OK, good evening everybody and welcome to tonight's webinar with the webinar vet. My name's Sophie McMurra and I have the pleasure of chairing tonight's webinar. So we have the wonderful Caroline Boothroy talking to us about an overview of renal disease in dogs and cats.
Before I introduce Caroline, if we do have any new members, I'll just point out that you can ask questions throughout the webinar, and if you'd like to do so, just hover over the toolbar at the top or bottom of your screen, click the Q&A box and send your questions through to me. So you can send these at any time throughout the webinar. It won't disturb the talk at all.
It'll just come through to me and I can ask Caroline at the very end. OK, so I've had the pleasure of working with Caroline for many years at Northwest Veterinary Specialists. So this is a multidisciplinary referral centre which Caroline joined in 2007.
She became a dedicated medicine nurse in 2014, and then moved on to become a dedicated oncology nurse in 2016. She passed her certificate in small animal nutrition in 2010 and became a veterinary technician specialist, which is also known as a BTS in Small Animal Internal Medicine in 2014. And she's currently collecting cases for her second BTS in oncology.
Excellent patient care is a real passion of Caroline's and she loves to look after patients as she would like somebody to look after her own pets. And after working with Caroline for so long, I know that you're in excellent hands tonight. So I will hand over to you and I hope you enjoy it.
Thank you very much, Sophie. That was very kind. So welcome everyone to my talk this evening on the overview of renal disease.
So I've got, there's quite a lot of slides that I've got to try and get through this evening. I wanted to get as much in there as possible for you guys. So I apologise if I talk pretty quickly on this.
I'm hoping that everything you need to know is in the notes, but if you do have any other questions, my email is in the notes and it's at the end of this presentation as well, so do, do please contact me and I'll do my best to answer them for you. So we'll start with the basics on, kidney function. So it has many functions, within the body and to maintain homeostasis within the body, and this is to remove any metabolic or nitrogenous waste.
It can respond to changes in water levels, so, varying hydration levels. It helps to maintain the electrolyte balance so as to whether or not it's going to secrete or reabsorb like potassium or sodium. It can help to control acid base status as well.
And then it also produces substances that can help regulate blood pressure and red blood cell production. So the kidneys, there should be 2 kidneys, and each of them kidneys will have 1 ureter, and then both of them ureters will actually then go into the bladder. They are located in the dorsal part of the abdomen and the right kidney is slightly cranial to the left one.
So the kidney has it's, it's nerve supply and it's primarily from the sympathetic portion of the autonomic nervous system. So this means it is basically working without any conscious thought. It just kind of keeps ticking over and does its own thing.
The kidney blood supply requires, has about 20-25% of the cardiac output and the kidney has a really high oxygen requirement therefore has has that massive output cardiac output. So the blood flow starts at the aorta, it goes into the renal artery, then into the interlobular arteries, into the capillaries, and then into the glomeruli, where all the filtration takes place, back to the capillaries, into the inter lobular veins, back into the into the renal vein and then to the vena cava. There are some, the macroscopic structures of the kidney are the hilllus, and this is where the vessels and everything else enter and exit the kidney.
The capsule is the protective layer, and then the cortex is the outermost protective layer. The medulla contains all the collecting ducts, and the pelvis is where any urine that has been formed drains into the pelvis and then this goes into the ureter. So onto the little macroscopic structures, the nephron is the functioning part of the kidney, and there's about 1 million of these little guys in the function of the kidney is compromised, but about 75% of these nephrons have been damaged.
And the nephone is responsible for filtration of blood and urine, filtration of blood and then the urine production. So breaking the, the nephron down a little bit further into the little tiny components. So the glomerulus or the Bowman's capsule, there's high pressure in this Bowman's capsule and this forces any fluid or small molecules out of the arterial blood.
The proximal convoluted tubule contains lots of microphyi, and this helps to increase the surface area. And this area is responsible for the reabsorption of water, sodium, chloride and glucose. And this is when the we start to con concentrate the levels of urea in the urine.
The descending part of the loop of Henley is permeable to water, but is unable to reabsorb any sodium out of this solution. The ascending loop of Henley is impermeable to water, er but it contains proton pumps, so this can actively reabsorb any sodium back into, back, back into the blood. The distal convoluted tubule doesn't contain any microvilli, and this is an area again responsible for reabsorption of sodium and potassium, or then secretion of potassium potassium if the potassium level is too high.
And it can also balance the acid base status by varying the amounts of hydrogen ions that are excreted. The collecting duct is the end part, and this is what this, this part receives multiple receives urine from multiple nephrons. And this is under the influence of the anti-diuretic hormone which is able to change the permeability of the duct to water.
So more ADH hormone means more water that is then reabsorbed back into the blood. So there's a couple of different types of renal disease, there's chronic disease, acute disease, and then sometimes we will see an acute acute case on a chronic disease too. So chronic kidney disease is the most common, common renal disorder in dogs and cats, and it might actually be a congenital condition, so you kind of think this would be your 20 year old cat that's coming in, but we can actually see the young animals as well as part of a a a con a congenital condition.
It's characterised by an irreversible and progressive loss of kidney function, and this can cause changes to the shape and size of the kidney. And we need to manage this with lots of supportive care, and that we we're able to actually stage, the level of kidney disease, using the iris iris scheme. So kidneys, when they are in chronic kidney failure, tend to be small and irregular and finely pitted, .
Compared to a normal kidney, and you can see the difference here, the one on the right would be the kidney and chronic disease, and then the one on the left would be a normal one. So renal dysplasia is another is a congenital form of chronic kidney disease, and this is when we do see this in really young patients. And it's, I find it really, I find it's one of these really sad cases.
It is caused by developmental anomalies, and an ultrasound may show some small, irregular shaped kidneys. But we tend to use biopsy to confirm the diagnosis, and these poor patients do tend to die before they're about 2 years old. So once we have a diagnosis of chronic kidney disease, I said the International Renal Interest Society have come up with some wonderful, steps to help us stage these guys.
