PMC7338606_01
Renal biopsy data for Case 1: (A) light microscopy 40x silver stain Double contours and segmental scar; (B) light microscopy 40x silver stain Double contours with endocapillary hypercellularity and segmental scar; (C) light microscopy 40x hematoxylin and eosin cellular crescent with segmental karyorrhexis; (D) light microscopy 40x hematoxylin and eosin tubulointerstitial inflammation; (E) immunofluorescence IgG staining; (F) immunofluorescence showed C3 staining > IgG staining. (G) Electron microscopy, subendothelial deposits (red arrows); (H) electron microscopy, subepithelial deposits (red arrows); (I) electron microscopy, mesangial deposits (red arrows).
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F1
On renal biopsy (Figure 1), the dominant finding by light microscopy was an MPGN pattern of injury that was predominantly chronic with segmental sclerosis, extensive global glomerulosclerosis, and parenchymal scarring.
PMC7338606_02
Renal biopsy data for Case 2: (A) light micrographs demonstrating a diffuse and global membranoproliferative glomerulonephritis pattern of injury periodic acid Schiff (PAS) stain; (B) Jones silver stain (40x magnification) demonstrating glomerular basement membrane double contours; (C,D) immunofluorescence micrographs demonstrating diffuse global bright mesangial and capillary loop C3 staining; (E,F) electron micrographs demonstrating numerous mesangial, subepithelial, and intramembranous deposits. Several subepithelial deposits show "hump-like" morphology. Capillary loop double contours with cellular interpositions are also present.
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F2
These parameters remained essentially unchanged for 2 years, at which time a renal biopsy (Figure 2) was performed.
PMC7338606_03
Renal biopsy data for Case 3: (A-C) First renal biopsy demonstrating (A); light microscopy with Jones silver stain demonstrating membranoproliferative pattern of injury 40x; (B) immunofluorescence demonstrating dominant C3 binding in a segmental confluent granular to pseudolinear pattern; (C) electron microscopy showing dense deposits within segments of the basement membrane, it also shows electron dense deposit-like aggregates in scattered subepithelial and intramembranous areas; (D-F) second renal biopsy re-demonstrates a membranoproliferative pattern of injury, C3 dominant binding on immunofluorescence and dense deposits.
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F3
Kidney biopsy at that time revealed DDD with 45% active crescents and marked acute tubulointerstitial injury (Figures 3A-C). The tubulointerstitium showed interstitial inflammation with focal intratubular neutrophils and cellular debris suggestive of acute pyelonephritis, as well as evolving parenchymal scarring (Figures 3D-F).