Effect of allopurinol in decreasing proteinuria in type 2 diabetic patients

Diabetic nephropathy is the most prevalent cause of end-stage renal disease. Besides factors such as angiotensin II, cytokines, and vascular endothelial growth factor, uric acid may play a role as the underlying cause of diabetic nephropathy. We evaluated allopurinol effects on proteinuria in diabetic patients with nephropathy.

In a double-blinded randomized controlled trial on 40 patients with type 2 diabetes mellitus and diabetic nephropathy (proteinuria, at least 500 mg/24 h and a serum creatinine level less than 3 mg/dL), allopurinol (100 mg/d) was compared with placebo. Administration of antihypertensive and renoprotective drugs (angiotensin-converting enzyme inhibitors and angiotensin receptor blockers continued for both groups, without changes in dosage. Proteinuria was compared at baseline and 2 and 4 months between the two groups.

Each group consisted of 9 men and 11 women. There were no difference between two groups regarding age, body mass index, duration of diabetes mellitus, systolic and diastolic blood pressure, fasting blood glucose, blood urea nitrogen, serum creatinine, serum potassium, and urine volume. Serum levels of uric acid (P = .02) and 24-hour urine protein (P = .049) were significantly lower in the patients on allopurinol, after 4 months of receiving allopurinol, compared with the control group.

Low-dose allopurinol can reduce severity of proteinuria after 4 months of drug administration, which is probably due to decreasing the serum level of uric acid. Thus, allopurinol can be administered as an adjuvant cost-effective therapy for patients with diabetic nephropathy.