So it means that we can look and kind of say, OK, the, the creatinine is this level, the SDMA is here, and then if they either stages 123 or 4. They then give us some guidelines or recommendations about what we should be doing for these guys, as in stage 3, we should follow all of the previous stages and then kind of, yeah, you can just monitor all of this. So acute kidney failure is the sudden onset of renal outflow or excretory failure, and this then leads to the accumulation of uremic toxins, clinical signs of uremia, and then a dysregulation of fluid, electrolyte and acid base balance.
And this is potentially reversible if it is caught quick enough and we actually get on top of it quick enough again. So again, 3 stages, 3 potential it can break this down into 3 areas and this can be pre-renal, renal or intrinsic or post renal. So pre-renal, this tends to be an insufficient blood flow to the glomeruli, so it means that there's just not enough flow getting to them.
And this can be caused by a thromboembolism, as in DIC shock or trauma, excessive vasoconstriction. Adrenal insufficiency, significant hypertension, or heart failure. And the main one is tends to be dehydration, extreme dehydration leading to hypovolemia and that we just need to rectify.
So with this, with prevenal, we tend to see an elevated urea and creatinine, but the urine we will find will actually be concentrated because if the, the body is, dehydrated, the body will then want to try and conserve as much fluid as it, it can do, so it will absorb lots of water back in by the kidneys, therefore making the urine very concentrated. So we need to replenish the fluid volume and restore the blood pressure. So renal or intrinsic, Talks about any injury or trauma to actually to the kidney, and this can be caused again by decreased perfusion, so if they the dehydration or the hypovolemia has been more severe or has gone on for a lot longer than for pre-renal.
Some toxins or even medications prescribed medications can cause this infections or microthrombi again as in DIC. So I said this can be caused by . Poor profusion, so it can, this occurs as in pre-renal disease, but it's typically a lot more severe and a longer duration.
So toxins, these can damage any part of the kidney, mainly the renal tubules, as these are very sensitive and even some of the some of the prescribed medications can cause injury. And we need to attempt to decontaminate these patients to try and minimise the impact of whatever they've taken. Infections, pyelonephritis is an infection of the renal pelvis, and this can come from in a complicated UTI or from sepsis or discospondylitis.
Some patients that have diabetes mellitus or chronic kidney disease tend to be predisposed. And ideally we want to get a a sample direct from that renal pelvis so for culture and sensitivity so we can get some appropriate antibiotics on board. Leptospirosis is another infection, and this is caused by a bacteria, and this can cause renal and hepatic injury.
These bacteria colonise and multiply in the renal tubules and cause the injury there. It's also toxic and it has a toxic effect on the renal cells. And do remember that this is a zoonotic condition, so if you're ever suspicious that this patient has got leptospirosis, you need to be barrier nursing straight away.
And we need to offer these, get these guys onto some antibiotics and lots of supportive care. Lyme disease is another infection that can be transmitted by ticks, and it can cause pyrexia, lethargy lethargy and polyarthritis. And if it is severe, it can cause protein losing nephropathy.
So post acute renal failure tends to be where there's a complication after the kidneys, and this is either a blockage or rupture of the urinary tract. So we can have a ureteral obstruction, so we can have ne nephroliths that have been produced in the kidney, can either migrate or fragment away from in the kidney and then block the ureters, and this prevents urine leaving the kidney. And if this just happens, we can place a suburethral bypass device to bypass the ureter and then we do need to maintain these.
Urethral obstruction, so we, we're not able to the, the, the urine has come from the kidney down, down the ureter into the bladder, but it can't actually then leave the bladder. It can be caused by neoplasia, urulus, or just a, a sludge, or this, it, it can be idiopathic in some cats as well. A bladder that is unable to empty, is a true emergency and you've all seen these blocked cats that come in and they're so painful, and we need to, we need to help these guys out.
This is an image of a, I think it was a dog that had this, a urethral transitional cell carcinoma. And for these guys, sometimes we're able to try chemotherapy to reduce these, these tumours. Or sometimes we've had to place a, a permanent, urethrostomy tube as well to help them, so we can actually then manually empty their bladder.
Uli or sludge can also cause blockages, so they can block into the urethra, either that just a sludge or even just the stones too. With some stones we might be able to block, flush them stones back into the bladder and then take them to surgery. And we need to be careful, especially when we get these great big bladders like this with cystocentesis, because we don't want to cause, a rupture of this bladder by popping a needle in there.
So rupture of the urinary tract can also cause a post renal kidney failure as well, because once this, the bladder has ruptured and the urine ends up into the abdomen, this is when we can end up with the the the urine and everything is then reabsorbed, hence that's why we end up with a kidney failure. And this can occur following trauma, urethral obstruction or bladder ureulus. And this surgery needs to be done, pretty quickly.
We need to ident, we need to identify where the rupture is and then go to surgery. And you can see in this picture, this dog had, had had a ruptured bladder, and you can see all the, the, the bladder stones that are actually just, free in the, the patient's abdomen. So patients that whether they have an acute or chronic disease, we can have, it's, a patient that has a chronic disease, and can, can kind of be doing OK.
And then after an acute insult, maybe they've ended up dehydrated, or they, there's something has just not been right with them. They've end, dehydrated, hypovolemic. They end up with an acute, acute kidney failure on top of their chronic disease.
So once we've got that acute failure under control and we've got that rectified, we shouldn't really then expect any further improvement because they've they're already in kidney failure. And so once we've got to a certain extent, then we probably won't get any further. So the clinical signs of chronic kidney disease will be nausea and or vomiting.
They will be maybe hyperexic or anorexic, PU and PD and they will be they will be producing quite dilute urine. Most of these patients will be hyper hypertensive, which can then sometimes be characterised by seeing the blood in the eye or maybe having some other ocular, problems. Owner might be noticing some weight loss or muscle loss, and these are great charts from the World's Small Animal Veterinary Association that you can actually then body condition score, patients and muscle condition score.
And they have them for both cats and dogs, and they're just on their website and you can download them as a PDF, . And this is something that you should be looking at every time you've got an a patient coming in for the clinics. Document the body condition score, document the muscle condition score so you can see if there are actually any changes when that patient starts to come for revisits.
