A world-wide coronavirus pandemic is in full swing and, at the time of writing, there are only few treatments that have been successful in clinical trials, but no effective anti-viral treatment has been approved . Because of its lethality, it is important to understand the current strain's effects and mechanisms not only in the respiratory system, but in other affected organ systems as well . Past coronavirus outbreaks caused by SARS-CoV and MERS-CoV inflicted life-threatening acute kidney injuries (AKI) on their hosts leading to significant mortality rates, which went somewhat overlooked in the face of the severe respiratory effects . Recent evidence has emphasized renal involvement in SARS-CoV-2, stressing that kidneys are damaged in COVID-19 patients . The mechanism by which this virus inflicts AKI is still unclear, but evidence from other coronavirus strains may hold some clues . Two theories exist for the proposed mechanism of AKI : 1) the AKI is a secondary effect to reduced blood and oxygen levels causing hyperinflammation and 2) the AKI is due to cytotoxic effects . Kidneys express angiotensin-converting enzyme-2 (ACE2), the confirmed SARS-CoV-2 target receptor as well as collectrin, an ACE2 homologue, that localizes to the primary cilium, an organelle historically targeted by coronaviruses . While the available literature suggests that kidney damage is leading to higher mortality rates in COVID-19 patients, especially in those with pre-existing kidney and cardiovascular diseases, the pathogenesis of COVID-19 is still being investigated . Here, we present brief literature review supporting our proposed hypothesis of a possible link between SARS-CoV-2 cellular infection and cilia.