Relationships among adiponectin gene polymorphisms, proteinuria and increased blood pressure in the context of placental diseases.

The etiology and pathogenesis of preeclampsia remain unclear. Little is known about the possible impact of adiponectin gene polymorphisms on the pathogenesis of preeclampsia. In this study, we analyzed the association of two adiponectin single-nucleotide polymorphisms (SNPs) with preeclampsia. One hundred eighty-eight Han Chinese pregnant women were enrolled (81 normal-term, 20 mild preeclampsia and 87 severe cases). Serum adiponectin level, and adiponectin exon 2 SNP +45T/G (rs2241766) genotype and intron 2 SNP +276G/T genotype (rs1501299) and their allele distributions were tested with enzyme-linked immunosorbent assay and PCR-restriction-fragment length polymorphism, respectively. There were no significant differences among the three groups (P>0.05) in genotype distribution or allele frequencies of either SNP. Systolic pressure and 24-h urinary protein were lower in TT homozygotes than those in TG+GG patients at SNP +45T/G in the severe preeclamptic group (P<0.05). Furthermore, blood pressure, serum adiponectin level and 24-h urinary protein were lower in GG homozygotes than those in TG+TT patients at SNP +276G/T in the severe preeclamptic group (P<0.05). The risk of high blood pressure (≥160/110 mm Hg) and of high serum adiponectin in T-allele carriers at +276G/T in the severe preeclamptic group were 5.345 and 5.818 times higher, respectively, compared with GG patients. These data suggest that adiponectin +45T/G and +276G/T polymorphisms are associated with important clinical manifestations of preeclampsia and that polymorphism +276G/T is associated with serum adiponectin level. Taken together, these findings suggest that adiponectin gene polymorphism is involved in the pathogenesis of preeclampsia.