Circulating CD89-IgA complex does not predict deterioration of kidney function in Korean patients with IgA nephropathy

Jong Hyun Jhee, Hye Young Kang, Meiyan Wu, Bo Young Nam, Tae Ik Chang, Su Young Jung, Seohyun Park, Hyoungnae Kim, Hae Ryong Yun, Youn Kyung Kee, Chang Yun Yoon, Jung Tak Park, Tae Hyun Yoo, Shin Wook Kang, Seung Hyeok Han

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7 Citations (Scopus)

Abstract

Soluble CD89 (sCD89)-IgA complex plays a key role in the pathogenesis of IgA nephropathy (IgAN). However, there is a lack of evidence supporting this complex as a good biomarker for disease progression. This study aimed to evaluate the usefulness of sCD89-IgA complex for risk stratification of IgAN. A total of 326 patients with biopsy-proven IgAN were included. sCD89-IgA complex was measured by sandwich-enzyme-linked immunosorbent assay. The study endpoints were a 30% decline in estimated glomerular filtration rate (eGFR). sCD89-IgA complex levels were inversely and weakly associated with eGFR at the time of biopsy (r=-0.12, p=0.03). However, the significance between the two factors was lost in the multivariate linear regression after adjustment of clinical factors (β=0.35, p=0.75). In a multivariate Cox model, the highest (hazard ratio [HR], 0.75; 95% confidence interval [CI], 0.35-1.61; p=0.45) and middle (HR, 0.93; 95% CI, 0.46-1.89; p=0.84) tertiles of sCD89-IgA complex levels were not associated with an increased risk of developing a 30% decrease in eGFR. Furthermore, the decline rates in eGFR did not differ between groups and C-statistics revealed that the sCD89-IgA complex were not superior to clinical factors in predicting disease progression. This study found no association between sCD89-IgA complex levels and disease progression in IgAN. Although sCD89 can contribute to the formation of immune complexes, our findings suggest that the sCD89-IgA level is not a good predictor of adverse outcomes and has limited clinical utility as a biomarker for risk stratification in IgAN.

Original languageEnglish
Pages (from-to)75-85
Number of pages11
JournalClinical Chemistry and Laboratory Medicine
Volume56
Issue number1
DOIs
Publication statusPublished - 2017 Nov 27

Bibliographical note

Funding Information:
Author contributions: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission. Financial support: This study was supported by a faculty research grant of Yonsei University College of Medicine for 2015; Dr. Wu M is supported by China Scholarship Council. Employment or leadership: None declared. Honorarium: None declared. Competing interests: The funding organization(s) played no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.

Publisher Copyright:
© 2018 2018 Walter de Gruyter GmbH, Berlin/Boston.

All Science Journal Classification (ASJC) codes

  • Clinical Biochemistry
  • Biochemistry, medical

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