126 | Chronic kidney disease in 2026: What’s changed, and why do we need to know about it as vet nurses?

PodcastNursingChronic DiseaseRenal
Written By Laura Jones

Today we’re revisiting a disease really close to my heart - chronic kidney disease. 

As you may know, my intro to CKD in general practice was ‘3 days of fluids, home if the bloods got better, PTS if not’ and then I had a very rude awakening as a new referral RVN when my 4 year old cat was diagnosed.

All of a sudden, I had a relatively young, supposedly healthy cat with marked renal disease - and I realised just how much influence we have as nurses and technicians in the care of these patients (and their families).

And while we’ve chatted about CKD on the podcast before - all the way back in 2024 - this year, in 2026, a LOT has changed.

We’ve now got new tests, brand new treatments, and new guidelines to follow. The IRIS guidelines, treatment recommendations, and iCatCare guidelines have all had a brand new refresh for 2026 and the way we support these patients - and their families - is getting a major upgrade.

So in this episode, we’re chatting all about how to nurse CKD the right way. We’ll recap what CKD is, why it happens, and then look at the treatment and nursing these patients need - and where our skills fit into it all.

Let’s start at the beginning - with what chronic kidney disease is, how it impacts our patients, and what we need to know about it as veterinary nurses.

The kidney basically acts as the body’s ‘recycling centre’, filtering blood, recycling needed substances, and eliminating waste products and excessive substances.

Each kidney contains hundreds of thousands of nephrons. A nephron has two main parts. The glomerulus filters the blood, and the tubules - divided into the proximal and distal tubules, and the loop of Henle - reabsorbs what the body needs. What's left becomes urine, which drains through the collecting duct, into the renal pelvis, to the ureter, and then to the urinary bladder.

However, making urine is only part of the kidney's job. It also:

  • Maintains fluid balance and electrolyte concentrations

  • Helps regulate acid–base balance

  • Produces erythropoietin, which drives red blood cell production

  • Produces renin, which starts the renin–angiotensin–aldosterone system and helps regulate blood pressure

  • Manages calcium and phosphate balance, and with them bone metabolism

When kidney function falls, any of these can go wrong. A CKD patient might have dehydration, hypokalaemia, acidosis, anaemia, hypertension or mineral and bone changes, and often several of these challenges will be present concurrently. This means that managing CKD is usually a case of managing a list of issues, rather than one simple disease - which means a lot of considerations for us as nurses. 

But chronic kidney disease is often diagnosed late - and that makes supporting these patients even more challenging.

The kidneys have a lot of reserve. When nephrons are lost, the remaining ones will compensate for that loss, as much as they can. They each filter more blood, under higher pressure, and this maintains overall kidney function - for a while.

Over time, though, the raised pressure inside the glomerulus damages the remaining nephrons. It also lets protein leak into the urine, causing proteinuria - which further injures the nephrons as they try to reabsorb this protein back into the bloodstream.

This compensation mechanism also means that our patient’s renal changes are often more significant than their blood results show. The patient’s results will lag behind the disease - previously, we’ve been taught that around 66-75% of nephrons are lost by the time USG decreases and creatinine becomes abnormal. also means blood tests lag behind the disease.

The updated guidelines point out something interesting that emphasies the way we think about this - creatinine has a non-linear relationship with glomerular filtration rate (the rate at which blood flows through the glomerulus in the nephron). This actually means that GFR (our marker of renal function) can fall a long way before creatinine becomes abnormal.

All of this means that by the time a patient is azotaemic, a large proportion of kidney function has already been lost - and this is why early detection is an absolutely essential part of supporting these patients.

There’s another important part of CKD to chat about - and that’s CKD-mineral and bone disorder, or what we used to refer to as secondary renal hyperparathyroidism.

CKD-MBD is an important complication of CKD - and when it happens, it can cause significant problems for our patients.

As GFR falls, the kidney excretes less phosphate, and phosphate starts to build up in the bloodstream. This is why we see hyperphosphataemia commonly in patients with CKD.

When a patient becomes hyperphosphataemic, the bone responds by releasing something called FGF23 - fibroblast growth factor 23. This tries to increase phosphate excretion, but when there are fewer working nephrons, this doesn't work well.

