Wilms? Tumor-1 (WT1) Protein in Urinary Exosomes Predicts Risk of Developing Proteinuria in Type-1 Diabetes

Aradhana Mohan,Aditya Upadhyay

doi:10.4172/2155-6156.1000510

Abstract

Objective: Previously, we reported presence of Wilms’ tumor 1 (WT1) in urinary exosomes in ~50% diabetic (T1D) population without proteinuria as oppose to 100% in T1D population with proteinuria. Here, we investigated if T1D subjects with detectable WT1 in urinary exosomes (UE) progress to proteinuria faster in a 2 year follow-up study. Method: 52 T1D subjects without proteinuria (age 20 μg/min in WT1-positive group as oppose to none in WT1 negative group. Moreover, binary logistic regression analysis revealed a significant relation of WT1 presence in UE with increase in urine microalbumin >5 μg/min as indicated by significant Odds ratio of 9.9 (95% CI of 92.686, p=0.04). Both groups had statistically similar diabetes duration, age, % HbA1c and estimated GFR at the baseline. Conclusion: Thus, presence of WT-1 in urinary exosomes could potentially predict risk of developing proteinuria in type 1 diabetic patients.

Highlights

Diabetic nephropathy (DN) is one of the severe complications that affect population with diabetes [1]
The clinical hallmarks of DN includes an initial period of glomerular hyperfiltration, progressive albuminuria, hypertension, followed by a gradual decline in renal function concluding, after 5–15 years, with End-Stage Renal Disease (ESRD) [1,2,3]
Its presence is appropriate in patients with advanced diabetic nephropathy but it has limited ability to predict the earliest stages of DN

Summary

Introduction

Diabetic nephropathy (DN) is one of the severe complications that affect population with diabetes [1]. Conclusion: presence of WT-1 in urinary exosomes could potentially predict risk of developing proteinuria in type 1 diabetic patients. We have reported detection of significantly higher level of WT1, a podocyte marker and transcriptional factor, in urinary exosomes of patients with proteinuria and its almost complete absence in non-diabetic healthy controls [16].

Results

Conclusion