I gained 92 pounds over the course of a few months before I finally understood what was happening to my body.
I was 23, wrapping up graduate school, rushing to finish my capstone ahead of the deadline — because that’s apparently how you handle a graduate degree — and ready to conquer the world. I came back from a beach trip in August of 2016 and noticed I was a little heavier than usual. As any former athlete would do, I assumed I needed to work out more. Two-a-day workouts became my new normal.
I kept gaining weight.
Once I noticed my legs were swelling — and pitting when I pressed into them — I knew something was actually wrong. I saw my primary care doctor, who initially thought I’d had too much salt in a few meals. Fast food, probably. Dietary choices causing edema. Nothing serious.
The swelling continued.
Urgent care. Blood testing. Minimal findings. Back to primary. More blood work. A suspicion it might be my kidneys. A referral to a nephrologist. A kidney biopsy. And finally, a diagnosis I had never heard of in my life.
Minimal Change Disease (MCD).
What is MCD?
Glad you asked — everyone else has.
Your kidneys are filters. They’re supposed to keep the good stuff — protein, nutrients — inside your body and send the waste out. In MCD, that filter breaks down. Without warning. Sometimes without an obvious trigger. When it breaks, protein pours out into your urine instead of staying where it belongs.
The result is swelling. Fatigue. Brain fog. Weight gain that happens faster than you can track it. My feet had to stay elevated constantly just to keep fluid from pooling in my toes. I wore compression socks around the clock. Sleep was nearly impossible. Food lost its appeal entirely. My body was retaining fluid faster than I could process what was happening — legs, abdomen, face, places you don’t expect to swell. I didn’t look sick the way people picture sick. I looked like a completely different person.
92 pounds. I’ll let you sit with that number for a second.
The treatment is high-dose prednisone — a powerful steroid that works, but carries its own significant consequences with repeated use. Bone density loss, adrenal suppression, increased infection susceptibility, metabolic changes, and long-term cardiovascular impact that compounds with every course. The goal is to beat the relapse back into remission and hope it stays there.
Sometimes it does. Sometimes it doesn’t.
Mine mostly hasn’t.
The Relapses
Over the last decade I have had nine relapses — and I am currently in an active one as I write this. Ten rounds of high-dose prednisone. If that sounds like a lot, it is.
By some combination of disease biology, environmental factors, and what I now suspect were COVID-era behavioral changes that inadvertently reduced my allergen exposure — I was given a 4.5-year remission window. No relapses. No medication. October 2020 through February 2025. I genuinely thought I might be done with this thing. My doctor mentioned that some people in my position simply grow out of the disease.
I have largely stopped believing that about myself.
February 2025 created what I now think of as the perfect storm. Our daughter was born on February 8th — the greatest day of my life, and also, as it turns out, a significant physiological and psychological stressor on an immune system already four and a half years removed from its last treatment course. Atlanta’s tree pollen spiked to more than double the count that preceded my last February relapse. Sleep deprivation became a new full-time job. And somewhere in the middle of all of it, my disease woke back up.
I’ve relapsed three times since — including twice while on a second medication added specifically to prevent it. Wild.
The Question I’m Now Asking
Here’s where the story gets interesting — and honestly, where I think it starts to matter beyond just my own situation.
While in the middle of relapse number nine, I started pulling a thread I had never pulled before — going back through my medical records, lab work, and every piece of relevant environmental data I could find for the last ten years.
What I found was consistent enough that I couldn’t ignore it.
Every single relapse I’ve had occurred during a period of elevated pollen, elevated mold, or both. In nine years I have never once relapsed in December or January — the two months when Atlanta’s allergen calendar goes quiet. My antihistamine use has escalated from occasional to daily over the last few years. And recent blood work revealed a total IgE — the antibody your immune system produces in response to allergens — nearly 15 times the upper limit of normal. That number was drawn while I was already on steroids known to suppress most immune markers.
I have never been treated for allergies.
There is published, peer-reviewed research showing that elevated IgE independently predicts delayed MCD remission and earlier relapse. There is a documented molecular connection between the immune pathway driving allergic disease and the one that drives MCD. And there is a growing body of evidence suggesting that untreated allergen burden may not be coincidental in a patient like me — it may be one of the reasons the fire keeps reigniting.
The Hypothesis
I am not saying allergies caused my kidney disease. That’s not what the science supports, and I’m not going to claim it.
What I am saying is this: my immune system appears to be constitutionally overactive — constantly running at an elevated baseline due to a daily allergen burden that has never been addressed. My working theory is that this chronic immune activation may lower the threshold at which my Minimal Change Disease triggers. When the system is already under pressure, it may not take much to push it over the edge.
Given that elevated IgE is a documented predictor of MCD relapse frequency in published literature, I am pursuing a straightforward hypothesis: if I can bring my IgE down — through treatment, lifestyle changes, dietary adjustments, environmental controls, or some combination of all of them — it may reduce how often my kidneys relapse. If my immune system operates at a lower baseline, the bar for triggering a relapse may be harder to reach.
I may never be able to prove this conclusively. Geographic relocation is one variable I’m considering, and I’ll be the first to acknowledge that isolating its impact from a clinical standpoint is nearly impossible. But the data is real, the research is real, and the treatment gap is real. At minimum, treating a confirmed allergic disease I’ve had for a decade and never addressed seems like a reasonable place to start.
Maybe I’m my own lab rat.
I’m documenting this entire journey — the research, the appointments, the data, the decisions, the outcomes. The hard days and the breakthroughs. All of it, as it happens, not in hindsight. If I’m wrong, at least I tried. In the world we live in today, information is more accessible than it has ever been — and I intend to use every bit of it.
Currently on the investigation list: Chronic Autoimmune Urticaria and Mast Cell Activation Syndrome — two conditions that have been raised as potential additional factors given my labs and symptom history. Whether they end up being part of the picture or not, I want to know.
The journey continues.
— LP
Logan Pethel 
Leave a comment