Moreover, the potential for overt AKI having a deleterious role in driving PKD pathogenesis is supported by studies showing that ischemic AKI superimposed on postnatal mice with induced Itf88 or Kif3α homozygous deletion (leading to deciliation) or with a one-allele loss of Pkd1 accelerates cyst progression compared to non-ischemic mice36, 52, 53. Here, KIF3A is linked to acute kidney injury.