FGF23 also lowers calcitriol, the active form of vitamin D - and at the same time, phosphate binds calcium and lowers ionised calcium. The result is lower calcium levels - which stimulates the parathyroid glands to release parathyroid hormone.

Over time this leads to soft tissue mineralisation, including within the kidney itself. Patients can develop often painful lesions in the soft tissue, and weaker bones (due to a lower calcium density within the bone). On top of this, mineralisation of the kidney tissues will cause further renal injury, worsening CKD.

This is why we adjust dietary phosphate intake so carefully in our renal patients - to prevent CKD-MBD from happening. And for us as veterinary nurses and technicians, discussing diet is an enormous part of our role - so understanding why we do it, and having those conversations confidently, is really important.

It’s also why we now use FGF23 testing much more in practice. FGF23 used to be mainly a research marker, rarely used in clinical practice - but that’s no longer the case, as we’ll chat about later when it comes to treating CKD. 

So that’s what CKD is, and what problems it causes. But why do our cats and dogs develop chronic kidney disease?

While there are some established causes, in the majority of cases it is an idiopathic condition.

Causes of CKD in Cats

In most cats with CKD, a renal biopsy - when performed - shows chronic tubulointerstitial nephritis. This is inflammation and fibrosis around the tubules, where healthy tissue is gradually replaced with fibrous scar tissue. The underlying trigger for this usually can't be identified.

However, several risk factors for CKD are well-documented, including age, tubular lipid accumulation, comorbidities such as hyperthyroidism, proteinuria, ureteral obstruction, and periodontal disease.

Interestingly, according to the new iCatCare guidelines, Cats as a species also seem predisposed to CKD, and the authors discuss whether being an obligate carnivore contributes, through high dietary protein and phosphate and a higher dietary acid load. 

Identifiable causes in cats include:

  • Polycystic kidney disease, with Persians being the classic breed affected.

  • Hereditary amyloidosis, seen in Abyssinian, Somali, Siamese and Oriental cats.

  • Neprholiths and ureteroliths. Most feline kidney stones are calcium oxalate and can't be dissolved - while stones that stay in the kidney don't appear to drive progression, a stone that moves and obstructs a ureter can cause severe post-renal AKI, leading to CKD.

  • Hypercalcaemia, which can cause nephrocalcinosis.

  • Pyelonephritis, renal infection.

  • Toxins such as lilies.

  • Neoplasia, including renal lymphoma and renal carcinoma.

I also want to mention a well-known syndrome in cats called ‘big kidney, little kidney’ - firstly because you may hear the term thrown around especially during an ultrasound in an affected patient, and secondly because this is precisely how Nigel ended up with CKD - and it’s more common than you think.

If one ureter becomes obstructed while the other kidney works normally, the cat doesn't become azotaemic and the problem can go unnoticed. The obstructed kidney scars and shrinks over time, and the other kidney enlarges to compensate. If the remaining kidney then becomes obstructed, the cat often presents acutely unwell - but by that point, marked renal dysfunction is present (and usually has been for some time).

So that’s cats - but why do we see CKD in dogs?

CKD is much less common in dogs than in cats, and the causes differ.

Glomerular disease and proteinuria play a larger role in dogs - causing what we call protein-losing nephropathy or PLN. There are also several familial and breed-associated kidney diseases - such as Shar Peis, English Bull Terriers and Cairn Terriers, so CKD in a young dog should prompt thinking about congenital or inherited disease.

Other causes include infectious disease, for example leishmaniasis in dogs that have travelled or been imported, along with leptospirosis, infections such as pyelonephritis and kidney damage after an acute kidney injury such as grape and raisin toxicity.

How are acute kidney injury and CKD related?

Acute kidney injury and CKD used to be thought of as separate conditions - and while we’re going to chat more about AKI in the next episode, I want to briefly mention it here too.

We’re now moving away from thinking of them as unrelated diseases, and towards a two-way relationship between them. CKD makes a patient more likely to have an AKI, and an AKI can start or speed up CKD - which makes sense, because when we think about the patients we see in practice, acute-on-chronic disease (or chronic-on-acute, for that matter) is much more common than we might think.

The updated 2026 guidelines describe two patterns of progression - one is a slow, continuous decline, but the other includes episodes of acute injury on top of chronic disease. Some of these episodes are clinically obvious (our ‘traditional’ acute-on-chronic kidney disease), but others actually go unnoticed. 

