Diabetic nephropathy

Diabetic nephropathy is one of the most important comorbidities in diabetic patients. The incidence of our country also showed an upward trend and has now become the second cause of end-stage renal disease, second only to a variety of glomerulonephritis. Because of its complex metabolic disorders, once the development of end-stage renal disease, often more difficult than the treatment of other kidney diseases, timely prevention and treatment for the delay of diabetic nephropathy is of great significance.

Common causes

And genetic, hyperglycemia caused by metabolic abnormalities and so on

Common symptoms

Chronic hyperglycemia, proteinuria as the main clinical manifestations

Etiology and pathogenesis

The etiology and pathogenesis of diabetic nephropathy is unclear. At present, it is considered that multiple factors are involved in the pathogenesis under the combined effect of certain genetic background and some risk factors.

1. genetic factors

In men, the incidence of diabetic nephropathy is higher than that of women; studies in the United States found that diabetic nephropathy was more likely to occur in African and Mexican-born whites than in whites in the same living conditions; some families were predisposed to diabetic nephropathy in the same race, Suggesting that genetic factors exist. Type 1 diabetes, 40% to 50% of microalbuminuria, type 2 diabetes in the observation period, only 20% to 30% of diabetic nephropathy, suggesting that genetic factors may play an important role.

2. Renal hemodynamic abnormalities

Early diabetic nephropathy hemodynamic abnormalities can be observed, showed high glomerular perfusion and hyperfiltration, renal blood flow and glomerular filtration rate (GFR) increased, and increased protein intake increased The degree of more significant.

3. Hyperglycemia caused by metabolic abnormalities

Hyperglycemia mainly caused by renal hemodynamic changes and metabolic abnormalities lead to kidney damage, including metabolic abnormalities leading to kidney damage mechanisms include: ① renal tissue disorders of glucose metabolism, can be formed by non-enzymatic glycation terminal glycation Metabolites (AGES); ② polyol pathway activation; ③ diacylglycerol - protein kinase c pathway activation; ④ glycosaminoglycans metabolic abnormalities. In addition to the metabolic abnormalities involved in early hyperfiltration, more importantly, to promote glomerular basement membrane (GBM) thickening and extracellular matrix accumulation.

4. hypertension

Almost any diabetic nephropathy is associated with hypertension, occurring in parallel with microalbuminuria in type 1 diabetic nephropathy and in type 2 before diabetic nephropathy. Blood pressure control and development of diabetic nephropathy are closely related.

5. Abnormal metabolism of vasoactive substances

The occurrence and development of diabetic nephropathy may have a variety of metabolic abnormalities of vasoactive substances. These include metabolic abnormalities such as RAS, endothelin, prostaglandin, and growth factors.

Clinical manifestations and disease staging

Diabetic nephropathy is one of the complications of systemic microangiopathy in diabetic patients. Therefore, diabetic nephropathy often simultaneously combines with other organ or systemic microangiopathy such as diabetic retinopathy and peripheral neuropathy. Type 1 diabetic patients with diabetic nephropathy mostly in the onset of 10 to 15 years, while type 2 diabetic patients with diabetic nephropathy is a short time, and older, combined with more underlying diseases.

Diabetic Nephropathy According to the course of diabetic nephropathy and pathophysiological evolution, Mogensen has suggested that diabetic nephropathy is divided into the following five phases:

1. Glomerular hyperfiltration and renal hypertrophy

This initial change consistent with high blood sugar levels, blood sugar control can be partially relieved. There is no histopathological damage in this issue.

2. Normal albuminuria

GFR is higher than normal. Kidney pathology manifested as thickening of GBM, increased mesangial matrix, increased urinary albumin excretion (UAE) after exercise (> 20 μg / min), returned to normal after rest. If in this period can be a good control of blood sugar, the patient can be stable in the long term.

3. Early stage of diabetic nephropathy, also known as "sustained microalbuminuria"

GFR began to decline to normal. Renal pathology glomerular nodular lesions and arteriolar hyaline degeneration. UAE continued to rise to 20 ~ 200μg / min and thus microalbuminuria. Current patients with elevated blood pressure. The ACEI or ARB drugs can reduce urinary albumin excretion, delay the progression of kidney disease.

4. Clinical diabetic nephropathy

Pathological appearance of typical K-W nodules. Persistent massive albuminuria (UAE> 200μg / min) or proteinuria greater than 500mg / d, about 30% of patients with nephrotic syndrome may appear, GFR continued to decline. The characteristic of this period is that urinary protein does not decrease with decreasing GFR. Once the patient enters the IV stage, the disease tends to develop in a progressive manner. If not actively controlled, the GFR will drop by an average of 1 ml / min monthly.

5. End-stage renal failure

GFR <10ml / min. Urine protein decreased due to glomerular sclerosis. Uremic symptoms are obvious, need dialysis treatment.

The above stage is mainly based on type 1 diabetic nephropathy, type 2 diabetic nephropathy is not obvious.

Proteinuria and diabetic nephropathy are closely related. Microalbuminuria not only means that the glomerular filtration barrier disorder, but also that systemic vascular dysfunction and found to be closely related to cardiovascular complications.

Nephrotic syndrome of diabetic nephropathy Compared with the general primary glomerular disease, the degree of edema is often more obvious, often accompanied by severe hypertension. As the disease glomerular capillary transmembrane pressure, combined with severe damage to the function of the glomerular filtration membrane protein barrier, so some patients with end-stage renal failure may also have a large amount of proteinuria.

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