Influence of beta3 integrin gene Leu/Pro33 polymorphism on primary glomerulonephritis.

BACKGROUND

Beta3 integrin subunit is expressed as alpha(IIb)beta3 integrin on platelets and as alpha(v)beta3 integrin on a variety of cells including renal endothelial, mesangial and tubular cells. Leu33/Pro33 polymorphism of beta3 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 beta3 integrin Leu33/Pro33 polymorphism is not a risk factor or a marker of progression in primary glomerulonephritis.