In a study of cats with acute-on-chronic kidney disease, ischaemia - lack of blood flow and oxygen delivery to the kidney - and ureteral obstruction were among the most common causes. However, in 66% of cases, no cause was found. 

And for us as veterinary nurses and technicians, we need to be thinking about how we can protect the kidneys in our patients - especially during anaesthesia, pain management, or rehydration - to minimise opportunities for AKI, or CKD progression. 

Diagnosing and staging renal disease in 2026 - where do we fit in as veterinary nurses?

While we’re not diagnosing these patients as nurses and technicians, assisting with this process is an enormous part of our role. 

We’re often the ones taking bloods, performing urine analysis, measuring blood pressure, weighing these patients, and performing things like body and muscle condition scoring. And these results are vital for our clinicians, since they’ll directly influence the treatment decisions they make.

The most important principle in diagnosing chronic kidney disease? Early detection.

We chatted a bit about this, and its importance, in episode 125 where we spoke about our senior pets.

Looking specifically at CKD, the 2026 iCatCare guidelines recommend health screening (weight, bloodwork and urine analysis) for cats aged seven and over, even when they seem well. They advise that cats aged seven to ten should be checked yearly, and cats over ten ideally twice a year.

And just as a reminder, the studies we chatted about in the last episode that came from Ghent University found that 8% of apparently healthy older cats already had CKD at IRIS stage 2 or above. Of the cats that were healthy at their first screen, 24% of those aged 11 and over developed azotaemia within two years. 

So this means there’s enormous value not just in one-off testing, but in repeated screening over time - even in seemingly ‘healthy’ individuals.

One of the earliest indications is weight loss. In fact, one study of over 500 cats found a median weight loss of 8.9% in the 12 months before CKD was diagnosed, and weight loss was already present three years before diagnosis. When questioned about that weight loss, the caregivers often put this down to age - reinforcing that point we made last episode about age not being a disease, but significantly increasing the risk of disease.

Senior clinics and routine weighing in consults are a good opportunity to pick this weight loss up. Recording weight and muscle condition score at every visit, and flagging unexplained weight loss to the vet, are small but really important ways that we can detect CKD early.

So how is CKD actually diagnosed?

There's no single test for CKD, and instead we’re looking at a combination of blood results, imaging findings, urine analysis and physical examination.

The diagnosis is usually built from several changes:

  • Creatinine above the reference interval, together with inadequately concentrated urine or azotaemia that persists on repeat testing.

  • Urine specific gravity - in cats, a USG below 1.035 should raise suspicion of reduced concentrating ability unless the cat is on a very wet diet or has another reason for dilute urine (this change often comes before creatinine rises).

  • Proteinuria, measured as a urine protein to creatinine ratio (UPC) rather than a urine dipstick.

  • Imaging, which can show small, irregular kidneys with poor corticomedullary definition and rule out problems such as ureteral obstruction.

Creatinine

Creatinine comes from muscle, so a patient with poor muscle condition (sarcopenia) can have a creatinine within the reference interval and still have significant kidney disease. I’ve also seen patients look like their disease is improving as their creatinine is getting ‘better’ on paper - but due to their muscle wastage progressing as their disease advanced, so this is something to be aware of too.

According to the 2026 guidelines, older cats tend to have lower creatinine, and suggest the upper reference limit should be lower for them - so interpret the result with that in mind.

SDMA

SDMA is less affected by muscle mass, which is useful in sarcopenic patients, but other factors influence it. For example, hyperthyroidism can raise SDMA independently of kidney function, and so can lymphoma. Diabetic cats also often have lower SDMA. 

For older cats, the feline guidelines describe a proposed cut-off of 18 µg/dl instead of the standard 14 µg/dl - and both SDMA and creatinine should be interpreted together, as different factors affect each parameter - meaning that interpreting them together gives a clearer picture of what’s really going on with the patient.

Urine Analysis

As well as examining urine concentrating ability and proteinuria, urine sediment examination should be performed as part of the work-up as well. It can identify crystals, bacteria or signs of pyelonephritis that would change management, and is another important area where we can utilise our skills as veterinary nurses.

