Renal agenesis is a medical condition in which one (unilateral) or both (bilateral) fetal kidneys fail to develop. Unilateral and bilateral renal agenesis in humans, mice and zebra fish has been linked to mutations in the gene GREB1L. It has also been associated with mutations in the genes RET or UPK3A in humans and mice respectively. Type Bilateral Bilateral renal agenesis is a condition in which both kidneys of a fetus fail to develop during gestation. It is incompatible with life. It is one causative agent of Potter sequence. This absence of kidneys causes oligohydramnios, a deficiency of amniotic fluid in a pregnant woman, which can place extra pressure on the developing baby and cause further malformations. The condition is frequently, but not always the result of a genetic disorder, and is more common in infants born to one or more parents with a malformed or absent kidney. Unilateral This is much more common, but is not usually of any major health consequence, as long as the single kidney is healthy. However, this kidney tends to be hypertrophied, ectopic and prone to infection and damage. It may be associated with an increased incidence of Müllerian duct abnormalities, which are abnormalities of the development of the female reproductive tract and can be a cause of infertility, blocked menstrual flow (hematocolpos), increased need for Caesarean sections, or other problems. Herlyn-Werner-Wunderlich syndrome is one such syndrome in which unilateral renal agenesis is combined with a blind hemivagina and uterus didelphys. Up to 40% of women with a urogenital tract anomaly also have an associated renal tract anomaly. Adults with unilateral renal agenesis have considerably higher chances of hypertension (high blood pressure). People with this condition are advised to approach contact sports with caution. A possible complication later in life of unilateral renal agenesis is Focal Segmental Glomerular Sclerosis (FSGS) which will cause nephrotic syndrome, potentially resulting from glomerular overload. Genetics In 2008 researchers found autosomal dominant mutations in the RET and GDNF genes to be linked to renal agenesis in unrelated stillborn fetuses through PCR and direct sequence analysis. In the study, DNA from 33 stillborn fetuses were sequenced for mutations in RET, GDNF and GFRA1. Nineteen of the fetuses had BRA, ten had URA and 4 had congenital renal dysplasia. Seven of the 19 BRA fetuses were found to have a mutation in the RET gene (37%), while two of the ten