Hello, I’m Dr. Hocheol Shin, or “Dr. Shin.” I study feline kidney health and aging at Greycoat Research.

I earned my Ph.D. studying cancer and immunology, and I’m now building on that experience to explore how we can help cats stay healthier for longer.

In “Reading Papers with Dr. Shin,” we’ll explore research related to feline health together. We’ll look a little deeper into how things work, what the studies actually found, and what those findings might mean for our cats. I’ll explain any unfamiliar terms as we go.

Ready to open today’s paper with Lulu?

< Three-Sentence Summary >

1. Much of the nitrogen left after amino acids are used is converted to urea and excreted through the kidneys. Changing protein intake can change that amount.
2. Producing less urea and preserving kidney function are different outcomes. Even a large human trial did not show steadily better results as protein intake fell.
3. Cats need both waste management and adequate nutrition. The benefits of renal diets cannot be reduced to a rule that less protein is always better.

< Getting Started >

“Reduce protein to ease the kidneys’ workload.”

Owners often hear this when managing kidney disease. Yet cats are carnivores with substantial protein requirements. Being told to reduce protein in an animal that needs it can sound confusing.

First, we need to unpack that word, workload. What happens after a cat eats protein, and which products do the kidneys handle? If less of those products are made, does kidney disease also progress more slowly?

These are the two questions in this article.

< Why Do the Kidneys Come Into the Protein Story? >

Digestion breaks dietary protein into amino acids. The body uses them to build and maintain muscles and other tissues, and to make enzymes, hormones, and other essential substances.

Amino acids can also provide energy. Their nitrogen must then be handled. The liver converts much of it to urea, which the kidneys excrete in urine.

BUN, or blood urea nitrogen, measures the nitrogen contained in urea in the blood. Changing protein intake can therefore change how much urea is produced and affect BUN.

Did BUN fall because less urea was made, or because the kidneys excreted it more effectively? The same numerical change can have different explanations. Hydration and other factors matter too.

< Researchers Tested Protein Restriction in People >

The MDRD study, reported by Klahr and colleagues in 1994, involved 840 people with chronic kidney disease. Participants entered one of two studies according to kidney function, with different protein intakes and blood-pressure targets. Average follow-up was 2.2 years.

The group with less advanced disease compared a usual-protein diet with a low-protein diet. The more advanced group compared a low-protein diet with a very-low-protein diet that included amino acid and related supplements.

The researchers did more than measure BUN. They followed glomerular filtration rate, or GFR: the rate at which the kidneys filter blood.

The findings did not amount to “the less protein, the better.” In the first study, the estimated overall decline in GFR at three years did not differ significantly between diet groups. The low-protein group had a faster initial decline over four months, followed by a slower decline. The researchers interpreted the later pattern as suggesting a possible small benefit.

In the more advanced group, further protein restriction did not significantly slow progression or delay end-stage kidney disease or death.

< What About Cats? >

Having reasons to adjust protein in people does not mean we can give cats the same diet. Cats have different protein and amino acid requirements.

Researchers have also examined amino acid concentrations in cats with kidney disease. Goldstein and colleagues compared fasting blood samples from 38 cats with chronic kidney disease and 24 healthy cats. Some amino acids, including arginine and tryptophan, were lower in the cats with kidney disease, while others were higher.

That does not automatically mean the lower amino acids needed supplementation. The authors considered most differences small. They also found no evidence that short-term use of commercial protein-restricted diets adversely affected plasma amino acid concentrations.

The study shows why protein metabolism in kidney disease cannot be explained solely as eating more and accumulating more. The body also uses and processes amino acids after they arrive.

In the renal-diet trial from the previous article, uremic episodes and kidney-related deaths were reduced. We can use that evidence while also checking whether a cat is getting adequate nutrition.

< Personal Thoughts >

When using the phrase “easing the kidneys’ workload,” I think it helps to say exactly what decreased. Was less urea produced? Were there fewer uremic episodes? Did kidney function decline more slowly? These did not all give the same answer in today’s studies.

Adjusting protein is also different from eating less food. A change in nutrient proportions should still allow the cat to obtain enough energy. When total food intake falls, calories and other nutrients can fall alongside protein.

Feeding a cat with kidney disease therefore means managing waste products while supplying the materials needed to maintain the body. Continually lowering one protein number cannot solve both tasks by itself.

One explanation often appears at this point: cats cannot reduce protein breakdown when they eat less protein. Is that actually true? The next article compares the early enzyme experiments with later measurements of whole-body metabolism.

< References >

1. Klahr S, Levey AS, Beck GJ, et al. The effects of dietary protein restriction and blood-pressure control on the progression of chronic renal disease. New England Journal of Medicine. 1994;330:877–884.
2. Goldstein RE, Marks SL, Cowgill LD, Kass PH, Rogers QR. Plasma amino acid profiles in cats with naturally acquired chronic renal failure. American Journal of Veterinary Research. 1999;60:109–113.
3. Ross SJ, Osborne CA, Kirk CA, et al. Clinical evaluation of dietary modification for treatment of spontaneous chronic kidney disease in cats. Journal of the American Veterinary Medical Association. 2006;229:949–957.

< About the Author >

Hocheol Shin, Ph.D. Greycoat Research

B.S./M.S./Ph.D. in Biological Sciences, KAIST (Korea Advanced Institute of Science and Technology)

Research background in cancer immunology, tumor microenvironment, and translational oncology. Currently engaged in companion animal health and longevity research.

[Educational Disclaimer]

This article is for educational purposes only and is not a substitute for professional veterinary advice, diagnosis, or treatment. It is not intended to diagnose, treat, cure, or prevent any disease.

Please consult your veterinarian before making changes to your cat’s diet, supplements, or care routine.