Hypokalemia can manifest as a cervical ventroflexion, we'll see these cats just holding their head down, and then this plan planter grade stances where they will be walking kind of on the hocks rather than on their toes. So they can end up with halitosis with and with severe azotemia, they can end up with ulcers on their tongue and the oral mucosa. And this was a 10 month old Pomeranian puppy that I had renal dysplasia, and you can see all these ulcers all around his tongue and all over his all over his lips as well.
They might have a poor hair coat, and kind of you'll, you'll all know these guys when they come in and they, they look a little bit unkempt and their just their coat looks a little bit, just a little bit worse for wear. They can have some neurological abnormalities with altered mentation, stumbling, seizures, or even muscle tremors as well. So the clinical signs with acute kidney injury can vary depending on kind of on, on the course.
So I've kind of come through a few of these and most of these guys do tend to be in normal body condition and have a normal hair coat. They tend to be of a normal, a normal patient, whereas something has gone wrong, they've gotten into, into some poison, or they've, they've not tolerated their medication well, or they've ended up really dehydrated or something has gone, something's not been quite right. And they will then present dehydrated, probably nauseous and vomiting, lethargic.
Again, maybe hyperexic or anorexic. And dependent, most of them will end up bradycardic if they've got a urinary tract obstruction, and they shall be due to the hyperkalemia. And if they got, if there's a potential from Lyme disease, they might be pyorexic, lethargic with some polyarthritis as well.
Some of the acute kidney injuries, patients will have a small non palpable, non palpable urinary bladder, and these kidneys will be enlarged asymmetrically and they'll be painful and firm, and these are the, these guys will be quite uncomfortable. Again, they will have this uremic breath and severe they get the severe a Tbia can lead again to the ulcers on the tongue and oral mucosa, and this was a cat that had ingested lilies, and these ulcers thankfully improved when the cat actually improved as well. So if the acute kidney injury has been caused by an obstructed bladder, we'll see that these patients will be straining.
Owners might actually say they've been going back into the litter tray, and they're actually, they're not producing any urine, but we think they're constipated, so we need to kind of get a full, a full picture of what's going on. They will be vomit maybe vomiting and they'll have a horribly painful abdomen because their bladder will be enormous. So the diagnostics that we have available for assessing kidney disease, make that, we will usually go for ultrasound.
And this is great for a structure assessment. And then we can use it for sampling, so we can use it for FNAs of the kidney biopsy, cystocentesis or pyelocentesis when we take the sample direct from the renal pelvis. Radiography will be able to show us radiopa urulus in either the bladder, kidney, or the ureter, and you can see this in the kidney here and these are little nephilus.
And then we can perform contrast studies as well if we're concerned that there might be a urinary tract rupture, and the contrast will then show us where the rupture actually is. CT scans are great because they can tell us the extent of any neoplasia, if there is a tumour involved. And then it can also tell us if there is actually any meta metastasis to the thorax as well.
And this The structure here with the green arrows is a kidney tumour. FNAs are very useful. We do this under ultrasound guidance, and this just means we're popping a needle, through the skin into the kidney, and it means we can take some cells, from various places around the kidney to get a sample, send that off for cytology, and hopefully be able to start, and hopefully they'll be able to get a diagnosis and then make a plan of action.
Histopathology, can either be, taken by, a biopsy using ultrasound guidance and a tubec needle. Or we can go for surgical excision of the kidney if we know actually there's something going on there. Kidney isn't right.
We've already got maybe some information from, cytology, and then we can send the whole kidney for full analysis too. So blood pressure gives us a clear indication of the peripheral circulation. The kidneys can regulate their own blood pressure as long as the main arterial pressure is within about 60 to 160.
And it can tell us if this patient is hypotensive or less than 60 milli of mercury, or hypertensive. And we need to maintain this blood pressure so it's important cos it's so important that these vital organs are perfused correctly. So it's a nice little overview of the renin angiotensin system.
I'm sure you've all got this all engraved in your brains. So if the body notices a drop in blood pressure or a drop in fluid volume, renin is released from the kidney. And this acts on angiotensin from the liver to cause to turn into angiotensin one.
ACE angiotensin converting enzyme, or ACE is released from the lungs, and this acts on the angiotensin 1 and converts this to angiotensin 2. This angiotensin 2 then acts on the adrenal gland to stimulate the release of the aldosterone, and this then acts on the kidneys to stimulate the reabsorption of sodium chloride and water, and then can also act directly on the blood vessels, stimulating vasoconstriction and therefore increasing blood pressure and circulating volume. So non-invasive blood pressure, we need to make sure that we pick the correct cuff size, and it's about 40% of the circumference of whichever limb or the tail that you're going to use.
Make sure you're sat in a nice quiet and stress-free area. There's no point in trying to do this in a busy prep room when there's lots of comings and goings. Nice quiet room, nice and nice and calm.
The cuff should be level with the right atrium, so if the patient is sat down, you should really, if you're using a front leg, you should lift the leg up as well. And we can use the Doppler or oscillometric machines. So the Dopplers are really nice.
I'd like using these. If you do use these and you, the, the, the nice little whooshing sound can be very therapeutic for us, but it can be quite stressful if you're using it with cats. So I do, or make sure that we always use the headphones so that they're not disturbed by that as well.
The osciometric is great because this can, it's a little bit easier to use and some of these newer machines are much more accurate, especially for cats. Invasive blood pressure is the gold standard for blood pressure monitoring, but it can be quite difficult to to perform. So we could either do as an instant blood pressure reading, and we can pop a needle direct into an artery and get a reading that way.
Or we could place an an a a catheter and then do a con a continuous monitoring, and then we, we can have this just running continuously. So these are the normal blood pressures for cats and dogs. And if we're suspicious, and we've we've started taking some blood pressure readings and that you're reading quite a lot higher than what we've got in that normal table.
The higher that this blood pressure gets, the more risk of target organ damage, there is. So yeah, there's either a minimal, mild, moderate, and severe risk. So you've got to try this out.
This is why we want the patients in a nice quiet environment, because you can look at a cat sometimes and go, yeah, yours is gonna be really high, just because they, they can see how stressed and upset that they are. So we need to make sure they're nice and quiet, and even if it's that we need to keep going back and doing repeated readings just to make just to kind of see if we are continuously getting high readings. This hypertension is common in chronic kidney disease and if it is continuously high, we do need to start some therapy for that because hypertension can actually accelerate further damage to the kidneys.
