Kidney Week

Abstract: FR-PO1042

Urinary CD163 Levels Reflect Crescentic Glomerulonephritis in ANCA-Associated Vasculitis

Session Information

• Glomerular Diseases: Immunology and Inflammation - II
  October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Glomerular Diseases

• 1202 Glomerular Diseases: Immunology and Inflammation

Authors

• Aendekerk, Joop, Maastricht University Medical Center, Maastricht, Netherlands

Joop Aendekerk,

• Timmermans, Sjoerd, Maastricht University Medical Center, Maastricht, Netherlands

Sjoerd Timmermans,

• Heeringa, Peter, University Medical Center Groningen, Groningen, Netherlands

Peter Heeringa,

• Paassen, Pieter Van, Maastricht University Medical Center, Maastricht, Netherlands

Pieter Van Paassen,

Background

Early recognition of renal flares in ANCA-associated vasculitis (AAV) can be challenging, particularly among patients with persistent or recurrent urinary abnormalities. Kidney biopsies are therefore often needed to detect active vasculitis. Urinary soluble CD163 (usCD163) has been shown to reflect early renal disease. Animal studies demonstrated that increased usCD163 reflects early stage necrotizing and crescentic glomerulonephritis (GN). However, this needs confirmation in humans to establish its role as a marker of active renal AAV. Also, it is unknown whether tubulointerstitial and/or vascular damage can affect usCD163 levels. Therefore, we analyzed usCD163 in relation to histologic data on kidney biopsy.

Methods

Thirty-two patients with AAV underwent a kidney biopsy because of suspected renal vasculitis (de novo, n=13; renal flare, n=19); concurrently, urine samples were collected. None of the patients were receiving immunosuppressive treatment before biopsy. usCD163 was analyzed by ELISA and corrected for creatinine excretion. Kidney tissue samples were classified according to the ANCA GN classification and scored for tubulointerstitial and vascular damage.

Results

Increased usCD163 levels were found in 27 (90%) out of 30 patients with crescentic GN but not those with normal kidney tissue (n=2) or controls (n=6), underlining usCD163’s specificity; median usCD136 levels did not differ between de novo and relapsing patients (302 versus 521 ng/mmol, P=0.1). In patients with crescentic GN, usCD163 correlated with the number of affected glomeruli (R²=0.61, P<0.001), but no differences were found according to ANCA GN class. Neither tubulointerstitial nor vascular damage affected usCD163 levels. Patients classified as sclerotic class however, progressed more often to the composite endpoint of CKD5, ESRD, and death as compared to those classified as focal, crescentic, and mixed class (n/N= 6/11 and n/N=3/18; P<0.05). No association between usCD163 and the composite endpoint were found.

Conclusion

usCD163 is linked to crescentic GN in de novo patients with AAV, as well as during relapses. Both tubulointerstitial and vascular damage do not affect usCD163 levels, suggesting that usCD163 specifically reflects crescentic GN and should be used as a marker of active renal disease in AAV.