Diabetic renal damage is divided into 5 periods

Phase Ⅰ: glomerular hyperfiltration. With increased glomerular filtration rate (GFR) and increased renal volume, newly diagnosed insulin-dependent diabetes mellitus patients have this change, while renal blood flow and glomerular capillary perfusion and internal pressure Are increased. This initial change in the involvement of the diabetic kidney is consistent with the high blood sugar level, is reversible, after insulin treatment can be restored, but not necessarily fully back to normal. This period did not suffer from pathological histology.

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Phase II: Normal albuminuria. Urine albumin excretion rate (UAE) was normal (<20μg / min or <30mg / 24h), and the UAE increased after exercise and recovered. The glomerular glomerulus has a structural change, glomerular capillary basement membrane (GBM) thickening and mesangial matrix increased, GFR more than normal and consistent with blood glucose levels, GFR> 150mL / min patients with glycosylated hemoglobin often > 9.5%. GFR> 150 mL / min and UAE & gt; 30 [mu] g / min were more likely to develop clinical diabetic nephropathy. Diabetic nephropathy Ⅰ, Ⅱ patients with normal blood pressure. Ⅰ, Ⅱ patients GFR increased, UAE normal, so the second phase can not be called diabetic nephropathy.

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Phase III: early diabetic nephropathy. The results showed that UAE was higher than 20 ~ 200μg / min (30 ~ 300mg / 24h). At the initial stage of UAE20 ~ 70μg / min, GFR began to decrease to near normal (130mL / min). High filtration may be one of the causes of persistent microalbuminuria in patients, and of course long-term metabolic control. This period of patients with mild blood pressure, lower blood pressure can be partially reduced urinary microalbumin discharge. Patient GBM thickening and mesangial matrix increased more obvious, there have been glomerular nodular and diffuse lesions and small arterial hyaline, and has begun to appear glomerular waste. According to a group of long-term follow-up results, the incidence of this period of 16%, occurred in the course of> 5 years of diabetes, and with the course of the rise.

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Ⅳ period: clinical diabetic nephropathy or dominant diabetic nephropathy. This period is characterized by a large number of albuminuria, UAE> 200μg / min or persistent urinary protein daily> 0.5g, non-selective proteinuria. Increased blood pressure. The patient's GBM was significantly thickened, the mesangial matrix widened, the abandoned glomerular increased (mean 36%), and residual glomerular compensatory hypertrophy. Diffuse type of urine protein in patients with glomerular pathology consistent with the degree of severe daily urinary protein> 2.0g, often accompanied by mild microscopic hematuria and a small amount of tubular, and nodular patients with the amount of urine protein There is no relationship between the degree of pathological damage. Clinical diabetes mellitus protein characteristics of urine, unlike other kidney disease protein, not because of decreased GFR decreased. With a large number of urine protein loss can occur hypoproteinemia and edema, but the typical diabetic nephropathy "triple sign" - a lot of urine protein (> 3.0g / 24h), edema and hypertension, seen only about 30% of diabetic nephropathy patient. Diabetic nephropathy is more severe, poor response to diuretics, the reason 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 changes the tissue Na +, K + operation, whether it is type I patients with insulin or stage Ⅱ patients with hyperinsulinemia, long-term high insulin levels that can change the Na + metabolism, so that patients with diabetes retention Na +, especially Is in the case of high Na + diets. This period of patients decreased GFR, the average monthly decline of about 1mL / min, but most patients with serum creatinine level is not high.

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Ⅴ: renal failure period. Diabetic patients once the development of persistent urinary protein development for clinical diabetic nephropathy, due to extensive glomerular basement membrane thickening, glomerular capillary lumen and more of the glomerular waste, renal filtration function decreased, Leading to renal failure, the final patient's GFR more than 10mL / min, serum creatinine and urea nitrogen increased, with severe hypertension, hypoproteinemia and edema. Patients generally have azotemia caused by gastrointestinal reactions, such as loss of appetite, nausea and vomiting, and secondary anemia and severe hyperkalemia, metabolic acidosis and low calcium tetany, but also secondary uremic neuropathy And myocardial lesions. These serious complications are often causes of death in diabetic nephropathy patients.

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