July 21, 2022

Kidney compilation, with Prof Jill Maddison, Dr Rosanne Jepson and Dr Clint Yudelman

Kidney compilation, with Prof Jill Maddison, Dr Rosanne Jepson and Dr Clint Yudelman
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Season 1

It’s been a while since we’ve released one of our clinical episodes on here, so we thought we’d create this lovely little compilation of kidney content for you. These are some of our biggest ‘AHA!’ moments from a series of episodes that we've done over on the clinical podcast over the past few months on those tricky little beans that stop us from being poisoned by our own waste products.

We start with some wisdom from small animal medicine guru Prof Jill Maddison about making sense of azotaemia and USG. Spoiler alert - it's not as straightforward as you might think, and there are DEFINITELY a few traps to avoid that Jill outlines in this conversation. Next is Dr Rosanne Jepson, another medicine specialist and associate professor at the Royal Vet College and a leader in the field of nephrology and especially hypertension to guide us through everything blood pressure.  And tying a bow on it all is Dr Clint Yudelman from Insight Mobile Diagnostics to help us make sense of the relationship between calcium and kidneys. 

 

And if you want MUCH more of Prof Maddison then join us live in Noosa in November when she joins forces with Prof David Church for what promises to be the most fun vet event of the year. Details are here - but don't book there - email us at vetvaultpodcast@gmail.com to tell us that you heard about the conference on here and we'll send you a listener-only discount code.  

Go to thevetvault.com for show notes and to check out our guests’ favourite books, podcasts and everything else we talk about in the show. 

If you want to lift your clinical game, go to vvn.supercast.com for a free 2-week trial of our short and sharp highly practical clinical podcasts.

We love to hear from you. If you have a question for us or you’d like to give us some feedback please get in touch via email at vetvaultpodcast@gmail.com.

 

Head of IT filters and welcome back.It's been a while since we released one of our clinical episodes on you.So we thought we'd make you a lovely little compilation of some of the biggest aha moments from a whole series that we did over the past few months on those tricky.Little beans that filter out blood for us and stop us from being poisoned by our own waste product.
We're talking of course, about the kidneys, we've spoken to some really brilliant mind on these really complicated little organs and we thought we'd bring you some of the best bits.First off, we've got a few bits of wisdom from small animal medicine, Guru, Prop, Joe medicine about making sense of act, Mia and urine, specific gravity and before you go.
Yeah, I've got this it's not a straightforward as I thought and they are definitely a few traps to avoid the Jill outlines.In this conversation, they have doctors and Jepsen who is another medicine specialist and associate professor at the Royal bed college with a lot of research under a belt around kidneys, and specifically hypertension.
So, of course, We talked to her about hypertension and kidneys, and then we finish off with another topic.That makes heads hurt around.Kidney failure.Calcium with specialist dr.Glen Gillman, from inside mobile Diagnostics.Now, these are not easy topics and on the full episodes, we dive a lot deeper still, but if you haven't listened to a clinical content before you were know this, but this is kind of a thing.
We love to take on the stuff that we and most out of it.Get a bit stuck on in general practice.And then we find somebody who really knows their stuff and ask the questions that we know you want to ask us well to see if we can get it to make some more sense.Why?Because we've learned that it's those things, the things that you don't quite understand it, vet school, all those conditions and cases that make you go.
No, not that case.When you see it arrived in practice, those things actually wrote away at some of the joy of clinical practice.And then on the flip side, once that light bulbs switches on.And you have that moment of I guess, It actually starts to look forward to some of those cases and work becomes more fun.
We have our subscribers.Tell us this time and time again stuff.Like I can't wait to see my next case of dka or I've got my mojo back for work.We haven't checked it out yet.You can try it for free at v v in the super cast.com.Oh and our subscribers also get beautiful.
Summarized show notes to refer back to each of the episodes because we know that some of these hard topics need a second pass or a quick revised.When you actually do see that case, okay?Please enjoy this little journey through the glomerulus.And into the nephron.
