109 | Here's how to make a REAL difference to your CKD patients as a busy vet nurse

NursingPodcastRenal DiseaseChronic Disease
Written By Laura Jones

In this episode, we’re chatting about something every single one of us deals with, whether you’re working in general practice, referral, or out-of-hours - and that’s chronic kidney disease.

CKD is one of the most commonly-diagnosed conditions in our senior patients - in both cats and dogs. Despite how often we see this disease, our role as nurses in caring for these patients is often quite limited, and there’s still a big disconnect between how we treat these patients in practice and what the evidence suggests about their management.

Today I’m bringing you an evidence-based overview of CKD, focusing on the International Renal Interest Society (IRIS) guidelines on its management. We’ll explore why CKD is so hard to diagnose early - and why it’s so important that we do - alongside how we can use things like staging to plan both effective treatment AND nursing care for our patients. So you can spend less time feeling like you’re just watching CKD patients sit on fluids, and more time using your skills and truly advocating for your patients.

Let’s get into it.

So what is chronic kidney disease, why is it hard to spot early, and why is early detection so important?

I’m not going to dive into the ins and outs of CKD here, since this episode is focused more on how we treat and nurse these patients. That being said, I firmly believe that part of nursing is understanding how the diseases we see impact our patients - so let’s recap the most important aspects of chronic kidney disease.

I’ve actually covered CKD here already as part of our renal and urinary series - all the way back in episode 12, nearly 100 episodes ago! So if you haven’t listened to that episode, I’d recommend heading there and listening to that next. But here’s the cliff notes version:

Chronic kidney disease is the most common form of renal disease we see, and it’s a gradual, progressive and irreversible loss of renal function. It occurs due to many causes - some we identify, like polycystic kidney disease in predisposed breeds, but most are idiopathic.

Regardless of the cause, the impact on our patient is the same. As more and more nephrons (the functional units of our kidneys responsible for filtering blood, excreting waste, and reabsorbing water and essential substances like electrolytes) stop working, our patients lose the ability to regulate their hydration, electrolyte balance and acid-base balance, and metabolic waste products accumulate within the body.

Since the kidneys are also responsible for things like BP management, red blood cell level and calcium/phosphorus balance (alongside other body systems), we can also see significant consequences including systemic hypertension, chronic non-regenerative anaemia, and metabolic bone disease (aka secondary renal hyperparathyroidism).

Our patients typically present with varied degrees of dehydration, hypokalaemia and metabolic acidosis. Alongside this, increasing levels of nitrogenous waste (BUN/creatnine) make our patients feel systemically unwell, causing things like nausea, vomiting and inappetence, which compounds dehydration further.

So why is detecting chronic kidney disease early so vital?

Because CKD is a progressive, irreversible condition, nephron loss will continue and the disease will continue to progress until quality of life is significantly impaired. We can’t reverse the disease, but we CAN slow it, manage its consequences, and improve quality of life - and the more time we have to do this, the better.

That is where early detection comes in - and where newer diagnostic tests such as SDMA have made a huge difference to these patients.

By the time a patient develops the classic clinical signs of CKD - the inappetence, the weight loss, the PUPD, the vomiting - they’ve already lost a significant amount of renal function. In fact, by the time their USG drops below normal they’ve lost around 66% of renal function - and when creatinine levels increase above normal, they’ve lost around 75%.

This isn’t because we’re doing anything wrong - it’s just how the kidneys work. The kidneys have an extraordinary ability to compensate for nephron loss; as more nephrons are lost, the remaining functional ones will hypertrophy and increase their workload to maintain kidney function.

The relationship between the blood markers we’ve originally used, like creatinine, and the patient’s renal function is what we call curvilnear. In English, this means that a substantial amount of renal function has to be lost before creatinine increases. And that’s why using creatinine alone to detect CKD can give us a false sense of security in the early stages of this disease.

So what early signs of CKD should we be looking out for?

Patients with stage 1 CKD have by definition a normal or near-normal GFR, meaning they won’t have obvious clinical signs of disease in most cases. Instead, we’ll see things like structural changes on imaging (eg renal cysts), or perhaps a decreased USG. These patients will have a normal creatinine level - so they’ll need to be moniored in other ways.

For us as nurses and technicians, early detection should be something in the back of our minds for every single senior pet clinic we perform, or every time we see an at-risk breed (eg a Persian cat at risk of PKD). At-risk patients require careful monitoring to spot signs of their disease as early as possible - giving us more time to manage them and support their quality of life.

What is IRIS staging and how is it performed?