Can also cause damage to the eyes, the brain and nervous system, heart, and as I said to the kidneys because this, any hypertension will significantly worse any existing kidney disease. Patients that are hypertensive but then need to go under anaesthesia. We need to monitor, we need to maintain their blood pressure at a lot higher.
Level than what we would do with with say normal patients, hyper perfusion will occur for them before it reaches 60 millimoles of mercury, so we do need to maintain them a little bit higher. So the aims of hypertension management is to firstly reduce the blood pressure using medication. And then we need to also treat the underlying disease as well and hopefully the combination well either one or the combination of the two will actually help to bring that blood pressure back down into the normal ranges.
So patients that are hypertensive, and if this is if the mean arterial pressure is becoming less than 60 milli of mercury or less than 90 systolic, this means that renal blood flow drops and then this can actually then lead to the acute kidney injury. This is why we're so careful when patients are anaesthetized, and that we do maintain at least I mean above 60. So then if this does happen, the anti-diuretic hormone is released to increase the water reabsorption, and this stuff then increases the circulating volume and improves the blood pressure.
So we have fluid therapy and medications that we can use to increase the blood pressure, and then we do need to monitor the response and then there's no point in just giving one bottle of of fluids and hoping that that's, that's a job done. So this is just to kind of show you from like hyper hypertension and hypovolemia, if the mean arterial pressure is starting to drop, kind of like the levels of fluid loss that we would expect to be associated with that, so we kind of then need to know actually how much fluids do we need to get back into these guys. So moving on to blood tests, so the SDMA blood test is a novel marker of the glomerular filtrate rate.
And this isn't affected by muscle mass, which some of the other blood tests may be. It detects chronic kidney disease earlier than, using the traditional, evaluation of urine and creatinine. Creatinine will only increase if it's 75% of the nephron function is lost, whereas SCMA will increase with 40% loss of function and a 25% decrease in this GFR.
Our studies have shown that it will show about 9 months earlier in dogs and 17 months earlier in cats, which is great, and it means you can pick this up so much earlier. So azotemia is defined as the urea and creatinine levels above the defined reference ranges and said that it needs to be at least 75% of these nephrons need to be impaired. Ua is the end waste product of amino acid metabolism, or the protein metabolism.
So as we see, the amino acids are metabolised to ammonia. This is then converted in the liver to urea, and then the urea is then excreted in the urine, but most, somewhat a little bit of it is then actually reabsorbed. So the renal function and it can be assessed on the ability to remove this nitrogenous waste.
So if there has been a renal, an impairment to the renal function, this means that insufficient waste is removed and then an increased urea. Some urea is reabsorbed in the proximal tubule with alongside water and, and then in the collecting ducts with anti-diuretic hormone influence. And it does tend to follow water, in the excretion in kidneys, and the kind of the, reabsorption and the excretion.
So if a patient is dehydrated, there'll be decreased perfusion, then decreased tubular urine flow rate, and then this leads to then increased water and the urea reabsorption. So again, if there's been renal dysfunction, there'll be reduced excretion. So there's other non-renal factors, and specific non-renal factors that can cause an elevated elevated urea that can be, dehydration because this means, there's been increased renal absorption alongside that water, increased dietary protein protein or the patient hasn't been fasted prior to sampling, or if there's a high rate of endogenous protein metabolism, such as if you hyperthyroid cats.
Creatinine is influenced by skeletal muscle mass, so an increased creatinine could indicate renal dysfunction, as there has been reduced excretion, or it could actually, show that this patient has, if, if it is a patient with an increased muscle mass, it could just solely be down to that. So do remember that if you've got a poorly muscled animal plus renal disease, sometimes it'll be possible to see a normal creatinine as well. It's less influenced by recent meals as well.
There's no tubular reabsorption or secretion in great amounts for of creatinine, but and it's less affected by dehydration than urea, but we should look at the the specific gravity alongside that as well. Hypercalcemia can occur due to chronic kidney disease or the acute kidney injury. And it can be secondary to other diseases as well, neoplasia such as lymphoma or anal gland adenocarcinoma, and it can be idiopathic in cats.
High levels are toxic to the renal tubules and can cause a PUPD and renal failure, and the hypercalcemia can also affect a number of the other body systems too. Hypershashamia can occur due to increased increased intestinal absorption or decreased excretion by the kidneys. Chronic kidney disease is the most common cause, and we need to be able to manage this either by diet modification or using phosphate binders.
The glomerular filtrate rate is the gold standard for assessing the filtration and excretion function of the kidney. As they, if you remember back to the CT picture that where that excuse me, the, the dog had a . A renal tumour.
So we had to remove one tumour, that the one kidney, leaving this patient with one kidney left. So we needed to assess whether or not this one kidney was actually able to, to cope with any chemotherapy medications that we needed to administer for her administer to her. These GFR samples.
Require collection of time blood samples and maybe urine samples as well. Hypo and hyperkalemia both need to be corrected. Hypokalemia can be due to increased losses, and this tends to be more in chronic kidney disease because as I said, the increased losses.
Hyperkalemia, it tends to be reduced losses due to a urinary tract obstruction and urinary blockage. Chronic kidney disease can cause anaemia due to a reduction in the production of the hormone erythropoietin, which stimulates the production of red red blood cells, and it does tend to be well tolerated due to the chronic nature and we only really tend to treat this if it is starting to become too low and the patient is actually starting to have clinical signs. So if we need to assess some urine, we can use the dipstick analysis and a microscopy for to look for bacteria and crystals.
Cultural and sensitivity is ideal. We can use that for cystocentesis or pyelocentesis, just again to make sure that we get the correct antibiotic if they do have an infection. Specific gravity should be measured using a refractometer and not on the dipsticks.
And you should calibrate these refractometers daily using distilled water. I tend to do this every time, before every time I use it for a specific gravity, just to make sure that it is, it is still, suitable for use. And ideally sample, before we've put these on, intravenous fluid therapy or any medications as well.
