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J Am Soc Nephrol. 2016 Sep;27(9):2906-16. doi: 10.1681/ASN.2015050511. Epub 2016 Mar 3.

Urinary Soluble CD163 in Active Renal Vasculitis.

Author information

Trinity Health Kidney Centre.
Department of Immunology, Trinity College Dublin, Dublin, Ireland;
HRB Clinical Research Facility, St James's Hospital, Dublin, Ireland;
Department of Nephrology, and.
Department of Medical Biology and Pathology, University of Groningen, University Medical Center Groningen, The Netherlands;
Department of Renal Histopathology, Beaumont Hospital, Dublin, Ireland;
Labmed Directorate, St James's Hospital, Dublin, Ireland; Department of Histopathology, Trinity College Dublin, Ireland;
Nephrological Center, Medical Clinic and Policlinic IV, University of Munich, Munich, Germany;
Department of Renal Medicine, Cork University Hospital, Cork, Ireland; and.
School of Medicine, University College Dublin, Dublin, Ireland.
Trinity Health Kidney Centre,

Erratum in


A specific biomarker that can separate active renal vasculitis from other causes of renal dysfunction is lacking, with a kidney biopsy often being required. Soluble CD163 (sCD163), shed by monocytes and macrophages, has been reported as a potential biomarker in diseases associated with excessive macrophage activation. Thus, we hypothesized that urinary sCD163 shed by crescent macrophages correlates with active glomerular inflammation. We detected sCD163 in rat urine early in the disease course of experimental vasculitis. Moreover, microdissected glomeruli from patients with small vessel vasculitis (SVV) had markedly higher levels of CD163 mRNA than did those from patients with lupus nephritis, diabetic nephropathy, or nephrotic syndrome. Both glomeruli and interstitium of patients with SVV strongly expressed CD163 protein. In 479 individuals, including patients with SVV, disease controls, and healthy controls, serum levels of sCD163 did not differ between the groups. However, in an inception cohort, including 177 patients with SVV, patients with active renal vasculitis had markedly higher urinary sCD163 levels than did patients in remission, disease controls, or healthy controls. Analyses in both internal and external validation cohorts confirmed these results. Setting a derived optimum cutoff for urinary sCD163 of 0.3 ng/mmol creatinine for detection of active renal vasculitis resulted in a sensitivity of 83%, specificity of 96%, and a positive likelihood ratio of 20.8. These data indicate that urinary sCD163 level associates very tightly with active renal vasculitis, and assessing this level may be a noninvasive method for diagnosing renal flare in the setting of a known diagnosis of SVV.


ANCA; glomerulonephritis; immunology; nephrology; renal injury; vasculitis

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