Details

Autor(en) / Beteiligte

• Yokoe, Yuki
• Tsuboi, Naotake
• Imaizumi, Takahiro
• Kitagawa, Akimitsu
• Karasawa, Munetoshi
• Ozeki, Takaya
• Endo, Nobuhide
• Sawa, Yuriko
• Kato, Sawako
• Katsuno, Takayuki
• Maruyama, Shoichi
• Yamagata, Kunihiro
• Usui, Joichi
• Nagata, Michio
• Sada, Ken-Ei
• Sugiyama, Hitoshi
• Amano, Koichi
• Arimura, Yoshihiro
• Atsumi, Tatsuya
• Yuzawa, Yukio
• Dobashi, Hiroaki
• Takasaki, Yoshinari
• Harigai, Masayoshi
• Hasegawa, Hitoshi
• Makino, Hirofumi
• Matsuo, Seiichi

Titel

Clinical impact of urinary CD11b and CD163 on the renal outcomes of anti-neutrophil cytoplasmic antibody-associated glomerulonephritis

Ist Teil von

• Nephrology, dialysis, transplantation, 2021-07, Vol.36 (8), p.1452-1463

Ort / Verlag

England: Oxford University Press

Erscheinungsjahr

2021

Link zum Volltext

Quelle

Oxford Journals 2020 Medicine

Beschreibungen/Notizen

• Abstract Background The detection of leukocyte-derived CD11b (α subunit of integrin Mac-1) and CD163 (scavenger receptor) in urine may reflect renal inflammation in antineutrophil cytoplasmic antibody-associated glomerulonephritis (ANCA-GN). The objective of this study was to evaluate the clinical significance of urinary CD11b (U-CD11b) and CD163 (U-CD163) in ANCA-GN. Methods U-CD11b and U-CD163 were examined using enzyme-linked immunosorbent assay in ANCA-GN urine samples from our institutional cohort (n = 88) and a nationwide cohort (n = 138), and their association with renal histology was subsequently analyzed. Logistic regression analyses were performed on a nationwide ANCA cohort to determine the associations of the two urinary molecules with renal remission failure at 6 months or with yearly estimated glomerular filtration rate (eGFR) slope over a 24-month observation period. Results U-CD11b and U-CD163 were significantly associated with cellular crescent formation and leukocyte accumulation in glomerular crescents. With regard to interstitial inflammation, both levels of U-CD11b and U-CD163 at diagnosis remarkably increased in ANCA-GN compared with the levels observed in nonglomerular kidney disorders including nephrosclerosis, immunoglobulin G4-related disease and tubulointerstitial nephritis; however, the presence of U-CD11b alone was significantly correlated with tubulointerstitial leukocyte infiltrates. Although neither U-CD11b nor U-CD163 at diagnosis was associated with remission failure at 6 months, multivariate analysis demonstrated that the baseline U-CD11b levels were significantly associated with the increase in eGFR following immunosuppressive therapy. Conclusions Although both U-CD11b and U-CD163 reflect renal leukocyte accumulation, U-CD11b at diagnosis provides additional clinical value by predicting the recovery rate after the treatment of ANCA-GN.