We kick off with Prop, Joe medicine, and a monologue on renal physiology, that might make your head go.But it's really important that you listen to this, the sake of your patients.I think the thing about a is at emia is and where the problem lies is that, for whatever reason we all get taught, renal physiology very badly at University.
I don't care what university it is.I got taught it badly, we teach it badly, there's something about how it gets taught, that's really poor.And of all of the tests that we have that we do.What about we?You need to understand the pathophysiology of changes of many tests to understand how to interpret them but with Urea creatinine and urine specific gravity.
You really need to understand the pathophysiology and the problem with as RT Mia is that exactly what you're saying you do, it's kidney disease.And so there's this implication this assumption that if an animal's as a team, Eric that it's got kidney disease.
And so, that's just not true.And it's understanding what causes those at emia what causes inappropriate.Urine concentration.And when do the two come together and when do they not?And so it's easier and cats because there are fewer non renal disorders that cause as artemia and impaired urine concentration.
But it's more challenging in dogs because there are diseases that will cause a CT Mia and impaired urine concentration.That are not structural kidney disease.That's not a sentence.You hear very often.It's easier and cats.Almost nothing is easier.
It okay.Yeah, exactly.Exactly.You know, usually cats and it is, we've talked about the do diagnosing, pancreatitis is a nightmare and all sorts of things, liver disease has a nightmare.But in, in cats, it is a bit more straightforward because there aren't the complicating, the same, the same pathophysiology applies.
It's just, they're not the complicating disorders that can pretend to be kidney disease if you like that aren't kidney disease, okay?So, should we start with that?With saying, what are the The most common misconceptions and misunderstandings that veterinarians have about.
Is it to Mia and urine specific gravity?Okay, so I think probably at the heart of it is that veterinarians don't necessarily understand that the causes of Azar T Mia.And the causes of inappropriate urine, specific gravity are different in most disorders, except for structural kidney disease.
So, in structural kidney disease, The animal is as a team attack and has impaired ability to concentrate their urine and to dilute their urine and it's because they have fewer nephrons and the nephrons are damaged etc etc.So that's absolutely fine but the drivers for a SRT Mia is the glomerular filtration rate which is the flow of the of the filtrates through the kidney and that's what drives our team yet.
So if that slows down you get as a team out and you get that will slow down for a number of reasons.We know it can slow down if has reduced blood flow to the kidney, so that will happen.If you've got shocked or you've got dehydration, it will slow down.If you've got constriction of the afferent arteriole that goes into the glomerulus and that happens in hypercalcemia it will slow down if you have serious glomerular disease but without tubular disease, it will slow down if you have structural kidney disease.
So you have loss of nephrons and it will slow down.Obviously if you have a post or an obstruction, that's stopping Urine flow.So there's all those things that we'll do that.Whereas impaired urine concentration is all about what's happening in the tubules and so it's all about our, the tubules able to do what they're supposed to do with water to preserve water.
If the body needs it and excrete.It if the body doesn't and that can be influenced by a whole range of things.Yes, the number of nephrons but things like antidiuretic hormone, the effect of Calcium potassium, so hypercalcemia hypokalemia hyponatremia on the actual function of the sodium potassium pumps and the concentration of sodium and urea in the medulla and distinction.
And so, the cop that that's the really complex bit of of renal function that everyone's heads, go back, because it involves and I'm not sure I can explain it into huge detail either, but it does involve.Mechanisms that the kidney uses to keep the medulla really concentrated so that water can flow in, or out at various parts of the Nephron when the body needs it.
But even without that, I mean, as soon as you start to say that you recognize that there are going to be factors that will impair the ability of an animal to concentrate its urine appropriately.So when we think about an animal that is polyuria polydipsia, for example.
We divided them into two groups or three groups.Really one group is what we call the primary polydipsia dog.So, these are the dogs that want to drink, so they drink, and it's a head thing.So it can be what we call psychogenic, but it can also, it's probably the main driver in dogs that have Cushing's Disease.
