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


The Latest on Twitter

Kidney Week

Abstract: FR-PO1052

Complement and Cytokine Characterization of C3GN

Session Information

Category: Glomerular Diseases

  • 1202 Glomerular Diseases: Immunology and Inflammation


  • Steers, Nicholas J., Columbia University, New York, New York, United States
  • Chatterjee, Debanjana, Columbia University, New York, New York, United States
  • Lam, Wan yee, Columbia University, New York, New York, United States
  • Demaria, Natalia D., Columbia University, New York, New York, United States
  • Bomback, Andrew S., Columbia University, New York, New York, United States
  • Appel, Gerald B., Columbia University College of Physicians and Surgeons, Scarsdale, New York, United States
  • Gharavi, Ali G., Columbia University, New York, New York, United States

The complement pathway is an innate immune defense mechanism, when uncontrolled can cause damage to host tissues including the kidney upon uncontrolled activation of the alternative complement pathway (ACP). C3GN is characterized by deposits in the glomerulus made up entirely of complement C3 protein without the presence of immunoglobulins.


We determined the cytokine and complement profiles derived from the plasma of 40 C3GN cases, and 15 healthy controls (HC), utilizing the Luminex assay.


Analysis of the plasma from 40 C3GN patients compared to HC revealed significant decreases in the complement pathway proteins C3 (424+336 vs 673+118 μg/ml), C4 (233+71 vs 392+115 μg/ml), C4b (10.9+4.3 vs 15.9+3.1 μg/ml), C5 (15.8+8.3 vs 24.3+6.4 μg/ml), CFH (247+60 vs 285+44 μg/ml), and Properdin (19.2+5.3 vs 25.2+5.6 μg/ml). In-depth analysis of the plasma derived from C3GN patients identified significantly low C3 levels (2*SD below Average HC) in 21 patients, in which 72% of these had significantly low levels of plasma C5. Key components of the ACP are CFH and properdin, and we only identified 10 patients with significantly low levels CFH (7 associated with low plasma C3), and 11 with significantly low levels properdin (8 associated with low plasma C3). Global cytokine analysis in C3GN plasma determined significant increases in proinflammatory cytokines TNFα detected in 100% of C3GN patients (17.9+8.9 pg/ml) and IL-1α detected in 82% of C3GN patients (80.3+80.1 pg/ml) compared to HC ((100%) 7.2+3.6 and (40%) 29.7+29.9 pg/ml, respectively). Cytokine analysis demonstrated bi-modal patterns with increased percentage of C3GN patients having elevated levels of pro-inflammatory cytokines, IL-6 and IL-12p40 was more prevalent in the plasma of C3GN patients (45% and 50% respectively), compared to HC (26% and 26% respectively)


The plasma of C3GN patients demonstrates activation of the ACP and elevated levels of proinflammatory cytokines that are associated with stimuli know to activate the ACP. Our data set is being expanded to include additional samples and will be correlated with the clinical status of patients. In-depth profiling of immunological markers and the specific relationships will able to design a panel specific to individual complement associated glomerular pathology.