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: PUB149

Clinical Characteristics, Histopathological Findings, and Kidney Outcomes in C3 Glomerulopathy

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Arabi, Ziad, King Abdulaziz Medical City in Riyadh, Riyadh, Riyadh Province, Saudi Arabia
  • Alanazi, Abdullah Mordhi, King Abdulaziz Medical City in Riyadh, Riyadh, Riyadh Province, Saudi Arabia
  • Alotaibi, Khalid Ayidh, King Abdulaziz Medical City in Riyadh, Riyadh, Riyadh Province, Saudi Arabia
  • Elhassan, Elwaleed A., King Abdulaziz Medical City in Riyadh, Riyadh, Riyadh Province, Saudi Arabia
Background

C3 glomerulopathy (C3G) is a rare complement-mediated kidney disease with heterogeneous presentation and variable renal outcomes. We aimed to characterize the clinical, histopathological, and renal outcome and explore the relationship between serum C3 levels and disease severity.

Methods

Out of 1,127 native kidney biopsies performed between 2016 and 2026, nine patients were identified. Data included demographics, kidney function, proteinuria, complement levels, histopathology, treatment, and one-year renal outcomes.

Results

Nine patients with biopsy-confirmed C3G were identified (mean age 37 years; 56% male). Clinical presentation was heterogeneous: 33% had preserved kidney function, 22% presented with acute kidney injury, 11% with rapidly progressive glomerulonephritis, and 33% required renal replacement therapy. Mean baseline eGFR was 49.7 mL/min and mean UPCR was 4.82 g/g.
Low serum C3 was present in 44% and was associated with lower baseline eGFR (20 vs 73.4 mL/min). Severe presentations were more frequent with low C3, although advanced kidney dysfunction also occurred with normal C3. Proteinuria did not consistently correlate with severity (Figure 1).
Histologically, a membranoproliferative pattern predominated (78%). Moderate-to-severe interstitial fibrosis/tubular atrophy was present in 55%, and strong C3 staining (3+) in 78%. Most patients received steroids and mycophenolate mofetil. Renal outcomes remained heterogeneous despite partial proteinuria improvement.

Conclusion

(C3G) demonstrated marked clinical and pathological heterogeneity in this cohort. Low serum C3 appeared associated with more severe renal involvement, although normal C3 did not exclude advanced disease. Degree of proteinuria alone did not reliably reflect disease severity. These findings highlight the limitations of conventional biomarkers in assessing disease activity in C3G and underscore the need for improved complement biomarkers and targeted therapies.

Figure 1 Clinical Heterogeneity in C3 Glomerulopathy