Influence of β ₃ Integrin Gene Leu ³³/Pro ³³ Polymorphism on Primary Glomerulonephritis

Abstract

Background: β₃ integrin subunit is expressed as α_IIbβ₃ integrin on platelets and as α_vβ₃ integrin on a variety of cells including renal endothelial, mesangial and tubular cells. Leu³³/Pro³³ polymorphism of β₃ integrin has been associated with altered platelet functions, cardiovascular complications and the incidence of acute rejection episodes in renal transplantation. We investigated its influence on IgA nephropathy (IgAN), focal segmental glomerulosclerosis (FSGS) and membranous glomerulonephritis (MGN). Methods: We studied 251 patients with biopsy-proven primary glomerulonephritis (IgAN n = 127, FSGS n = 71, MGN n = 53) followed up for 6.3 ± 5.3 years and 100 control subjects. Patients were classified according to the slope of reciprocal serum creatinine into slow (n = 162) and fast progressors (n = 89). Leu³³/Pro³³ polymorphism was determined by PCR amplification followed by restriction with the endonuclease Bcnl. Results: The genotype frequencies were similar in patients and controls (n.s.). Initial renal function, proteinuria and blood pressure did not differ significantly between patients with different genotypes (n.s.). The genotype frequencies were similar in slow and fast progressors (n.s.). Furthermore, Leu³³/Pro³³ polymorphism had no impact on renal survival in the Kaplan-Meier analysis (n.s.). Conclusion: Our results indicate that β₃ integrin Leu³³/Pro³³ polymorphism is not a risk factor or a marker of progression in primary glomerulonephritis.