127 | Acute kidney injury in dogs and cats: myths, misconceptions, and how we should REALLY nurse these patients in 2026

PodcastNursingRenalEmergency + Critical Care
Written By Laura Jones

In today’s episode, we’re continuing our renal and urinary revisited series. Last time we took a big look at CKD and all of the new evidence around its treatment, and this time we’re turning our attention to acute kidney injury. 

AKI is one of the diseases I see go wrong a LOT, because there are still - I think - a lot of misconceptions and myths about how we treat it, especially when it comes to things like fluid therapy.

If you’re like me, you probably grew up as a VN thinking that kidney disease = treatment with aggressive fluid therapy. The idea behind this was that high rates of IV fluids would ‘flush’ the kidneys and bring the numbers down - and we applied it to almost every azotaemic patient that came through the door.

Looking back, I wonder how many of those patients had fluid overload that I didn’t spot - because I didn’t know to look for it. And now, it’s one of the biggest areas I tell nurses to take initiative on and monitor for when caring for their kidney patients - because we see it all the time.

We last chatted about AKI over 100 episodes ago, and since then, there’s been new evidence on how we manage it. In fact, a few months after that episode went live, the International Renal Interest Society (IRIS) published the first ever consensus guidelines on diagnosing and managing AKI in dogs and cats. We’ve had some great updates on top of that since, too, and all of that means we've got a much clearer picture of how these patients should be cared for - and where our skills as veterinary nurses and technicians fit in to it all.

In the last episode we also touched on the fact that AKI and CKD aren't the completely separate diseases we used to think they were - and we’re going to chat a lot more about that today.

Across the next half an hour or so we'll look at what AKI actually is, how it's related to CKD, how we tell the two apart, and why we manage them so differently. And then we'll look at some of the biggest myths and misconceptions around AKI - and what they mean for us when we're nursing these patients.

But before we do that, what actually is acute kidney injury?

AKI is now defined as an injury to the kidney tissue, with or without a decrease in kidney function. That injury can range from a mild insult that doesn’t actually cause bloodwork changes (meaning its virtually undetectable), all the way to overt kidney failure.

If you’ve been nursing for some time (like me!) you’ll probably remember AKI being called ‘acute renal failure’ previously. That term has really fallen out of use, being replaced by AKI for the best part of the last 10 or so years. And the reason we’ve stopped calling it ARF is because it only described those extreme cases at the end of the range. AKI also includes the patients whose kidneys have been damaged but are still coping, which is arguably where we want to catch them, because in these cases we have the most opportunity to intervene.

Community-acquired versus hospital-acquired AKI

We’ve traditionally split AKI according to where in the BODY the ‘injury’ takes place, but we can also describe AKI according to which LOCATION the injury takes place in.

Community-acquired AKI happens outside the hospital.

For example, think of a dog that's eaten grapes, a cat that's been exposed to lilies, or a patient that's become severely dehydrated. There's usually a delay of a few days between the insult and presentation, so by the time we see these patients, they're often already azotaemic.

Hospital-acquired AKI, on the other hand, develops while the patient is with us.

It used to be considered uncommon in veterinary patients, but it's being recognised more and more - partly because we're monitoring more closely, and partly because we're treating more critically ill and geriatric patients with multiple comorbidities.

This isn’t necessarily iatrogenic (ie caused by something we’ve done) - though it can be. But if we think about some of the more critical patients we see, such as our septic patients, or patients with complex diseases such as IMHA, many develop AKI while in hospital as a consequence of their primary disease process.

Patients at higher risk of this include those with pre-existing kidney disease, heart disease or sepsis, those receiving nephrotoxic drugs, and those undergoing anaesthesia. IRIS recommends that hospitalised patients with these risk factors have their kidney function monitored at least once daily, because their clinical signs, at least initially, will usually relate to whatever they were admitted for rather than their kidneys.

