, stones, pyelonephritis, cystitis or nephritis. Consider the diagnosis of kidney biopsy if necessary.

【Treatment measures】

First, diabetic nephropathy has no special effects. It is manifested by the majority of nephrotic syndrome. Most of them should not be used in glucocorticoids, and cytotoxic drugs or thunder vines have no obvious effect.

2. Actively control blood sugar, including dietary treatment, oral hypoglycemic drugs, and insulin. When nitrogen disease occurs, the dose and type of insulin and oral hypoglycemic drugs should be adjusted according to blood glucose.

3. Limit protein intake (≯0.8g/day). If necessary, add essential amino acids or α-ketone acid.

Fourth, with hypertension or edema but normal renal skills, a small dose can be selected. Those with no renal function should choose tadpole urine or pyride tablets; those with height edema, in addition to strictly restricting the intake of sodium, should be appropriately expanded; if the blood pressure is too high or inadequate, and the active expansion of diuretic conditions will not improve without improvement. Those can consider dialysis treatment.

Fifth, actively reduce blood pressure to less than 18.6kPa. It is recommended to prefer ACEI to improve GFR and reduce urinary albumin excretion rate while lowering blood pressure, but to prevent functional GFR decline; Vascular tension II receptor antagonist.

6. Actively treat hyperlipidemia and hyperuricemia.

7. Application of anti -platelet aggregation and adhesion drugs, such as Pan Shengding, dwarf, aspirin or heparin. The correct use of traditional Chinese medicine for syndrome differentiation, especially for controlling blood sugar and improving microvascular lesions.

8. CCR can consider replacement treatment when CCR is 10 ~ 15ml/min or serum creatinine 530 ~ 710 μMON/L.


The basic pathological characteristics of urine and nephropathy are glomerular base membrane uniform fertilizer and thickness accompanied by increased glomerular membrane cell matrix, glomerular pockets and glomerular membrane cells to increase hypertrophy and increase permeability. Its pathogenesis includes:

① High protein diet exacerbates the deterioration of diabetes and nephropathy: Diabetes patients are mainly due to the strict restrictions on the intake of carbohydrates, mainly based on the supply of high protein fiber foods. Pathological damage.

② The impact of hypertension: Diabetes patients have many reasons such as lipid metabolic disorders and atherosclerosis and many other reasons. There are many people with hypertension. Almost all of these patients can see urine micro protein, indicating that kidney damage is common.

③ High blood glucose: Long -term and excessive blood sugar increases, which can cause increased capillary permeability, plasma protein exogenous, causing capillary base membrane damage, glomerular sclerosis and kidney tissue atrophy.

Urine kidney damage is divided into 5 phases

Phase I: Gensoza high filtration expires. Characteristics characterized by the increased glomerular filtration rate (GFR) and increased renal volume, and the newly diagnosed insulin -dependent diabetes patients have changed. At the same time Both increase. The initial changes in the suffering of this bran urinary kidney are consistent with the level of hyperglycemia. It is reversible. It can be restored after insulin therapy, but it may not be fully restored to normal. There is no damage to pathological organizational science in this period.

Phase II: Normal albumin urine period. This period of urine albumin excretion rate (UAE) is normal (<20 μg/min or 9.5%. Patients with GFR> 150ml/Min and UAE> 30 μg/min will become more likely to develop into clinical diabetic nephropathy in the future. The blood pressure of patients with diabetic renal damage Ⅰ and III patients is normal. Phase Ⅰ and II patients have increased GFR and UAE is normal. Therefore, the second phase cannot be called diabetic nephropathy. Phase III: Early diabetic nephropathy. The main manifestation is that UAE continues to be higher than 20 to 200 μg/min (equivalent to 30 ~ 300mg/24h), and GFR starts to fall to nearly normal (130ml/min) at the initial UAE20 ~ 70 μg/min. High filtration may be one of the reasons why patients continue to trace white proteinuria, and of course there are factors for long -term metabolic control. Patients with a mild blood pressure in this phase, reducing blood pressure can partially reduce the discharge of micro -white protein. The patient’s GBM thickening and the increase of membrane matrix are more obvious. There are already glomerular node belt types and diffuse lesions and small arterial glass -like changes, and glomerular wasteland has begun to appear. According to the results of a group of long -term clinics, the incidence of this period is 16%, which mostly occur in diabetic patients with 5 years of disease and rise with the course of the disease.

