Hello everyone, and thank you so much for Logging on to this webinar where we are going to cover some of the new thoughts around how fluid therapy can help and may not help our dogs and cats with kidney disease. So let's go ahead and get rolling here. First thing you remember, and this should all be kind of clear.
The goal is for all these statements that are going to appear on the slide to be kind of obvious and for you to understand them when we're done with the talk. OK. First of all, is that fluids do not improve kidney function, OK?
Second, excess fluids can actually cause or worsen kidney disease. And then we're going to hopefully understand when to use them. What type of fluid, how much, how fast to administer and for how long.
So that's kind of the road map for our talk here. So before we get into how to treat kidney disease, focusing on fluid therapy, let's review best way to diagnose kidney disease. So, I'm a big fan of using every tool in the kit, and as we've gone through the years, we've gotten better and have newer ways of identifying kidney disease earlier.
Including now with urystatin B, a way to identify kidney tubular injury, which when the kidneys are impacted, sometimes and most often the tubules are affected first, then the most vulnerable part of the nephron. So the ability to identify tubular injury can give us a jump on finding a kidney problem in a patient because these markers in the urine. All kidney tubular injury markers are in the urine, may be present for up to 2 days before we would see an increase in our blood markers of kidney function, GFR like BUN creatinine and SDMA.
So best ways to diagnose kidney disease early in my view are include all all available GFR biomarkers. And there'll be others, hopefully that will even be more sensitive and more specific than the currently available ones that we have. And remember that these are GFR biomarkers.
So when we have an increase, Our question shouldn't be what kind of kidney disease does this patient have? It should be, why is this patient's GFR decreased, and that will prompt us to investigate for pre-renal, renal, and post renal causes, because if we can find and fix a pre-renal cause or a post renal cause, we may avoid the development of renal disease, OK? Kind of a theme throughout the talk will be how important the urinalysis is in assessing kidney status, and ideally we want to include the specific gravity dipstick and sentiment exam when we get a urinalysis and that sentiment exam, ideally should be done within 30 minutes of collection, OK?
And First off is you really cannot interpret an increase in GFR biomarkers without specific gravity. So here we have two dogs, both of them are aotemic. One of them has a kidney problem.
OK, so same degree of azotemia, but the one that has the poorly concentrated urine is the one that concerns us. So when you have azotemia. You have to assess specific gravity to determine whether you have pre renal or renal.
Issues, OK. And for the iris guidelines, specific gravity in a dog should be above 1030 when the dog is azotemic and above 1035 when a cat is azotemic, yeah. So if, as the dog on the left here who has a highly concentrated urine, when azotemic, that's pre-renal azotemia, rehydrate the dog, the dog's dehydrated.
Our dog on the left, because the specific gravity is below the 10:30 cutoff for an azotemic dog, this dog has renal azotemia, and we should pursue the various causes of that, whether it's infection or toxin or chronic kidney disease. What clues about kidney function do we have looking at the dipstick? Well, there are two that I can think of.
One is glucose. The job of the proximal renal tubule is to reabsorb all filtered glucose. So that is why there should be no glucose in the urine of a normal dog or cat.
If we have glucose in the urine, usually that's because we have high blood glucose, and that's diabetes, OK? When the blood glucose is normal, and we have glucose in the urine, that is telling us the proximal tubules aren't working. And that could be from an inborn metabolic problem like tubular glucose urea or part of the Tanconi syndrome.
Or it could be due to a Acute insult to the kidney, like. Infection, toxin, ischemia, shock, lepto, jerky treats, for example. OK.
The other function marker on the specific on the urine dipstick is. Protein. When we have protein in the urine, that can be pre-renal if we have high globulins or high globulins or other proteins in the serum like myoglobin or haemoglobin.
So, or that can be post renal, whether it due to haemorrhage or inflammation in the lower urinary tract and post renal protein is the most common reason to have protein in the urine. So anytime you see protein on a dipstick, then make sure you look at a sentiment exam to investigate for inflammation or haemorrhage in the lower urinary tract. But if you've ruled out pre and post renal proteinuria, you've got renal proteinuria.
