Can diabetes lead to kidney disease?

Diabetic nephropathy is one of the common chronic complications of diabetic patients, and it is also a serious microvascular complication, which is one of the main causes of death of diabetic patients. The main pathological features of diabetic nephropathy are. Glomerular sclerosis, its development process only shows the permeability change in the primary stage. If diagnosed and treated early, kidney disease can be reversed. Once persistent proteinuria occurs, it means that it has developed into clinical nephropathy. It's hard to reverse it at this time. Of course, effective treatment can still delay the development of the disease, but it will cause great pain and economic burden to patients, so diabetic patients should pay special attention to the early diagnosis of diabetic nephropathy.

It is often said that diabetic nephropathy cannot be found early. In fact, this conclusion is arbitrary Mogensen, a Danish medical scientist, believes that patients with type I diabetes develop nephropathy after 6 ~ 10 years, and patients with type II diabetes develop nephropathy after 1 1 ~ 20 years. However, because the onset of type 2 diabetes is hidden and the course of disease is difficult to infer, the time of type 2 diabetes complicated with nephropathy can be any time before or after the diagnosis of diabetes. Therefore, it should be noted that once type I diabetes is diagnosed within 6 years, we should pay attention to the relevant examinations of diabetic nephropathy for early diagnosis and treatment. Specific examination items for early diagnosis of diabetic nephropathy are recommended as follows:

(1) renal color ultrasound examination or iodine-o-iodohippurate sodium renogram examination. Both of these tests can find renal volume and renal blood flow. In diabetic nephropathy, renal volume increases and hyperfiltration occurs. This may be related to renal vasodilation, especially afferent vasodilation, increased renal blood flow and increased glomerular capillary venous pressure in diabetic patients. Effective renal plasma flow (ERPF) and renal index (R 1) can be obtained by renogram examination and microcomputer processing. If combined with glomerular filtration rate (GRF), it can be a good way to judge diabetic patients with nephropathy. That is, glomerular filtration rate and renal index are normal, indicating normal renal function; All of them rose to renal hyperfiltration state; The glomerular filtration rate is normal and the renal index is decreased, which belongs to recessive diabetic nephropathy. Both of them were reduced to clinical diabetic nephropathy.

(2) Determination of microalbumin. Before clinical proteinuria, urinary albumin excretion has increased subclinically, which is called microalbuminuria. At rest, the urinary albumin excretion rate (UAER) of healthy young people rarely exceeds 15 μ g/min, and the upper limit of 95% urinary albumin excretion rate of healthy people is 20 μ g/min, so the urinary albumin excretion rate is more than 20 μ g and less than 200 μ g/min (>: 20 μ g/min).

(3) Determination of urinary N- acetyl -P-O-D glucosaminidase (NAG) and trace transferrin (TRF): The molecular weight of N- acetyl -β-D glucosaminidase is 30000 ~ 140000, which is a high molecular glycoprotein. It is an important lysosomal hydrolase widely existing in human body, and there are many N- acetyl -β-D glucosaminidase in kidney, especially in proximal convoluted tubule epithelial cells. Normally, it cannot be filtered out of the glomerulus. After kidney disease, N- acetyl -β-D glucosaminidase in blood can be filtered out by glomerulus, which increases N- acetyl -β-D glucosaminidase in urine. Medical research has found that the increase of urinary N- acetyl -β-D glucosaminidase/urinary creatinine ratio is earlier than the change of urinary protein output. Therefore, the determination of urine N- acetyl -β-D glucosaminidase activity is more helpful for the early diagnosis of diabetic nephropathy. The molecular weight of transferrin is 77,000, which is close to albumin (Alb), and it is a protein with medium molecular weight. However, the negative charge of transferrin is obviously smaller than that of albumin, so it is easier to pass through the negatively charged glomerular filtration membrane. Some people think that urinary transferrin appears earlier in patients with type 2 diabetes, and the change of urinary transferrin/creatinine ratio is more sensitive and meaningful than that of albumin/creatinine ratio. Therefore, trace transferrin urine may be more sensitive to the early diagnosis of diabetic nephropathy than proteinuria. Patients with type I diabetes have a similar situation.

(4) Determination of urinary albumin fragments (UAF). After treating urinary albumin with mercaptoethanol, three fragments can be separated by electrophoresis. It is considered that there are albumin fragments in urine of diabetic patients with microalbuminuria, and 30% of diabetic patients with microalbuminuria negative are still albumin fragments positive, so the determination of albumin fragments can be used as an early indicator to predict the occurrence of diabetic nephropathy before microalbuminuria appears.

The above methods are helpful for early detection of diabetic nephropathy. Different patients and hospitals can choose one or more of the above methods according to the actual situation, so as to find and treat diabetic patients early, so as to control the occurrence and development of diabetic nephropathy.