30 December 2004
Background: β<sub>3</sub> integrin subunit is expressed as α<sub>IIb</sub>β<sub>3</sub> integrin on platelets and as α<sub>v</sub>β<sub>3</sub> integrin on a variety of cells including renal endothelial, mesangial and tubular cells. Leu<sup>33</sup>/Pro<sup>33</sup> polymorphism of β<sub>3</sub> 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). Leu<sup>33</sup>/Pro<sup>33</sup> 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, Leu<sup>33</sup>/Pro<sup>33</sup> polymorphism had no impact on renal survival in the Kaplan-Meier analysis (n.s.). Conclusion: Our results indicate that β<sub>3</sub> integrin Leu<sup>33</sup>/Pro<sup>33</sup> polymorphism is not a risk factor or a marker of progression in primary glomerulonephritis.