And that can be due to either glomerular disease or tubular damage. So again, looking at protein can help you assess kidney status, yeah. Then I would like to remind people of what not to pay attention to on these dipsticks, and that is specific gravity, forget it.
And then the indicators we have of urinary tract infection are white cells in the urine, just not that useful in dogs or cats. OK. Other tubular injury markers and they're all found in the urine, you can see here on the slide.
Probably the most specific one we have is granular cast. When we see granular cast in the urine sediment, then we have evidence of acute kidney injury, but we don't always. So the issue with these traditional markers is they're not 100% sensitive.
So if we combine norglycemic glucose era and granular casts, right? 30% of dogs with AKI have those findings. So they're not always present.
And then they're not all that specific either because other diseases can cause some of these findings in the urine. So, we're looking for always better tests, and now we have the availability to look at a marker for tubular injury in the urine that is sensitive and pretty specific as well, and that's the statin B. And this is an intracellular protein.
That in the kidneys is found in the tubule cells, and when those cells are damaged from ischemia or toxin or inflammatory cytokines, then they leak and the ystatin B that's intracellular enters the urine and we can measure that as a marker for active it's happening right now to be injury. We would consider. Measuring statin B when we suspect our patient has a toxic insult to the kidneys, some primary insult to the kidneys, or when there is a severe systemic disease that could be impacting the kidneys either by causing poor perfusion like shock, GDV or systemic inflammation, sepsis, severe pancreatitis, and those inflammatory cytokines can damage the tubules.
Now, The part of the nephron that's most vulnerable to any of these insults is the tubule because it's the most metabolically active part of the nephron and has the highest energy requirements. So anything that compromises that in the kidney overall is likely to be likely to affect the tubules first and then therefore these tubule tubular injury markers in the urine may be our earliest indicator of a problem. And then Other tips for diagnosing kidney disease early is to detect it before it's even azotemic.
OK, not all with either acute or chronic kidney disease are isogenic and if we can identify. It prior to the development of whatever the kidney disease is prior to it becoming aotenic, clearly the better chance we have a good outcomes. Yeah.
So, for detecting pre-aotenic CKD, here are a couple of strategies for that. If we establish each patient's individual normals when they're young and healthy by looking at their baseline lab work, CBC biochemical panel, urinalysis. And we trend those values over time, we may detect trends that tip us off we've got a developing problem even before the values become abnormal.
So if we see creatinine creeping up over time or STMA trending up over time, even though still normal, we would want to investigate. Same if we see the specific gravity decreasing over time. If we have a decrease in body weight in, especially in an older cat, there's a lot of diseases that older cats get that are associated with decreased body weight, but CKD is one of them, and we know that in the 12 months prior to the diagnosis of CKD, on average, cats lose 9.8% of their body weight, but that weight loss can start up to 3 years before the diagnosis.
So if you're seeing a trend. In a decreasing body weight in a cat. Keep CKD on the list of possible causes and start investigating, monitoring more frequently, looking at blood pressure, etc.
Also, you can have pre-azotemic or non-azotemic CKD if it's proteinuric. So proteinuric CKD exists, and if it's in stage one, so pre-azotemic by definition, because azotemic CKD is stage 2 and beyond, so persistent renal proteuric is CKD. And it might not be aotemic.
So again, urinalysis is critical there to identify protein with AKI. You know, we might see these markers in the urine of tubular injury up to 2 days before the GFR markers in the blood increase. So getting that urine and assessing for norglycemic glucoseuria as we discussed, renal protonuria and looking at cystatin B can identify this type of kidney injury early.
All right. So, Let's, now that we've kind of covered ways to get to a diagnosis of kidney disease as quickly as possible. Let's, let's get to the part of the talk that you guys all tuned in for, fluid therapy and what's new.
First of all, fluid therapy is not the mainstay of treating azotemic patients, OK? Sounds a little. Unusual, but the job of fluids in any exogenic patient is to support those kidneys by correcting any abnormalities, and we'll talk about which so that the kidneys can heal.
