bubble_chart Overview

Diabetic nephropathy refers to glomerulosclerosis primarily caused by abnormal glucose metabolism in diabetes, accompanied by urinary protein levels exceeding the normal range.

bubble_chart Diagnosis

1. Medical History and Symptoms

A history of diabetes is present, and the clinical manifestations of renal damage are positively correlated with the degree of glomerulosclerosis. When microalbuminuria appears, the diabetes history is usually 5–6 years, and the clinical diagnosis is early diabetic nephropathy, with no obvious clinical symptoms. Approximately 80% of patients progress to clinical diabetic nephropathy within 10 years, characterized by urinary protein excretion greater than 0.5g/24h, typically without significant hematuria, and clinical manifestations such as edema and hypertension. Once persistent proteinuria occurs, accompanied by loss of appetite, nausea and vomiting, and anemia, it suggests the onset of chronic renal insufficiency.

2. Physical Examination Findings

Varying degrees of hypertension and edema are observed, and in severe cases, ascites or pleural effusion may develop. Most cases are accompanied by diabetic retinopathy.

3. Auxiliary Examinations

(1) Qualitative urine glucose testing is a simple screening method for diabetes, but false negatives or positives may occur in diabetic nephropathy. Therefore, blood glucose measurement is the primary diagnostic criterion.

(2) Urinary albumin excretion rate (UAE) of 20–200μg/min is an important indicator for diagnosing early diabetic nephropathy. When UAE persistently exceeds 200μg/min or routine urine protein tests are positive (urinary protein excretion >0.5g/24h), diabetic nephropathy is diagnosed. Urinary sediment usually shows no significant changes; a high white blood cell count suggests urinary tract infection, while abundant red blood cells may indicate hematuria due to other causes.

(3) In advanced diabetic nephropathy, endogenous creatinine clearance decreases, and blood urea nitrogen and creatinine levels increase.

(4) Radionuclide renal dynamic imaging shows an increased glomerular filtration rate (GFR), and ultrasound reveals enlarged kidney volume, consistent with early diabetic nephropathy. In uremia, GFR significantly declines, but kidney volume often does not shrink noticeably.

(5) Fundus examination, supplemented by fluorescein angiography if necessary, may reveal microaneurysms and other diabetic retinal lesions.

4. Differential Diagnosis

Other potential causes of proteinuria must be excluded. When hematuria is prominent, careful exclusion of renal papillary necrosis, renal tumors, stones, pyelonephritis, cystitis, or nephritis is necessary. Renal biopsy may be considered for definitive diagnosis if required.

bubble_chart Treatment Measures

1. There is currently no specific treatment for diabetic nephropathy. For those presenting with nephrotic syndrome, glucocorticoids are generally not recommended, and cytotoxic drugs or Root Leaf or Flower of Common Threewingnut also show no significant therapeutic effect.

2. Active blood glucose control is essential, including dietary therapy, oral hypoglycemic agents, and insulin administration. In cases of azotemia, timely adjustments to insulin and oral hypoglycemic doses and types should be made based on blood glucose levels.

3. Protein intake should be restricted (≤0.8g/day). If necessary, essential amino acids or α-keto acids may be supplemented.

4. For patients with hypertension or edema but normal renal function, low-dose thiazide diuretics may be considered. In cases of renal insufficiency, loop diuretics or indapamide tablets are preferred. For severe edema, strict sodium restriction should be enforced, and appropriate volume expansion with diuresis may be applied. If blood pressure remains excessively high or cardiac insufficiency persists despite aggressive volume expansion and diuresis, dialysis may be considered.

5. Actively lower blood pressure to below 18.6 Kpa. ACE inhibitors are the first-line choice, as they not only reduce blood pressure but also improve GFR and decrease urinary albumin excretion—though functional GFR decline should be monitored. Diuretics, calcium channel blockers, cardioselective β-blockers, and angiotensin II receptor antagonists may be added as needed.

6. Hyperlipidemia and hyperuricemia should be actively treated.

7. Antiplatelet and antithrombotic agents such as dipyridamole, ticlopidine, aspirin, or heparin may be used. Properly administered Chinese medicinals, guided by pattern identification, can be particularly effective in controlling blood glucose and improving microvascular complications.

8. Replacement therapy may be considered when Ccr is between 10–15 ml/min or serum creatinine reaches 530–710 μmol/L. {|107|}