A rare case of equine renal tubular acidosis

When a Friesian mare stops eating and drinking, the cause turns out to be a rare equine kidney disease with a common antidote.

One skipped meal was all it took to make me worry about my Friesian mare, Amber Van De Dollen. In the four years I had owned her, she had been bright, loving and always appreciative of food. So when I brought her into her stall one July evening last year and she ignored her hay, grain and water to stand quietly in the corner, I knew something was wrong.

The cure of renal acidosis is found in the grocery store.

I immediately took her temperature, which was normal, then listened for, and heard, normal gut noises. I searched her face for a clue to how she felt, and she stared back at me, bright-eyed and calm. I couldn’t find anything wrong beyond her untouched meal. I was worried, but I wasn’t quite sure what I should do or even whether I should call my veterinarian. I went to bed that night hoping I was just overreacting.

But my heart sank the next morning when I peered hopefully into Amber’s stall, only to see that her hay, grain and water remained untouched. I prepared a bran mash, a favorite treat of hers, but she just lipped at it halfheartedly. I’d seen enough; I headed to the phone to call our veterinarian, Carla Francheville, DVM, of Sunny Coast Veterinary in Punta Gorda, Florida.

When Francheville arrived she ran through some possible reasons a horse might not want to eat, a list that included gastric ulcers, colic, a viral infection or dental pain. Then she inspected Amber from poll to hoof, passed a nasogastric tube to look for reflux, used a speculum to look at her teeth, and even did a rectal palpation. But she found no sign of any problem.

With little else to do, Francheville drew some blood for testing and told us to keep an eye on our other horse, D’Avant, for similar signs. If he fell sick, too, we could suspect a common cause, such as some type of contagious infection or maybe a toxic plant in their pasture.

By that evening, Amber still hadn’t eaten or drunk, and Francheville told us she was worried the mare would become dehydrated. She came back out to the farm to administer intravenous fluids and told us to call her in the morning with the good news that Amber was her ravenous self again. Unfortunately, we weren’t able to do that.

Still no answers

Amber continued to ignore her food and water for days, while D’Avant remained healthy. The first round of blood tests came back completely normal, and then so did a second round, as Francheville continued to search for clues. By this time, Amber had had a catheter put in place, and my husband and I were delivering intravenous fluids several times a day to stave off dehydration. Francheville visited daily to feed Amber a slurry of senior feed, electrolytes and probiotics through a nasogastric tube. Our mare, always an easy keeper, wasn’t losing weight, but she required round-the-clock care.

Baffled, Francheville consulted with the clinic at the University of Florida, but without seeing Amber in person the experts there said they couldn’t offer suggestions beyond what we had done. Each day, Francheville and I discussed taking my horse there. In my mind, however, shipping Amber to the university clinic would mean the situation was dire and we were out of other options.

Meanwhile, I reached out to fellow Friesian enthusiasts. I asked officials at the Friesian Horse Association of North America if they had ever heard of one of “our” breed acting in a similar manner. They said they hadn’t but referred me to Klaas Wiersma, DVM, a Canadian veterinarian with extensive experience with Friesians.

The first possibility he raised was botulism, poisoning that causes progressive paralysis of the nervous system first manifested as an inability to chew. Botulism typically develops after a horse consumes contaminated feed. But that didn’t sound right: Horses with botulism want to chew but can’t. Amber could chew but didn’t want to.

Wiersma said he’d keep thinking and ask other veterinarians familiar with the breed. By now it had been nine days since Amber had eaten or drunk anything on her own. My husband and I had closed our business to tend to her 24 hours a day. We were physically exhausted and no closer to an answer. I told Francheville that it was time to head to the university clinic.

“She is very distressed”

The shipper who had brought Amber to us years earlier cleared his schedule to haul her the four hours to Gainesville the next day. Although my mare had hardly ever traveled, she was a champ about it.

I remember checking in at the front desk and hearing the receptionist page the on-call clinician: “Amber is here with Mrs. Strong, and she is very distressed.” It took me a second to realize that the “distressed” one she was talking about was me. The staff compassionately allowed me to accompany Amber.

