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

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....

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Published inClinical chemistry and laboratory medicine Vol. 56; no. 1; pp. 75 - 85
Main Authors Jhee, Jong Hyun, Kang, Hye-Young, Wu, Meiyan, Nam, Bo Young, Chang, Tae-Ik, Jung, Su-Young, Park, Seohyun, Kim, Hyoungnae, Yun, Hae-Ryong, Kee, Youn Kyung, Yoon, Chang-Yun, Park, Jung Tak, Yoo, Tae-Hyun, Kang, Shin-Wook, Han, Seung Hyeok
Format Journal Article
LanguageEnglish
Published Germany De Gruyter 27.11.2017
Walter De Gruyter & Company
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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.
AbstractList 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. Methods: 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). Results: 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. Conclusions: 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.
Abstract Background: 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. Methods: 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). Results: 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. Conclusions: 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.
BACKGROUNDSoluble 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.METHODSA 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).RESULTSsCD89-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.CONCLUSIONSThis 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.
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.
Author Kang, Hye-Young
Han, Seung Hyeok
Kim, Hyoungnae
Yun, Hae-Ryong
Kang, Shin-Wook
Jung, Su-Young
Park, Seohyun
Nam, Bo Young
Chang, Tae-Ik
Yoo, Tae-Hyun
Jhee, Jong Hyun
Park, Jung Tak
Kee, Youn Kyung
Wu, Meiyan
Yoon, Chang-Yun
Author_xml – sequence: 1
  givenname: Jong Hyun
  surname: Jhee
  fullname: Jhee, Jong Hyun
  organization: Department of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Republic of Korea
– sequence: 2
  givenname: Hye-Young
  surname: Kang
  fullname: Kang, Hye-Young
  organization: Severance Biomedical Science Institute, Brain Korea 21 PLUS, Yonsei University, Seoul, Republic of Korea
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  givenname: Meiyan
  surname: Wu
  fullname: Wu, Meiyan
  organization: Department of Nephrology, The First Hospital of Jilin University, Changchun, P.R. China
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  givenname: Bo Young
  surname: Nam
  fullname: Nam, Bo Young
  organization: Severance Biomedical Science Institute, Brain Korea 21 PLUS, Yonsei University, Seoul, Republic of Korea
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  givenname: Tae-Ik
  surname: Chang
  fullname: Chang, Tae-Ik
  organization: Department of Internal Medicine, National Health Insurance Service Medical Center, Ilsan Hospital, Gyeonggi-do, Republic of Korea
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  givenname: Su-Young
  surname: Jung
  fullname: Jung, Su-Young
  organization: Department of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Republic of Korea
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  givenname: Seohyun
  surname: Park
  fullname: Park, Seohyun
  organization: Department of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Republic of Korea
– sequence: 8
  givenname: Hyoungnae
  surname: Kim
  fullname: Kim, Hyoungnae
  organization: Department of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Republic of Korea
– sequence: 9
  givenname: Hae-Ryong
  surname: Yun
  fullname: Yun, Hae-Ryong
  organization: Department of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Republic of Korea
– sequence: 10
  givenname: Youn Kyung
  surname: Kee
  fullname: Kee, Youn Kyung
  organization: Department of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Republic of Korea
– sequence: 11
  givenname: Chang-Yun
  surname: Yoon
  fullname: Yoon, Chang-Yun
  organization: Department of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Republic of Korea
– sequence: 12
  givenname: Jung Tak
  surname: Park
  fullname: Park, Jung Tak
  organization: Department of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Republic of Korea
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  givenname: Tae-Hyun
  surname: Yoo
  fullname: Yoo, Tae-Hyun
  organization: Department of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Republic of Korea
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  givenname: Shin-Wook
  surname: Kang
  fullname: Kang, Shin-Wook
  organization: Severance Biomedical Science Institute, Brain Korea 21 PLUS, Yonsei University, Seoul, Republic of Korea
– sequence: 15
  givenname: Seung Hyeok
  surname: Han
  fullname: Han, Seung Hyeok
  email: hansh@yuhs.ac
  organization: Department of Internal Medicine, Severance Hospital, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 120-752, Korea
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Keywords CD89
IgA nephropathy
estimated glomerular filtration rate (eGFR)
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Snippet 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...
Abstract Background: Soluble CD89 (sCD89)-IgA complex plays a key role in the pathogenesis of IgA nephropathy (IgAN). However, there is a lack of evidence...
BACKGROUNDSoluble CD89 (sCD89)-IgA complex plays a key role in the pathogenesis of IgA nephropathy (IgAN). However, there is a lack of evidence supporting this...
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SubjectTerms Antigen-antibody complexes
Biomarkers
Biopsy
CD89
CD89 antigen
Confidence intervals
Enzyme-linked immunosorbent assay
Epidermal growth factor receptors
estimated glomerular filtration rate (eGFR)
Glomerular filtration rate
IgA nephropathy
Immunoglobulin A
Pathogenesis
Patients
Risk
Statistical analysis
Title Circulating CD89-IgA complex does not predict deterioration of kidney function in Korean patients with IgA nephropathy
URI http://www.degruyter.com/doi/10.1515/cclm-2017-0090
https://www.ncbi.nlm.nih.gov/pubmed/28672768
https://www.proquest.com/docview/1978464473/abstract/
https://search.proquest.com/docview/1915881770
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