Objectives: Pre-eclampsia is an important cause of maternal and fetal morbidity and mortality worldwide. Hyperhomocyst(e)inemia in pregnancy is associated with an increased risk of preeclampsia in most studies. Nutritional and genetic factors regulate homocyst(e)ine levels. A missense mutation 677 C→T in the gene for methylenetetrahydrofolate reductase (MTHFR) has been associated with an increased pre-eclampsia risk in some, although not most, previously studied populations. Methods: To further understand the role of this polymorphism in the etiology of pre-eclampsia, we genotyped a total of 125 pre-eclamptics and 179 normotensive pregnant Peruvian women. Results: The wild-type allele frequency among cases and controls was 54% and 58%, respectively. Twenty per cent of cases and 17% of controls were homozygous for the 677 C→T MTHFR genotype (T/T). After adjustment for confounding by covariates including maternal age, nulliparity, prepregnancy body mass index and use of prenatal vitamins, women homozygous for the 677 C→T MTHFR genotype (T/T) experienced a modest, statistically non-significant increased risk of preeclampsia (adjusted OR 1.6, 95% CI 0.7, 3.8). Maternal folate deficiency was associated with a statistically non-significant doubling in risk of pre-eclampsia in this population (adjusted OR 2.0, 95% CI 0.9, 4.3). Conclusions: There was no evidence to suggest that pre-eclampsia risk is positively associated with the T/T genotype overall, or in the context of folate deficiency.