I had steeled myself for a long and difficult time at the clinic with days of uncertainty followed by terrible news and weeks of treatment. Imagine my shock then when, barely an hour after we’d arrived, Johanna Elfenbein, DVM, DACVIM, came to tell me she knew what was wrong with my horse—and even better, she could fix it.

Amber, Elfenbein explained, had renal tubular acidosis, an exceptionally rare condition with only a handful of documented cases in horses. It occurs when, for unknown reasons, the kidneys stop removing acid (typically in the form of hydrogen ions) from the blood. The resulting buildup of acidity (acidosis) affects metabolic chemical reactions throughout the body. In people, renal tubular acidosis is typically diagnosed when it leads to urinary stones and bone demineralization. In horses, the most common signs are frustratingly vague: depression, poor performance, weight loss and loss of appetite.

Renal tubular acidosis is diagnosed through a “blood gas” test that determines the acid-base status of a horse’s blood. It’s a simple test to perform, but with two catches: It requires specialized equipment most primary veterinarians do not have, and for accurate results the blood must be tested within 20 minutes of being drawn. Francheville had done repeated blood tests on Amber, but she’d had to send the samples out to a laboratory, which took several days.

I marveled to Elfenbein about how she even thought to look for this condition in my horse. She smiled and told me she had just taken her examination to become a certified diplomate in large-animal internal medicine. One of the exam questions had been about renal tubular acidosis.

Sudden reversal

The primary treatment for renal tubular acidosis is probably in your kitchen pantry right now. Sodium bi-carbonate—baking soda—corrects the acid-base imbalance in the blood. Amber stayed at the university for three days, during which time she was given sodium bicarbonate in an intravenous solution, along with electrolytes, fluids and glucose to compensate for the meals she had missed for so long.

Within the first 24 hours, she perked up and began eating on her own. My eyes flooded with tears as I watched her contentedly munching on her hay. Another round of blood tests revealed that her acid-base balance had returned to normal.

Occasionally horses with renal tubular acidosis also have kidney damage, explained Martha Mallicote, DVM, who was coordinating Amber’s ongoing treatment, although it’s not clear whether the acid buildup is a cause or an effect of the disease. We would have to do a kidney biopsy to know for sure, but considering that Amber’s blood tests and urinalysis had revealed no other signs of kidney damage, Mallicote didn’t think a biopsy was necessary. I agreed.

Amber was ready to go home. I, however, was a little nervous about leaving the wonderfully supportive university environment. Mallicote explained that renal tubular acidosis can recur at any time. Not enough is known about the disease to say why or how this might happen, she said, but I’d likely see the same signs: loss of appetite and lethargy. Then we would know to check her blood acidity immediately.

Mallicote also suggested a preventive measure: If I gave Amber a little baking soda each day, I might be able to stop a recurrence from happening. That sounded like a terrific plan to me.

Now, a year later, Amber is still eating with enthusiasm. Twice a day, I make a mixture of baking soda, water and Karo Syrup and deliver it to her through an oral syringe. Once a month, Francheville visits and draws blood, and my husband and I drive to a small-animal clinic in the next town with the equipment to run a blood-gas test. So far, the results have all been normal. I could stop the baking soda treatments and see whether Amber remains normal without them, but I’m not going to try that.

Looking back, I’m still amazed at how an illness that looked so dire and took so long to diagnose turned out to have such a simple solution. Other equine veterinarians and horse owners I’ve spoken to since have never heard of renal tubular acidosis—it’s just that rare. I have to wonder how many horses stop eating and, as a result of dehydration and malnutrition, get very sick yet never have this disease properly diagnosed. The thought that someone might put down a beloved horse for something so easily treated breaks my heart.

I’ve also had a change of heart about taking a horse to a university hospital. I had always thought of the university as a last resort—where horses go when they aren’t going to make it. Taking Amber there, in my mind, was the beginning of the end. But my fears only delayed her diagnosis and treatment.

Now, I’ve done a complete turnaround on that topic: I have every faith in my regular veterinarian—who did everything appropriate during Amber’s crisis—but the next time I have a sick horse and the answer isn’t immediately obvious using the resources we have, we’ll head to Gainesville. I think the receptionist will remember me.




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