For example, it's the main driver in caps that have hypothyroidism Soze.In other words are drinking because they want to in inverted commas and they don't have any problem with concentrating their urine.Most of Whereas you've got the other group of animals that have got polyuria polydipsia because they have to drink, because they can't concentrate their urine appropriately.
And so, they have to drink sufficient.They're losing too much water, and they have to drink sufficient water to compensate for that because they can't concentrate their urine.And those animals can be divided into those.That have actual structural kidney disease that have chronic kidney disease, for example, or those that have a non renal cause of Of being unable to concentrate their urine appropriately.
And those are the animals that if they don't drink either, because they're denied water, or they become unwell, and they're not drinking, they're the ones that will get dehydrated and get really unwell.And so, that's the really fundamental concept is that if you have an animal, that has to drink.
So it has primary polyuria.The big question is, is this animal got kidney disease actual kidney disease or I should have known renal disease and the misconception is well if it stays at emic it must be kidney disease but that's not true either.
Firstly because any animal that has an impaired ability to concentrate its urine.If they become dehydrated they can easily get prerana laser t Mia but they can't concentrate their urine properly because of whatever disease that they've got.So that's the first thing.
And the second thing is, even if they're not dehydrated, there are some disorders that can Can cause a CT Mia, without it being structural renal disease, and the two major ones are hypercalcemia and hyponatremia.
So the hypercalcemia caused by, you know, primary hyperparathyroidism or caused by lymphoma, you know, paraneoplastic syndrome, for example, or sometimes vitamin D intoxication.And that's not Nefra, cows enosis.
So that's one of the confusing things people think if they're hypercalcemia Reason why there is a teamwork is because they've got Nefra cows enosis but most of them.Don't the reason why there is a teamuk is because calcium constricts that arteriole that What's called the afferent arteriole that goes into the glomerulus and therefore slows the blood into the glomerulus which then slows the glomerular filtration rate.
So there's that group so that and that's very reversible with the modification of the hypercalcemia and then hypo Ona tree Mia for whatever reason, so be it Addison's disease, be it got lost.Be it.They're probably the two major ones.Hyponatremia, impairs the kidneys ability to concentrate because sodium is incredibly important.
The concentration of sodium is incredibly important in the medullary interstitium in driving the osmotic.Gradient that helps the kidney retain water.So if you have a hyponatremic animal, they don't have Enough sodium there.So even if they need to preserve water, they can't.
And so, they produce too much water and they become.And then with animals that have got profound hyponatremia, they also have a blunted stimulus to antidiuretic hormone because they're hyponatremia because one of the stimulus has to switch on your antidiuretic hormone and till a body not to produce so much urine is the level of sodium in the blood.
And so if they're hyponatremia at that, Affects blunted.That's that's an awful lot in a few sentences of a very complex topic, so I'm sure everyone is just going.Oh my God.So let's say it's not a very well monitored, dog.
I haven't done.It's been busy.I haven't done a decent history.We run a wellness Bob Lutz for some reason.In my older Animal 80, it has, I create good teen level.So we've got to pay attention.I just want to make sure I understood what you said earlier about the percentage of percentages of nephron loss.
So the first thing that's going to go is going to be your specific gravity.Am I right before you become a certificate?So by virtue of that, if I see I created great.In and I go, right?Let's measure creatinine, sorry, let's do that.As I let me check during SG, F HG in an animal is normal.
Then then it, then it can't be structural kidney disease.Am I like?And I was depends on what you define as normal.So okay, let's define normal.Yeah, so normal, can be anything.So, a, normal specific gravity in a dog, in particular, it can be anything, it can be one point, oo1, it can be 1.06.
So it's normal depending on the situation.Ation so normal depending on the situation.So if you had an animal that genuinely had an increased creatinine and you did a urine specific gravity then for a dog to be absolutely sure that that kidney is functioning.
Normally the urine specific gravity would be need to be more than 10:30 10:35 and for a cat it needs to be more than ten.Thirty five.Ten forty below that.Anything below that could be inappropriate for that dog.It could be yeah.
