Q&A: Managing anemia, appetite loss, and phosphorus in feline chronic kidney disease

Chronic kidney disease (CKD) is one of the most common conditions veterinarians manage in cats and treatment often requires addressing multiple aspects of the disease. In this Q&A adapted from an earlier interview with dvm360, Mark J. Acierno, DVM, MBA, DACVIM (SAIM), shares practical guidance on treating anemia and appetite loss in cats with CKD and discusses how FGF-23 can be used to tailor phosphorus restriction.

Editor’s note: This dvm360 Q&A has been edited and consolidated from a verbal interview to better fit a written format while retaining the substance of the original conversation.

dvm30: What are the most effective ways to manage anemia in a feline patient with CKD?

Acierno: Traditionally, we've treated anemia using drugs like Epogen and darbepoetin. Epogen has its own problems in that, although it's inexpensive and has been around for a long time, it can cause antibodies to develop in cats. The cat will not only destroy the exogenous Epogen you're giving, but also destroy the endogenous Epogen, making the anemia even worse.

So, people looked at darbepoetin. Darbepoetin is not associated with the same autoimmune response because it's a molecule that's been clustered with a lot of things, like carbohydrates. For people, the idea was that they'd have to inject themselves less often, which is a real bonus, but for us, it's important because it hides the molecule from the immune system.

Darbepoetin is fairly expensive, but there's been a realization that the anemia that happens, happens not because the cells that produce Epogen have died off. Those cells are still in the kidney doing their job, but so many other cells have died off that the Epogen-producing cells don't detect the need for it, because the kidney is no longer using as much oxygen, so they don't release it. Now we have a drug that interferes with that process—Varenzin-CA1, a conditionally approved drug that works by getting the body's own production of Epogen back on track.

dvm30: What is the best way to control nausea and stimulate the appetite of a feline patient?

Acierno: There are a number of things we can do. I like to break it down into both feeding management and medications. For management: small, frequent meals, and rotating the diet. Often, we'll send a cat home with a particular brand of food, and the owner will tell me, "Well, they ate it for a while, then they stopped." So I send them home with a whole smorgasbord and have them rotate through the options. Small, frequent meals may mean that the idea of feeding a meal in the morning and a meal at night might have to change because when we’re are sick, we don't feel like eating a big meal. So cats may nosh throughout the day, and that may add up to a meal and that would be great. Those are some management strategies we can use.

There are also medications we can try. For a long time, a lot of us used maropitant, which is a very good anti-nausea medication. The problem is that, in at least one small study, it didn't really improve the cat's appetite or cause weight gain. Mirtazapine—there's an FDA-approved topical transdermal formulation for cats called Mirataz—not only decreases nausea but also seems to cause cats to gain weight. So we can use a combination of treatments and feeding strategies.

There's also a drug called Elura, similar to Entyce for dogs, which has been shown to increase appetite in cats. So, we have a number of management strategies, and a couple of different drugs, to control nausea and increase appetite.

dvm30: Are there any other treatment options for feline patients with CKD?

Acierno: Fibroblast growth factor 23, more commonly known as FGF-23, is something we should talk about.

For a long time, the big question was: When do we start a phosphorus-restrictive diet?

Oftentimes, people would wait until phosphorus levels got out of normal range before starting a diet to bring it back down. What we've discovered through a number of studies is that long before phosphorus in the plasma begins increasing, the body maintains a normal phosphorus level by dumping excess amounts into the urine, and that dumping is caused by FGF-23. FGF-23 production is stimulated by phosphorus elevations and it tells the kidney to get rid of the phosphorus, so the kidney dumps it.

But studies show that dumping phosphorus into the urine actually damages the kidneys. So now we have FGF-23, which we can measure and use to determine the best time to start phosphorus-restricted diets.

The literature points to a level greater than 400 as a time to start restriction, but it helps us even more than that, because we can start phosphorus restriction and then remeasure FGF-23. If it hasn't come down, we haven't done our job and we need more aggressive phosphorus restriction, with things like phosphate binders.

Mark J. Acierno, DVM, MBA, DACVIM (SAIM), is a professor and the associate dean for clinical affairs at Midwestern University's College of Veterinary Medicine in Illinois.