Among the 578 patients with idiopathic membranous nephropathy, 12 (2%) patients were identified as THSD7A-positive: ten patients were THSD7A-positive alone, which accounted for 16% (ten of 64) of PLA2R-negative patients; two patients were dual-positive for both anti-THSD7A and anti-PLA2R antibodies and showed enhanced expression of both antigens colocalized in glomeruli.
Renal biopsy revealed MN and immunohistochemistry (IHC) showed enhanced staining of THSD7A as well as PLA<sub>2</sub>R along the glomerular basement membrane whereas the serum level of THSD7A and PLA<sub>2</sub>R were both within normal range.
The thrombospondin type-1 domain containing 7A (THSD7A) protein is known to be one of the antigens responsible for the autoimmune disorder idiopathic membranous nephropathy.
Here, we studied the presence of anti-PLA2R and anti-THSD7A antibodies in patients with biopsy-proven IMN (n = 212), secondary membranous nephropathy (SMN, n = 118), and other kidney diseases (n = 84).
In idiopathic membranous nephropathy (IMN) the immune complexes are formed by circulating antibodies binding mainly to one of two naturally-expressed podocyte antigens: the M-type receptor for secretory phospholipase A2 (PLA2R1) and the Thrombospondin type-1 domain-containing 7A (THSD7A).
Idiopathic membranous nephropathy (IMN) has recently attracted much attention due to the development of auto antibodies, anti-phospholipase A2 receptor and anti-thrombospondin type I domain-containing 7A on podocytes, the establishment of immune networks complexes in circulation as well as the development of autoreactive immune cells against kidney, in both innate and adaptive participants.