And this is particularly important for us to consider as veterinary nurses and technicians, because we’re the ones monitoring these patients closely in the hospital. This means we’re often the ones picking up on those subtle changes first, flagging them to the vet, and adjusting care as needed under vet direction. 

And then we’ve got our ‘traditional’ classifications - prerenal, renal and postrenal.

As we’ve already touched on, the causes of AKI are grouped by where the ‘injury’ or problem is within the body.

  • Prerenal AKI is caused by reduced blood flow to the kidneys - for example hypovolaemia, other causes of shock such as sepsis, heatstroke, cardiac disease, etc, alongside things like Addison’s and thromboembolic disease. It's often volume-responsive, which means it improves once perfusion is restored.

  • Intrinsic (renal) AKI is caused by injury to the kidney itself. This includes toxins such as ethylene glycol, lilies in cats and grapes and raisins in dogs, nephrotoxic drugs such as NSAIDs and aminoglycosides, and infections such as leptospirosis and pyelonephritis.

  • Postrenal AKI is caused by an obstruction to urine flow, or a leak - urethral or ureteral obstructions, or a ruptured urinary tract (bladder, ureter or urethra) causing a uroabdomen. 

Another important point on the topic of where in the body is this: both prerenal and postrenal AKI can lead to renal/intrinsic renal AKI, complicating matters further. A kidney can only cope for so long with decreased perfusion before the tissue within that kidney suffers, for example.

Also, even with thorough investigations, the exact underlying cause of AKI isn't always found. In fact, in one study looking at causes of canine AKI, there was no specific cause identified in almost ¼ of cases.

So that’s what acute kidney injury is, and what causes it. But what happens during AKI? 

AKI also moves through four phases or stages. Now these are not formal stages in the CKD sense, and they’re not tied to things like blood results - instead, they describe how AKI progresses.

While they don’t change how we nurse our patients, it’s imporant we’re aware of them as and knowing these helps us understand the changes we see in our patients, and our aims when treating them.

  1. Initiation - the initial insult damages the tubular cells within the nephrons. At this point, there may be no changes in bloodwork or clinical signs at all.

  2. Extension - ongoing hypoxia and inflammation cause further tubular cell death. Damaged cells can slough off into the tubules, which we may see as casts in the urine sediment if you’re examining a sample under the microscope, or reviewing external results.

  3. Maintenance - at this point the injury to the kidney has reached maximum damage. The tubular cells start to regenerate, but azotaemia and uraemia are usually present, and urine output may be very high or very low. This phase can last days to weeks.

  4. Recovery - the cells mature and regain their function, and the patient often becomes polyuric. This phase can last weeks to months.

The important part here is that, as long as the basement membrane of the tubule is intact, those tubular cells can regenerate. And that's the fundamental difference between AKI and CKD - an injured kidney has the potential to recover, whereas the nephron loss we see in CKD is irreversible (hence the term ‘injury’, rather than ‘failure’).

So are AKI and CKD separate conditions, or are they part of the same disease spectrum?

We were always taught AKI and CKD as two completely separate conditions - one sudden and potentially reversible, the other slow, progressive and permanent. And while that's still broadly true, we know now more about the relationship between the two.

We’re now starting to think of these conditions as being part of one big kidney disease continuum, as we chatted about last week, with AKI and CKD sometimes overlapping in the same patient.

Some of the strongest evidence for this came from research into biomarkers of kidney injury. Markers like NGAL were originally being studied as early markers of AKI. But when researchers measured them in animals with apparently stable CKD, they were consistently higher than in healthy animals - suggesting there's ongoing, active damage happening in these ‘stable’ kidneys.

So IRIS - the International Renal Interest Society, and the provider of much of our kidney disease education and guidelines - now suggest these conditions may be linked, and that the main difference between them may be the rate at which the disease progresses.

A helpful way to imagine this is to think about how much working kidney tissue a patient has over time. 

Some patients lose a big chunk of their kidney function in one single, severe injury. Others have lots of small acute injuries, where each one takes away a little more. Others have a sustained, ongoing injury, but all of these different injuries can cause the same result for our patient - varying degrees of chronic kidney disease.