So the specific gravity is an indication of tubular function and it might increase a little tiny bit if the patient does have glucose in your ear or pro in your ear, but not, not, not a whole lot. In dehydrated patients again due to anti-diuretic hormone increasing the reabsorption of water, and this then leads to an increased urine specific gravity. Animals that have chronic renal disease may have poorly concentrated urea urine rather than isoheur urine.
But the closer it becomes to these really low values of the isohenuric urine, it become, it becomes the greater amount of kidney function that has been lost. So protein, there tends to be a a small amount of allumin and other proteins in urine as a normal. And there's a selective permeability of these membranes to minimise protein filtration.
Most accurate way to assess protonuria is using the protein creatinine ratio. You can use the dipsticks and that will give you a kind of a +1, + 2, but this is the more accurate way of measuring it because it compares protein and creatinine levels. It allows for variation in hydration status, so therefore the amount of urine that is produced per time.
And it isn't affected by collection method, either fasted or fed, or the time of collection as well. This is just kind of show you how it's broken down, so sample 1 and sample 2 have come from the same patient. Sample one was 500 mLs.
There's 5 molecules of creatinine, 4 of protein. So this is a 44 grammes of protein in a 500 mL, solution. So it's 8 grammes per litre.
Sample 2 leads to 4 grammes per litre, whereas this is the same patient. Whereas the urine protein creatinine, it's got they've got exactly the same regardless of the, the volume that has been produced. And it still shows 4 grammes of protein to 5 grammes of creatinine, which leaves then a a ratio of 0.8.
So the treatment aims for any of the patients with either chronic or acute disease is to improve the pet's quality of life by treating the clinical signs of eremia. These patients are gonna be feeling pretty crummy, so we need to make sure that they're feeling better as well. We need to stop or slow down any progression, and we need to minimise any disturbances or fluid losses, any electrolyte changes or any minimal changes as well.
So we might need to use some antiemetics, Mirropotin is licenced for once a day use, and it might also provide some pain relief as well, and it is licenced IV as well. Metoclopramide can be used as a CRI IV given as a bolus IV or given orally. And Dansetron can be added into that as well if the combination of them two are not working, but that is expensive and off licence, so it's not something that we tend to use all that often.
Appetite stimulants can work very well, but you do need to make sure that you've dealt with all of the other reasons for, anorexia, and make sure pain has been addressed, nausea has been addressed. Is that patient scared? Are they, are they sat in the back of the kennel?
Is it a little cat sat in the back of a kennel because there's a dog barking and it can hear this? We need to make sure that we're addressing everything, but, appetite stimulants can work very well. We need to protect their gut as well.
Elevated levels of urea can cause, dys anorexia, can cause gastritis and GI ulceration, and even GI bleeding as well. So we do need to protect them guts too. Anantacids such as salfate and omeprazole can neutralise gastric hydrochloric acid.
Just to try and, Treat for these ulcers. So calcium and phosphate also need to be managed too, just because if the if the product of both of them together is greater than 60 to 70. This is when renal mineralization can occur and then this leads to progression of the chronic kidney disease.
So we need to take steps to lower the phosphate levels, and this can either be through restriction of dietary phosphorus, and this is mainly with the renal renal diets, or we can use phosphate binders, and this has to be administered with food. We need to be careful with some of the some of the phosphate binders because they, they some of them contain calcium, and this can actually then worsen any if any hypercalcemia that calcemia if the patient already is hypercalcemic. Hypercalcemia that needs to be rectified as well and tends to be use saline diuresis, as a fluid of choice because it doesn't contain any calcium, as does Hartman's.
We can use diuretics and corticosteroids can be useful, and we need to treat the cause and to make to try and get this back under control. So if this patient is common as lymphoma or anal gland adenocarcinoma with a really elevated calcium, we need to treat that. And once we've started to treat that, hopefully that calcium will come down and hopefully minimise the impact on the kidneys.
So pronephri is a a supplement that can be used, and this is a phosphate binder and can help to bind some of the mic toxins, and it can help to maintain the kidney architecture and help with blood pressure maintenance as well. Benazapril is an ACE inhibitor, so this stops, the angiotensin 1 going to the angiotensin 2. And this can be used .
For as an additional treatment for CKD as well. So telmisartan Semenra is an angiotensin 2 receptor blocker, and this can block the AT1 receptor and aldosterone synthesis and secretion is reduced, and then this and reduced causing vasodilation, and then decreased potassium and increased sodium excretion, so this stops, here, so it stops everything else happening afterwards. The cementra comes in two different formulations and the 10 milligramme per mL solution has been approved for control of systemic hypertension in cats.
And this has been shown in studies to reduce the blood pressure by about 23 mm medications. And we do need to monitor the blood pressure and adjust the dosing as required. The 4 milligramme per mL solution has been approved for the reduction of protonuria associated with CKD in cats.
And there's been plenty of studies done comparing the two, but it has been shown that . Only the telamisartan, only the reduction of an oh sorry. In one study, telemosartan and benazepril were compared in both of them actually reduced the urine protein creatinine.
But only the the reduction by telemaan actually reached a statistical significance. We may need to add in erythropoietic agents, so if this chronic anaemia has started to cause any clinical signs, and this by using these agents, it just means that we're stimulating erythropoiesis in the same way that it would happen naturally, and it just means that we're stimulating the stem cells and the the bone marrow to to produce more red blood cells. We've tended to use it weekly to increase the PCV to a percentage that we is is more suitable for a patient.
And then once we've achieved this, then we reduce the frequency of administration to maintain the PCV. We need to make sure that the patient has got suitable iron stores as well, and for this to work properly, and we tend to use an injectable iron dextro rather than the oral products. So I can see yeah, it's just to help, help with the haemoglobin, just to make sure that it's what when when we're trying to stimulate the red blood cell production, that it's got the full backup of iron as well.
So fluid therapy, we're trying to increase and maintain this colloidal osmotic pressure to try and make sure this blood pressure is staying as it should be. We need to replace fluid losses, so we need to replace the deficit that is already present. So if this patient has come in as vomiting and diarrhoea and has already started to be a percentage dehydrated, say 789, 10% dehydrated, we need to be replacing everything that they're losing.
But then we also need to remember about ongoing losses as well. So if that patient is continuing to have diarrhoea or vomiting. And we need to maintain, so we need to aiming to maintain that circulating fluid volume.
