Table 1.

Pathomechanisms of LN inside the kidney

Glomerular Pathology	Tubulointerstitial Pathology
Mesangial and subendothelial, immune complex deposits, complement activation	Immune complex deposits in periglomerular vessels
Fc, Toll-like, and complement receptor activation	Complement activation
Activation of renal cells and infiltrating leukocytes (subepithelial IC causes LN class V and podocyte injury with massive proteinuria)	Activation of endothelial cells, luminal adhesion molecules
Local cytokine expression	Leukocyte recruitment
Recruitment of leukocytes	Local antibody production by B cells including tertiary lymphoid organ formation
Proliferation of endothelial and mesangial cells	Cytotoxic and Th17 T cells
Filtration barrier damage causing proteinuria and hematuria	Proapoptotic cytokines
Renal cell necrosis causing focal scaring	Proximal tubular cell damage causing proteinuria
Proliferation of parietal epithelial cells and crescent formation	Tubular/vascular atrophy
Periglomerular inflammation	Hypoxia → inflammation
Global glomerulosclerosis	Insufficient tubular and vascular repair plus ischemia promotes interstitial fibrosis