“…Referring to the highest tested PFOA concentration (2 mg L −1 ), the reported architecture disarrangement agrees with the known morphopathological evidences of glomerulonephrosis (i.e., the morphofunctional alteration of the glomerular filtration barrier), with particular regard to podocyte effacement [ 9 , 11 , 48 , 58 , 66 , 67 ]. Though PFOA and other PFAS can accumulate at high concentrations in the kidney and potentially affect renal function, no previous research has specifically addressed the effect of these pollutants on the glomerular filtration barrier [ 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 ], making it difficult to interpret and compare the observed alterations and speculate about the possible underlying pathophysiology. Interestingly, none of the lesions seen in other anatomical districts (namely mitochondrial cristolysis, vesiculation, swelling, and ballooning, autophagosomes occurrence, rough endoplasmic reticulum degranulation, disarrangement and enlargement in hepatocytes [ 54 ]; increased number and volume of cytoplasm vesiculations in cells of the first proximal tubular segment, mitochondrial focal vesiculation in cells of the distal tubular segment and of the collecting ducts in kidney [ 22 ]; rough endoplasmic reticulum enlargement and fragmentation, cytoplasm vacuolation, enhanced phagolysosomes formation in thyroid follicles [ 45 ]) were appreciated at the level of glomerular filtration barrier, suggesting a somewhat different pathogenesis compared to the previous tissues.…”