Hetmans are 0.9% saline preferred, and therapy based on the severity of dehydration or volume depletion. And it's common for some of our acute kidney injury patients that we will use a rate of up to 10 mL per kg per hour.
This is really high. So we do need to make sure that we are monitoring them for volume overload. So these would be classified as signs of like weight gain.
Any restlessness or tachyona, we need to be doing for auscultation and listening to the lung sounds, if you're hearing any crackles or any coughing, we need to inform the vet and look to reassess that rate. And if we have supplemented that fluid with potassium, we need to be careful with at the rate that we infuse that and I'll discuss that a little bit later on. So patients that are hypokalemic, we do need to supplement them with potassium, and we do tend to just add this into their fluids.
I always like to, once I've added it, once I've worked it all out and got that double checked, I like to work out just to make sure that we're not over infusing. This is the maximum in fluid infusion rate of 0.5 mil per kg per hour.
Make sure that you correctly label a fluid bag, with a drugs label, and they know exactly how much is in there. We tend to label it as, say 20 millimoles per litre. And that's how we would label that, even if it was on a 0.5 litre bag, just so we know exactly, and it's just less confusing.
And we do need to make sure that we don't bowl us any of these potassium chloride supplemented fluids. We have a little chart so we can see actually if the potassium is 2.5 today, we need to add 40 millimoles of potassium into 1 litre of fluids.
And then we have it all broken down just to try and make it as easy as possible for the person who comes after you to actually be able to make that rate, that, that, the next bag of fluids up. And the chart then comes with a a hand a little, part to the table to say this is actually the maximum infusion rate for this, solution as well. If we overinfuse or give this potassium too quickly, we can start to cause some bad arrhythmias as well.
So what this patients going home, and we're starting to think actually we need to supplement them at home, oral supplementation is available. Cainox is a liquid solution, and that's got additional vitamins and amino acids as well. GMLK is a again, his potassium and his tablets or a powder, so that can be added into food.
Patients that have come in hyperkalemic as in say over 5.7 millimoles per litre. So firstly, what, what you need to stop and think, actually, did I contaminate my blood sample with EDTA when I've added the blood into the tubes?
If you can 100% say no, I've not contaminated it, go ahead and treat for the hyperkalemia. If you think, oh, I might have done, take another sample and recheck that. The the salts in the EDTA tubes contain potassium, so it can artificially increase your, potassium when if it is, you do contaminate the blood.
So the elevated potassium can be caused by conditions that inhibit renal elimination, and patients that end up hyperkalemia can have problems with the cardiovascular system, can lead to some brady arrhythmias. That then leads to potentially weakness, collapse, and death. And it can also affect the nervous system as well.
Correction of this is required, and we can ad administer neutral insulin to induce translocation of this potassium back into the cells. And then we need to follow with glucose, as a bolus or ERI because we're giving them insulin, we're going to lower their glucose. We need to make sure that we don't lower it too much.
We can also administer calcium gluconate and that can be administered slowly over 10 minutes. And this can antagonise the effect of the potassium on the cardiovascular system, but it doesn't actually do anything to reduce the potassium, it just protects the heart. Fluid therapy at home, these patients need to be encouraged to drink plenty of water, so this is when we say to the owners, get some water fountains, lots of water bowls around the house.
And some owners can be taught how to give subcutaneous fluids if they're, if they're keen to do that and it helps, perfect. There are fluid ports available so we can put a subcutaneous port in. But there has been reports of port induced soft tissue sarcomas as well, but yeah, I think it's see how, see what the owner's wanting to to do.
Hemodialysis is limited in availability, but this can actually then help to eliminate any toxins and any undesired substances from the blood. So this is something that is available. We're gonna want an IV catheter in these guys, and there's lots of places that you can place IVs.
And some of these acute kidney cases can be in for days and weeks. So we need to make sure that we're looking after these veins and if we get these catheters placed, and we replace them well. Ideally for some of these acute kidney cases, we can place a jugular catheter and these can be maintained for a lot longer than a normal peripheral catheter.
These are ideal for blood sampling, we can provide them with fluid therapy, and if we need to, we can give them parental nutrition as well, which can only be ad administered by a via a central line. For jugular catheters, we need to make sure that we're checking these sites at least once a day. We do it as a twice a day routinely and that they're dressed and protected, to prevent any any damage to them and to keep them from becoming infected.
We need to monitor urine output and we aiming for 1 to 2 mL per kg per hour. So for acute kidney failure, a urinary catheter is ideal, so we can monitor the, the urine that is actually being produced. And if the urine output falls or stops, you need to find out why.
Is it just a case of, the kidneys have become that, that traumatised, they have been that damaged, that there is just no urine being produced at all. Or is it that the fact that the kidney is, is limiting water because the patients because they're actually dehydrated, or is it just because there's nothing in the urinary bag because the, the catheter is kinked or something along them lines too? We need to make sure that we can be any renal hyper perfusion if they are dehydrated.
Diuretics can be used as long as the hypo perfusion has been corrected. But if we do give diuretics, then we do improve the urine output. It doesn't necessarily mean that the kidneys have magically been fixed, but it does mean that we've got a more favourable prognosis because it does mean that we can manage the fluid therapy and the electrolytes a little bit better.
Cathetters are great, your catheters are great because it means that we're not having to manually express these guys and if they've got a painful kidneys, painful abdomen. Once you've got a catheter in, you will, you will see blood at some point, hopefully not as much blood as in the syringe, but you will see blood at some point. And again, I'm, I'm just gonna keep harping on about this.
Investigate if there's no urine, if there's no urine in that bag, why? These catheters can help keep patients clean and comfortable, and we remember regular urinary catheter care as well. Patients should really wear a buster collar to prevent them, chewing at the catheter.
This poor little chap was very poorly, so I wasn't actually interested in that catheter at all. If you've got a patient who is potentially with got leptospirosis, we could use a closed system, for, collecting the urine, and then we can collect the urine into one bag, and then we can use the syringe to then measure out the urine back into another bag so we're not actually having to handle or pour urine into bags, into jugs to measure. We need to make sure that everyone knows how to use a three-way tap properly so that we don't inadvertently close off the wrong tap and actually cause a an iatrogenic cureinary obstruction.
