Lupus nephritis and related renal disease: review from case series.

Abstract

Renal lesions due to systemic lupus erythematosus (SLE) are defined as lupus nephritis (LN), a renal disease characterized by the deposition of immunoglobulin (Ig)G-based immune complexes in the kidney and the appearance of double-stranded DNA and Smith antibodies. In particular, deposition of IgG3, which has strong complement binding properties, under the endothelium or in the mesangium activates the classical complement pathway of C1q, C4, and C3, leading to renal damage. This step is followed by migration of inflammatory cells, including neutrophils and monocytes, which induce inflammation in the glomerular capillaries and cause mesangiolysis and endothelial cell damage, resulting in endocapillary proliferative nephritis. LN is classified as class I to IV depending on the degree of inflammation or as class V in cases of subepithelial deposition of immune complexes in glomeruli. Deposition in the renal small arterioles by the same mechanism induces thrombus formation, resulting in lupus vasculopathy. Deposition in the tubular basement membrane and peritubular capillaries leads to tubulointerstitial lupus nephropathy. The appearance of antiphospholipid antibodies leads to acute and chronic forms of antiphospholipid antibody nephropathy (APSN) due to thrombus formation. This article reviews cases of the typical diverse renal lesions in LN.