Diabetic nephropathy is the single most important factor in the etiology of chronic renal failure in adults. Diabetic nephropathy can occur in both type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM), and the incidence of diabetic nephropathy is higher in T1DM patients, at 30 %C40 %. Diabetic nephropathy occurs in about 34.7% of T2DM patients. So early detection of diabetic nephropathy is very important. Diabetic nephropathy can be divided into the following V stages: Stage I: increased glomerular filtration rate, increased renal volume, increased renal blood flow, glomerular capillary perfusion pressure and internal pressure. The glomerular basement membrane and thylakoid membrane are normal. It can be recovered with appropriate treatment. Stage II: i.e. normal albuminuria stage. Glomerular filtration rate is normal or increased, urinary albumin excretion rate is normal (less than 20 micrograms/min or 30 mg/24 hours), excretion increases after exercise or stress, and returns to normal after removal of the trigger. The glomerular basement membrane is thickened and the thylakoid matrix is increased. Blood pressure is mostly normal. Stage III: Early diabetic nephropathy. Glomerular filtration rate is approximately normal, urinary albumin excretion rate is consistently higher than normal, and blood pressure is mildly elevated. The glomerular basement membrane is thickened and the thylakoid matrix is significantly increased. Glomerular nodular and diffuse lesions and small arterial vitelliform lesions are present and glomerular wasting has begun to occur. Patients in this stage have mildly elevated blood pressure, and lowering blood pressure can partially reduce urinary microalbumin excretion. Stage IV: Clinical diabetic nephropathy. Large amounts of albumin, urine protein quantification consistently greater than 0.5 grams per 24 hours for non-selective proteinuria, and in severe cases greater than 3.5 grams per 24 hours for urine protein, hypoalbuminemia, edema and hypertension, often with varying degrees of nitrogen retention and diabetic fundopathy. The glomerular basement membrane is further thickened, the thylakoid matrix is further increased, and the glomerulus is deserted. Stage V: i.e. end-stage renal failure. Urinary protein excretion is reduced due to glomerular wasting, glomerular filtration rate is less than 10 ml/min, with hypertension, hypoalbuminemia, edema, elevated creatinine and urea nitrogen, loss of appetite, nausea and vomiting, anemia, metabolic acidosis, hypocalcemia and hyperkalemia, secondary uremic neuropathy and cardiomyopathy. The most critical of these V stages is stage III: early diabetic nephropathy, which is the earliest stage to detect diabetic nephropathy, so that effective intervention and treatment will have a significant effect on interrupting the further development of diabetic nephropathy. The early onset of diabetic nephropathy often has no obvious symptoms, and by the time patients discover it, it is usually in the middle or late stage of nephropathy, which makes treatment difficult and brings pain to patients. Therefore, we should screen urine microalbumin in every patient with initial onset type 2 diabetes and type 1 diabetes for more than 5 years, with a view to early diagnosis, early treatment and early benefit.