ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: SA-PO275

Renal CD141+ Dendritic Cell Infiltration in IgA Nephropathy

Session Information

Category: Glomerular

  • 1005 Clinical Glomerular Disorders

Authors

  • Chen, Titi, University of Sydney, Westmead, New South Wales, Australia
  • Cao, Qi, Centre for Transplant and Renal Research, Westmead Millennium Institute, University of Sydney, Sydney, New South Wales, Australia
  • Rao, Padmashree, Westmead Millenium Institute for Medical Research, Parramatta, New South Wales, Australia
  • Zheng, Guoping, The University of Sydney, Sydney, New South Wales, Australia
  • Wang, Yiping, Centre for Transplantation and Renal Research, Westmead Millennium Institute, The University of Sydney, Westmead, NSW, New South Wales, Australia
  • Harris, David C., Sydney Medical School - University of Sydney, Terrey Hills, New South Wales, Australia
Background

Previous studies have shown that the severity of interstitial inflammatory infiltrates, which include myeloid dendritic cells (DCs), correlates with progression of IgA nephropathy. CD141+ DCs have recently been identified as a unique myeloid DC subset that plays a significant role in the induction and regulation of immunity. This DC subset has been studied in mouse models, but studies in humans are lacking. We aim to investigate the relationship between CD141+ DC infiltration and clinicopathologic features in IgA nephropathy.

Methods

Thirty adult patients with a sole diagnosis of IgA nephropathy were included in this study. Patients were excluded if they had received glucocorticoids or immunosuppressant therapy before renal biopsy. The histological classification was scored according to the Oxford classification. CD141+ DCs were identified through immunofluorescence staining and visualised using confocal microscopy.

Results

In normal human kidney, CD141+DCs were rarely present. Patients with IgA nephropathy had significantly higher number of CD141+ DCs than normal control (P=0.021) and CD141+DCs were mainly present in the interstitium. Higher CD141+ DC density was significantly associated with worse serum creatinine (r=0.81, P=0.015) and proteinuria (r=0.75, P=0.049). Higher CD141+ DC density was also associated with increased severity of tubular atrophy/interstitial fibrosis (P=0.025), but not with mesangial hypercellularity, endocapillary hypercellularity, segmental glomerulosclerosis, or number of crescents.

Conclusion

Our data highlight the close correlation between the density of CD141+ DCs and clinicopathologic features of IgA nephropathy progression. Further studies will be conducted in human samples and murine models to investigate whether CD141+ DCs mediate kidney injury, and the possible mechanisms involved.