This links back to what we chatted about in the last episode, where the new CKD guidelines describe episodes of acute injury on top of chronic disease - many of which go unnoticed.

There's another term you might start to hear more of, and that's acute kidney disease, or AKD.

In human medicine, AKI is defined as an abrupt decrease in kidney function over less than 7 days, acute kidney disease develops over 7 to 90 days, and CKD is present after more than 90 days. 

The IRIS guidelines describe every dog and cat that has had an AKI as passing through a period of AKD between days 7 and 90. This is the window where the kidney either recovers, partly recovers, or moves on to CKD - and if we think about it, that makes sense, because we’ve traditionally described patients as having CKD when renal dysfunction has been present for at least 3 months.

So that’s AKI, CKD, AKD, and the relationship between them all. But how do we assess kidney function, and which tests do we use?

A big part of this is understanding what our tests are actually telling us, and this is an area where there has been quite a bit of change over the last few years - because we’ve now got newer tests in our kidney patients.

Broadly speaking, we can split our results into functional markers and injury markers.

Creatinine, SDMA and urea are functional markers. They reflect glomerular filtration rate, and as we chatted about last episode, creatinine has a non-linear relationship with GFR, so a big drop in GFR may only cause a small rise in creatinine early on.

Injury markers, on the other hand, are different. 

These are parameters measured in the urine, showing damage to the nephrons. Usually, they indicate proximal tubular damage - as the proximal tubules are the most ‘active’ part of the kidney (they ‘recycle’ the most substances).

Because of this, injury markers can increase before, or even without, any change in our functional markers. Several are being studied, including NGAL, KIM-1 and cystatin B. Cystatin B is now commercially available, and being used more and more commonly in the diagnosis and investigation acute kidney injury (and CKD).

These tests allow us to separate two main questions about the kidneys: first, how well are they working overall, and second, are they actively being damaged or injured right now?

For example, a patient with stable stage 2 CKD might have raised functional markers, but no evidence of active injury. However, a patient who had a hypotensive episode under anaesthesia might have completely normal functional markers, but evidence of active injury. Those are two very different patients, but if we only looked at BUN and creatinine, one of those patients would look absolutely fine.

So how do we tell AKI and CKD apart?

In many patients, this is fairly straightforward, but in others it can be really difficult, especially because we know the two conditions overlap a lot. And it’s difficult mostly because we use the same markers - creatinine and SDMA - to diagnose both.

Alongside diagnostic results, our vets will be using information from the history and examination to differentiate the two. And as well as bloods, they’ll use urine analysis and imaging findings (particularly ultrasound) to help with that differentiation.

History and physical examination

Patients with AKI typically have no history of chronic illness, and present with a sudden onset of fairly non-specific signs such as vomiting, diarrhoea, inappetence and lethargy. Their signs are often more severe than the azotaemia alone would explain, because AKI often occurs as a consequence of an underlying disease process - meaning their clinical signs can be quite varied. 

On examination, they often have good body and muscle condition, and their kidneys may be normal-sized or enlarged, and painful.

If we compare this to patients with CKD, they typically have a slower, more progressive history, including PUPD, reduced appetite, and weight loss. But as we chatted about last episode, caregivers often miss these signs or put them down to age - so if they're not in the history, that doesn't rule CKD out.

Bloodwork and urine analysis

We can’t differentiate AKI and CKD based on single results, but looking at a few in combination can help us get a better idea of which our patient has.

Severe azotaemia in a patient with no history of illness points towards AKI, or an acute flare of CKD.

Phosphate tends to rise gradually alongside creatinine in CKD, thanks to those compensatory mechanisms we talked about with CKD-MBD. In AKI, those mechanisms haven't had time to kick in, so phosphate is often disproportionately high compared with creatinine.

Calcium tends to be normal to low in AKI and normal to high in CKD - unless hypercalcaemia has caused the AKI, for example through things like vitamin D toxicity.