And if you That.So if you've got a CT Mia and you've got that urine specific gravities.And either that animal is dehydrated or has got decreased renal perfusion for some reason.It might have heart failure.For example, as long as you again, you know, you got to get your Greyhounds out of here or it's got something in its urine.
That's creating sort of an osmolarity thing and so it can be dehydrated, but have high concentration.So we sometimes say that and diabetics for example, because they I won't have a dilute urine.Why?Because the glucose is pushing up the SG.Yeah, yeah, yeah.
And it also, they can they have a driver to produce more urine, but they don't necessarily have an impaired ability to suck back the fluid, so they can be quite concentrated.So, if you have that case, so you have an increased creatinine in this animal, then you do your own specific gravity and it's highly concentrated.
Well then probably what that's telling you is that your dog is dehydrated probably assuming it doesn't have Failure, which hopefully you would have recognized.I think it's more.It's more often that those profiles are go in.The supposedly, well, animal are going to throw problems is much more likely to relate to liver enzymes and probably calcium just because the way calcium is, then then as a team, but okay, that's the case.
But that's if you if you have that animal and you do the urine specific gravity and it's anything less than 10:30.So, one of the myths is that it can only be renal failure.If it's, I saw The nurik which is a specific gravity one point, oo, 8 to 1 point 0, 1, 2 and that's a myth as well because I saw us an area just means that the glomerular filtrate hasn't been concentrated nor diluted in its Passage through the kidney.
But the question it can get concentrated in its passage to the kidney but it may not be enough for what the body needs.So you can have animals that have renal failure with a specific gravity of 1020.You can have cats with renal failure with a specific gravity up to 10:30.What they can't have in.
This is the other thing that's misunderstood is that they cannot have high costs in your area.They can't have dilute urine because it takes just as much nephron function to dilute urine to actively dilute urine to move more water out than solutes are retained.
As it is to concentrate it.So if you have an animal that is PPD or is as a team akande, they have a urine specific gravity, that's less than one point.Oo. 8 and you're sure you re Frank time it is you know calibrated properly.Etc etc.
So if it's down at point oo5 or four or three or two or one, the one thing you know, is that that animal does not have structural renal disease.The one thing they can have that involves the kidneys, they can have pyelonephritis, because pyelonephritis, although it's sort of mucks up the rule about structural versus functional.
But pyelonephritis, doesn't cause impaired urine concentration by damaging Nephron.It causes it by changing the osmotic gradient in the kidney, because the E.coli, which it usually is changed as the osmotic gradient just like happens in pie Metron, for example.
So, you know, in part Metron and in pyelonephritis, the bacteria, affect the function of ADH and affect the osmotic gradient in the kidney.So pyelonephritis is that is the very reversible It has to be, you have to call it renal disease because it is renal disease, but it's not structural loss of nephron, some of them can, of course, you know, if it's really bad they'll go on to have structural loss of nephrons but that's very reversible.
Okay, I just want to clarify, so you say that that thing is when we get an animal, it's easy to make and then we checked the SG and it is Eyes.Austin, Urich The Assumption to go.Yep, this structural renal disease, not necessarily true.There are still other causes that and that's not necessarily true.
So if it yet so if you have an isotonic animal and the urine specific gravity is not highly concentrated and or it's got a history of PPD then in the cat just to make things simple.In the cat, it is probably most likely going to be Chronic kidney disease probably.
Now, you know, I'm not saying never because it in the dog then it depends on whether you're dealing with an animal who is dehydrated or not, so if they're not dehydrated, right?So there's nothing that you can see that they're dehydrated their skin.
The lastest is fine.That mucus membranes are nice and moist.There's nothing.Nothing that suggests to this animal is dehydrated.They don't have anything that suggests hypovolemia that don't have anything that should suggest.Kris renal perfusion, then the two things you have to check for absolutely must check for is their sodium level, whether they're hyponatremic and their calcium level.
