BACKGROUND AND OBJECTIVES: Oxidative stress is a significant contributor to the pathogenesis of diabetic nephropathy. Carnosine is a natural radical oxygen species scavenger. We investigated the effect of carnosine as an adjuvant therapy on urinary albumin excretion (UAE), the tubular damage marker alpha 1-microglobulin (A1M), and oxidative stress in pediatric patients with type 1 diabetes and nephropathy. METHODS: This randomized placebo-controlled trial included 90 patients with diabetic nephropathy, despite oral angiotensin-converting enzyme inhibitors (ACE-Is), who were randomly assigned to receive either 12 weeks of carnosine 1 g/day (n = 45), or matching placebo (n = 45). Both groups were followed-up with assessment of hemoglobin A1c (HbA1c), UAE, A1M, total antioxidant capacity (TAC) and malondialdhyde (MDA). RESULTS: Baseline clinical and laboratory parameters were consistent between carnosine and placebo groups (P > .05). After 12 weeks, carnosine treatment resulted in significant decrease of HbA1c (8.2 ± 2.1% vs 7.4 ± 1.3%), UAE (91.7 vs 38.5 mg/g creatinine), A1M (16.5 ± 6.8 mg/L vs 9.3 ± 6.6 mg/L), MDA levels (25.5 ± 8.1 vs 18.2 ± 7.7 nmol/mL) while TAC levels were increased compared with baseline levels (P < .001) and compared with placebo (P < .001). No adverse reactions due to carnosine supplementation were reported. Baseline TAC was inversely correlated to HbA1c (r = -0.58, P = .04) and A1M (r = -0.682, P = .015) among carnosine group. CONCLUSIONS: Oral supplementation with L-Carnosine for 12 weeks resulted in a significant improvement of oxidative stress, glycemic control and renal function. Thus, carnosine could be a safe and effective strategy for treatment of pediatric patients with diabetic nephropathy.
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Elbarbary et al. (2017) studied this question.
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