Managing feline kidney disease: The 2026 Consensus Guidelines

In general terms, how has the clinical approach to fila and chronic kidney disease changed between then and now?

Thank you for doing this interview with me.

I'm absolutely delighted to be here and to be here with Sam.

So to answer your question, I'm going to talk about the most recent things in diagnosis and atiologies and risk factors, and then also management.

So in terms of diagnosis, then I think what hasn't changed is our use of creatinine.

So it is our most widely used and established surrogate marker of GFR.

We know lots about how to use it.

We've got lots of information on it.

But what has evolved perhaps is our understanding of the benefits of the repeated measurements of creatinine.

creatinine.

So using a cat where it serves as its own baseline to look for progressive increase in creatinine concentration that might alert us to the possibility of either progressive disease or the development of azotemic chronic kidney disease.

Ten years ago, we did have SDMA available.

And at that time, the initial studies were suggesting that SDMA had a greater detection for decreased renal function than creatinine.

But we've had lots more studies since that time.

And so now we know that actually the correlations between SDMA and GFR and creatinine and GFR are probably similar.

SDMA is less affected by muscle mass than creatinine.

And so it can be beneficial when we're using it in those cats with chronic kidney disease that may have lost muscle mass, those underweight cats.

So perhaps we want to consider SDMA in our interpretation of our renal profile more in those cats.

But we do also know now that it's affected by other non-renal factors.

And most importantly for our older cat population, and that's going to be hyperthyroidism.

So we need to interpret it with caution in a cat where we may think that there's underlying hypothyroidism.

And now we've also got increasing evidence that perhaps the standard commercial assay cutoff, the 14 micrograms per deciliter, may not be appropriate for the older cat population either.

And perhaps we should be using a higher diagnostic cutoff of 18 micrograms per deciliter in our older cats.

In terms of the etiologies and risk factors for chronic kidney disease in cats, then we've got increasing evidence, both in humans and wild and domestic cats, because we know that wild cats too also get a lot of tubular interstitial nephritis and chronic kidney disease.

We've got increasing evidence that dietary phosphate is playing a role in the development and progression of chronic kidney disease.