Editing Potter sequence (section)

==Causes==
{{Further|Oligohydramnios}}
The Potter sequence is due to restricted ability for certain organs to grow due to severe [[oligohydramnios]].{{cn|date=August 2024}}

In one study, the causes leading to Potter sequence were bilateral [[renal agenesis]] in 21.25% of cases; [[polycystic kidney disease|cystic dysplasia]] in 47.5%; [[obstructive uropathy]] in 25%; and others in 5.25%.<ref>{{cite web|url=https://rarediseases.info.nih.gov/diseases/4462/potter-syndrome|title=Potter syndrome|website=Genetic and Rare Diseases Information Center (GARD) at the [[National Center for Advancing Translational Sciences]]|access-date=2017-11-16|archive-date=2017-11-16|archive-url=https://web.archive.org/web/20171116185801/https://rarediseases.info.nih.gov/diseases/4462/potter-syndrome|url-status=dead}} Last updated: 2011</ref>

===Bilateral renal agenesis===
{{Main|Renal agenesis}}
Bilateral renal agenesis has been estimated to occur at a frequency of approximately 1:4000 to 1:8000 fetuses and neonates. However, recent analysis has estimated that the condition may occur at a much greater frequency. The condition has been reported to occur twice as commonly in males as in females, suggesting that certain genes of the [[Y chromosome]] may act as modifiers. However, no candidate [[gene]]s on the Y chromosome have yet been identified.{{citation needed|date=April 2021}}

BRA appears to have a predominantly genetic [[etiology]] and many cases represent the most severe manifestation of an [[autosomal dominant]] condition with incomplete penetrance and variable expressivity. There are several genetic pathways that could result in this condition. In 2017 researchers identified heritable autosomal dominant mutations in the gene [[GREB1L]] in two unrelated families as being the cause of both BRA and URA utilizing [[exome sequencing]] and direct sequence analysis.<ref name="Brophy PD, Rasmussen M, Parida M, Bonde G, Darbro BW, Hong X, Clarke JC, Peterson KA, Denegre J, Schneider M, Sussman CR, Sunde L, Lildballe DL, Hertz JM, Cornell RA, Murray SA, Manak JR 2017 215–228">{{cite journal| pmid=28739660 | doi=10.1534/genetics.117.1125 | volume=207 | title=A Gene Implicated in Activation of Retinoic Acid Receptor Targets Is a Novel Renal Agenesis Gene in Humans | year=2017 |vauthors=Brophy PD, Rasmussen M, Parida M, Bonde G, Darbro BW, Hong X, Clarke JC, Peterson KA, Denegre J, Schneider M, Sussman CR, Sunde L, Lildballe DL, Hertz JM, Cornell RA, Murray SA, Manak JR | journal=Genetics | issue=1 | pages=215–228| pmc=5586373 }}</ref> This is the first reported genetic lesion implicated in the activation of [[retinoic acid receptor]] (RAR) targets that has been associated with renal agenesis in humans. The majority of other possible candidate genetic pathways are [[autosomal recessive]] in nature and do not coincide with the frequency or penetrance at which BRA typically occurs in the human population. Additionally, candidate genetic pathways would be expected to involve genes expressed in the developing [[urogenital]] system (UGS). Often, these same genes and/or pathways of interacting genes are also expressed in the developing UGS as well as the [[central nervous system]] (CNS), gut, lung, limbs, and eyes.{{citation needed|date=April 2021}}