Now more and more people suffer from diabetic nephropathy, the treatment of diabetic nephropathy is urgent, but there are still many people do not understand diabetic nephropathy. Today we are going to introduce the stages of diabetic nephropathy.
Diabetic nephropathy can be pided into 5 stages:
Stage I: glomerular filtration rate increased, kidney volume increased, renal blood flow increased, glomerular capillary perfusion pressure and internal pressure increased. The glomerular basement membrane and the mesentery are normal. After proper treatment, it can be recovered.
Stage II: normal albuminuria. The glomerular filtration rate was normal or increased, and the urinary albumin excretion rate was normal (less than 0.02 mg per minute or 30 mg /24 hours). After exercise or stress, the excretion increased and the returned to normal after stimulation was removed. The glomerular basement membrane is thickened and the mesangial matrix is increased. Blood pressure is usually normal.
Stage III: early diabetic nephropathy. Glomerular filtration rate was approximately normal, urinary albumin excretion rate was higher than normal, and blood pressure was slightly elevated. Glomerular basement membrane thickening and mesangial matrix increased significantly. There were glomerular nodular and diffuse lesions and arteriole hyaline degeneration, and glomerular degeneration had begun to occur. Blood pressure of patients in this period show mild elevation; lowering blood pressure can partially reduce the excretion of urinary albumin.
Stage IV: clinical diabetic nephropathy. A lot of albumin, urine protein was consistently more than 0.5 grams for every 24 hours are non selective proteinuria; severe patients have proteinuria more than 3.5 grams per 24 hours; they may have hypoalbuminemia, edema and hypertension, often with varying degrees of nitrogen retention and diabetic retinopathy. The glomerular basement membrane is thickened, the mesangial matrix is increased, and the glomerulus becomes obsolete.
Stage V: end-stage renal failure. Urinary protein excretion reduces due to lomerular obsolescence; glomerular filtration rate is less than 10 ml / min; if companied with hypertension, hypoalbuminemia, edema, blood creatinine and increased urea nitrogen, loss of appetite, nausea and vomiting and anemia, metabolic acidosis, hypocalcemia and hyperkalemia, can induce secondary uremic neuropathy and myocardial lesions.
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