So we’ve got our results - what now? Let’s talk about staging chronic kidney disease in dogs and cats

Staging only happens after CKD has been diagnosed - this is where we’re determining the severity of their CKD according to their creatinine and SDMA result, amongst other things. The patient’s treatment, monitoring, and care is all influenced heavily by their CKD stage - so knowing how we stage these patients is really important.

Patients are staged as either stage 1 (non-azotaemic CKD), 2 (mild azotaemia), 3 (moderate azotaemia) or 4 (severe azotaemia) according to their results - and these are results taken when the patient is stable and appropriately hydrated, not immediately after an acute period of illness.

Once we’ve staged the patient, they’re then substaged.

This substaging is performed by proteinuria and blood pressure - because these are the two factors that can be treated to slow CKD progression.

Patients are either non-proteinuric, borderline proteinuric or proteinuric depending on their UPC, and normotensive, prehypertensive, hypertensive or severely hypertensive depending on their systolic blood pressure.

These should be persistent changes - so multiple urine samples, taken at least 2 weeks apart, and not when a UTI or urinary inflammation is present which can increase protein levels.

Similarly, blood pressure should be reliable, with every measure taken to reduce stress which could contribute to ‘white coat hypertension’ and falsely increase SBP.

How do we know if the patient’s disease is progressive or stable?

A 2026 study described in the feline guidelines found that serial creatinine, phosphate and body weight measurements in the first three months after diagnosis help separate cats with stable CKD from those with progressive CKD. 

Median survival was 894 days for stable CKD and 287 days for progressive CKD - which is an enormous difference - and more than 60% of cats with progressive disease died within a year of diagnosis.

So being able to tell these two apart is really important, and again, it’s an area where we’re ideally placed to help as nurses and technicians. 

The iCatCare guidelines recommend repeating creatinine two to four weeks after diagnosis to help determine how progressive the patient’s CKD is - and we can help by seeing these patients ourselves in between vet visits, performing those tests, chatting to clients after diagnosis, and determining whether the patient’s clinical signs are progressing at home. 

So your patient has chronic kidney disease. What now? Here’s what the brand new guidance for treating CKD in 2026 has to say

We can broadly divide our CKD treatment into two groups: first we have treatments that slow progression and preserve kidney function, and then we have treatments that manage clinical signs and support quality of life.

In stages 1 and 2, most patients have few clinical signs, so the emphasis is on slowing progression. Clinical signs become more common from stage 3, and by stage 4 IRIS considers treatments aimed at quality of life more important than those aimed at slowing progression.

This is a useful way to explain to caregivers why the plan changes over time, and why a vet may decide not to put as much emphasis on pushing for things like bloodwork improvements in a stage 4 cat who is eating well and comfortable - because the priority is exactly that, keeping them eating and comfortable.

There are a lot of changes in how we treat CKD in the recent guidelines - so let’s run through them.

The role of diet in patients with CKD

Diet has the strongest evidence of any CKD treatment. In cats, feeding a veterinary renal diet prolongs survival and reduces the risk of uraemic crises - and there are countless studies, going back years, that prove this.

The main reason for this is phosphate manipulation. Renal diets typically contain about 80 to 130 mg of phosphorus per 100 kcal, while some non-renal diets contain 400 to 600 mg. In one study described in the feline guidelines, each 0.32 mmol/l increase in serum phosphate was associated with an 11.8% increase in the risk of death. Renal diets usually also include omega-3 fatty acids and added potassium, along with B vitamins and antioxidants - to minimise oxidative renal injury, and replace electrolytes and vitamins lost through polyuria.

The new guidance contains lots of great practical information about feeding cats with CKD, including: 

  • Even feeding at least 50% renal diet is associated with improved survival - so if your patient isn’t eating 100% renal food, as long as they’re eating over half, it is worth continuing.

  • Maintaining body weight and muscle is a priority. If a cat isn't eating enough, an early renal diet with slightly more protein may be a better choice than a traditional renal diet - as the protein level is higher - regardless of their CKD stage.

  • Wet food provides more water, while dry food has around four times the calories per gram - so we need to balance the desire to increase water intake with their caloric intake. A cat struggling to eat enough volume may do better with some dry food.

  • Appetite in CKD varies from day to day, so having more than one suitable diet that the cat accepts is helpful - that way we have options if the patient becomes picky.

