The Impact of Histologic Variants on FSGS Outcomes
Table 1
Pathological features of different FSGS histologic variants [13].
Histological variant
Pathologic features
NOS
(i) Focal and segmental consolidation of the glomerular tuft by increased ECM*, leading to obliteration of glomerular capillary lumen (ii) May have segmental capillary wall collapse without overlying podocyte hyperplasia (iii) Exclude perihilar, cellular, tip, and collapsing variants
Perihilar
(i) At least 1 glomerulus with perihilar hyalinosis with or without sclerosis with >50% of sclerotic glomeruli possessing perihilar lesions (ii) Perihilar lesions located at glomerular vascular pole (iii) May be glomerular hypertrophy in adaptive FSGS (iv) Exclude cellular, tip, and collapsing variants
Cellular
(i) At least 1 glomerulus with endocapillary hypercellularity (including foam cells, macrophages, and endothelial cells) involving >25% of the glomerular tuft, leading to occlusion of the capillary lumen (ii) Exclude tip and collapsing variants
Tip
(i) At least 1 segmental lesion involving the “tip” domain (the outer portion of the glomerular tuft next to the origin of the proximal tubule) (ii) Either ECM adhesion or confluence of podocytes with parietal or tubular epithelial cells (iii) Exclude collapsing variant and perihilar sclerosis/endocapillary hypercellularity
Collapsing
(i) At least 1 glomerulus with collapse and overlying podocyte hypertrophy and hyperplasia (ii) Hyperplastic podocytes may fill urinary space, resembling crescents (iii) May have tubular injury and microcysts
