TNF and hypertensive disorder: This further confirmed the independent association of Met235Thr, T>C (-344) and G>A (-1903) SNPs with CRI and suggests that these SNPs though known to modulate RAAS activity, does not operate through hypertension as a crucial mechanism but via stimulation of chemokines like TGF β1, TNF α and IL1 [48,49], thus warranting further investigations of such genes.