And that may be because you're giving specific therapy like treating pyelonephritis with appropriate antibiotics. Yeah. And these quotes come from, I think, a very useful guideline for practitioners, which are the 2024 American Animal Hospital Association fluid therapy guidelines.
Well worth a read. OK. So what are those treatable abnormalities that we might use fluids for in kidney patients while the kidneys heal themselves?
Well, with CKD, I think this is a pretty good list. Most of these cats, especially, can be dehydrated if their appetites are decreased or they have such extreme PUPD hypokalemia, we can address that with fluid therapy, supplemented with potassium, and we see hyperkalemia in about 30%. Of CKDAs.
Some have severe severe metabolic acidosis or asidedemia, which we might be able to correct with fluid therapy and bicarbonate if we need to. Anaemia can be corrected with fluid therapy using blood products, all right, for your CKD patients with AKI. There could be a raft of abnormalities that we need fluids to, you know, correct while we're allowing the kidneys to heal.
And let's just take for example, a dog with an adrenal crisis may have all of these abnormalities may be hypovolemic, hyperkalemic, hypoglycemic and hypercalcemic and fluids clearly are going to be useful in correcting these abnormalities, OK? In general, when it comes to how fast to administer fluids, it all depends on how fast the animal lost them. Rapid losses get replaced rapidly.
Gradual losses get replaced gradually. And so what does that really mean in clinical practise? Well, it all basically boils down to the difference between hypovolemia and dehydration.
All right. So hypovolemia is a loss of fluids from the intravascular space, and this is the fluid that perfuses. The tissues with oxygenated blood, right?
This is bad, right? So this would be shock or haemorrhage or GED or sepsis, right? These animals are hypovolemic.
Their organs aren't being perfused. And you can identify this and monitor it by looking at perfusion parameters like heart rate, pulse quality, capillary refill time, membranes, mucous membranes, blood lactate, and urine output, right? The fluid of choice for correcting hypovolemia is an isotonic crystalloid given intravenously or intraosseously, the two most rapid methods of administering fluid, and we want to use an isotonic crystalloid because its composition mimics that of plasma, so we don't cause deviations and problems.
The rate at which we want to give in the volume, this is what's changed. We no longer give a shock dose of fluids to a dog or cat within one hour, so one blood volume within one hour to treat shock. We do incremental boluses and monitor our perfusion parameters.
Along the way and do that until we're satisfied and that may be less than a shock dose of fluids in some or more in others. So we kind of tailor to what our patients need, starting with a 10 mL per kg bolus in a dog and a 5 mL per kg bolus of. Isotonic crystalloids in a cat given over 15 to 30 minutes.
And with hypovolemia, we want to correct it quickly because again, this is what is perfusing the tissues and organs with oxygenated blood. Dehydration, on the other hand, is a loss of food from the interstitial space that occurs more gradually, right? And this can be identified with your physical exam parameters that we're all familiar with like skin trigger, most reliably assessed over the rib cage and mucous membrane moisture.
We also correct dehydration with an isotonic crystalloid by any number of methods, intravenously is fine, sub-Q is fine. If you've got a stable patient that can be treated as an outpatient. If you've got a feeding tube in place, oral water through the feeding tube is fine.
And the amount of fluids that we give to restore hydration is based on our familiar formula, which is body weight in kilogrammes per dehydration that you determine from the physical exam as a decimal times 1000. That's the mills to replace, and this is done because the dehydration occurred slowly, more slowly, over 4 to 6, up to 12 to 24 hours. When the dehydration becomes severe enough, the animal may also be hypovolemic, not only lost fluid from the interstitial space, but also in the intravascular space.
But this means we're like 10 to 12% dehydrated. The animals are really in bad shape. Most of our kidney patients aren't that dehydrated, so they aren't hypovolemic, just dehydrated and can Have these lower volumes of fluid given more slowly to restore that.