Anaemia is more typical of CKD - especially the later stages of CKD - though AKI patients can become anaemic too, from things like inflammation or gastrointestinal bleeding.

In the urine, active tubular damage in AKI can cause glucosuria with a normal blood glucose, and casts in the sediment. But only around 30% of animals with AKI have either of these - so if we don't find them, that doesn't rule AKI out.

Imaging

On ultrasound examination in CKD the kidneys are typically small and irregular, with poor corticomedullary definition. AKI kidneys usually keep their normal architecture, and are often enlarged.

There are exceptions to this, for example amyloidosis, lymphoma and polycystic kidney disease can all cause enlarged kidneys in CKD, but in general we expect to see smaller kidneys in CKD than in AKI. 

Ultrasound is also essential for picking up ureteral obstructions and hydronephrosis, a common cause of AKI (and associated CKD) in cats.

What about acute-on-chronic kidney disease?

The trickiest patients are those with acute-on-chronic disease, because they have features of both. Some have advanced CKD with a relatively small acute decompensation, while others have early CKD with a severe acute injury.

This is where previous blood results are incredibly valuable - and it's another reason the senior screening we chatted about in episode 125 matters so much. We need those baseline results to compare to, so this is another area where we can really champion renal monitoring and care as veterinary nurses and technicians.

OK, so our patient has AKI. How do we know how bad it is? Let’s talk about grading.

In the last episode, we chatted about how CKD patients are staged once they're stable and hydrated. AKI has its own system, and it's called grading rather than staging.

The terminology is important - staging AKI refers to where in the cycle of damage and recovery the kidney is, but grading refers to the severity of bloodwork changes we see.

We need a separate system to traditional CKD staging, because AKI has the potential to recover. These patients don’t stay in one static stage - instead they can move up the grades as their injury gets worse, and back down again as their kidneys recover.

The IRIS AKI grades are based on serum creatinine levels, and are as follows: 

IRIS AKI Grade Serum Creatinine
Grade I Less than 140 µmol/l (less than 1.6 mg/dl)
Grade II 141 to 220 µmol/l (1.7 to 2.5 mg/dl)
Grade III 221 to 439 µmol/l (2.6 to 5.0 mg/dl)
Grade IV 440 to 880 µmol/l (5.1 to 10.0 mg/dl)
Grade V More than 880 µmol/l (more than 10.0 mg/dl)

Each grade is then subgraded by whether the patient is oliguric or non-oliguric, and whether they need renal replacement therapy.

How does managing AKI differ from managing CKD?

Managing AKI and CKD are entirely different, and understanding this difference is essential for us when caring for these patients as nurses and technicians.

Some of the things we do routinely for our CKD patients are exactly the things we avoid in AKI - especially when we talk about things like diet and fluid therapy.

CKD AKI
Main aim Slow progression and support quality of life Support the patient while the kidneys recover, and prevent further injury
Fluids Maintain hydration long term, sometimes at home Correct deficits quickly, then match input to output
Protein Renal diet with restricted phosphate Protein restriction not indicated
ACE inhibitors and ARBs Used for proteinuria and hypertension Avoided
Phosphate binders Added if diet alone doesn't reach target Not used until enteral feeding starts
NSAIDs Cautious use possible in stable patients Contraindicated
Monitoring Weeks to months between rechecks Several times a day

Fluid therapy in acute kidney injury

In CKD, fluid therapy is usually about supporting hydration long term. In AKI, IV fluid therapy is a mainstay of treatment, but it's very targeted - we need correct the deficits, then match ins and outs to avoid overload. We'll come back to this in a moment, because it's at the heart of one of our biggest myths.

Nutritional support in patients with kidney injury

In CKD, renal diets are one of our most important treatments - but in AKI, the focus is completely different.

