BACKGROUND: Albumin is a potent antioxidant as it chelates transitional metals and contains antioxidants like thiol and bilirubin. In neprotic syndrome, the defining parameter is proteinuria with hypoalbuminemia. Therefore albuminuria in nephrotic syndrome may increase toxic transitional metal ions and also can cause loss of albumin associated antioxidants causing oxidative stress to the individual. METHODS: We investigated this possibility and estimated some markers of oxidative stress in 20 nephrotic syndrome patients and healthy controls along with urinary thiols, urinary bilirubin and plasma free iron in both cases and in the controls. RESULT: We found oxidative stress in 20 nephrotic syndrome patients and the markers of oxidative stress correlated significantly with proteinuria, but the urine of nephrotic syndrome patients (28.33+/-4.2 micromol/g creatinine)contained significantly less thiols compared to the healthy controls (88.45+/-10.6 micromol/g creatinine) and no biliribin. The patients plasma also showed free iron (0.7+/-0.05 micromol/l), a parameter undetectable in the healthy controls. CONCLUSION: We suggest that oxidative stress and presence of free iron in the patients were responsible for less thioluria and no bilirubinuria. A detailed study of oxidative biology in a large cohort of nephrotic syndrome patients is necessary to confirm the presence of free iron as appropriate chelation of free iron may benefit the long-term prognosis of the disease.
BACKGROUND:Albumin is a potent antioxidant as it chelates transitional metals and contains antioxidants like thiol and bilirubin. In neprotic syndrome, the defining parameter is proteinuria with hypoalbuminemia. Therefore albuminuria in nephrotic syndrome may increase toxic transitional metal ions and also can cause loss of albumin associated antioxidants causing oxidative stress to the individual. METHODS: We investigated this possibility and estimated some markers of oxidative stress in 20 nephrotic syndromepatients and healthy controls along with urinary thiols, urinary bilirubin and plasma free iron in both cases and in the controls. RESULT: We found oxidative stress in 20 nephrotic syndromepatients and the markers of oxidative stress correlated significantly with proteinuria, but the urine of nephrotic syndromepatients (28.33+/-4.2 micromol/g creatinine)contained significantly less thiols compared to the healthy controls (88.45+/-10.6 micromol/g creatinine) and no biliribin. The patients plasma also showed free iron (0.7+/-0.05 micromol/l), a parameter undetectable in the healthy controls. CONCLUSION: We suggest that oxidative stress and presence of free iron in the patients were responsible for less thioluria and no bilirubinuria. A detailed study of oxidative biology in a large cohort of nephrotic syndromepatients is necessary to confirm the presence of free iron as appropriate chelation of free iron may benefit the long-term prognosis of the disease.