What type of fluid you want to go for, like we mentioned, an isotonic crystalloid and good old lactated ringers is perfectly fine. It's isotonic. It has a buffer.
It contains calcium, which criticalists like because with critical illness, hypocalcemia is not uncommon and is not a great prognostic sign. It has potassium. Lactated ringers has potassium, but a small trivial amount, so it's perfectly safe to use in hyperkalemic patients like our dog with an with an adrenal crisis or a blocked cat.
And the lactate in lactated ringers may actually be inflammatory. There are other options other than lactated ringers that would be fine for restoring volume and hydration, and you can see the list here. These are also isotonic.
They have Buffers acetate, gluconate, not lactate, and magnesium, not potassium, fine. Sodium chloride best to avoid because it's acidified, no buffer. The high sodium content may, especially in animals with kidney disease, not be optimal, and the really high chloride content relative to these other fluids can cause renal vascular constrictions.
So best to avoid sodium chloride. So, when it comes to restoring volume and hydration, a replacement fluid. Isotonic, any of those ones we just talked about.
If an animal needs to be on fluids after it's normal bulimic and has normal hydration, say because it's just not eating or it needs to have additives in the fluid like potassium to correct severe hypokalemia. Ideally switch to a maintenance, not a replacement fluid, and maintenance fluids are hypotonic, basically have have half the sodium as replacement fluids, and that's just easier on the kidneys, more physiologic to what's happening throughout the day in normal patients, and you can actually buy maintenance fluids or make them by diluting whatever. Replacement fluid you use, lactated ringers, for example, 1 to 1 with 5% dextrose and these fluids will also need potassium supplementation.
Are you gonna harm an animal by leaving them on, say, lactatings for 5 days in the hospital? So short term, is that really gonna be harmful? Probably not.
But in the kidney patient, that sodium content could be a little bit of a concern. And if we're just gonna really refine or fluid therapy, it's best in that situation to switch to a maintenance fluid. Just remember that with lactated ringers, because it has calcium, we don't want to put things that could precipitate with calcium in the same line, like blood products with the citrate or bicarb.
So if you're using lactated ringers and you need to give these other products, it needs to be through a separate line. OK. All of these fluids that we're talking about move freely between the fluid compartments in the body, and only 25% of them remain in the vascular space after 30 minutes of administration.
Where they go is what all the kind of fuss is about that has led to some changes in the recommendation in fluid therapy for kidney and other diseases, and it all has to do. With the increased understanding of the importance of this thing called the endothelial glycocalyx. OK.
What this is is sort of think of it as a protective sieve, a mesh that coats all endothelial surfaces, and it's composed of Various proteins, so glycoproteins, proteoglycans, glycos aminoglycans, and also plasma proteins like albumin, fibrinogen, and antithrombin. When this thing is healthy, fluids stay where they belong. When this thing is denuded, then the endothelium is exposed, so platelets can adhere, white blood cells can go through and exacerbate inflammation.
And fluids can go through in larger volumes, increasing the amount of fluids in the interstitium. All right? What is it that damages the glycocalyx or inflammation in general and everything here on this list is inflammatory, and sepsis for sure, trauma is inflammatory.
If you have a cat with cardiomyopathy that has aortic thromboembolism, reperfusion can cause damage to the glycocalyx. As can just giving larger than necessary volumes of crystalloids, crystalloids or clear fluids denude or damage the glycocalyx. So we really want to be careful there and kidney disease per se is inflammatory.
So animals with kidney disease are predisposed to endothelial glycocaly damage. That can complicate things if we overdo fluids. If we do have damage to this glycocalyx, you can see the problems that can result in in our for purposes of our discussion in kidney patients is mainly capillary leakage.
If we have more fluid in the interstition in the kidney, in a dog or cat, we have issues because the kidneys surrounded by a rigid capsule. If interstitial fluid builds up. In that kidney because of overzealous fluid therapy, overhydration, or giving too many fluids while we're resuscitating a hypovolemic animal, then the pressure in that kidney will also increase and that increased.