  • A new diet should not be introduced while the cat is unwell or hospitalised, because food aversions can develop. Instead, we should feed the cat's familiar food in the hospital and transition at home once they're eating well.

  • Diet transitions should take at least one to two weeks, offering small amounts of the new food alongside the old food. Many cats accept the two side by side better than mixed together.

Phosphate binders and monitoring phosphate restriction

Depending on the patient’s IRIS CKD stage, they’ll have different serum phosphate targets. 

Phosphate restriction is achieved with diet initially. If phosphate stays above target after four to six weeks, a phosphate binder can be added - these should be mixed with each meal, since they bind the phosphate in the diet they are mixed with.

The new guidance recommends using FGF23 testing to help decide whether a cat would benefit from phosphate restriction, and then in assessing and adjusting phosphate management ongoing.

Calcium monitoring and management in CKD

Hypercalcaemia is common in CKD - around 20% of cats with azotaemic CKD have ionised hypercalcaemia at diagnosis, and a further 26% develop marked or persistent hypercalcaemia within 12 months. 

And - really interestingly -  around half of cats with azotaemic CKD show rising calcium after starting a phosphate-restricted renal diet, which is one of the reasons why we’re now using many more ‘early renal’ type diets - because by overly restricting phosphate, we tip the Ca-P balance and can cause hypercalcaemia.

Hypercalcaemia increases the risk of nephrocalcinosis, which appears to be associated with faster CKD progression - so we want to strike a balance between restricting phosphate and slowing disease progression but without overly restricting it and causing hypercalcaemia.

Regular calcium (ideally ionised calcium) monitoring is an important part of CKD management, with appropriate dietary adjustment as needed.

Blood pressure assessment and management in CKD

Hypertension is common in CKD and can damage the eyes, brain, heart and kidneys. Ocular changes are present in up to 80% of hypertensive cats - even in the absence of blindness and retinal detachment. And all of this means that every CKD patient should have their blood pressure measured at diagnosis and as part of routine monitoring.

Of course, this naturally presents us as veterinary nurses and technicians with a great opportunity to utilise our skills through things like clinics, obtaining measurements for our clinicians and providing advice and support.

Our aim is to keep the patient’s systolic BP below 140-160mmHg, treating as appropriate with either amlodipine or telmisartan for cats, or an ACE inhibitor +/- amlodipine for dogs.

The goal is to achieve a gradual, sustained reduction in blood pressure without evidence of hypotension, rechecking blood pressure regularly to ensure it remains within that ideal window.

Treating and managing proteinuria in CKD

Persistent proteinuria is associated with progression and shorter survival in cats and dogs, so where this is present, it is treated accordingly with drugs that inhibit the RAAS. An angiotensin receptor blocker such as telmisartan is used most commonly, though ACE inhibitors such as benazepril can also be used.

These drugs should not be started in dehydrated or unstable patients in either species, they can cause rapid decreases in GFR which could worsen renal dysfunction. Patients should be monitored carefully after these drugs are started, and if acute worsening of the patient’s signs develop, they may need to be temporarily stopped.

Managing anemia in the CKD patient

As CKD progresses, erythropoietin production falls and anaemia develops - in turn causing lethargy, weakness, inappetence and potentially reduced oxygen delivery, including to the kidneys themselves.

These changes can impact disease progression - in fact, a 2025 study found that cats with a PCV below 27% had poorer health-related quality of life scores.

So where anaemia is present, it needs to be treated - depending on the severity of that anaemia.

There are two main drug options for this. The first is darbepoetin - a synthetic version of erythropoietin. This is injected, weekly at first, with blood pressure and PCV checked before each injection. Concurrent iron injections (usually monthly) are often needed.

There is now a new, licensed, oral treatment for CKD-associated anaemia. Molidustat belongs to a class of drugs known as HIF-PH (prolyl hydroxylase) inhibitors, which work by increasing the body's own erythropoietin production. 

Supportive treatment in CKD - what else do we need to think about?

The more targeted treatments we’ve discussed above are only one part of managing CKD. There is a LOT of supportive care and treatment to consider, including:

  • Nausea management

  • Appetite stimulation and supportive nutrition

  • Hydration support

  • Potassium supplementation

  • Treating constipation (where present, secondary to dehydration)

There are a variety of agents used to do this both in and out of the hospital, across injectable and oral antiemetics, appetite stimulants such as capromorelin and mirtazapine, enteral feeding tubes, intravenous or subcutaneous fluids and more.

