Role of antiphospholipid antibodies in kidney disease: Risk factors, immunopathogenesis, and diagnosis

Figure 1  Main targets of antiphospholipid antibody-induced injury in antiphospholipid syndrome nephropathy.

Figure 2 Morphological features of chronic antiphospholipid syndrome nephropathy. A: Low-power view showing subcapsular focal cortical atrophy, a characteristic lesion of chronic antiphospholipid syndrome nephropathy (APSN) (hematoxylin & eosin, 100 ×); B: Low magnification view showing the same lesion on trichrome stain (Masson’s trichrome, 100 ×); C: Another biopsy with chronic APSN showing ischemic solidification of some glomeruli as a result of chronic ischemia (Periodic acid-Schiff [PAS], 200 ×); D: Another area from the latter biopsy showing fibrous intimal thickening observed in chronic forms of APSN (PAS, 200 ×).

Figure 3 Pathogenesis of antiphospholipid syndrome: The dual hit theory explained. Schematic representation of the two-hit theory in antiphospholipid syndrome-mediated renal injury. “First hit” involves the presence of antiphospholipid antibodies in the circulation. “Second hit” refers to any triggering event that leads to thrombus formation when circulating antiphospholipid antibodies bind to β2 glycoprotein I (B2GPI), triggering complement activation, recruitment of inflammatory cells, and thrombus formation.