Intrarenal pressure will decrease renal blood flow and GFR and this is why we can cause or exacerbate kidney disease by getting fluids in excess. So we have to remember fluids are a drug. Excess fluid or volume overload is the most common drug overdose in our patients and that that results in problems, increased interstitial fluid, not only in the kidneys that we discussed, as we've discussed, but in other organs like GI tract and the lungs, OK?
So, how do we avoid this? Well, as a summary of kind of what we talked about before, if you have a kidney patient who's hypovolemic, get on it, fix it quickly with replacement fluids intravenously or intraosseously. If your CKDA is dehydrated, you got more time, go slower, either the IV subQ or interval route.
Keep up with any ongoing losses. So some kidney patients are vomiters or have diarrhoea or are so puberty that they cannot keep up by drinking adequate amounts of water, and in order to determine How much fluid to replace in a vomiting or diarrhoea patient or lung with pubBD if you can't measure urine output, you just weigh an absorbent pad and a change in weight of 1 gramme. Equals 1 mL to replace.
We also then need to provide maintenance, so the total fluid requirement of the patient is the sum of all of these components, OK? And then you stop. All right, and you continually monitor and adjust fluid rate and volume based on your parameters that we talked about earlier.
We want to use an isotonic crystalloid with a buffer as we've mentioned, synthetic colloids in general are sort of out of favour and kind of especially in animals with kidney disease because That population may be more at risk for the adverse renal effects of these fluids such as head of starch, and also possibly some problems with hemostasis, so best to avoid those. How are you doing? How do you know whether you're giving the right amount of fluids or overdoing it?
Wait. Accurately weigh the patient, and this may be 4 times a day when they're acute and unstable, or as they stabilise once or twice a day. And our goal is to maintain body weight.
Replace whatever body weight loss has occur from dehydration and stay there, cause remember any sort of rapid increase in body weight is due to a change in total body water. And at 5% increase, you should be thinking, oh well, I should really reassess whether the patient needs all these fluids or do I need to cut back at 10% increase in body weight over a short period, that is the threshold at which we might see complications due to volume overload, hypervolemia. And those patients decrease or stop fluids and then reassess.
What we don't do anymore is this forced diuresis by giving multiples of maintenance in the hopes that it will speed elimination of a nephrotoxin, which it probably doesn't. There's not a lot of evidence that that actually happens, or that it will decrease the creatinine or SGA faster, get rid of your reemic toxins and make the animal feel better. We, we're kind of done with that for reasons that should be obvious.
If we overdo the fluids, we may actually cause or worsen kidney disease. If we do not see improvement in our renal parameters, Within 12 to 24 hours, we don't have a fluid responsive azotemia. So there's no point in pushing fluids further in those patients.
OK. If you see an animal that has azotemia, and that aotemia gets worse on fluids. In in the past, I think a lot of our instincts would be, oh, more fluids, OK?
But now, given the new thought around all of this, we want to consider either decreasing or stopping fluids, and there are two ways to know whether you should do that or not. One is just weigh the animal like we talked about, and if you're seeing that 5, or especially 10% increase in body weight, stop the fluids at least temporarily reassess, yeah. Or if the amount of fluids that the animal got in the interval in which you saw the isotemia worsen, so let's say 8 a.m., you get sic creatinine, they're elevated.
8 p.m. They're more elevated.
Well, determine how many. Mils of fluid the animal received in that interval, the total volume of fluids administered in that 12 hour interval and compared to what maintenance would have been in that same interval. And if the amount the animal got exceeds maintenance, it might be time to consider decreasing or stopping the fluids.
And if you're seeing evidence of volume overload that you don't like serious nasal discharge, after discharge to keep the regurgitation, then you might want to also give Lasix. OK. So let's put this new thinking around fluids to work in a chronic kidney disease patient and an acute kidney injury patient.
OK. We've got a cat. We've all seen these.
