Hi everyone. My name is Sarah Stuart. I'm here today to talk to you about the diagnosis and management of acute acute on chronic and chronic kidney disease in dogs and cats.

I found quite often during my time, teaching at the Royal Veterinary College that the distinction between these different clinical scenarios can often Be a challenging point for clinicians at all levels of their education journey. So I hope through the discussions we'll have tonight in this lecture, you'll have some good take home points to help you the next time you have unexplained azotemic patient presenting to you in your practise. So, on that note, I did want to first begin with a clinical case.

So, we have a patient I saw, about a year and a half ago at the Royal College named Pascal, and he's a 15 year old male neutered domestic long hair. He presented to us with a previous diagnosis of early stage 2 chronic kidney disease, which was first diagnosed by his primary care veterinarian about 8 months ago. He was not hypertensive, non-proteinuric, was started on Purina F canned food, and owners didn't quite follow up with their recheck schedule as advised, so we hadn't sort of seen him since that time.

So he then presented to us with acute onset lethargy, vomiting, and inappetence through our emergency service overnight. The emergency service team found on their exam that he was about 5 to 7% dehydrated. He had a slightly reduced body condition score of 4 out of 9 and a moderately reduced muscle condition score of 1.5 out of 3.

We will talk about muscle condition score a bit later in the talk, if you're not familiar with that, so stay tuned. On abdominal palpation, it was possible to appreciate small irregular but non-painful kidneys. So some initial blood work was taken at admission.

We noted a PCD of 22% with a mildly elevated, total solids of 88%. So our BUN and creatinine have, BUN has disappeared, but I'll say it was off the off the charts, creatinine is also markedly. Elevated at 800.

We're able to get a urine sample before starting any IV fluid administration, and that showed Iosce area at 10009, with an inactive sediment. So no evident white blood cells, bacteria, or casts looking that that quickly inhouse. So the owner's perspective, they had some financial constraints, but they were very keen to, to do whatever was possible to try and get Pascal out of the hospital, ideally with, you know, a good outcome.

So, The working diagnosis when Pascal was transferred to us in the medicine service, given his prior history of CKD was concerned that we might have be dealing with progression of his disease, in which case there might not be a lot we could do to help him. We could have a significant pre-renal component, we'll talk about that shortly. That might have been due to a concurrent illness, potentially like pyelonephritis, but generally because of his pre-existing chronic kidney disease, there was concern from the ER service that he might have a, a poorer prognosis, so that was sort of what the owner had gotten as her, initial setup before being transferred to us.

So. For now, keep Pascal's case in the back of your mind. You can pause this presentation and maybe take a moment or two to write down a problem list and some prioritised differentials, and maybe what your treatment plan, and diagnostic plan would be for him.

And then as we go through the presentation, we can, we'll revisit his case and we'll see if what you've come up with for Pascal matches what ended up happening to him in hospital. So, They're going in now to begin talking about kidney disease. We have to first start by, making sure we understand what glomerular filtration rate is because this is what we use to talk about and refer to the severity of renal dysfunction.

So what is GFR? Glomerular filtration rate is the rate at which the kidneys are filtering our blood, and it represents the volume of plasma filtered in the by the kidneys per unit of time. So this is the single most useful test of renal function.

We don't often run GFRs in our veterinary patients though, so we tend to use other lab work parameters as approximators of GFR. So those would most commonly be things like creatinine and more recently SDMA, but we do have to keep in mind the potential limitations of those tests and for what we use most often, we have a sort of exponential increase in that, the more advanced stages of kidney disease we get to. So the worry is we might have a creatinine that stays within the normal reference range just up until we've lost a significant amount of kidney function, in which case then it's going to start rising exponentially.

So where GFR is helpful, if we did have a case, say where we weren't really certain if there was significant renal dysfunction, we could run a GFR to try and detect evidence of renal dysfunction earlier than creatinine maybe would indicate for us. So how are we utilising GFR in the context of this talk? It's really to determine the degree of dysfunction we have in the kidneys.

So moving on to introduce acute kidney injury or AKI. This is an acute abrupt decrease in kidney function, which has the functional effect of resulting in reduced GFR. We also see a reduction.

In the tubular functions, so the concentrating ability of the kidneys, and production of urine depending on the severity of that. So CK AKI is a continuum of damage to the kidneys. So we can see in our image here below, we've got potential for different stages of, of this disease process to .

Continue to go back and forth. So if we have patients that are have an underlying predisposing factor for AKI that could lead to some damage, we could have some complications. Those complications could increase your risk of getting more AKI, that could result in a worsened GFR and we can, if this cycle cannot be broken, ultimately we may lead to irreversible damage to the kidneys and death.

So we have a few different things that can cause acute kidney injury, and the ways in which we sort of think about that. So pre-renal, renal, and post renal causes. So, we'll talk about these a little bit separately, shortly, but if we think, you've probably heard this terminology before in the context of discussing chronic kidney disease and how we refer to azotemia.

So these two systems will be very similar. So, for pre-renal causes of acute kidney injury, this is issues with hemodynamics. So typically if a patient becomes significantly hypovolemic, so if we've had a sudden loss of fluids through acute vomiting, diarrhoea, or blood loss, the body is going to start to conserve blood flow to the critical organs, the brain and heart.

That means Like the kidneys and the gut will start to get a little bit shortchanged after a few hours, and if that pre-renal sort of hemodynamic issue is not corrected quickly enough, we will actually be able to intrinsically damage the kidneys. But when a patient is first presenting in a clinical state like that, even if they are showing signs of an AKI it might potentially be completely reversible if that was all a pre-renal component. Post renal causes of AKI are if we have something that is obstructing the flow of urine out of the body.

Most commonly that would be a urethral obstruction due to a stone. So those are gonna be pretty straightforward to diagnose, so we'll, leave post renal causes now to, to one side and really focus in. On the renal causes of acute kidney injury.

So the first of those would be things like ischemia. So if we had that pre-renal phase of reduced perfusion to the kidneys going on for long enough, ultimately that will lead to ischemic renal damage. We can have conditions causing inflammation in the kidneys that might be infectious or sterile in origin, so things like, glomerulonephritis, which could be immune mediated or could be secondary to infectious disease, so that could be things like tick-borne illnesses like, like Lyme nephritis, or we could see, infectious agents caused by bacteria like leptospirosis.

And we may also see a whole variety of nephrotoxins, so, antifreeze, which we have in our image here is what people most think of, but we of course have, examples of lily toxicity in cats, potential for grapes and raisins, and the, the working theories it's probably the tartaric acid in those for dogs. We won't read through you read you through the whole list of nephrotoxins, but. Certainly anytime I have a patient coming in with an unexplained AKI I will revisit that entire list, refresh myself to make sure there's no new causes that have come out in the literature recently, and I will run through that list with the owners, probably on multiple occasions.

If they aren't sure if there was an exposure, sometimes in the panic of the first presentation, they might not recall, so we keep revisiting just in case something jogs their memory. We can see renal lymphoma causing acute illness, and dysfunction in the kidneys, much more commonly in cats versus dogs. And then we can see hospital acquired causes of AKI.

So that would most commonly be seen in patients that have significant degree of systemic illness. So maybe they've come in, with a sepsis. Septic abdomen due to a perforated intestine.

They're very sick. We've gotten them through surgery, but due to all of the systemic sequelae of that disease process, we start to see damage to other organs. So again, usually those will be more straightforward cases of AKI to diagnose but still good to have on our radar.

