Abstract

AimThe study aimed to test the hypothesis that indoleamine 2,3-dioxygenase (IDO) plays a pathogenic role in type 2 diabetic nephropathy (DN). MethodsOne hundred individuals were recruited in our study from January 2012 to December 2013, including group A (control group, 24 healthy adults), group B (20 patients with latent glomerulonephritis), group C (32 type 2 DN patients, estimated glomerular filtration rate (eGFR) >30ml/min per 1.73m2), group D (24 maintenance hemodialysis, MHD patients). Clinical parameters such as gender, age, urine samples, serum creatinine, eGFR, L-tryptophan, L-kynurenine and 24h urinary protein were collected and analyzed. Group C was further divided on C1 (eGFR >60ml/min per 1.73m2) and C2 (eGFR 31–60ml/min per 1.73m2). ResultsAge was not related to IDO activity (r=0.27, P=0.057), while eGFR was significantly related to IDO activity (r=−0.54, P=0.002). IDO activity was significantly higher in the group C1 than group A (P=0.003), group B (P=0.008), and lower than in group D (P=0.003). ConclusionsIDO activity increased with severity of chronic kidney disease and negatively correlated with eGFR. Moreover, IDO activity was significantly increased in type 2 DN when eGFR was >60ml/min per 1.73m2, which suggested that IDO may closely correlate with the pathogenesis of type 2 DN.

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