I've written about the ciliary hypothesis of cystic kidney disease before, and it is one of my personal research interests: defects in renal primary cilia are the common pathogenesis of renal cyst formation. Despite large advantages in understanding cystic kidney diseases, however, there remains one really large, looming question: what exactly does the cilia do in normal physiology? Some studies suggest that the cilium is a rigid antennae, functioning to sense urine flow, but it is still not clear how this connects with the pathogenesis of cystic kidney disease.
One potential clue to cilia function has come from recent studies which demonstrate that the cilia grows longer in response to kidney injury. Previously, these results have been limited to animal studies; a recent article in JASN by Verghese et al however illustrates that cilia lengthening occurs in human kidneys subjected to ATN! Their study design was fairly clever: they performed cilia staining on serial biopsies of donor kidneys at the time of harvest (prior to any ATN changes having taken place) and then at 6-days post-transplant (after which ATN-like changes were present). They found a striking doubling in average cilia length following ATN (compare the image on the right to the one on the left; the cilia is the green thread-like structure sticking into the lumen of the tubule).
Why is cilia length increasing? Is it simply an abnormal reaction to tubular injury? Or could increasing the length of the cilium somehow be an adaptive response which aids in the recovery of nephron function? The answer is not clear from this study alone, but understanding this phenomenon could turn out to be an important step forward in figuring out the precise role of renal cilia.
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