Despite this nice list of differentials, unfortunately in many cases of acute kidney injury presentations, we don't ever definitively identify an underlying aetiology. So we'll continue revisiting differentials with the owners in the hopes that it a history fact might pop up after a few days, but in many cases we sort of have to treat the effect of whatever happened, if our exhaustive diagnostic searches don't reveal anything. So moving on now to defining chronic kidney disease.

If we say had an acute kidney injury that ended up causing irreversible renal damage, that could lead to fibrosis or scar tissue formation within the kidney, we're gonna be losing functional glomeruli and renal tubules that are doing the day to day jobs. The kidney to be excreting wastes and preserving water and electrolytes. So if we see that permanent damage, it's going to result in a reduction in renal function, reduction in renal urine concentrating ability, and glomerular filtration rate.

So again, back to the first topic we were chatting about. The name does what it says on the tin. So chronic kidney disease implies it's going to be a chronic process.

This isn't something that's going to happen overnight, but if we did have an acute insult to a kidney, maybe that happened, subclinically. We didn't actually see that patient in the hospital. We had a day or two of, sort of unexplained illness.

It is possible that we can have an acute insult causing CKD that was never detected, or that we have an underlying primary chronic process, something like a simmering chronic inflammatory situation that never causes a true AKI but causes damage that results in chronic dysfunction over time. So I did also want to take a moment to define emia here cause sometimes we do run into confusion about chronic kidney disease versus euremia and using the same term to sort of imply both things. So uremia is defined as the clinical syndrome of renal failure, where we start seeing clinical consequences of the kidney's dysfunction.

So we have clinically significant azotemia. So if we're thinking about the iris stage system, which we'll talk about shortly, but I'm sure you're all familiar with, we don't tend to see clinical signs of uremia until we have we're at sort of the high end of stage 2 and above. And we would also with the remic patient expect to see multisystemic clinical signs that are resulting from the kidneys not functioning appropriately, so that patient might be presenting with things like weight loss.

Appetite changes, maybe some intermittent vomiting and diarrhoea. We would expect to see PUPD, but again, many owners, if we have cats that are avoiding out of doors, they may not be picking up on things like polyuria, dogs that are doing their business out in the yard, so, and if we have a multi-pet household where they were sharing a water bowl, quite often owners aren't necessarily aware that PUPD has appeared. In with severe aremia, we might start to see things like neurologic abnormalities, where we have such a high buildup of renal toxins that can actually, start causing, sort of inflammatory changes within the brain.

But the key here is when we're saying a patient is presenting with uremia, they're not only in, they don't only have chronic kidney disease, they actually have the clinical syndrome of renal failure. So we can see amia occurring with severe acute kidney injury, acute on chronic kidney disease, and chronic kidney disease usually in those later stages. So we've defined acute kidney injury and chronic kidney disease.

Now we need to talk about how we classify them. So, I'm sure you're all familiar with the Irish International Renal Interest Society websites, one of the best veterinary resources out there and all free. So I'll give you tonight's going to be a bit of a highlight of everything that Iris has to offer, but I definitely recommend you, go and use peruse the site at your leisure, read through some of the articles we'll be talking about, and refer back to it, so you don't have to memorise everything in Iris.

Go back to the site, whenever you need to remind yourself. So, Iris has developed a grading system for acute kidney injury. Grading implies that something has the potential to change rapidly.

Acute kidney injury, as we said at the beginning, is a continuum. We can have patients that, their renal function is changing sometimes hour by hour in the ICU if say we have a septic patient that is rapidly declining. On the other hand, CKD, we've designed a staging system.

Staging implies that something is chronic and has been relatively static for a period. So Iris defines, sort of a chronic stable change as being present for a minimum of 2 weeks. So if we are assessing a patient with acute kidney injury, I can.

Take a sort of in the moment grade of their kidney disease. So 8 o'clock, you know, we're having a a a grade 2 episode going on. It's possible by 8 a.m.

The next morning that patient's disease will have progressed, we may have moved to a higher grade of AKI that's gonna require more intervention. On the other hand, for chronic kidney disease staging, I have to see that, you know, before I'm gonna start implementing treatment recommendations and giving a prognosis to the owner, I need to see that those values are stable and we can say, yeah, I'm confident that patient is in stage 2 or in stage 3, so that's going to require at least 2 sets of blood work 2 weeks apart that are not showing a significant difference. So how are these classification systems helpful for us clinically?

There's a couple of reasons. So they can help us standardise the severity of disease, which, for us on a day to day basis, I think is most helpful for giving owners appropriate prognostic and treatment options for the severity of disease their pet is presenting with. So, with a case like Pascal, we have to kind of have a chat with the owner about what do we think the chances of us getting him out of the.

Hospital are and then if we get him out of the hospital, how long do we potentially expect his life span to be? So if owners are making decisions for, say, a 5000 pound estimate, going in for multiple days of hospitalisation, Obviously we don't have a crystal ball, we can never tell them with certainty, but these systems, and all of these sort of evidence that they've generated in the literature to say a patient with X stage of disease to Lives for this long or has this degree of percentage recovery that can be very useful information for clients. It's also important for us on a research basis, because if we are doing studies, we have to make sure that if we're assessing an intervention, we're comparing all the patients in that treatment group, with the same level of disease.

So making sure that we have a classification system that we can stick them into at an accurate point in time. So, we're gonna introduce the grading system for acute kidney injury here. This system helps us characterise the severity and monitor progression of AKI when we're in the hospital.

So as we said, we'll get probably multiple grades for a patient during a hospital stay, that will change rapidly potentially over time. The grading scales based on a combination of the fasting blood creatinine concentration. So ideally we want to pull this after at least 12 hour fast, the patient's rate of your information, and whether or not we need to consider a renal replacement therapy.

So renal replacement therapy is things like intermittent hemodialysis. Continuous renal replacement therapy or peritoneal dialysis, basically an intervention where we are temporarily taking over the function of the kidneys because they are completely non-functional, not able to excrete any waste products, excess potassium, excess phosphorus, and water. So for what the other thing that is important to think about for acute kidney injury and sort of terminology, often we'll say a patient is presenting in acute renal failure, and what that image immediately calls up in our mind is a patient that's coming in very sick, usually very aotemic, and for I think a lot of students that I encounter in the hospital, that is sort of the picture they have in their mind of a patient with acute kidney injury.

But it's important. Remember, AKI is a continuum. We can have patients with AKI that have no clinical signs of it yet.

We just have mild increases in the creatinine, sometimes even within the normal reference range. So the key here is sort of resetting our, detection to have the, the concept that we're going to keep an eye out, and we have our eyes peeled for any patients that could have an early AKI because if we can catch that. In sort of intervene, administer appropriate treatment, then we have a chance of stopping that from progressing further, and ultimately, you know, having that patient present in 36 hours with an acute renal failure.

So the earlier we can recognise that an acute kidney injury episode is is present, the better we can hopefully get our patient outcome to be. So just to run through this grading system, so we can see here for grade one where we have a creatinine less than 140. This patient is non-emic and in most cases we wouldn't have the possibility of an EK on our on our radar just looking at that number, but say if this is a patient that's come in and I know we've just had a significant hypovolemic episode, we lost a lot of blood, that would be a patient that I would be worried about.

We might have the potential for . Sort of a, a grade 1 AKI I'm gonna need to be rechecking that patient's blood work fairly frequently while they're in hospital. Grade 2, where we're moving up to mild azotemia, grade 3 moderate, and then as we go up to 4 and 5, we're starting to get into, very severe elevations in creatinine, as well as the clinical signs associated with uremia and functional renal failure.