They come in, they, they have CKD but they present having acute and chronic kidney disease because something else made them sick or they just stopped eating, vomited, got dehydrated. So we've got this CKD cat, dehydrated, inappetent. You can't palpate, you're in the bladder, so it's alleguric and the azotemia baseline that you know this isotemia is worse.
The rest, the azotemia is more severe than baseline. This, this is what I would have done in the past to make everyone's job easier. I would have just asked a nurse to start IV fluid that.
I would have picked an interval of say 2 to 4 times maintenance just based on my looking at the animal. Instead of doing the math that we talked about earlier, due to calculating dehydration percent and all of that, yeah, just put them on 2 to 4 times maintenance, then we're gonna park him there. And then we check the next day.
24 hours later, hydration is normal, great, urine is being produced great, so that was physiologic oliguria, but not eating, and the kidney values have not improved. So this is another key decision point that I think we need to rethink compared to what we might have done in the past, you know. In the past, well, maybe just we under maybe that 3 times maintenance wasn't enough.
Maybe it needs 5 times maintenance. Let's do that. Let's increase the fluids that might drive those, you know, estimating creatinine values down quicker, maybe improve appetite.
This is completely not what we should be doing these days, OK? It should be clear by now, hopefully, because If we haven't seen the kidney values improve within 24 hours of of appropriate fluids, what do we have? Non-fluid responsive azotemia.
So there's no point. In fact, it's kind of like harmful to think about increasing the fluids in that patient. We just have to support, correct any other abnormalities, potassium, pH abnormalities, while the kidneys heal, nutrition, all of that.
All right. So here's what we do now. Once hydration is present and volume is restored, then maintenance fluids until the animals eating, no more than that.
Administer potassium, correct other electrolyte or mineral abnormalities, acid-based abnormalities along the way. Once they're hydrated and still not eating, that's the time to consider maybe an appetite stimulant or ideally. With if the animal has not eaten within 48 hours, I mean that's kind of like the time to consider placing some sort of feeding tube that's super easy to put in a nasogastric or nasal esophageal tube for not only nutrition, but also hydration, water.
OK, so this would be the new approach. You would do your calculations, how what percent dehydration. Add that amount of fluids to maintenance, any ongoing losses, that's the fluid this cat gets on presentation, reassess.
If the ao team is not improving, then not fully responsive, just maintain hydration, keep up with ongoing losses and and all of all of that to the maintenance fluids. And then whatever other specific therapy for the primary renal insult, if there is one, you better make for that as well, and then don't forget. Try not to let your sick patients go longer than 2 days, including the time prior to presentation before getting some nutrition.
And then we want them to at least have, well, we're shooting for resting energy requirements, but something is better than nothing. OK? OK, so that's how we would reassess and maybe rethink our fluid therapy for a CKD patient.
What about an AKI patient? Here we have a dog who's been exposed to a Nephrotoxin, potentially raisin ingestion maybe at some point in the last 8 hours, but looks great. So this would be also the same basic thing you might see in a dog that only comes home and instead of finding a box of raisins, finds some a a bottle of a non-steroidal and doesn't know if the dog ate it or how many, whatever.
And the dog looks great. Vital signs normal, no dehydration, no anything. What are we gonna do?
Well, we're gonna get some baseline lab work, right? This is way too early for the possible toxin ingestion to result in azotemia. Remember that can take up to 2 days after exposure, but this may not be too early to see evidence of tubular damage cause that shows up first.
So we look at our GFR biomarkers, are functional markers in the blood of this dog or BUN creatinine estimate normal, yeah, right now, normal. Look at the urine ystatin B though high. This dog did get into raisins and that did cause This dog, it's idiosyncratic.
Not all dogs that ingest raisins or grapes will develop toxicity, but some do. So you assume they all have, and you want to assess for that. And so here we have evidence that this particular dog did have a toxic event related to this raisin ingestion that's affecting the kidney tubules, but nothing is touching the kidney function parameters at this point.
So we look at the rest of the urinalysis, which is free catch. Nothing here to write home about. It's got a 1049 specific gravity.
The other changes I'm happy to associate with a tribute to just it being a free catch sample with contamination. OK. What do we have?