Now, having said that in the cat, the one thing I probably should.Yeah, the one thing that will be very confusing is that cats who have cons disease.So hyper, all the steering is MM will present A Hazard teaming, they will be hypokalemic, which of course they can be in renal disease and they can really look like kidney disease.
But they've got hyper hyper or the steering is.MM.And that's not it's not a common disease but it's certainly not totally unheard of.So the disease that you would confuse most likely to confuse with renal disease in the cat would be hyperaldosteronism.
So it's the one you have to watch for.They will often present with their hypokalemia being their driving pathology that's causing their clinical sign.So weakness, for example, whereas in the dog, the disorders that Need to worry about is anything causing hyponatremia significant hyponatremia.
So, Addison's disease would be 150 gender quota system.Gut loss of sodium.There are lots of things that will do it.Usually in those animals, they'll be other things going on.That make it pretty obvious and you will have picked this up.But and then the other one is hypercalcemia for whatever reason.
And that can either be hypercalcemia that's driven by a PTA, increase pth, parathyroid hormone level.So they will have a normal or low phosphate or it can be the ones that are like vitamin D in toxicosis that will have both increased calcium and increased phosphate.
And they're the ones that are at risk of going on to develop Nefra Cal samosas, whereas the other ones aren't so, and if you look at the prevalence of diseases, like high poder, Anacortes ISM hyperparathyroidism paraneoplastic hyperparathyroidism in Lymphoma versus Primary renal disease in dogs.
You know, I can't give you the numbers, but all of those diseases are just as likely as primary renal disease, particularly if it's an older dog, maybe not so much of it's a younger dog where you're dealing with congenital renal disease.So the balance of probabilities just on the fact that these diseases are not rare.
Means that if you assume that you have an Acer teamuk, dog that has inappropriate urine concentration and you assume without doing.Thing else has got renal disease, you're probably going to be wrong 2/3 of the time.There are a lot of dogs in heaven.
Now who've been put to sleep because of renal disease which probably didn't have it.Okay, everyone still following will make the show notes available to you.Just go to the clinical section of our website, that's delivered volts.com and there will be a button there that you can click to get them somewhere.
We'll figure it out.And if you'd like to hear more from Jill.Remember that she's joining us and about 50 of you live and we talked In the Flesh life, not zoom life in Noosa for our first ever live event, 22 to 25, November, Jill and prof.
David church right here in Noosa, for some V down learning as well as some Fayetteville stuff, fun.So put on your smart heads, wax of your surfboards and bring your walking shoes.It's going to be epic.Link will be in the episode description but our listeners will get 300 bucks.
Off the full price.Just email us at video broadcast at gmail.com and we'll send you the discount code.Okay, dr.Jefferson and kidney cats with high blood pressure.What's your go-to for hypertension?And do we differentiate dogs and cats again in my head?
I have tensions not as a big deal in dogs or is that a misconception?That's more cats and dogs, right?Or we certainly see the ocular manifestations.Much more common in cats than we see in dogs.I actually think measuring blood pressure is harder in dogs than it is in cats.In terms of getting quality reliable readings.
I think it can be much more challenging in terms of medical management of hypertension.Then yes, Are some differences again, speaking in terms of what we have in the UK, we have to license product for the cat.And so we have a lot of pain and we have Thomas data and so a calcium channel blocker and do the Angiotensin receptor blocker.
And in the cat really, either of those products can be used equally in terms of being first line agents in the dog because we see more protein Uric, renal disease.We will often reach for either an ace.Inhibitor or Angiotensin receptor blocker.
Initially, because we'll be managing their proteinuria and then we tend to use a model penis, an additional agent.And in the biggest difference that we see between cats and dogs, is that cats typically are quite easy to control in terms of their hypertension and using a single agent.
Whereas dogs are much more similar to humans in that multimodal treatment is quite often necessary.So we quite often need to use more than one.Drug for a dog.And would that be a matter of starting off with one?Say?And I think a bitter or the blocker.