We do have some subgrades for, the AKI grading system as well, so those are gonna be based on, the urine production rate, whether we are non-alleguric, so most of the patients that we see with AKI will come in with polyuria, so we've lost the ability to concentrate urine, but the kidneys still. Can manage to excrete liquids. If we are starting to see progressive damage and that ability is starting to get impacted, we can move into a phase of oligo and urea, so that's usually where we're making less than 1 millilitre per kilogramme per hour of urine.

And that for me is sort of the immediate warning bell that we need to start getting very proactive about monitoring that patient, having conversations about possible referral for renal replacement therapy if we don't see a turnaround or a response to our fluid challenges within the next sort of 6 to 12 hours. If we do have a patient that progresses to that stage or that presents in a phase of an Urea, meaning we're not making any urine, or they're presenting with severe hyperkalemia that we can't manage or volume overload. The patient can't excrete fluid and that's actually causing a degree of pulmonary edoema.

All of those would be immediate indications for emergency referral for renal replacement therapy and would be classed as a subgrade too. So how do we, we've we sort of established with this AI grading system that urine output is very important to track. So how are we going to do that?

The gold standard is going to be placing a urinary catheter. This is the most accurate way to measure, but it's something we actually try not to do, so if we can avoid it because we do have potential risk of. Introducing infection.

And if we have a patient that already has renal dysfunction, if we then give them an ascending pyelonephritis, it's going to be a difficult situation. We also know that, if we are, say, administering empiric antimicrobials, maybe there's a possibility this patient could have an acute kidney injury due to pyelonephritis, and I'm treating empirically while my culture is, is pending. If we have an indwelling urinary catheter, we are increasing the risk that we might be breeding a multi-drug resistant infection, in that scenario.

We also, especially if we have a female patient, we're going to have to do heavy sedation or even a general anaesthetic to place the urinary catheter. For males, it will obviously depend on their temperament, but generally if I have a patient that's had a significant acute kidney injury, if I can avoid anaesthetizing them, doing anything that might reduce renal blood flow for a period, I want to do that. So quite often, unless we are extremely worried a patient is going into oligura and urea territory, and we need an absolute number to track, we will approximate urine output by doing things like weighing litter boxes and inco sheets, collecting and measuring voided urine.

Keeping track of serial body weights and water intakes, palpating the bladder, and then one of the other tools that can be helpful is actually serial bladder ultrasound. So, there is a nice recent paper that sort of walks you through this, but essentially, you can use any of your, standard in small animal clinic ultrasound units, get a longitudinal and transverse view of the bladder, take our height and length measurements, plug them into this formula, and that will give us quite a reasonable. Approximation of the fancier three dimensional modelling that we can do to, it's the most accurate way to measure this, but, say if you have a patient, a large dog, it's really difficult to palpate the the bladder and, you know, they're just urinating on themselves in the kennel, so we can't really quantify volumes.

This can be a useful tool to help track more objectively how much urine we're making and if we think we're in polyuria versus oliguria territory. So let's say we'll talk a little bit later in the presentation about treatment and fluid plans, but here moving into sort of segueing towards chronic kidney disease, we wanted to just briefly mention what if we had a patient with AKI we've gotten them through the the worst of that insult, are we, are we done? Are we sort of in a, in a safe place now that they're non-mic, they're eating, drinking, they're ready to go home.

Unfortunately not, because we know that during that AKI period, the kidneys will have sustained an insult. The question is whether they have the capacity to completely recover from that or whether that insult did cause some permanent damage to, say, the glomerular basement membrane. We've now got something that's gonna result in scar tissue formation and fibrosis in the kidney, that may then result in development of stage one chronic kidney disease that could progress from there.

So the important take home here after you've had any patient with an acute kidney injury, we doesn't mean that we are out of the woods if you've had a complete clinical recovery and normalisation of azotemia. We've got to keep an eye on them. We're not necessarily out of the woods yet, so.

And I will be rechecking their blood work and physical exam 3 months after an episode and then probably every 6 months for, you know, the next 12 to 18 months just to make sure that if we start seeing any ticking up in our renal values, we're gonna be on top of it right away. So, moving now into we mentioned we might develop something like stage one CKD in the last side, so this is a good segue into introducing the iris staging system for chronic kidney disease. Again, we can only apply the staging system to patients with chronic renal disease.

So we established chronicity by checking blood work at least 2 weeks apart and Seeing that we haven't had any substantial change, so the values are stable. If I check and the values are significantly worsened, that tells me we may still have an active disease process going on. Maybe I need to do some more diagnostic workup.

And then once I've done that, if I've identified and treated something, I can then recheck blood work, see if it's stable, and then give, give an appropriate iris stage. So I won't read all the values out to you, but If you you can pause here, take a close look at everything. There are some subtle differences between the canine and feline scales.

Often I recommend just printing off a copy of this and having it above one of your desks or on a wall in the clinic, so you can easily refer to it and make sure that any patients in your practise that have azotemia on their blood work or suspicion of CKD we can get their correct iris stage in the record. We do have a new addition to the Irish system that was put in a few years ago, so utilising SDMA symmetric dimethyl arginine. So like creatinine, this is another approximator of GFR that tends to be most useful when we're either diagnosing patients very early in their disease process where the creatinine maybe hasn't had a chance to exponentially increase yet, or patients with chronic kidney disease that have a significantly reduced muscle mass.

So we know creatinine is. A byproduct of muscle metabolism. So many of our patients with chronic kidney disease may have significant cachexia and muscle wasting.

So if we look only at their creatinine, we might potentially underestimate the stage of CKD that they have and maybe aren't implementing all of the treatment recommendations that we should be for that stage. So you'll see if we have a significantly elevated STMA that might actually push a patient into a higher iris stage than they would be based on their creatinine alone. We also substage chronic kidney disease based on the presence of proteinuria or hypertension, so it's important that we get that set of baseline of baseline readings whenever a patient is diagnosed with chronic kidney disease and that we continue to reassess all of these at recheck points, and we'll talk towards the end of the presentation about how often we want to be doing these rechecks.

So, now segueing into the area that often poses the diagnostic challenges for these cases, the acute on chronic kidney disease. So this is when we have an event that is triggering acute kidney injury in a patient that already has preexisting occult or subclinical chronic. Kidney disease, resulting in a rapid worsening of their renal values.

So we do know that patients with preexisting chronic kidney disease will be more sensitive to any, potential renal insult because their kidneys, we, we've lost a lot of glomerulli already. We don't have much wiggle room. So with patients like this, any patient I know that has CKD, I'm going to be more cautious about things like putting them under general anaesthesia, making sure that I'm gonna be monitoring their, blood pressure very closely, keeping them on IV fluids for a few hours before and after.

I'm gonna try and avoid using potentially nephrotoxic drugs like say, Amicain or gentamicin in these patients, anywhere we can mitigate a risk, we will try to do that. When we have patients presenting with acute and chronic kidney disease, the diagnostic challenge for us is that that could look like a pure new acute kidney injury, especially if we don't have any prior history on that patient. They haven't been to the vet in 3 years.

We don't know if they had pre-existing, you know, stage 2 early Irish CKD, and conversely they could present looking like an end stage CKD and we might give, say a more pessimistic prognosis than would be appropriate. So really our task and sort of the, the main focus of this talk is really trying to help us differentiate between these two ends of the scenarios. So why is this important?

We know that acute kidney injury is potentially reversible. If we find it quickly, treated appropriately, we may be able to have that patient have normal renal function after. There is potential if, if the AI is bad enough that we could cause a permanent insult, but there's always a chance that we'll have complete recovery.