Now we understand why early detection is tricky, we need to think about what happens once CKD has been diagnosed. Because the staging system is not just used for diagnosing CKD - it tells us how to manage these patients, and it’s something we’ll regularly revisit throughout the patient’s life.

IRIS staging is done in steps. First, the patient is assigned a stage based on their fasting blood creatinine and/or SDMA. Then, they're substaged based on proteinuria and blood pressure. And together, all of that gives us a really clear picture of where the patient is in their disease, and how we’ll treat and nurse them as a result.

One really important thing to mention about staging: It must be performed on a stable, hydrated patient. 

If a patient comes in in an acute crisis, eg severely azotaemic, dehydrated, or collapsed, that's not the moment to stage them because we won’t get a true picture of their baseline renal function at that time.

This means we need to stabilise them first, rehydrate them, and then reassess. Dehydration alone can push creatinine and SDMA up significantly, and staging on that result would over-stage the patient. IRIS recommends ideally assessing on at least two separate occasions in a stable, hydrated patient.

The four stages of CKD (and what we need to know about them as vet nurses)

Stage 1 patients have early or non-azotaemic CKD.

In Stage 1, creatinine is within normal limits (below 125 µmol/L in dogs, below 140 µmol/L in cats), and SDMA is below 18 µg/dL. But there is some other evidence of  CKD - maybe persistent proteinuria, maybe abnormal imaging, maybe a persistently elevated SDMA above 14 µg/dL, or increasing serial values. Clinical signs are usually absent or very mild. Think of this as the ‘we've caught something early’ stage - it’s actually the ideal stage to catch, because this is where we have the most opportunity to slow progression.

Stage 2 patients have mildly azotaemic CKD.

Stage 2 is where we start to see mild azotaemia. In dogs, creatinine is between 125 and 250 µmol/L; in cats, 140 to 250 µmol/L. SDMA is in the 18 to 35 µg/dL range. Clinical signs are usually still mild or may even be absent, but patients require increasing treatment and monitoring.

Stage 3 patients have moderate CKD.

By Stage 3, azotaemia is moderate. Dogs and cats both fall in the 251 to 440 µmol/L creatinine range here. SDMA is 36 to 54 µg/dL in dogs, 26 to 38 in cats. Clinical signs are more likely to be present, with things like increased thirst and urination, weight loss, reduced appetite common. These patients have more pronounced treatment and nursing needs, including periods of hospitalisation.

By the time our patients reach stage 4, they have severe CKD.

Stage 4 patients have severe azotaemia with a creatinine is above 440 µmol/L in both species, and an SDMA above 54 µg/dL in dogs and above 38 in cats. Patients are often systemically unwell with increasing risk of uraemia, and treatment and nursing support are typically more intensive.

When do we use SDMA in these patients, and when do we use creatinine?

SDMA, or symmetric dimethylarginine, is a breakdown product of methylated proteins that's released from all nucleated cells. Unlike creatinine, it's not significantly affected by muscle mass, which matters a lot in patients who are already losing lean muscle because of their disease. SDMA may detect reductions in GFR earlier than creatinine (research suggests it can detect reductions of as little as 20% in kidney function).

For this reason it’s a great test for early detection, but it can also be challenging to interpret, particularly if creatinine and SDMA results don’t agree. For example, sometimes creatinine will be within the normal range but SDMA will be elevated, or vice versa. 

In practice, we typically tend to use SDMA more for early detection than ongoing monitoring in an already-azotaemic patient. However, the guidance from IRIS is that if there's a persistent discrepancy, you treat for whichever result is highest. So if you had a SDMA result consistent with stage 2 CKD but a creatinine consistent with stage 3 (and those results are repeatable) - you’d assume the patient is stage 3.

Once we’ve staged our patient’s azotaemia, we substage them according to proteinuria and blood pressure.

First, we’ll look at proteinuria.

Assessing proteinuria matters because it’s both a symptom of CKD AND an independent risk factor for progressive renal injury/disease.

As the kidneys lose protein via the urine, they try to reabsorb that protein back into the bloodstream to minimise loss. This injures the kidneys, damaging them and progressing CKD over tiem.

We measure proteinuria using the urine protein to creatinine ratio, or UPC. And the substaging categories are:

  • Non-proteinuric: UPC below 0.2 in both dogs and cats

  • Borderline proteinuric: UPC 0.2 to 0.5 in dogs, 0.2 to 0.4 in cats

  • Proteinuric: UPC above 0.5 in dogs, above 0.4 in cats

Ideally, substaging should be based on at least two urine samples over at least two weeks, to confirm that the proteinuria is persistent rather than transient, because transient proteinuria can occur with things like UTI or stress. 

