Abstract: PO1406
Collapsing FSGS Is Strongly Associated with Microvascular Injury
Session Information
- Glomerular Diseases: Fibrosis and Extracellular Matrix
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1201 Glomerular Diseases: Fibrosis and Extracellular Matrix
Authors
- Van de Lest, Nina A., Leids Universitair Medisch Centrum, Leiden, Zuid-Holland, Netherlands
- Dijkstra, Kyra L., Leids Universitair Medisch Centrum, Leiden, Zuid-Holland, Netherlands
- Chua, Jamie S., Leids Universitair Medisch Centrum, Leiden, Zuid-Holland, Netherlands
- Wolterbeek, Ron, Leids Universitair Medisch Centrum, Leiden, Zuid-Holland, Netherlands
- Bruijn, Jan A., Leids Universitair Medisch Centrum, Leiden, Zuid-Holland, Netherlands
- Scharpfenecker, Marion, Leids Universitair Medisch Centrum, Leiden, Zuid-Holland, Netherlands
- Bajema, Ingeborg M., Leids Universitair Medisch Centrum, Leiden, Zuid-Holland, Netherlands
Background
Recent studies have suggested that the collapsing variant of focal segmental glomerulosclerosis (FSGS) might be a common secondary feature in renal disease influenced by microvascular injury. Here, we investigated glomerular and arteriolar microvascular injury in patients with collapsing FSGS, including primary FSGS and HIV-associated FSGS, and compared these lesions to patients with other variants of FSGS.
Methods
Biopsies of patients with FSGS were collected, including primary FSGS in native biopsies or transplant biopsies, as well as HIV-associated FSGS. Cases of FSGS secondary to renal diseases known to be caused by microvascular injury were excluded. We assessed all glomeruli in a biopsy for the presence of lesions associated with FSGS or ischemic injury, assessed microvascular lesions in glomeruli and arterioles, and studied interstitial lesions.
Results
We included 53 cases of FSGS, of which 19 cases with collapsing FSGS, 18 cases with FSGS not otherwise specified (NOS), 11 cases with FSGS tip, 3 cases with perihilar FSGS and 2 cases with cellular FSGS. Compared to other variants of FSGS, glomerular endothelial swelling of the vascular pole was more common in patients with collapsing FSGS (11% vs 0.0%; p=0.05). Associations between thrombotic injury and FSGS variant were not found. Arteriolar abnormalities were seen in 58% of collapsing FSGS and 38% of other variants of FSGS (p=0.17). When evaluating the concomitant occurrence of FSGS lesions and microvascular injury in individual glomeruli, we found that collapsing lesions and FSGS NOS lesions were associated with endothelial swelling in the same glomerulus (OR=22; p<0.001 and OR=3.8; p<0.01, respectively). Endothelial swelling was more common in glomeruli with collapsing lesions than glomeruli with FSGS NOS (OR=2.7; p=0.044). Collapsing FSGS was also associated with endocapillary hypercellularity (OR=4.3; p<0.001).
Conclusion
Here, we demonstrate that collapsing FSGS lesions are strongly associated with microvascular injury such as endothelial swelling and endocapillary hypercellularity, and often co-exist in the same glomerulus. In addition to collapsing FSGS occurring as a secondary phenomenon in renal microangiopathies, these results indicate that endothelial injury could also be involved in the pathophysiology of collapsing FSGS due to primary podocyte injury.