However, chronic kidney disease that is permanent and irreversible. We've destroyed the nephrons, they're not coming back. So we know because of this acute kidney injury will have a potentially better long term prognosis than chronic kidney disease will.

So we want to know which of these we're dealing with right at the outset or as close to that as as is possible. So what sort of things might trigger an acute on chronic event? One of the most common can be pyelonephritis, so we know that patients with underlying renal dysfunction, early chronic kidney disease, they are more susceptible to ascending urinary tract infection as we have dilute urine, it's not as inhospitable an environment for bacteria to grow in as a very highly concentrated, you know, USG above 1050 urine in a cat.

If one of these patients. Has significant dehydration, hypovolemia, or ischemia. So say we've had a severe transient gastroenteritis, we've had significant volume losses as a result of that, and that patients come in dehydrated after a 48 hour history of vomiting and diarrhoea.

We might find that they're significantly aotemic as a result of that. Some of it could be a pre-renal component, but if it was going on long enough and knowing we don't have much wiggle room to work with in a patient that already has CKD. There's an increased risk that we're going to rapidly move from the pre-renal to renal, kind of phase of acute kidney injury.

If we treat our patients with any medications that reduce GFR, patients that already have chronic kidney disease and a reduced GFR don't have much wiggle room. So, while we know that treatment of protonuria is important for management of RCKD patients, we tend to be quite careful with, the prescription of ACE inhibitors and tensin receptor blockers will often start at a lower dose and gradually increase to effect if I need to prescribe those, but say if you do have a patient with pre-existing kidney disease that is has to be started on an ACE inhibitor for management of acute onset congestive heart failure, we're gonna have to be very closely monitoring that patient. And then any nephrotoxins, so just like all of the, sort of nephrotoxins that could cause a pure acute kidney injury, if you have a patient that already has preexisting CKD get into those, they're gonna present in a very similar way.

So clinical presentation, sometimes it will be obvious that a patient's coming in with pre-existing chronic kidney disease. So in the case of Pascal, we already had a prior diagnosis, so we have a piece of information that is, is there to help guide us, but we don't always get the luxury of that information. So if say a patient hasn't been to the vet in 3 years, you know, we may not have any inkling that there is a problem.

So we'll have to rely on some other tools to help us differentiate. So if we get one of these mystery patients coming in, acute severe uremia, no prior medical. We need to figure out is it AKI is it acute on chronic?

Is it progressive CKD that you know the owners just didn't pick up on any of those early signs, and prognosis will be very different, so hopefully we will guide the owner correctly. So going back to Pascal. We've kept him in hospital for 48 hours of IV fluid diuresis.

We've done some diagnostics, so, based on the things that we've chatted about and those possible triggers for, AKI and an acute on chronic episode, we know we probably want to screen for things like pyelonephritis, so we've done a urine culture that was negative. We did see that his BUN and creatinine, they had, we've corrected his dehydration, but those numbers have not significantly. Changed yet.

We've corrected his dehydration deficit and he's gained about 5% of his body weight, but he's still inappetent, still looking somewhat under the weather, and we haven't seen much improvement in those renal values. So from here, thinking about, you know, are we dealing with acute on chronic versus a progressive end stage chronic CKD at this point, given that we haven't seen much of an improvement in his renal values despite correcting his fluid deficit. So what will we advise the owner, so you can, you know, pause the presentation here, make a few notes, see, see which of these options you think would be most appropriate for this case and why?

Should we keep going with IV fluids, give him another day or two, reassess the renal values, should we recommend doing further. Diagnostic workup, or, you know, is it really looking like this is probably heading in the direction of a progressive CKD? Should we taper off the IV fluids and, sort of, you know, knowing the owner has financial constraints, start sort of setting her up that that's the more likely outcome at this point.

So Now we'll talk about some of the tools that we can use to help better differentiate acute kidney injury from chronic kidney disease. So we'll be using, we'll talk through each of these elements individually, but really trying to apply them in such a way that, we're using detective skills, to help us with some of the uncertain cases. So for history and clinical presentation, for the classic acute kidney injury, often those patients are coming in with an acute or para acute illness.

We might have a sudden onset of PUPD inappetence, nausea or vomiting, and patients coming in with acute kidney injury, they're not used to being azotemic, so we might have, you know, quite a significant clinical syndrome of euremia apparent without numbers for creatinine and BUN that are necessarily markedly off the charts. For CKD, we will probably, if the owners picked up on it, have more of a chronic history of PUPD maybe with further questioning, we can see that, yeah, we have been having to take them outside more often for their for dog walks. They've been urinating for a longer stream for a longer period of time or for cats we're having to change the litter box more frequently.

The owners might report some evidence of chronic weight loss, or patient feeling bonier, like they've maybe lost a bit of muscle when they're, petting them over their dorsal spinous processes. We might have more of a chronic waxing waning appetite, and if the patients coming in with, absolutely off the charts, these aemia numbers, so for Pascal, say creatinine of 800, which she presented with, we could have, you know, if they're coming in and not seeming. As ill as we would necessarily expect.

Maybe they're still eating and, you know, right after we rehydrate them, their appetite goes back to normal. That for me would maybe be a little clue that I wonder if this patient's body has been a bit used to more of a chronic azotemic state, and as a result, they're happy to continue eating and drinking, sort of despite those higher numbers. So for physical examination findings, for AKI again this is an acute process, so we might have a patient that has more normal body condition, muscle conditioning, a good, you know, normal glossy hair coat, whereas if the patients had a cult subclinical chronic kidney disease, and, you know, we're now presenting a I might be more suspicious that it's an acute on chronic episode or a progressive end stage episode if we've got things like poor body condition, significant muscle wasting, very unkempt hair coat that suggests the patient hasn't been grooming properly.

If on palpation, I can appreciate small irregular kidneys or that big kidney little kidney effect. Generally, patients with chronic kidney disease don't tend to have, any pain on palpation of the kidneys, whereas for acute kidney injury, depending on the aetiology, some toxins, and some things like ureteral obstruction, can result in, in pain, pyelonephritis as well. So, Dehydration is a bit of a harder parameter, so, usually our AKI patients will come in dehydrated and potentially even hypovolemic.

The CKD patient, it will kind of depend where they are in their phase of presentation. With CKD that's quite advanced, often say patients with renal dysplasia, sort of our younger patients that have been very easy attainment for a long time, we may even see symptoms of rubber jaw where we start getting, sort of mineral and bone disorder, clinical signs as a result of having chronically elevated phosphorus. I wouldn't expect to see that in an acute kidney injury patients, so it takes time for those changes to develop.

So just to review, muscle condition scoring if any of you are less familiar with this. So, if you Google the WSAVA, the World Small Animal Veterinary Association, you can download and print off these charts, but essentially we, assess muscle condition based on palpation of, you know, above the the apexxial muscles over the spine as well as the points of the hip, and the muscles of the thigh. So this is something we record in our medical record for every patient along with body condition, it certainly be a helpful parameter if we are trending patients over time, and often it may be the first sign that we have an early onset chronic kidney disease, you know, indicator that something is not quite right, just on your physical exam, say at a wellness appointment, that could be a reason to help convince an owner to say, actually, I think we should do some, some blood work at this visit, even though Fluffy's been clinically well, because, you know, the last time we saw you 6 months ago, we had a normal muscle condition.

You know, now we're, we're moderately decreased. Let's see if there's a reason for that. So next tools that we can use in addition to our history and physical exam, will be diagnostic imaging.

