PMC8631422_01
Patient 1. Light microscopy shows an intact glomerulus without hypercellularity or thickened glomerular capillary walls (A). By electron microscopy, there is prominent widening of the subendothelial space by edema, cell debris, and amorphous proteinaceous deposits (B). X10,000.
fimmu-12-780107-g001.jpg
PMC8631422_01_fimmu-12-780107-g001.jpg
f1
TMA was diagnosed (see  Table 4  and  Figure 1 ) and subsequent assessment for MAHA and secondary causes of TMA was unremarkable.
PMC8631422_02
Patient 2. Light microscopy shows an intact glomerulus without hypercellularity or thickened glomerular capillary walls (A). By electron microscopy, there is prominent widening of the subendothelial space by edema, cell debris, and amorphous proteinaceous deposits. Partial basement membrane reduplication is present (B). X8,000.
fimmu-12-780107-g002.jpg
PMC8631422_02_fimmu-12-780107-g002.jpg
f2
TMA was diagnosed (see  Table 4  and  Figure 2 ) and subsequent assessment for MAHA, underlying genetic mutations, and secondary causes of TMA was unremarkable.
PMC8631422_03
Patient 3. Light microscopy shows an intact glomerulus with prominently thickened capillary walls and segmental mesangial hypercellularity (A). By electron microscopy, there is prominent widening of the subendothelial space by edema, cell debris, and amorphous proteinaceous deposits. Basement membrane reduplication is complete (B). X8,000.
fimmu-12-780107-g003.jpg
PMC8631422_03_fimmu-12-780107-g003.jpg
f3
Table 4  and  Figure 3 ).