AKI patients are in a severe catabolic state. In one study, dogs with AKI fed 1.3 times their resting energy requirement still lost around 1.2% of their body weight every day. Because of this, IRIS suggests their calorie intake should be more than 1.5 times RER (of course adjust this to the individual patient, considering their risk of refeeding syndrome and metabolic consequences), and that nutritional support should start if anorexia has lasted, or is expected to last, more than 48 hours.

Protein restriction isn't indicated in AKI, and may even be harmful to recovery. Highly digestible diets are preferred instead - generally speaking, the best diet for them is the one they want to eat in hospital. 

If a renal diet is needed, this decision is made after discharge, once the patient is re-staged and we know the extent of any CKD present. 

Medications in AKI - which do we avoid and why?

There are a few key medication differences to be aware of. ACE inhibitors and angiotensin receptor blockers, which are common in CKD, should be avoided in AKI - amlodipine is the first-line choice for hypertension instead. Phosphate binders aren't used until the patient is eating or being tube fed, because they work by binding phosphate in food. And while we chatted last episode about cautious NSAID use in stable CKD, NSAIDs are contraindicated in AKI, with opioids being the first-line choice for analgesia.

Every medication should be reviewed for its potential to damage the kidneys and how it's eliminated, since many drugs that are excreted by the kidneys may need their dose or dosing interval adjusted.

And then there’s one AKI treatment we don’t use in CKD - dialysis.

Finally, there's one option for AKI that doesn't exist in the same way for CKD - extracorporeal therapy, aka renal replacement therapies or dialysis. There are two forms - haemodialysis and peritoneal dialysis. The theory behind them is that they take over the kidney's excretory function while it recovers, buying time for the tubular cells to regenerate.

It isn't available everywhere, and it can be costly, but the guidelines recommend speaking to a centre that offers it early on, rather than as a last resort. Typically, indications for renal replacement therapies include a creatinine above 442 µmol/l (5 mg/dl) that's still rising in a hydrated patient, oligoanuria that isn't responding to treatment, severe fluid overload, or electrolyte disturbances that can't be controlled medically.

Let’s talk about some of the common myths and misconceptions in acute kidney injury.

1: ‘We need to flush the kidneys’

This first one is a big one and probably the one we’ve all heard the most often.

For a long time, forced diuresis - giving IV fluids at multiples of the maintenance rate to ‘flush out’ the kidneys - was standard practice.

The logic seemed sensible. More fluid in, more urine out, more toxins cleared, and the kidney values come down. The problem is that giving more fluid doesn’t increase GFR, and acutely injured kidneys are usually not able to process that extra fluid.

The evidence now shows that high fluid rates, beyond what's needed to restore kidney perfusion, don't improve outcomes - but they do increase the risk of fluid overload, which is a big problem.

Why is fluid overload such a big problem?

When fluid builds up in the kidney tissue, the pressure inside it rises. This reduces lymphatic drainage, congests the small blood vessels around the tubules, activates the RAAS and increases inflammation - and ultimately GFR reduces. This is sometimes called congestive nephropathy.

So in trying to help the kidney, too much fluid can actually make its function worse.

Alongside the impact on the kidney, fluid overload can cause intestinal oedema and ileus, cardiac dysfunction, liver congestion, poor wound healing, pulmonary oedema and pleural effusion. It's also a key contributor to hypertension in these patients.

It's really common, too. Around 55% of AKI patients that need renal replacement therapy are already fluid overloaded when they arrive, and in dogs, fluid overload during hospitalisation is associated with lower survival to discharge and longer hospital stays.

So what do we do instead?

Instead of flushing the kidneys with high rates, we need to firstly restore perfusion, then rehydrate the patient, and then match their fluid input and fluid output. This is called a zero fluid balance, where the fluids going in replace urine output, gastrointestinal losses and insensible losses.

If a euhydrated patient is anuric, with no other losses, their IV fluids may actually need to be stopped, which feels wrong, but is absolutely the right thing for them.

This is an important area of nursing.