Phase II: Clinical diabetes nephropathy or explicit diabetes and nephropathy. This period is characterized by a large amount of albuminuria, UAE> 200 μg/min, or continuous urine protein daily> 0.5g, which is non -selective proteinuria. Blood pressure increases. The patient’s GBM is significantly thickened, the membrane matrix is ​​widened, the abandoned glomerular increases (average accounting for 36%), and the residual glomerular compensation is enriched. The diarrhea that damages patients is consistent with the pathological damage of glomerular diseases. In severe cases, daily urine protein volume> 2.0g, often accompanied by mild mirror hematuria and a small amount of tubular type, while nodular patients There is no relationship between the degree of pathological damage. The characteristics of clinical diabetic nephropathy are not like the urine protein of other kidney diseases, and do not decrease due to the decline of GFR. With a large amount of urine protein loss, hypoproteinemia and edema can occur, but the typical “three joints” of diabetic nephropathy -a large amount of urine protein (> 3.0g/24h), edema, and hypertension, only about 30%of diabetic nephropathy patient. Diabetic nephropathy edema is more serious and the response to diuretic drugs is different. In addition to the low plasma protein, at least part of the sodium sodium sodium in diabetic nephropathy is severe than other reasons. This is because insulin changes the operation of NA and K in the tissue. Whether it is the high insulin ledmia of the insulin or phase II patient in the injection of patients Ⅰ, long -term high insulin levels can change NA metabolism, so that diabetic patients 潴 NA, especially It is in the case of high NA diet. This phase of patients dropped by GFR, with an average of about 1ml/min per month, but most patients’ blood creatinine levels are not high.

Period: renal failure period. Once diabetic patients have developed into clinical diabetes and nephropathy, due to the widespread thickening of glomerular base membranes, glomerular capillaries, and more glomerular dehydration, renal filtration function decreases, and the kidney filtration function decreases. Causes renal failure. In the end, the patient’s GFR was more <10ml/min, blood creatinine and urea nitrogen increased, accompanied by severe hypertension, hyparmanemia, and edema. Patients generally have gastrointestinal reactions caused by nitrogen lesions, such as loss of appetite, nausea and vomiting, and secondary anemia and severe hypertropacteria, metabolic acid poisoning and low calcium convulsions. And myocardial lesions. These severe complications are often the cause of death caused by diabetic nephropathy uremia patients.

[Clinical manifestations]

Early proteinuria diabetic nephropathy has no clinical proteinuria. Only by radiological immune can detect trace proteinuria. The only manifestation of clinical diabetes and nephropathy was proteinuria, and proteinuria gradually developed from intermittentity to persistent.

Early edema clinical diabetic nephropathy generally does not have edema early, and a few patients may have mild edema before the plasma protein is reduced. If a large amount of protein urine, the plasma protein is low, and the edema is increased, mostly the progress of the disease to the late stage.

Hypertension In diabetic patients with type 1 nephrotic disease, the prevalence of hypertension does not increase than normal people; patients with type 2 diabetes are accompanied by high blood pressure, but if proteinuria occurs, the proportion of hypertension also increases; Patients with hypertension during nephropathy syndrome are accompanied by hypertension. This hypertension is mostly moderate and a few are severe.

There is a big difference in progress of kidney failure diabetes and nephropathy. Some patients have mild proteinuria for many years, but their renal function is normal; some patients have few urine proteins, can develop nephropathy syndrome quickly, and have gradually deteriorated renal function, and uremia occurs.

Patients with obvious nitrogen anemia may have mild anemia.