And then seeing how it goes and then potentially adding in something like I'm a lot of pain or do you kind of throw everything you've got and see how it goes and then potentially pull back on some things if it's stable.So we would do it incrementally, just as you said to begin with.So starts start with your is inhibitor or Angiotensin receptor.
Blocker, and then Monitor, and then add in the second drug in a dog.That's How likely is going to be necessary but I think it still can be useful.I think one thing that people don't often appreciators that with chronic kidney disease that increase in blood pressure has probably been happening over a very long period of time.
It's, we diagnose it suddenly because it's the point at which we start measuring blood pressure, but actually, it's been gradually increasing and that's very different from.For example, your acute kidney injury, patient that goes from having a normal blood pressure.Yesterday to having a renal insult, And then becoming hypertensive very rapidly.
So, in terms of controlling blood pressure and a chronic kidney disease patients, it's all about gradual, slow reduction.Obviously, I don't want them to be too high for too long, but at the same time bringing blood pressure down over one.Two, three weeks is probably absolutely fine.
As long as we're seeing a gradual slow reduction over that time period.So in those cases, would you be how funny Would you be taking them back to assess where they're at, in terms of those who are adding something in?Is that Matter of a couple of weeks.You want the in every week or how do you stage that?
Yeah so patient dependent definitely patient dependence.So a patient that presents for example with ocular injury you probably going to get them back sooner so maybe between three to seven days if you have patience with hypertensive encephalopathy than obviously you're probably going to be hospitalized in those patients happens.
Less commonly with chronic disease again than with acute, but I guess in some of the charity clinics that we work.If you sometimes it goes, two weeks between us being able to get those cats back in to see us.So I think I would say, ideally, you know, I would see them back on a weekly basis initially, if I could and more frequently, if I had clinical concerns for Target organ damage.
Yeah.And that kind of weekly check you primarily be reassessing blood pressure.Would you be repeating any other Diagnostics know to probably just blood pressure at least initially and then in terms of monitoring Hang of renal function parameters that again, is going to be on a patient by patient basis and depending on the stage of these as well.
So, you know and Iris stage 2 patients, you know, after diagnosis, maybe then you would see them back and repeat parameters, maybe after about a month, to make sure that things were remaining relatively stable, but thereafter, you might go to Every 3 to 4 months and then you might even extend out to six monthly of things are looking very stable in contrast.
Obviously like with your little dog, then.You know, things are changing rapidly, and that could be every Fortnight or it could be more frequent than that depending on what's happened to them clinically.And how many medications that were changing?I think the only other thing to say in relation to the blood pressure monitoring and monitoring of renal parameters would just be with the Angiotensin receptor blockers and ACE inhibitors which can have an impact on GFR.
So they drop glomerular.Capillary pressures.So we do Sometimes expect to see a small increase in creating with those.So if I was starting those in a later stage patient, I might want to Renown parameters a bit more sooner than I would, for example, starting at model peen.
And then, how would you do if that does happen?Because that's something that's always confused.Me, you read the label for your heart patients.On an Ace, inhibitor says, don't give it to patient's, kidney failure, but then you go.But if they have kidney failure, it's one of your treatment.Well yeah, yes, it's about stability and monitoring.
And tolerance.So if you've started a patient on an Ace inhibitor or ARB, and you see a small increase in creatinine, but clinically they're doing well, it's made no impact in terms of their activity, there are other clinical parameters.
Then, great, we'll stick with that but if you started it in a patient with let's say later our stage 3C kit CKD, you probably purposefully be getting them back to check on that.And if you've seen more than a 25% increase, Increase in creatinine, you're going to have to be balancing.
Is this going to continue to increase?Do I actually need to stop this drug because it's having an adverse effect on this particular patients renal function.And so, it's just something to be cognizant top.It's not that it would stop us from using them necessarily, but we would be a lot more cautious about it.
I think the important thing is to do it.It is very common in older cats.It's very common in cats with chronic kidney disease.I just passionately think that it Be standard of care, it should be part of the physical exam and every cat over the age of nine.Blood pressure machine should be in the consult room and it should just be built into part of a routine.
