Urinary Soluble CD163 Levels Predict IgA Nephropathy Remission Status.

Shaomin Gong,Xiao Liu,Yiqin Shi,Xiaoqiang Ding,Wuhua Jiang,Yang Li,Hong Liu,Zhen Zhang,Jialin Wang,Shi Jin,Ziyan Shen,Huili Zhou,Xialian Xu

doi:10.3389/fimmu.2021.769802

Abstract

Noninvasive biomarkers of disease activity are needed to predict disease remission status in patients with IgA nephropathy (IgAN). Soluble CD163 (sCD163), shed by monocytes and macrophages, is a potential biomarker in diseases associated with excessive macrophage activation. We investigated the association of urinary sCD163 (u-sCD163) with histopathological activity and clinical manifestations in 349 patients with biopsy-diagnosed IgAN. U-sCD163 was measured via enzyme-linked immunosorbent assay. In patients with IgAN, higher u-sCD163 levels were associated with histological lesions of greater severity, as well as more proteinuria and poorer renal function. Additionally, u-sCD163 was correlated with infiltration of tubulointerstitial CD163+ macrophages. High u-sCD163 levels (>3.57 ng/mg Cr) were associated with a 2.66-fold greater risk for IgAN remission failure in adjusted analyses. Adding u-sCD163 levels to the model containing clinical data at biopsy and MEST-C score significantly improved the risk prediction of IgAN remission status (AUC 0.788). Together, our results suggest that u-sCD163 may be a useful noninvasive biomarker to evaluate disease severity and remission status of IgAN.

Highlights

IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis throughout the world and is a leading cause of chronical kidney disease (CKD) and kidney failure [1]
Clinical data, and kidney histological evaluations based on u-Soluble CD163 (sCD163)/Cr levels (Table 1)
We further demonstrated that u-sCD163 levels are independent and strong predictor for IgAN remission status

Summary

Introduction

IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis throughout the world and is a leading cause of chronical kidney disease (CKD) and kidney failure [1]. 20–40% of IgAN patients develop end-stage kidney disease (ESKD) within 20 years from the time of diagnosis [2]. Patients can present with a range of traits, from asymptomatic microscopic haematuria to macroscopic haematuria and/or proteinuria. No specific therapy is available for IgAN. Development of strategies for early diagnosis and precise treatment for IgAN are urgently needed. IgAN diagnosis is based on kidney biopsy, an invasive procedure. Risk of bleeding and other clinical complications limits the application of biopsy. Noninvasive and sensitive biomarkers are necessary for evaluating disease severity in patients with IgAN

Objectives

Results

Conclusion