So there's a couple ways we can look at the kidneys, we can take radiographs, these are most helpful for indicating the overall size, and symmetry of the kidneys. So if we have significant big kidney little kidney where one is much smaller than the other in the, we've seen compensatory hypertrophy occur. Contralateral kidney, depending on what other organs are in the way, we may be able to appreciate that on radiographs.

If there are any stones impacting the urinary tract, radiographs, will show that as long as it's one of the radio opaque forms. So typically our calcium-based, and strew bit-based stones will show up very well. But radiographs are, are limited in the information they can give us.

We can't really get into the actual internal architecture of the kidneys. So the best tool for looking at that is going to be things like ultrasound. So with acute kidney injury, we, we may not necessarily see abnormalities, but with chronic kidney disease, we, we almost always will.

So we'll talk about those findings in the next slide. This image here is a sort of classic picture of a chronic kidney disease, kidney with reduced cortical medullary distinction. So we've got a cross section here through the kidney, you really can't discern where the cortex stops and the medulla begins, and that's cause we've had scar tissue deposition here, that has sort of changed and homogenised the kidney, so we've lost that, sort of classic, 22 textured appearance.

We can utilise more advanced imaging like CT scan and contrast CT angiography for assessing the kidneys, but in these clinical situations where we're worried about acute kidney injury, chronic kidney disease, we're often quite reluctant to recommend that because we're going to have to heavily sedate or anaesthetize a patient for those studies in most cases, and we know that that risks reducing renal blood flow, that could exacerbate the insult, but even more concerningly, In order to see anything on a CT scan, and sort of highlight lesions, we've got to give an iogenated contrast agent like Iohexol. And Iohexol is potentially nephrotoxic in and of itself, so I would be quite hesitant to administer Iohexo to a patient that has, say, you know, a creatinine of, of 300 or or above. So if in most cases ultrasound will give us all the information that we need, if we still have any queries then, you know, we'll probably.

Make a decision jointly with the owner to say we think risk versus benefit. Do we try treating and then reassessing versus do we really feel like we have to perform a CT now and understand the risk that that entails. I have unfortunately had some patients go into a sort of a severe acute kidney injury that has been oliguric and neuric after getting contrast, so it is something that can does have the potential to go badly, so make sure that we have that conversation with the owners ahead of time and document that.

So for ultrasound, which, as we mentioned, it's gonna be the modality that's most useful here, for acute kidney injury, I would potentially we might see absolutely nothing, just a normal kidney, but some indicators that there has been an acute injury could be mild bilateral renal enlargement. We have a little bit of swelling of the kidneys due to any sort of non-specific insult. We may have a small volume of perirenal effusion around the kidneys, but the overall architecture might be essentially unchanged, so, the cortex and the medulla and the distinction between the two will still be maintained.

With chronic kidney disease, we'll often see that the kidneys are measuring smaller than the normal reference ranges. We might have a symmetry where one kidney is markedly smaller than the other, and we might see abnormal architecture, so the normal smooth external view of the kidney becomes knobbly and irregular. Largely because we have scar tissue and things like renal infarcts that are then scarring and making that smooth surface irregular, we might lose that corticomedullary distinction, and we might start to see dystrophic mineralization in in sort of deposition of calcium deposits in the kidneys which can show up both on radiographs and ultrasound.

So moving on to blood work distinct distinctures, for chronic kidney disease we sort of have that typical hallmark of CKD being a non-regenerative anaemia, which is happening because the kidneys are producing erythropoietin, the hormone that helps to stimulate the bone marrow to make new red blood cells. The key take home to remember here is that we don't start to see significant impact on erythropoietin production until our kidney disease. It is quite advanced, so usually Irish stage 3 or above.

If you have a patient with early Irish stage 2 CKD and they've got a moderate to marked non-regenerative anaemia, I wouldn't be attributing that to the chronic kidney disease until I've done a very thorough workup for anaemia, probably doing things like a bone marrow aspirate after doing all my systemic imaging, if that didn't reveal a cause before I would conclude it's due to the kidney disease. We may see a higher magnitude of a presentation with CKD or an acute on chronic CKD episode because the patient's body has acclimated a little bit to living at higher levels, they're not presenting until they're becoming clinical, and those numbers have gone high enough that we're triggering clinical signs. Looking at, impact of urine, so if we have an acute insult to the kidneys, we might actually start seeing, renal damage to renal cells that will be, sort of excreted as granular or cellular casts, what we would call cylinguria.

We could also see normal glycaemic glucose area where we have glucose present in the urine with a normal, sort of systemic glucose on a biochemistry panel that indicates that we've got acute tubular damage happening, so we're actively leaking glucose and potentially also protein, into the urine. We may, if a patient's presenting with acute kidney injury and they're oliguric to auric, they may have elevated potassium, whereas with CKD we don't again tend to see that commonly unless we've got a patient that is presenting at the very end of their disease process and usually those will be quite obvious on clinical exams. Or if they've got an unusual sequelae like a hyperreinemic hyperaldosterinism, but usually that's kind of the referral type territory.

So most of the time we seeKT the issue is potassium is normal to to slightly low because we're excreting excess amounts of potassium in the urine. We may see an increased phosphorus to creatinine ratio in acute kidney injury, because in the chronic phase of disease, we tend to see phosphorus rising more in proportion to creatinine. So if you are getting blood work on a patient and you're not sure if we're acute versus chronic, if the phosphorus is markedly high and doesn't seem to match up with the creatinine, that could be a clue that we're more acute.

And then for calcium, we more often will see a normal to mildly increased calcium with chronic kidney disease, whereas with acute kidney injury, it's more often normal to low. The exceptions to that are, to toxins if we do have CKD or do have an acute kidney injury due to vitamin D toxic toxin ingestion or grape and raisin exposure, those two could, result in a mild hyperkalemia or a severe hyperkalemia in the case of vitamin D toxicity. So just to show an image of what that's those granular and cellular casts we mentioned could look like.

So, with acute kidney injury suspects, I will usually look at a freshly voided urine sediment in-house. These casts will dissolve quickly after urine has been excreted from the body. So if you send these to the lab overnight, all of the casts may have dissolved by the time.

The sample gets there and has a look. So, try to get in the habit of doing an in-house urine sediment exam, or utilising this newer technology on the market from, you know, a few companies like IEX and Novartis, that have machines that will automatically read out your urine sediments using AI technology and can tell you right away if you have casts or not. So one of the other things we want to pay attention to with our physical exam and assessment of clinical pathology parameters is not getting tricked by the effect of dehydration when we're assessing anaemia and whether that anaemia might be pushing us in the direction of chronic kidney disease versus acute kidney injury.

So we want to get in the habit of looking at the absolute values, not just anything that's flagged on the panel is abnormal. So if I have a patient coming in and their PCV isn't flagged, but actually it's, you know, the number is 25 and the low end of the range for your lab is, is 23 for a cat, that for me would be a concern in a dehydrated patient, if, if they've got a Normal PCV we and there's that 5 to 7% dehydrated, we should see that number actually at the higher end of the reference range. So as if these patients are coming in 5 to 10% dehydrated, we might not see their real degree of anaemia for 48 hours until we've completely rehydrated them, but if we're looking in, we have some of those early clues at first glance at presentation.

We might want to be chatting with the owners and setting them up about potential next steps that that might come. So here's some examples with those reference ranges. If we've got a dog presenting azotemic with a creatinine of 39 and it's 7% dehydrated, that would be a worry for me.

Similarly, a cat with 29% just at the low end of the reference range, those patients are probably actually moderately azotemic by the time we rehydrate them. So heading back to Pascal on his example, when he came in, we had a PCV of 22% and 88 grammes per litre when he was 5 to 7% dehydrated. After 48 hours of IV fluid diuresis and we've corrected that deficit, his PCB has gone down to 15% and 65 grammes per litre.