Then we’ll move on to hypertension.

CKD and hypertension are closely linked. Like proteinuria, hypertension is both a consequence and a driver of kidney disease. High blood pressure causes direct damage to the kidney's delicate vessels, and it can also damage other so-called target organs including the retinas, heart, and brain. 

We need to manage hypertension promptly to minimise both target organ damage and associated complications like retinal detachment, AND further renal damage.

The IRIS blood pressure substages are:

  • Normotensive: below 140 mmHg systolic

  • Prehypertensive: 140 to 159 mmHg

  • Hypertensive: 160 to 179 mmHg

  • Severely hypertensive: 180 mmHg or above 

Patients with severe hypertension are at significant risk of target organ damage, and require prompt treatment.

Blood pressure measurements should ideally be taken on multiple occasions and in a calm environment, because stress alone can elevate blood pressure significantly. IRIS recommends that persistence of hypertension should be demonstrated before treatment is started, except where there is already evidence of target organ damage.

So now our patients are staged, what does this mean for their management?

Right, so now we understand the staging system. But what does it actually mean for how we manage these patients? Well, we’ll use the staging system to guide our management decisions.

The treatment goals for CKD fall into two categories. First, treatments that slow progression of the disease and preserve remaining kidney function, and second, treatments that address quality of life and manage the clinical signs of CKD.

And the balance between these two changes as the disease progresses - in early stages, slowing progression is the priority, however in later stages, quality of life becomes the main focus.

Stage 1 and 2 (early CKD) is focussed on slowing progression.

In these early stages, clinical signs are often minimal or absent. The patient might look and act completely fine. So our management emphasis is on doing everything we can to slow progression and the patient’s remaining kidney function.

Some of the key interventions at these stages include:

  • Identifying and removing any nephrotoxic drugs

  • Investigating and treating any pre- or post-renal causes of azotaemia

  • Ruling out treatable conditions like pyelonephritis or renal urolithiasis

  • Starting a an appropriate therapeutic diet, depending on the individual patient - stage 2 is the ideal time to do this, as these patients often have a good appetite at home

  • Increasing water intake (since renal concentrating ability is already decreased)

  • Monitoring and managing blood pressure and proteinuria where present

  • Regulating phosphate levels

Stage 3 and 4 (later CKD) is focussed on maintaining quality of life.

As patients progress into Stage 3 and 4, their clinical signs are more obvious and include extra-renal signs such as nausea, vomiting and inappetence. With this, our nursing care is vast, and many patients require hospitalisation. 

In Stage 3, we see a wide spectrum of patients. Some wil have minimal signs, others will be visibly unwell. The early stage 3 patient might just be slightly thinner and drinking a bit more; the late stage 3 patient might be nauseated, losing weight rapidly, and struggling to maintain body/muscle condition.

By Stage 4, most patients have significant extra-renal signs, and quality of life becomes the priority. That said, the IRIS guidelines are clear that we don't abandon disease-slowing treatment altogether at this stage - but we balance it alongside, and sometimes in favour of, symptomatic management.

As nurses and technicians, our priorities for these patients include:

  • Mantaining hydration and monitoring/administering fluid therapy

  • Managing nausea, vomiting and inappetence

  • Ensuring appropriate long-term dietary management (not while the patient is hospitalised or inappetent)

  • Managing hypokalaemia where present

  • Managing anaemia of chronic disease where present

Managing hypertension and proteinuria (regardless of the patient’s CKD stage)

Our target systolic blood pressure in CKD patients is below 160 mmHg. For hypertensive or severely hypertensive patients, treatment will be initiated by the vet, and our role is in measurement, monitoring, and early detection of complications.

When monitoring response to antihypertensive treatment, we're watching for:

  • Changes in blood pressure: we’re aiming for below 160 mmHg, while avoiding hypotension which will impact renal blood flow

  • Increases in creatinine after starting antihypertensive treatment: small increases are expected - the guidance says up to a 45 µmol/L increase is normal. But a marked increase needs flagging with the vet immediately, as we may need to stop treatment

  • Signs of hypertensive ocular damage: including sudden blindness, hyphema (blood in the eye), or retinal detachment 

  • Neurological signs: mentation changes such as dullness or seizures can indicate hypertensive encephalopathy

Hypertensive patients require close monitoring long-term, at least every three months once stable. So these are patients we're going to be seeing regularly, and building a relationship with over time - something we’re ideally placed to do as nurses and technicians.

Proteinuria is treated using an angiotensin receptor blocker medication like telmisartan. These drugs should NOT be started in dehydrated or hypovolaemic patients, as they work by controlling renal blood flow, and renal blood flow may be reduced in these patients.