And of course, all of this requires an enormous amount of input, skill, and monitoring from us as veterinary nurses and technicians.

I also want to mention a newer treatment, renaltec, which is being used increasingly commonly in CKD - especially uraemic CKD. This is a carbon-based adsorbent that binds uraemic toxin precursors in the gut and has been shown to reduce serum uraemic toxins in cats with CKD. This is something we’re seeing used more and more in practice, and though there isn’t a lot of evidence around its use, it’s interesting to see how this area of treatment develops.

What about pain in CKD patients? Should we always avoid NSAIDs? What does the evidence say?

I think this is an interesting area because we’ve always been taught that all CKD = absolutely steer clear of non-steroidals. However, I’ve seen many patients with CKD and lower urinary disease over the years, and we’ve had that challenge of seeing them uncomfortable and really need NSAIDs, but the worry about whether that would make their kidney disease worse.

In reality, it isn’t as clear cut as all NSAIDs = bad in patients with CKD. In fact, according to the recent iCatCare guidelines, CKD should not be a reason to leave pain untreated. Current evidence suggests low doses of NSAIDs like meloxicam or robenacoxib can be used - though cautiously - in cats with stable CKD. 

By stable, they mean a patient with minimal change in body weight and creatinine over at least two months, with concurrent conditions such as hypertension, hyperphosphataemia and urinary tract infection controlled. 

It is our dehydrated, unwell, progressive CKD or stage 4 CKD patients who are absolutely NOT NSAID candidates.

And when using them in all cases, but especially in patients with CKD, caregivers should be told about possible adverse effects and the importance of keeping the cat drinking.

What about nursing cats and dogs with CKD - how do we support them as veterinary nurses and technicians?

There’s an enormous amount of nursing knowledge and skill that goes into supporting patients with CKD - be that in hospital, during procedures, or on an outpatient basis.

In the hospital, nutrition, monitoring, sampling, vascular access, nausea and fluid therapy are especially important considerations.

How we support these patients during anaesthesia is also really important. We need to avoid hypotension, vasodilation, renal hypoperfusion, and hypothermia - especially since many of these patients have often marked weight/body and muscle condition loss, meaning hypothermia is an even higher risk. Maintaining blood pressure above 90-100mmHg (systolic) or 60-70mmHg (mean) helps to avoid drops in GFR and renal ischaemia, which could contribute to AKI or worsen the patient’s CKD.

And then when the patient is discharged, that care doesn’t stop. There are SO MANY ways we can continue to use our skills with these patients long-term - from caregiver support and education, remote monitoring, nurse consultations, and much more.

So let’s recap everything we’ve chatted about today…

That brings us to the end of episode 126.

To recap, CKD is a permanent, progressive loss of renal function - and while we don’t know exactly why it happens in many cases, we know what it causes for our patients: dehydration, uraemia, anaemia, electrolyte abnormalities, acidosis, metabolic bone disease and more.

After diagnosis, the patient is staged once they are stable and hydrated, and then treated accordingly - both to treat symptoms and improve QOL, and slow progression of their disease.

There is an enormous amount of nursing to do in all of this - from early detection in our at-risk patients, to helping with sampling and diagnosis, caring for these patients in the hospital, and supporting caregivers and beyond.

If you want to read further, I’ll leave all of the new guidelines linked below - grab them and have a read over a coffee on your next break, because they’ve got a lot of great information in. There’s also a caregiver guide to CKD, which is fantastic and really worth having a few copies of in your consulting room - that way, you can give one to your client when their cat is diagnosed.

But most importantly? Remember how much your knowledge, skills, and experience caring for these patients makes a difference - because there are honestly so many ways these patients benefit from nursing, both in and out of the hospital.


Did you enjoy this episode? If so, I’d love to hear what you think. Take a screenshot and tag me on Instagram (@vetinternalmedicinenursing) so I can give you a shout-out and share it with a colleague who’d find it helpful!

Thanks for learning with me this week, and I’ll see you next time!

References and Further Reading

Laura Jones
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125 | This is why our senior cats and dogs are often overlooked - and what you can do about it as a vet nurse