So, definitely at a range now where we, we need to intervene. So he required a blood transfusion while in the hospital and a few other, interventions. But that's something knowing this owner has financial constraints, looking at his admission blood work with his degree of dehydration, we did have a chat with the owner, sort of our emergency service told them right.

At that point, he doesn't need blood at this at this second, but it's highly likely we will have to give him a transfusion in order to get him out of the hospital. So that gives you time to make sure the owner has the finances for that. You can source a blood donor, you can get your blood type sort all all performed, so always kind of having that assessment at the very beginning, so that we can give the owner the most accurate advice.

Hopefully we won't need it, but we want to be prepared to to give it if we have to. So looking at trends and blood work, this is another tool that can be really helpful for us in differentiating between acute versus chronic. If I have a patient who is just not having a significant reduction in their, azotemia after we're appropriately rehydrating.

Then that would be a, a bit of a flag for me that we might have an underlying chronic kidney disease. So if I, if this patient has previous blood work, I do want to track that down. It might involve calling another veterinarian that saw them previously 2 years ago or 6 months ago, so that we can see if there maybe was any pre-existing azotemia.

Once we have fully rehydrated the patient, I'm gonna be reassessing azotemia after, sort of that that 48 to 72 hour period. We're gonna continue diaring these patients until their renal values have either normalised, returned to their previous baseline, if we could establish that, knowing that they had CKD, or plateaued, meaning that we've been giving them fluids, we've reduced the, the magnitude of the numbers, but they're not in normal range, and then if we recheck our values after another, say 24 hours of diuresis, we haven't seen a significant change, that's probably as good as we're going to get for that patient. So if we have a scenario where we're struggling to tell the difference between the two, we may start to consider things like renal biopsy.

I, I'd say the amount of times I've had to reach for this to differentiate, I can probably count on, on one hand after, you know, 12 years of practise at this point. The risk obviously. Is that we're going to further damage kidneys that are already not functioning very well.

So, more, more practically, monitoring serially for evidence of renal recovery, will be the, the approach that we tend to take the most. Other tools that might help us convince ourselves that we're dealing with a chronic kidney disease case, probably the most useful is ultrasounding the parathyroid glands. So if we have CKD we will almost always have parathyroid gland hypertrophy, as a result of the phosphorus dysregulation and mineral and bone disorder that that is causing.

You can also, if you have a fairly azotemic patient, and we think we've been like that for some period, you could radiograph the jaws to look for demineralization or loss of the laminadura those are changes that will be seen in patients with chronic kidney disease that have long standing aotemia. So coming back to Pascal again, thinking back now to, you know, what we would have advised the owners at that time, were you, were you guys based on all the information we had thinking you sounded more like a progressive end stage CKD cat or an acute on chronic with a trigger that we couldn't identify. So for, for his situation, when he was transferred to medicine, some of our team members were a bit reluctant to, push hard for an ultrasound given the owner's financial constraints, but, I was on team ultrasound when we were in the hospital and kind of said, you know, we, we miss everything we don't look for.

So if we do say have a patient with pre-existing chronic kidney disease that's developed a ureteral obstruction in the one sort of Functional kidney, that could certainly be something that we could intervene on and have that patient improve, and we're not gonna find evidence of that without doing an ultrasound, to see if there's hydronephrosis or ureteral obstruction that we can visualise, or if a patient has developed something like renal lymphoma, that certainly could be another reason why we have an acute worsening that might not improve, with just administration of IV fluids and empiric antibiotics. So in Pascal's case, when we all Sounded his kidneys. This is what we saw.

So we have a thick, layer hypochoic layer sort of a perinephric rim around the kidney. This is classic infiltrates of renal lymphoma. So we took an FNA of this area, confirmed that diagnosis, to pay the owners had limited finances but did want to try and treat Pascal, so he started on chemotherapy and actually had a, a good clinical response.

So it was a good example. Of the case where, you know, we have a 15 year old cat coming in with a history of kidney disease, acute worsening, negative urine culture, you know, it could be easy to sort of dismiss that and say there's not a lot we can do. This is probably end stage disease, but actually insisting on an ultrasound right away so that we really know what are we actually dealing with.

Is there anything here that's potentially fixable? We were able to find something that, you know, gave us a better chance of getting him out of the hospital and You know, well, renal lymphoma, we don't have, you know, we, we're not gonna be able to cure that. We usually have a survival time of about 6 to 9 months.

It's still a better outcome than we would probably be seeing with end stage CKD case. So, just to talk a little bit now as we wrap up about treatment, so we're gonna have to, for a case like Pascal coming in, initially design a fluid plan based on how dehydrated we think the patient is. So we said that we estimated him as about at about 5 to 7%.

What was that based on? That's gonna be, his skin trigger, so we can see in the image here we've got a cat with quite a mark. Skin tint, a skin tint of this degree, I'd probably be expecting at least 7% dehydration.

We can feel the mucous membranes if they're tacky and dry. If we're getting more advanced dehydration, especially in old cats, we can start to see sunken eyes. So if I see that often that usually means we're at the higher end of the dehydration scale, so I'm approaching 10%.

And then hemo concentration, although with the caveat that in a patient with pre-existing chronic kidney disease that might have an acute insult, they might actually have a preexisting anaemia that now is pushed within the normal, the normal reference range that as we hydrate them is going to slide backwards. We always want to give patients the benefit of the doubt for dehydration because we can't detect dehydration less than 5%. So knowing that we could have a pre-renal component with any of these, sort of presentations, I will always try to correct for a dehydration factor of probably at least 5% if I even if I'm not fully convinced on my physical exam that I have something there.

Generally, if we're getting up to 12 to 15% dehydration, that's where, you know, we're we have the potential to succumb as a result of that severity. Anything that's 10 to 12%, they're going to, I'm setting up them up that they're gonna need to be in the hospital for quite some time. Some of these patients, especially the acute kidney injury patients may come in in signs of hypovolemic shock, if we've lost so much fluid volume through things like vomiting and diarrhoea, or excessive polyuria that the body hasn't been able to keep up with, so we will.

Assess for tachycardia hypertension. If I see those, I'm probably going to administer fluid boluses to try and immediately correct hypertension as quickly as we can, normalise heart rate and then continue to administer fluids as as indicated. So if we've given a number of fluid bonuses and we're not seeing the improvement in those parameters that we want, we may have to consider things like pressor support and getting colleagues from, sort of emergency and critical care involved.

That's a fairly difficult decision to make in some of these patients coming in with, signs of acute kidney injury or an acute and chronic insults because pressers will cause some Degree of peripheral vasoconstriction and redirection of blood from places like the GI tract and the kidneys to the, the heart and the brain. So, if we put them on pressures, we have the potential that we might further exacerbate, kind of a renal insult. So I really try, if at all possible, you know, feel like you've accomplished as much as you can on your fluid re resuscitation before doing that.

So for a fluid plan, just have this slide up here for your, for your reference, we won't sort of read everything out here, but if you need a sort of refresher on the old school, the full way for calculating up fluid plan, this is what we will be using. Generally the, the shortcuts we'll use in clinical basis, is to sort of, if I have a patient coming in that's significantly dehydrated without cardiovascular concerns, I'll usually be starting them at around 4 millilitres per kilogramme per hour, reassessing after 6 hours, and looking at things like your body weight, blood pressure, is the patient actively urinate? Has my PCP total solids dropped, and based on those clinical parameters, I can titrate that fluid rate up or down accordingly.