This approach relies completely on monitoring - and that's where we come in. We need to be weighing these patients regularly, monitoring their urine output, and looking for those subtle signs of fluid overload.

‘He's urinating, so he must be getting better’

Linked to all of this is another assumption we hear a lot - that if the patient is producing urine, the kidneys must be recovering.

First, we can only call a patient oliguric once they're fully hydrated, because a dehydrated patient won't produce normal amounts of urine. Once they're euhydrated, urine output below 1 ml/kg/hour over 6 hours should raise concern, and less than 0.3 ml/kg/hour over 6 hours is classed as oligoanuria.

Diuretics such as furosemide may be used to try to increase urine production in oligoanuric patients, which can help manage fluid overload and hyperkalaemia. But there's no solid evidence that diuretics change the outcome of AKI, and they don’t increase GFR - they just help manage overload.

At the other end of the scale, patients in the recovery phase can become really polyuric, producing more than 2 ml/kg/hour. These patients need their fluid rates matched to their urine output so they don't become dehydrated, close electrolyte monitoring (hypokalaemia is common during this phase), and they need to be really carefully weaned off IV fluids once their kidney values have stabilised. 

2: ‘His kidney values are back to normal, so he's cured’

Because we (generally, across the profession) put so much emphasis on our results, it can be easy to focus more on them than the kidneys themselves.

BUN and creatinine don’t rise until significant renal dysfunction - be that permanent or temporary - is present. And this means that our numbers can be ‘back to normal’ while renal dysfunction remains.

This means that recovery from AKI can take anywhere from days to months. Around 55% of dogs with AKI have a normal creatinine by the time they're discharged, and a further 20% normalise after discharge - sometimes several months later, as the remaining nephrons enlarge to compensate.

So does a normal creatinine mean the kidneys have fully recovered? Not necessarily.

Because creatinine is an insensitive marker of renal function, a patient can have a normal creatinine and still have a lower GFR than they did before their AKI. On top of that, an episode of AKI makes the kidney more vulnerable to future injury and progression.

That's why the IRIS guidelines recommend that every patient that recovers from AKI is monitored as an IRIS CKD stage 1 patient - because stage 1 CKD is a patient with normal creatinine but other evidence of renal dysfunction.

In practice, that means monitoring these patients through things like regular rechecks, and these rechecks are great opportunities for nurse clinics, as we chatted about in the last episode.

I want to end with a few more rapid-fire myths in AKI management. 

3: ‘He needs a renal diet straight away’

Not in AKI. As we covered earlier, protein restriction isn't indicated in the initial management of AKI, and may slow recovery because of how catabolic these patients are. In one study, dogs with AKI fed a high-protein recovery diet didn't produce any more urea than dogs fed a mildly protein-restricted diet - which suggests these patients may actually need more protein, not less.

4: ‘They’ll start eating again as their injury recovers’

I mean, true to a point, but that’s not a reason to withhold assisted nutrition or consider alternative ‘less invasive’ options such as force-feeding. Without getting on my soapbox (much) we know that force-feeding is ineffective, it can cause food aversion, and it increases the risk of aspiration pneumonia - especially in patients that are nauseous and vomiting. And these patients are already at risk of respiratory complications due to their high risk of fluid overload.

Instead, IRIS recommends enteral feeding via a feeding tube. General anaesthesia can be provided safely in most AKI patients as long as kidney perfusion is maintained, so an oesophagostomy tube is usually an option - but where it isn’t, a nasal tube can be easily placed under light sedation in most cases, by us as nurses and technicians.

Nausea management goes hand in hand with this. Nausea can persist even when a patient is on maropitant, so multimodal antiemetic therapy is often needed.

5: ‘The higher the grade, the worse the prognosis’

Not necessarily - the severity of azotaemia isn't an accurate indicator of whether the injury is reversible. The grade reflects the window of opportunity for recovery, not the likelihood of recovery.