Cardiovascular lesions of other organs such as heart failure, myocardial infarction, and neuropathy such as peripheral neuropathy can occur when the plant nerve is involved, and almost 100%of the retinal disease may occur when the plant nerve is accumulated.

1. proteinuria

At first, due to the increased voltage of glomerular filtration and changes in the charging on the filter membrane, only trace albumin appeared in the urine. It was selective proteinuria and no globulin increased. This state was sustainable for many years. With the increase of the glomerular base membrane filtrate, macromolecular substances can pass through non -selective clinical proteinuria. With the further development of the lesion, urine protein gradually becomes sustainable severe proteinuria. If the urine protein exceeds 3 grams /Day is the sign of poor prognosis. The severity of proteinuria in diabetic nephropathy is mostly developed in progress until nephrotic syndrome occurs. 2. Bloating

Patients with diabetic nephropathy generally do not have swelling. Before the plasma protein is reduced, a few patients may have mild puffiness. When the urine protein exceeds 3 grams of 24 hours, edema will appear. Obvious puffiness of the whole body is only found in the rapid developing of diabetic nephropathy.

3. Hypertension

Blood pressure is common among patients with diabetic nephropathy. Severe nephropathy is mostly hypertensive, while hypertension can accelerate the progress and deterioration of diabetic nephropathy. Therefore, it is very important to effectively control high blood pressure.

4. Renalized functional incomplete

Once urinary nephropathy starts, the process is performed, and nitrogen ledmia and uremia are its final ending.

5, anemia

Diabetes patients with obvious nitrogen disease may have mild to moderate anemia, and the treatment of iron is not effective. Anemia is caused by the formation of red blood cells, which may be related to long -term restricted protein diet and nitrogen disease.


The early prevention of this disease is very important. The common prevention measures are the following points:

① Those who have more than 5 years of diabetic patients should often check renal function, urine protein, and quantitative urine protein at 24 hours, and pay attention to measuring blood pressure, and do eye examination. ② When conditions permit, urine microfinance should be measured and β2-microfot protein measurement should be performed to detect diabetic nephropathy early. If the urine trace albumin increases, it takes 3 to 6 months to test it for 3 times to determine whether it is a persistent trace albuminuria. ③ If it is determined to increase the trace albumin and can exclude other factors that cause it, such as urinary infections, exercise, and primary hypertension, they should be highly vigilant. And pay attention to control blood sugar so that it is as close as possible. If blood pressure> 18.7/12kPa, the blood pressure should be positively reduced to keep blood pressure in the normal range. At the same time, you should also emphasize a low -salt and low protein diet, which is better for high -quality protein.

<!-2586: Diabetic terminal page


The prognosis of diabetic nephropathy is mostly bad. This is because the kidney disease is chronic for sexual damage. The clinical symptoms occur late. Generally, when urine protein occurs, the course of disease is more than 10 years. It has been affirmed that there is a “concealment period” in the early days of diabetic nephropathy. The glomerular goals have lesions, but there are no clinical manifestations. The only change is just increased urinary white protein. Clinically, once diabetic nephropathy occurs, the renal function will not be able to decrease in the renal function once it occurs. About 25%of patients can develop into end -stage renal failure within 6 years, 50%of patients within 10 years, and 75%of patients within 15 years. Urine protein> 3.0 grams died in 6 years. Poor diabetes control, high blood sugar, hypertension, and dietary high protein can accelerate the deterioration of kidney function in patients with diabetic nephropathy. In addition, observations in recent years have confirmed that smoking is also a risk factor for diabetic nephropathy. 19%of diabetic smokers have proteinuria, and only 8%have proteinuria. About 5%to 15%of people with diabetes have uremia, but 40%to 50%of those under 50 years of age. The prognosis of diabetic nephropathy is also related to the changes in its kidney pathological changes. Mainly, compared with nodular diabetic nephropathy, it is easy to develop into uremia.

(Intern editor: Wuying)

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