If we're not gaining any weight or producing urine, we know we're gonna need to increase that fluid rate probably by 1 to 2 mL per kg per hour and reassess frequently, because obviously the risk of volume overload is also always there, the higher that we get. I generally try to avoid, going above 6 mL per kg per hour in cats and 7 to 8 mL per kg in dogs unless patients are extremely polyuric and I can be monitoring them very closely, so sort of 24 hour care in the ICU because there is potential for fluid overload, being induced. Quite quickly if we're going at those really high rates, but some patients will need fluid rates that high, often things like leptospirosis, especially we can see quite marked polyuria, and if we don't keep up with that, the patient potentially can have precipitation of their acute kidney injury.

So. For maintenance fluid therapy, once the patient has been, we've corrected their dehydration, we do have to start thinking about, the amount of electrolytes that we're putting in. If we're giving a resuscitation fluid like plasma light, normosol R, lactated ringers, all of those have quite high levels of sodium and chloride.

So there is a risk that we could, develop hypernatremia, which we know has the potential to exacerbate, sort of acute kidney injury and damage. This is a particular risk in cats. So if I've had a patient that has been in, in the hospital for, you know, 48, 72 hours already, I've corrected their dehydration.

We may want to start thinking about should I switch them to something like half strength LRS or 0.5% NACL, to try and reduce the amount of sodium that we're giving them because really the more sodium we give over time, we're increasing the potential risk for volume overload with all of that. Sort of sodium and associated fluid retention.

It also there's some theoretical concerns that making a damaged kidney have to process and excrete a lot of excess sodium, may not be the most beneficial thing for for a kidney that we're really actively trying to support. So for monitoring our fluid therapy, the biggest danger I end up seeing for patients that we have in hospital for long periods of time on diuresis is volume overloading them after they've been in for 345 days. So, frequent serial physical exams is gonna be our best tool to mitigate that and really getting your nurses involved in that as well.

Often it's the nurse team, that's the first to tell us that there might be a problem. So I'll be evaluating things like body weight, skin. Cardiac auscultation to look for new murmurs, depending on my degree of concern and how high the fluid rate is, potentially every 4 to 6 hours.

We're gonna, if we have a patient on diuresis, we should be checking their electrolytes at minimum every 24 hours because with frequent diuresis at high rates, we risk causing hypokalemia, and if we're giving one of those resuscitation fluids with high sodium content, we could cause hypernatremia. So the more, the longer they're in the hospital, the more frequently we want to be checking this. Traditionally, we have administered IV fluids at the highest tolerable tolerable rates to try and maximise GFR and renal blood flow.

When we're treating patients coming in with azotemia and what we think is an acute or an acute on chronic insult. However, evidence from human medicine and from veterinary medicine has showed that volume overload actually is one of our biggest enemies. It significantly increases morbidity and mortality across the board, so more fluids does not necessarily mean a better outcome for the patient.

We wanna give just enough fluids to correct the deficit, and, you know, allow excretion of toxins, but if we give too much we can actually. Worse than acute kidney injury by causing edoema and venous congestion in the kidneys. We could cause volume overload and secondary congestive heart failure, which often when that happens, because we have to stop fluids and we may have to give diuretics, often those are the patients that we don't ever get out of the hospital because it becomes an impossible balance to try and tweak those two, and the cost of having to stay in the hospital for that initial or for for that ongoing, tinkering, some owners just can't, cannot keep up with that.

So monitoring for volume overload, in addition to the physical exams things we can look at, some of the other helpful tips we found is sudden reduction in appetite. So if you have a patient that's been in the hospital for 4 days on diuresis that came in inappetent, they perked up and started eating really well once we corrected their dehydration and his team started to go down, but then suddenly they stopped eating again, that would be a worry for me that maybe we're starting. To get gastric edoema, intestinal edoema, let's reassess our fluid status.

We can use things like serial, left atrium to aorta measurements, if you're comfortable doing those from sort of an ER medicine standpoint, doing that once a day when you're doing your main physical exam on the patient can be an early clue that the LAAO is trending upwards dramatically, we might want to back off on our fluids. Anytime I have a new heart murmur, I'm gonna be also quite concerned about that. By the time we see the classic signs of volume overload, so chemosis, nasal discharge, this, sort of gelatinous skin trigger or tip and dyspnea, it's too late.

We've lost our intervention window. So for me, if I have one of those patients, I feel like I've, I've, I've missed the early signs. So, it's also important that we monitor these patients for hypertension.

They may present with normal blood pressures, but once we correct their fluid deficits, that can, start to trend upwards. So we'll usually look at that every 24 hours when they're in hospital. So discussing, reassessing azotemia, so, how should we do this and how often?

It's really important that we're comparing apples to apples here. So if we're looking at a nova one day and the next day and then an external lab sample the day after that. We may have significant variation from machine to machine that makes it very difficult to actually see meaningful changes in the creatinine, trends.

So, generally, I recommend just send sending a sample to an external lab every 48 hours to really see clinically significant changes in your azotemia. That's where we're really making our big decisions. Based on kind of that frequency every 48 hours and ideally an external sample.

Of course, we will be checking electrolytes every, at least every 24 hours when patients are hospitalised to adjust that and those electrolyte, sort of panels might also have creatinine on them. So you can certainly look at it and give it, use it as a general guide, but for making big decisions, I've seen quite a few cases where, Those in-house creatinines have been a little bit misleading, and then actually when we get something back from the lab, there hasn't been a significant change, so we have a different sort of tone of conversation with the owner and if they've been thinking things were heading in the right direction based on the Nova and the external lab doesn't suggest that it can be a difficult conversation. So I'm just setting those expectations and always comparing the same type of test to another will help avoid that scenario.

So, if we have a patient that is oliguric or auric, we need to then think about how, how to approach that. So first thing we wanna do is rule out that we have, any sort of deficit in circulating volume that we are fully hydrated, so we're gonna fluid challenge as needed with intermittent fluid bolus, so usually for say a cat I would be giving 5 mL per kg boluss every 20-30 minutes, maybe repeating those over a few hour period. If the patient is already hydrated, we may move on to just matching ins and outs to maintain hydration while minimising the risk of volume overload.

If we are still oliguric, despite we, ruling out any occult dehydration deficit, then we may have to consider doing a trial of furosemide to increase urine output. It's important to remember though that this does not actually increase the GFR or Improve patient outcomes. All it does is buy us a bit more time to allow IV fluid therapy to continue and address any acid base and electrolyte issues that are arising, while we're waiting to see if the kidneys are heading in the direction of recovery.

But if there's been no improvement in urine output, so an increase to above 2 mL per kg per hour within 8 to 12 hours, that's the point where we have to refer for renal replacement therapy or consider euthanasia. So, Let's say now we've we've gotten through the hard part. We've successfully discharged one of these patients from the hospital, so we think we've we've got a degree of pre-existing chronic kidney disease.

How are we gonna best manage that? So this is a whole talk in and of itself, so I can direct you to the Iris treatment guidelines for all of the different stages of chronic kidney disease on the website. It's a really helpful document, but I've got sort of the, the basic interventions that we will always think about here starting from, for me the, the most important, so prescription renal diet where we are feeding a phosphorus reduced food, that's gonna be the most important intervention we can make that, and we have the highest level of evidence to support it prolonging lifespan.

We also want to be very proactive with phosphorus binders. So there are specific phosphorus sort of treatment guide goals for each iris stage of CKD, so we want to ideally get our patients within that recommended zone. If we have hypertension and proteinuria, we're gonna proactively manage those, if patients are at the advanced stages of CKD and they have clinical emia.

