C-reactive protein as a predictor of hypertension in the Hong Kong cardiovascular risk prevalence study (CRISPS) cohort

Abstract

OBJECTIVE: Inflammation contributes to the development and progression of hypertension. However, whether C-reactive protein plays a causal role in hypertension is questionable. We studied single-nucleotide polymorphisms (SNPs) in the C-reactive protein gene as a determinant of its plasma levels and the propensity to develop hypertension in a population-based prospective cohort of Hong Kong Chinese. METHODS: The genotypes of nine SNPs and plasma C-reactive protein were determined in 1938 unrelated subjects from the Hong Kong Cardiovascular Risk Factor Prevalence Study-2 (CRISPS-2) in 2000–2004. Among 1388 subjects normotensive in CRISPS-2, 1124 subjects had been followed up in CRISPS-3 in 2005–2008, in which 237 subjects developed hypertension. RESULTS: Subjects with prevalent or incident hypertension had significantly higher plasma C-reactive protein level (P , 0.001). Plasma C-reactive protein correlated positively with both systolic and diastolic blood pressures (P , 0.001). Six of the nine SNPs were significantly associated with plasma C-reactive protein level (P , 0.001). The SNPs rs3093068 and rs1800947 were independently associated with higher and lower C-reactive protein levels, respectively, in stepwise linear regression analysis (P , 0.001). Among subjects normotensive in CRISPS-2, plasma C-reactive protein was an independent predictor of developing hypertension in CRISPS-3 (P , 0.005). However, none of the SNPs was significantly associated with blood pressure, prevalent or incident hypertension. CONCLUSION: Genetic variants in the C-reactive protein gene are associated with plasma C-reactive protein level only, but not with hypertension. This suggests that C-reactive protein may not play a direct casual role in the development of hypertension although its plasma level is elevated before the onset of hypertension development.