Week 2 - Mary

I just finished my second week of the summer immersion program at Weill Cornell. Along with continuing to shadow Dr. Prince, I had the chance this week to shadow Dr. Shimonov at the Rogosin Institute, a nephrologist specializing in treating patients with ADPKD.

During one of his clinic days, I sat in on his routine checkup meetings with ADPKD patients at varying stages of the disease, ranging from those being monitored because of family history to those on dialysis and awaiting a kidney transplant. One case stood out in particular to both Dr. Shimonov and me: a patient had come in who was taking GLP-1 agonists for weight loss, and their liver volume had decreased substantially. While the change was most likely driven by a drop in liver fat content, it was striking all the same, since there are currently no drugs that can reverse the course of either liver or kidney PKD. The best option on the market right now is Tolvaptan, but even that only slows kidney growth. Seeing this firsthand made it easy to understand why Dr. Prince has been so enthusiastic about his longitudinal studies of volume.

 

Beyond shadowing, I also refined and expanded the background for my research project, which will examine how kidney volume changes over the course of a patient’s treatment. After a kidney transplant, renal function improves while the volume of the native kidneys decreases. No one is entirely sure why this happens, much like the GLP-1 case, but it is very reproducible. For a while, it was thought that the mTOR pathway might be the culprit, since it normally drives the cyst growth that enlarges these kidneys in the first place, and many transplant patients are placed on immunosuppressants that block it. 


One randomized pilot study even looked at whether an mTOR-pathway anti-rejection drug might be driving the effect. It compared ADPKD transplant patients on sirolimus, which inhibits mTOR, with those on mycophenolate and found that native kidney volume shrank by a similar amount in both groups, with no significant difference between them. In other words, the volume decrease showed up regardless of which immunosuppressant the patients received, which deepens the mystery rather than resolving it. What makes it even harder to explain is that, while it makes intuitive sense that a kidney transplant would ease the strain on the native kidneys, it is not obvious why the native kidneys would actually shrink rather than simply stay the same size. This is because once these fluid-filled cysts grow beyond a couple of millimeters, most detach from the parent nephron and become isolated from the urinary space, so they are no longer connected to the filtration system that the new kidney has taken over.


This question of how to pinpoint the correct drug treatment ties in nicely with the lecture Dr. Elemento gave on Tuesday. As he explained, if we can pinpoint the genetic differences that shape how cells and organoids expressing a PKD phenotype respond to different drug combinations, research in this area could move much faster, especially given that the original pharmaceutical for this disease was first developed to treat a different condition. With that framing in mind, my own research project will use Dr. Prince's advanced volume-measurement tool to examine the Weill Cornell cases. The goal is to measure volume changes and, beyond that, to examine whether there is a difference between the PKD1 and PKD2 subtypes, something that, as far as I can tell, has not been reported before. The novelty of our study will stems from an observation the lab has already made through routine radiology work: some patients who receive a kidney transplant do not show as dramatic a decrease in volume. The question we want to ask is whether there is a common feature shared across those patients.


I am very excited for the weeks ahead as the research gets underway and I continue to shadow both Dr. Prince and Dr. Shimonov.

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