We're going to want to prescribe potentially multiple medications for nausea. I think of nausea control like pain control, so multimodal where we're used targeting different receptors with different drugs, can often yield a better result. So I might have an advanced patient on Mirroetin and ondansetron and Mirtazapine as needed.

We need to maintain hydration, so some patients will require ongoing subcutaneous fluid therapy at home. If patients severely anaemic, we're going to correct that with transfusions in Darby Puatin, which we'll talk a bit more about in the next slide. And in some cases, it's not right for every pet and every owner, but placement of an esophageal feeding tube, can help significantly with these patients because we can administer a renal diet predominantly and then they can graze on whatever little snacks.

They want to around that, we can give phosphorus binders, we can give all the medications that we need to, and we can give ent water. So enteral water is gonna be more preferred, because we're not giving all the excess sodium along with it, and it's generally less of a risk for causing volume overload. So I think for me when I think about the quality of life for a cat with chronic kidney disease.

If I don't have to chase them around the house to give them their phosphorus binders and give them their 3 medications, and I can do all of that through the tube a couple times a day. Often those cats will actually be happier at home with their owners than they will if we're trying to get all those things in by mouth. So it's not for every cat, but it is something to to consider for for, you know, certain very invested clients.

So if we're dealing with significant anaemia in the advanced stages of chronic kidney disease, we do want to think about correcting that because we know that anaemia will make patients feel quite crappy, so people humans with CKD associated anaemia report low energy levels, low appetite, they just just feel blah. So generally the recommendation is to start this when anaemia is starting to impact quality of life, so that's gonna be any PCV less than 20%. We specifically recommend using Darbyuin.

We don't recommend using erythropoietin anymore, because erythropoietin has a higher risk of inducing autoantibody formation where, with prolonged use, the patient will mount antibodies to the erythropoietin molecule, and then we become completely transfusion dependent. So, Darbywein has very low rates of inducing autoantibodies, and it's also easier to give cause you only have to, to give it sort of at at at most once a week, whereas ythropoietin was about 3 times a week. When we're starting a course of ribwein, we do in most cases want to give 1 to 2 injections of iron Deextra 10 mg per kg DIM, 11 to 2 doses a month apart, to make sure that we actually got enough iron to produce new red blood cells.

So for dosing, we generally advise 1 mcg per kilogramme, but if I have a very small cat, I'll generally give, sorry, I've got a decimal point error there, should be giving 4.5 mcg total cat dose. I generally won't go below that because in my experience, if we're giving doses like just 2 or 3 mcg total dose for a very small cat, it doesn't tend to be enough to raise their, PCB substantially quickly.

Once. Started drupuin, we do want to see these patients back for recheck weekly, for a physical exam and a check of their PCB total solids. So once the PCD is increased to the middle of the normal reference range, we can try reducing the frequency of Darbuin to every 2 weeks for the next 1, maybe 1 to 2 visits.

So we sort of taper the medication out gradually, and we can keep doing that until we start seeing the PCV drop. At that point, we go back to the last sort of taper that we were at and we stay there. If we find after the first sort of two weeks on therapy that the PCD isn't going up, I would consider doubling the dose.

If we're still not going up, then I'd probably be saying that we need to do more workup just to make sure I'm not missing any other sort of multi-factorial causes of anaemia like an occult GI bleed. So if the PCV is remaining stable at Q2 week dosing, we can try to go to Q3 weeks. I have seen some patients that can tolerate every 4 to 5 weeks, but I'd say 3 to 4 week dosing is the average once we've got their PCV normalised and have them nicely stabilised.

So, recheck schedule for CKD patients, for stable patients that are in stage 1 and stage 2 iris, the recommendation is to recheck them at least every 6 months, for patients who are, maybe, you know, more recently diagnosed and we're not sort of sure how quickly they're gonna progress. I might be checking them every 3 months for the first year. Once we progress to stage 3, we advise checking every 3 months if the owners are able.

It's all what they're, you know, what, what's feasible within their financial means, but with CKD I'd much rather see them more frequently on an elective basis than having them come in through the emergency department in a crisis cause that will be more expensive. Once we're getting to stage 4, we've got to really be managing those. More proactively, so often I'm trying to get them in every 1 to 2 months so we can tinker with medications accordingly.

Anytime they're presenting with a new or unexplained clinical illness, we will want to see them right away to make sure that we say don't have an opportunistic ascending pyelonephritis. If they, they've had a new or acute worsening in their PUPD that could be an indicator of something like a pyelonephritis as well. And anytime I'm gonna be doing, sort of an elective anaesthetic or heavy sedation procedure, I want to get baseline blood work right before doing that, so that say if they did have a worsening afterwards, I know exactly what my baseline was, before that insult happened.

So for finishing off with prognostic factors, so AKI quite a serious disease, we see mortality rates of up to 45 to 60%, with negative prognostic indicators for aura, degree of azotemia, higher is worse, protonuria, patients that are all the uric or aneuric unsurprisingly have a worse prognosis, and if we cause volume overload, we know that that is a negative prognostic indicator. If they have multi-organ dysfunction, that will also be not a good thing. So, for acute and chronic kidney disease, we have some recent papers that have shown that the short term outcomes are actually quite similar to acute kidney injury.

So we've got about the same chances of getting them out of the hospital. It's often depending on severity around 50/50, but the longer term outcomes will be a bit more guarded, and that's gonna be related to how severe their underlying pre-existing kidney disease was before this insult happened. So, if we Look at these statistics, it's just an idea of, you know, advising owners.

So for a client like Pascal's owner, letting them know that, you know, there's a good chance we'll get him out of the hospital, but, you know, probably quite a low chance he's gonna survive more than a year, and that's even if we didn't have the, the renal lymphoma that we also found. So to help guide prognosis when I'm advising patients at the outset, I find having that initial Ultrasounds telling us what does the renal architecture actually look like is probably the most helpful, as well as things like how was their quality of life before they've come in with this acute illness where they having variable appetite, you know, some, some days where they weren't feeling quite as energetic, that might suggest to me that they've they've got more pre-existing chronic kidney disease, that may shorten lifespan, you know, more acutely. So finishing off with prognosis for chronic kidney disease.

This is gonna be very linked to a stage of the error system, but for early stage CKD it's important to also weigh impact of concurrent illnesses because a patient may succumb to something like underlying congestive heart failure much sooner than their kidney disease would actually shorten their lifespan. So we really kind of look at the prognosis holistically based on what iris stage they're in. So to summarise, key take home points is remembering that acute kidney injury is a continuum.

And it can be present even when renal values are within normal reference range, so really trending, look back at that Irish AKI grading system, if you have patients that are in the hospital and acutely ill, keeping close eyes on how their creatinines are trending and intervening if necessary. We need to be able to successfully differentiate acute kidney injury from acute on chronic and progressive CKD. This is gonna be key for prognostication and owner expectations.

The tools we can use for that differentiation will be a good thorough history and physical exam, the clinical presentation of the case and really teasing out. Did we have occult signs like muscle wasting, variable appetite, PUPD present, diagnostic imaging with ultrasound being the most helpful. Clinical pathology, blood work trends.

And finally, my best take home is go to the Irish website, really have a good look around their treatment guidelines will walk you through sort of every step that you need to take for whatever stage of kidney disease or acute kidney injury your patient is in, and it's gonna be updated very regularly, so it's one of one of the best free resources out there. Thank you all so much for your time, and I hope you'll enjoy, working through the revision questions after the lecture.