We've got this perfectly healthy looking dog, normal kidney function, normal hydration, with an increase of statin B. So we know he's got active, it's happening right now to bitter injury, like we do to raisins. What are we gonna do?
All right. Well, You know, we're gonna make this dog vomit and give one dose of activated charcoal. Decontamination is always your first go to with any toxin exposure unless the animals severely obtunded, you know, and could be at risk for aspirating.
But in general, the toxins that we encounter, if you see the patient, say 4 to 6 hours after ingestion or later, it might be too late for that decontamination to work, but raisins stay in the stomach for up to a day. Not rapidly broken down or reabsorbed absorbed by the GI tract. So in this case, within the first with radius and ingestion, within the 1st 24 hours, make them vomit, give them one dose of activated charcoal.
We don't have any evidence that repeated doses of charcoal are useful, so vomiting induce emesis, one dose of activated charcoal. And now we have some choices. OK.
The new way of approaching these patients means we have options. In the past, we would have just said, oh, you were exposed to a nephrotoxin, we're gonna get you in the clinic for 48 hours of IV fluids at 2 to 4 times maintenance, forced diuresis. That's over, OK?
The reason that that should be clear. So what are your options clinically now? So you can send this dog home.
And just have the owner come back for recheck in 2 to 3 days or sooner if they notice anything at all, decrease appetite, lethargy, vomiting, yeah. If you want to for a little bit of insurance, you can get sub key fluids before sending the dog home. I would do this probably because I've made the dog vomit.
Maybe he'll vomit a time or two again on the way home, or maybe just not feel like eating cause he's got the charcoal and was vomiting. I do not want this dog to become dehydrated at all, to add insult to injury, yeah, or if I was concerned. Just didn't like how this dog looked or had a, you know, clinical niggle in my gut about, I want to watch you.
I might keep him in the hospital on IV fluids, but at maintenance rates for a day or two. OK, so all these options are fine, depending on you and the owner and your clinical, you know, intuition. Any of the 1st 3 are fine, we're just done with the last one because this one.
Giving more fluids than necessary for longer can cause or worsen kidney function, OK? So we do get the dog back in. This dog was treated with 2 days of IV fluids in the hospital, fine as long as it wasn't excessive.
Also, antibiotics for possible urinary tract infection, which is fine as well. I probably would not have done that, because we had a free cat sample and everything was sort of the changes were minimal on that. So we just want to reassess.
So we have still perfectly normal functional markers in the blood, BUN creatinine and STMA, and our cystatin B is now normal. So this dog did great. This is what we see with the statin B in the mix.
It will increase quickly within hours of the onset of acute tubular insult, which is helpful, so it's sensitive, yeah. And it means when it's elevated damage is happening now, so you have to do something about that, right? And then it has a short elimination time.
So once the tubular injury is resolved, then you should see a rapid normalisation of the statin B within, say, a few days to a week or so. All right? So I think that kind of kind of summarises the new thinking to recap.
Fluids are not the mainstay of treating isotemic patients. They don't improve kidney function. The first evidence of kidney disease may be in the urine.
Tubular injury markers may proceed. Increases in GFR biomarkers in the blood by 2 days. So if you want to identify kidney disease early, we must include urine and look for evidence of tubular damage including cystatin B, and then When we need to decide if a given kidney patient eats fluids or not, look at the patient.
Hypovolemia, of course. Dehydration, of course, ongoing losses, keep up, give maintenance till they're eating or drinking, OK? We assess frequently using body weight, and when you get to 5%, or especially 10% increase in body weight, it's time to think about decreasing or stopping fluids.
And if azotemia is worsening on fluids, rather than Knee jerk reaction of increasing fluid weight to drive those values down further. Look at body weight and compare the amount of fluids the animal got to what maintenance would have been over the interval when kidney function worsened to see if the right call is less instead of more. OK.
And with that, I'm gonna let you guys go, but thanks so much for attending and we hope to see you at another webinar soon. Thank you so much.