It’s actually the underlying cause that is one of the biggest factors. In one study of dogs, 82.7% of those with volume-responsive AKI survived, compared with 47.8% of those with intrinsic AKI. Survival in cats with lily toxicity can be as high as 87.5 to 100% (depending on how quickly they're treated) while survival after ethylene glycol toxicity is around 12% in dogs and 8% in cats.

6: ‘If his bloods haven't improved after a couple of days, he isn't going to recover’

This one takes me back to that ‘3 days of fluids’ approach I mentioned at the start of the last episode. It’s also one that carries a lot of personal meaning, because when my own cat Nigel was hospitalised with AKI-on-CKD, his creatinine was still in the 900s after 4 days of IV fluids. A month later it was 400 - and all I did was give him enteral water (and nutrition, of course!) via an O tube while he was inappetant.

A lack of improvement in kidney function in the first few days of treatment does not mean the patient can't recover. Patients with severe AKI are typically hospitalised for around a week, and some need several weeks, so we can’t use those initial results to indicate outcome.

What does all of this mean for us when we're nursing AKI patients?

There's an enormous amount of nursing involved in caring for these patients - and much of the monitoring that guides their treatment comes from us.

Alongside the fluid balance monitoring we've already chatted about, the IRIS guidelines recommend:

  • Blood pressure at least 2 to 4 times a day. Hypertension affects up to 80% of dogs and 60% of cats with AKI, and IRIS recommends keeping systolic blood pressure below 160 mmHg to reduce the risk of complications such as seizures, encephalopathy and retinal detachment. Just like with our CKD patients, situational hypertension during measurement (from things like pain or stress) needs to be considered, and this is another area we play an essential role in as veterinary nurses.

  • Electrolytes at least twice daily to start with, and more often if there are severe abnormalities. Hyperkalaemia is a particular concern in oliguric patients because of its effects on the heart, while hypokalaemia is common in the polyuric recovery phase.

  • Acid-base status at least once daily in hospitalised patients, until it no longer needs active management.

  • Pain scoring every 4 to 6 hours using a validated scale, such as the Glasgow Composite Measure Pain Scale or the Feline Grimace Scale.

There are a few other things to keep an eye on too:

  • Heart rate and rhythm. Arrhythmias are common in uraemic patients, and those linked to severe hyperkalaemia or causing cardiovascular compromise need treatment.

  • Respiratory rate and effort. Around a third of AKI patients develop respiratory compromise - from pulmonary oedema, aspiration pneumonia, or pulmonary haemorrhage in dogs with leptospirosis.

  • Nutrition, recording calorie intake against the patient's target, caring for feeding tubes and monitoring nausea.

  • Blood sampling. Repeated sampling can contribute to anaemia in these patients, so it's worth keeping sample volumes to a minimum - and avoiding the jugulars if dialysis is a possibility. PICC lines or central lines (where appropriate) are a great use of our skills here, and can help preserve veins and avoid repeated venepuncture for our patients.

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

To recap, acute kidney injury is a sudden injury to the kidney, which may or may not cause a drop in kidney function - and unlike CKD, it has the potential to recover. We now think of AKI and CKD as part of the same continuum, where repeated or severe injuries can lead to chronic disease, and CKD leaves patients more vulnerable to further injury.

AKI is graded instead of staged in the CKD sense, and even a small rise in creatinine within the reference interval can mean a patient has an AKI. While some parts of their management overlap with CKD, many are completely different - especially things like dietary choice, and the use of some of our medications like RAAS-inhibitors.

We've moved away from ‘flushing the kidneys’, towards targeted fluid therapy that restores perfusion, corrects dehydration and then matches what goes in to what comes out. And a normal creatinine at discharge doesn't mean the kidneys are back to how they were before - these patients should be monitored as CKD stage 1 patients from then on, so our nursing care needs to continue past discharge from the hospital.

All of this relies on careful, consistent monitoring and nursing care - weight, urine output, blood pressure, pain scoring, nutrition and so much more. There are so many ways we can make a difference in the care of these patients, and so many skills we can use in the process!

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