Renal Tubular Acidosis
I still have a lot to learn about renal tubular acidosis (RTA). It’s not something you hear about everyday. The journey started when I was getting a CT scan for shortness of breath and an elevated D-dimer. I have an allergy to the contrast in both CTs and MRIs (thanks mast cells), so I had to have the premedication protocol and stay in observation.
Once my CT was done, bloodwork showed my CO2 (carbon dioxide) at 15 mmol/L and my lactic acid was over 4 mmol/L. Both of these levels were very much outside of the normal ranges. The doctor there asked if I had ever had a renal (kidney) work-up done. I told him that I didn’t have any known kidney problems, but I would look into it. My levels stabilized on its own after a couple of days and wasn’t a top priority at the time. Several months later, I had to have prednisone for an upper respiratory infection and I felt pretty terrible afterwards, so I went to the ER. My CO2 was low again and I started seeing a pattern from previous bloodwork. It seemed like I had what’s called steroid-induced lactic acidosis (low pH brought on by high lactic acid). While this is a different mechanism from renal tubular acidosis, it started my research into the subject.
The final straw was when I started a GLP-1, Mounjaro, for metabolic syndrome. I had been tolerating it well, up until I reached my 3rd dose of 7.5mg. About 10 minutes after taking it, I immediately felt so weak I fell to my knees. I got very dizzy and confused, so I decided to go to the ER. I couldn’t walk and had to be wheeled in by my husband. I felt like I couldn’t catch my breath, and of course, the medical gaslighting began once my oxygen level came back at 99%. I started feeling intense bone pain and numbness. I was given Valium, which helped some, and I was told my initial labs looked fine. They couldn’t figure out what was going on and were planning to discharge me, so I asked for a neurology consult. This is key to advocating for yourself. If your symptoms (such as an inability to walk) fit into a specialty (like neurology), it is well within your rights to request a consult.
The consult was done via telemedicine from a doctor in Florida, but he is the one that saved me. He requested a phosphorus level, which I found out had NEVER been tested before. It was at 0.8 mg/dL, which is a life-threatening level. I also found out my CO2 was 17 mmol/L, NOT normal. These two levels were the key to finding out I had RTA, likely present since I was born, as I later found a variant for RTA type 2 in my WGS (whole gene sequencing) on the SLC4A4 gene. Anti-inflammatories (such as NSAIDS, steroids, and quite possibly the GLP-1) caused the RTA to show itself.
After treatment with a bag of sodium bicarbonate and phosphorus, I went home and started researching. Low CO2 is a sign of metabolic acidosis (low blood pH) and can happen when the kidney’s tubules can no longer either reabsorb bicarbonate (type 2) or remove acid (type 1). Low phosphorus and low potassium are common findings because the kidneys waste these electrolytes when trying to normalize your blood pH. Type 1 is a major cause of calcium deposits in the kidneys and kidney stones.
There is also Type 3, which is a mix of Type 1 & 2. And there is Type 4, which is when aldosterone levels are low or the body has resistance to aldosterone. This type usually has high levels of potassium and is also caused by diabetic nephropathy, as well as certain medications, like NSAIDS.
Additionally, low vitamin D can cause RTA by increasing PTH levels. High PTH levels (a hormone from the parathyroid gland) causes bones to release calcium and phosphorus (thus leading to increased levels that are later wasted in the urine), as well as interfere with the kidney’s ability to reabsorb bicarbonate (type 2). The body can overproduce PTH, due to primary hyperparathyroidism or secondarily due to a cause, such as a tumor on the parathyroid gland, resulting in the condition.
One hallmark sign of renal tubular acidosis is what they call non-anion gap, hyperchloremic (high chloride) acidosis. Chloride is a negative ion (think back to chemistry class) which rises when bicarbonate is lost (since it’s also a negative ion) to try and keep the electrical charge in the blood neutral. Sodium, which is a positive ion, can cause the blood to be too positive when bicarbonate is lost, so the body tries to compensate. Many times if the loss is mild (also called “incomplete” RTA), CO2 is borderline or low normal and chloride is on the higher side. Chloride is tested in a standard CMP, alongside potassium (but not phosphorus – which has to be tested separately or with a renal panel).
I looked back into my lab history as far back as I could, and most of the time my chloride was 107 or greater, so on the high-end of normal. This allowed the compensated RTA to stay hidden for most of my life. However, this type of tug-of-war causes bone loss and short stature for many with the condition, not to mention fatigue, muscle weakness, palpitations, and brain fog from the electrolyte instability.
Take a look at your past labs and see if you have the following: borderline or low CO2 levels, borderline or low potassium, high or borderline-high chloride, or low vitamin D. Also, if you haven’t had a phosphorus level done, next time you feel weak or have shortness of breath (also called “air hunger” – a description that might make medical professionals think twice) make sure to have your CO2 and phosphorus checked. It might just help solve a medical mystery.
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