We could intermittently catheterize these patients, but that isn't really ideal, cos if we're having to do this every couple of hours, it's easy enough in males, but this won't stop dribbling or any overflow and then repeated catheterization isn't ideal. So for placement, we need to make sure that it's aseptic placement and we clip and clean around the area around the prep and the vulva, just to make sure that there's no contamination and that when we are cleaning the the doing the urinary cathetic care that we are using gloves at all times. So we do the only catheter care twice a day, and we use a diluteevervidine iodine solution to flush to wipe the catheter away from the patient, and we flush with saline.
So just gonna have to calculate urinary output. So if you've got a a collection bag and you've collected 1200 mL of urine for a 30 kg dog over 24 hours, you divide the 1200 mL of urine by 24 hours. This gives you 50 mL per hour.
Divide that 50 mL per hour by the patient's body weight. Which in this case is 30, and this gives you 1.6 mL per hour.
So we need to make sure that these guys are eating and drinking properly and we need to monitor the water intake, especially if they're not on fluid therapy, such as when they've gone home. And we need to make sure that ongoing losses are we do remember them as well and make sure that if their urine output is good, indicator if they're actually drinking enough. And remember, some patients will want a different type of bowl, they might want a glass, they might want ceramic bowl or a metal bowl or a glass bowl, they might want it holding for you, holding for them, .
And some patients will want a a fresh bowl of water every time they want a drink and you you kind of just have to pander to their requirements a little bit just to try and encourage them to, to drink enough. We can try and syringe water, but this isn't ideal at all because we're never gonna get enough water into these patients just by syringing. So we tend to either add a little bit of add some water to food and make a nice slop, and they tend to be quite like that.
Or you can add a spoonful of food to the water and just kind of have some flavoured water. And that also tends to go down quite well, er sometimes. If they've got a feeding tube in, you can use that for water too, and you can then actually work out their fluid actual fluid intake.
Feeding tubes are ideal for some of these patients, and the nasal esophageal tube can be used mainly just for short term use. It can be placed in a conscious patient, but only liquid food. And with the new liquid foods that are available, we don't need to be putting great big feeding tubes into cats and dogs anymore.
You can get that liquid food down, even just a tiny little tube. Esophageal tubes can be in for a lot longer for weeks to months if they're maintained properly, and we can get some, maybe the liquid food and maybe some blended foods down there as well. Kitty collar.com.
I've come up with some really nice little collars and they've got a little slit in here so you can pop the the tube through there and then you can change the the cotton wool pad around there every day as well. This is mainly for when they've been discharged. Gastrostomy tubes, probably less used for kidney patients but may, may well be needed.
And we can use liquid or blended foods, these tubes tend to be quite large, so blended foods tend to go down a lot easier. We need to look at these tubes at least twice a day. We tend to get owners to do it maybe once a day at home, and we use an iodine gauze around the insertion site.
And you need to make sure you keep an eye on these sutures. There's only one suture anchoring that into place, and then make sure that these sutures aren't starting to bunch up, which could indicate that they're too loose, which could then mean that the tube starts to slip and slide in. Once we've placed a tube, we always measure how much tube is left outside of the patient and make a record of that.
So if anything starts to change with that patient, we can make sure that the the tube hasn't started to slip in. And then we cover that up as well with a little bit of a a dressing just to protect the insertion site. So for nutrition, it needs to be low protein but high biological value to decrease the retention and the production of any nitrogenous waste.
High calorie to ensure adequate intake. We can add omega 3 in there and hopefully this can help to decrease some kidney inflammation. We need a normal or lower sodium level.
This is because of the link between sodium intake and hypertension. Ideally phosphate restricted, but only if that patient needs phosphate restriction. There's lots of different renal diets and some do have restriction and some don't.
And we need to make sure that they've got increased water soluble vitamins because they because these patients are polyuric, they're gonna be peeing them all out. Nutrition, I, I A good, a good quality diet can help improve the survival time and the quality of life, and we can come up with a home cooked plan for them and we can, there's lots and lots of different renal diets on the market, so if we do need to chop and change around a little bit, it is we we can do that. Make a plan once you've made a plan for the feeding amount, if if you've calculated that the patient needs say 200 grammes a day, but the owner starts feeding 400 grammes a day, they're actually getting double the phosphorus protein and the sodium that they actually require, so you could actually worsen the condition.
So we need to make a plan based on, on the patient's weight, the patient's ideal body weight, and kind of the their exercise levels and actually, so we can actually maintain the correct calories and actually provide a proper plan for them. As I said, lots of renal diets on the market, liquid foods, canned foods that can be blended. But remember, what does that patient usually eat at home?
If they are usually a dry food, offer them a dry food, ideally wet foods, but some will, I know, well, if it was my cat, I know she would, completely flat out refuse to eat her wet food. So I know if anyone tried to offer her wet food in a hospital, she wouldn't eat it. Offer her dry food, she will eat that.
So ideally, we'd want to start a prescription diet when these patients are feeling better and have gone home, and they're actually eating a little bit better. But again, this is, this tends to be up to the clinician as to when they want to start that food. But I would, I would much prefer it that they start this when they've gone home.
If you start offering patients these dedicated prescription diets when they're in the hospital, when they feel nauseous and feel rubbish. There is, they're gonna associate that food, that smell with when they felt awful. So then you, you run the risk of starting with food aversion.
So ideally when they're feeling better and at home. Balanceit.com is brilliant.
I've used this quite a few times for creating diet plans for many renal patients, and it just, it creates a home cooked plan and then you just have to add the supplement into it as well. It's an American company, so it takes about 2 weeks for the supplements to arrive. The the for renal plans it does tend to be quite carbohydrate heavy.
So there tends to be lots of rice or potatoes with a little sprinkling of chicken or fish on top. But we've had quite, I've had quite a success with quite a lot of patients with this. So I'm just gonna show you these pictures again to remind you, if they've got, sore mouths that we need to be thinking about feeding tubes for everything, for the food and the water and the medications.
