Expression of Foxp3 in renal tissue of patients with HBV-associated glomerulonephritis and their clinical and pathological characteristics.

Our study retrospectively investigated the expression of forkhead/winged helix transcription factor (Foxp3) in renal tissue and clinical features of patients with hepatitis B virus (HBV)-associated glomerulonephritis (HBV-GN). A total of 58 patients with HBV-GN were assigned to group A; 45 serum and renal tissue HBsAg-negative patients with nephritis were group B; 24 serum HBsAg-positive and renal tissue HBsAg-negative patients with slightly increased serum creatinine without nephritis were group C. Clinical manifestations, laboratory indices and renal biopsies were recorded. Expression of Foxp3, CD4 and CD25 in renal tissue was detected by immunohistochemistry. In group A, 74.1% were serum HBeAg-negative, with serum complement C3 level of 0.99±0.27 g/l, and deposition rates of renal complement C3 and C1q in renal tissue of 34.9 and 16.3% respectively; 25.9% were serum HBeAg-positive, with serum complement C3 level of 0.19±0.17 g/l, and deposition rates of renal complement C3 and C1q in renal tissue of 80 and 46.7%, respectively. A significant difference was found in C3 and C1q between HBeAg-negative and HBeAg-positive group (P<0.05). Increased urinary protein and decreased serum albumin were found in patients in group A with moderate levels of HBV DNA compared with patients with low levels of HBV DNA in the same group over 24 h (P<0.05). The numbers of Foxp3 lymphocytes, CD4 T cells and CD25 T cells in the tubulointerstitium of patients in groups A and B were 3.41±1.16 vs. 3.52±1.27, 2.78±0.15 vs. 3.12±0.17 and 2.90±0.20 vs. 3.09±0.18, respectively. The clinical manifestation of HBV-GN is nephrotic syndrome, and HBV DNA is correlated with urinary protein and serum albumin levels. Activation of C3 and C1q may be related to the pathogenesis of HBV-GN in serum HBeAg-positive patients. Downregulation of Foxp3 expression in regulatory T cells is related to the development and progression of HBV-GN.