Because these drugs rely on good renal perfusion to work safely, and in a dehydrated patient they can decrease glomeruluar filtration rate and therefore impair renal function. If one of our CKD patients comes in unwell and they're on a drug like benazepril or telmisartan, we need to flag this to the vet. The drug may need to be paused until the patient is rehydrated and stable.

Monitoring response to treatment involves serial UPC measurements, which we’ll combine with bloodwork to check renal parameters in most cases.

So what does all of this mean for us as veterinary nurses?

I want to take a moment before we finish the episode to talk about what all of this means for us as nurses and technicians - because while most of this staging info is what our vets will be focusing on, there is NO reason we can’t use this information to plan and deliver nursing care.

And I genuinely think this is important, because CKD is a condition that really demonstrates the value of nursing care over time.

These patients aren't just with us for a single hospitalisation. They're with us for months or (hopefully) years. We see them coming in for bloods, their blood pressure checks, their restaging reviews, to pick up more renal diet, for some subcut fluids every now and then, and everything inbetween. And because of that, we have a unique opportunity to build real relationships with these patients and their families, and to notice those subtle changes that might otherwise be missed.

We notice the cat who's lost another hundred grams since last month. The dog whose caregiver mentions he's a bit less keen on his food at the moment. The cat whose skin tent is a little more pronounced today. These things, and so many more, are why we should all be doing more long-term nursing with our renal patients.

What does our CKD nursing care look like?

Before we close out the episode I want to leave you with a really practical list of things to take away from what we’ve discussed and use with your own kidney disease patients.

Here’s what to think about, whether you’re managing them in the hospital or as an outpatient:

  • Accurate and consistent blood pressure measurement: using consistent technique, appropriate cuff size, and minimising patient stress

  • Urine sample collection: ensuring the method is appropriate, prompt processing and accurate labelling - especially for UPC measurement, where we’ll sometimes pool samples over multiple days

  • Weight and body condition scoring

  • Muscle condition scoring: CKD causes muscle wasting, and muscle condition score should be assessed alongside BCS using the WSAVA MCS tool

  • Food intake monitoring: amounts offered and consumed, daily in hospital and appetite at home

  • Hydration assessment: skin turgor, mucous membrane moisture, acute weight change, urine output monitoring

  • Fluid therapy management: correct fluid type, rate, monitoring for overload or inadequate replacement

  • Medication administration: considering supportive treatment like antiemetics and appetite stimulants alongside treatment for proteinuria/hypertension

  • Electrolyte awareness: monitoring for hypokalaemia and alerting the vet to any changes

  • Client communication and education: how to introduce a renal diet, how to increase water intake, home monitoring, signs to watch out for, when to call or come back in

And then there's the softer side of it - except that it's not soft at all, really, and I say that as someone who managed CKD in their own cat for 7+ years. 

Our clients are often managing a chronic disease in a beloved companion, often for a very long time. It can be easy for this to impact the human-animal bond and for our clients to start seeing their pet as a ‘patient’ over time. 

They may well be scared, tired, or feel guilty, and part of our role is in supporting them as well as the patient.

We can't cure CKD, but we can make an enormous difference to how supported they feel, and to the quality of life for their pet, and this is a huge area of potential for us as nurses and technicians.

So to close out today’s episode…

CKD is a complex, progressive disease that we cannot cure, but we CAN manage effectively, and we can make a real difference to quality of life through careful management.

The IRIS staging system gives us a really clear framework for doing this. Four stages based on creatinine and SDMA. Substaged by proteinuria and blood pressure. And at each stage, a specific set of management priorities - shifting from slowing progression in early disease to maximising quality of life in later stages.

The final points I want to leave you with today are:

  • CKD is often already advanced by the time we see obvious clinical signs, which is why serial monitoring and early detection matter so much

  • Staging must be done on a stable, hydrated patient, not when they present with signs of acute deterioration

  • SDMA is not a replacement for creatinine - these tests tell us different things, with SDMA generally being used more for early detection and diagnosis

  • Proteinuria and blood pressure substaging are vital in every CKD patient - even if the blood pressure is normal, documenting baseline values and trends are really important

  • A therapeutic renal diet is a treatment in itself, and introducing it before inappetence develops gives us the best chance of compliance

  • Take care with antihypertensives or proteinuria treatments in unwell patients - we need to avoid these where renal perfusion is a concern

  • Our role shifts from progression-slowing support in early disease to intensive symptomatic nursing in later stages, but despite that, through it all, our role is vital and cannot be overlooked.

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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