And that we do actually look after these ulcers as well to hopefully help them heal alongside with all of the treatments that we're giving them for the aotemia. A dilute called hexadine mouthwash can be used to clean the mouth. There is a risk of bacterial, this oral bacteria crossing over into the bloodstream, and causing sepsis, so this is why we do need to keep the mouth nice and clean too.
So this is the last section, just an anaesthesia and sedation considerations. So if the patient has come in, has it dehydrated, is it hypokalemic or hypokalemic, we need to make sure that all of this is corrected before we do sedate or induce anaesthesia. Their acid-based status, if this patient is acidotic, along with your and along with binduremic, this can have a real influence on how these anaesthetic drugs work, and they, they might not need the, like the, the normal dose, you might end up inadvertently overdosing them.
So we may end up needing to use a much lower dose or even titrating these two effects. As I mentioned before, if this patient is hypertensive pre-surgery, we're gonna need to maintain their blood pressure at a higher level during anaesthesia because hyper perfusion will occur much sooner before 60 milli of mercury, and then if we do start getting lower and lower, this is when we can worsen their kidney disease. So any hypotension must be treated rapidly in renal patients just to try and help these kidneys out a little bit more.
So do your normal checks, check anaesthesia depth, can you reduce their inhaled gases? Do they actually need more analgesia so you can turn down the anaesthetic gas. If it continues, we could give a fluid bolus, under the direction from your, from your vet.
And if the hypertension is still present after Ebolus, then we need to consider that we might need to use some drugs as well. So dopamine CRI can be used, it's very short acting, so it lasts only about 2 to 5 minutes, so it has to be given as a CRI. And there's plenty of other drugs, ephedrine, noradrenaline, and phenylephrine, that can be used to help increase blood pressure.
Hyperventilation can be caused by anaesthetic drugs, so an increase in carbon dioxide will cause respiratory acidosis, which can then worsen any pre-existing acidosis. So then this again can change how the drugs work. We may need to mechanically or manually ventilate these patients, especially if their entitled CO2 is going above 60.
These patients that are with chronic kidney disease do tend to be quite skinny with little, with not much fat on them, and this puts them at a greater risk of hypothermia during any procedures that you're sedating them, either sedating or anaesthetizing them for. Hypothermia can also have a reduction in the anaesthetic requirements and will alter or slow down any drug metabolism. So again, overdose and slow recoveries can result.
Try to keep your patient warm straight from the pre-meds, so if you've got your patient out on the table, get them wrapped up in some bubble wrap or some blankets, and if you've got access to our active warming, such as bear huggers or hot dogs, we can use this as well. So once these patients are ready, we've got them we've got them through . The chronic kidney disease, we've got them through the acute kidney injury.
We need to think about what are their goals for long term treatment. Are their owners happy to kind of go ahead with everything? Can we manage their hydration at home, especially with these chronic kidney disease patients?
Have we informed, make sure the owner knows how lots of little dips and hints and tips about how they can increase their water intake? Make sure these owners have got a proper nutrition plan, either for home cooked or for different prescription diets. A medication plan.
Sometimes these guys will be going home with lots of medications which can be really overwhelming for our owners. And so what I like to do is we have kennel sheets or a medication sheet. I like to print one of these off, write everything all on there just so that the owners can then follow it themselves and actually then schedule when they want to give medications, and it's just all then written down for them nice and easily.
We need to manage all of their clinical signs, so we're making sure that we're, we're correcting any pain, any nausea, anything else that's going on as well. And we need to schedule rechecks, so make sure that owner knows, do they need to come back in 2 weeks or 4 weeks for a checkup, for repeat blood tests and just to kind of do, do they have ulcers? Do we need to keep an eye on stuff like this?
And we need to monitor the quality of life as well. Are they eating well, are they gaining weight, are they losing weight? Are they gaining some muscle back or are they losing muscle, and just how they are actually, Kind of getting on at home as well.
So this is just a little word, just remember, veterinary nursing and veterinary practise life is tough, so remember to look after yourself as well as looking after your patients. So thank you very much for attending this evening. I'm sorry I probably talked really, really quickly because I had lots to get through.
I wanted to share with you. If you have any questions you can email me, or if you have anything you want to ask now, feel free. Thank you.
Brilliant, Caroline. Thank you very much, and you've managed to fit in so much into just one hour, so brilliant. And if you do have any questions, please pop, pop them through to us.
Just click the Q&A box at the bottom and ask away if we do have anything at all, just type it in there and I can read it out to Caroline. Caroline, do you tend to find that many owners will go for some cough fluids at home? I think quite a lot of owners, would be quite keen to do that.
I think if they're on board with starting treatment and, changing their diets and starting lots of different treatments, I think most owners would be quite on board with that, especially if you're able to then Take the time to teach them how to do this. It's the same with like diabetic clinics. We need to spend a bit of time with owners, teaching them how to draw up the fluids or, and how to actually inject the medications and stuff like that.
I think if we can spend the time with them, I think, I think they would be really keen to do that. Yeah. Oh, brilliant.
I suppose it makes them feel like they're doing their little bit to help as well. Absolutely. And if it means that we can Keep the patient out of the hospital and out of needing, intravenous medication and intravenous fluids.
If we can avoid that and keep them at home where they really want to be, that's the, that's the goal really. Yeah, I suppose it's particularly useful for those anxious patients, particularly cats. If they, you know, if they are quite scared coming in, then it's much nicer if they can have all the treatment done at home or at least the majority of the treatment.
Yeah, absolutely. I'm sure if you could, some of these cats would probably quite like to sit on their, maybe sit on their owner's knee, while they've got, maybe a little butterfly catheter going in, and we can just get a little bit of fluids going in. Hopefully, so much less, well, it would be much less stressful.
And yeah, just kind of sitting there chilling out, having some fluids, and then you get to spend, the owners get to spend a little bit more quality time with their pet as well. Yeah, absolutely. It's a really great idea.
So it doesn't look like we have any questions just yet. So on that note, I will just say thank you so much for all the listeners for logging in this evening and taking time out of your evening after I'm sure it's been a busy day. And thank you very much to you, Caroline, for delivering such an informative webinar.
It was absolutely brilliant, and I'm sure everyone has really enjoyed it. Thank you very much.