Physical exams that he's got.It should obviously be done first because you don't want to do your physical exam and then what do they do there?And give it take the temperature then, no, definitely not that way.But yes, because once you get confident in what you're measuring blood pressure, you will identify these patients and controlling hypertension.
Something that can make a big impact in terms of quality of life.And there are the subtle changes that I think owners perceive in older cats as well.The sort of Behavioral changes, which sometimes was we can't say for certain are hypertension related or it definitely clients who feel that their cats are better.
Once the hypertension is controlled, how good was that the rest of our series with there is an focused on managing as a team Mia in those, chronic kidney cases As well as a good old Deep dive on proteinuria or complicated topics go and check it out.
Next up, we've got dr.Clint Gilman and we are talking calcium before we jump in a quick shout-out for Clint.But first of all, a bit of background about Clint, Clint has a pretty sweet gig.He lives outside of Melbourne, on a beautiful Coastline with some spectacular Surf and he gets to explore that part of the world while Hugh drives around to go and help other clinics with their complicated medical cases.
We recorded this.He told me that he's doing.Doing way too much of the work, but, and not enough of the fun things, and the family things.So, he needs a colleague.So, if you are a medicine Specialist or, you know, of a medicine specialist, who's had enough of being stuck, inside a large, multidisciplinary hospital and enough of working weekends, and being on goal sometimes and you like the idea of being out and about to see your clients who are vets by the way.
No client consults and you like the idea of total work flexibility and probably more dollars than you currently getting paid and maybe should give Clinton.Please contact details in the episode description but for now, let's get back to calcium.I want to talk about calcium and if we talk about kidneys being complicated and cheapest, that's something that does my hidden completely, that calcium win, it relates to kidney.
So we've said in Jill's episode that hypercalcemia can't be the cause of AZT Mia.But then there's the flip side as well, where the sad kidney starts, causing calcium issues and then to the point where you start getting calcium, Um, deposited in the kidney there, and that's where my, that's why I get confused.
Can we talk about that?Yeah, yeah, I think helped him is a challenging aspect of kidney disease.Like, we can get calcium deposition, secondary to inflammation in any organ.And that can happen with.Chronic kidney disease.
Will often see mineralization of the caliph, he's or mineralization of the tissue and sometimes it's even hard to distinguish from natural lip.But yeah, do you might get a Chronic kidney disease patients that no McHale samich, but has calcium mineralization all of its calculus a but site secondary to the inflammation.
Not necessarily net for accounts enosis, which is where you get mineralization of the kidneys.Usually, with a concurrent High, phosphate directly as a result of the increased calcium concentration in the blood.Okay, see.That's right.Yeah, it's ragged vague.So that, that calcium concentration is that because of the kid is a secondary thing to the kidney failure, or is it, is that the scenario way?
That's the primary problem because of a parathyroid issue.Some correct correct.But, but it's probably more of vitamin D.Intoxication that leading to a high calcium and a high phosphate that then leads to Nefra calcium notices because normally you need a combination of a high calcium and phosphate to result in mineralization in the kidney.
And Parathyroid disease.Usually like primary hyperparathyroidism will have a high calcium but low-normal phosphate so you don't necessarily get their freak Elsa gnosis and disease that way and just to put vitamin D into context that's like a real dentist side issue but old old rodenticides their surroundings and actually is that still a thing?
Like what?Like I think very old the common cream that humans do so it's more like cats licking their owners possibly that has vitamin DD Cream thing caught on or occasionally eating a vitamin D tablets over human or something like that, that's pretty uncommon, but it can have so never calzone noses.
So pathological, calcium deposits in the kidneys that cause kidney problems.He said that's mostly going to be vitamin D.Yeah, you.Okay.Right.And, and again, so there's no pre-existing kidney disease that causes that.That's because of the kidneys, take a hit, secondarily.
It's that, that's where.And, and kind of Most chronic kidney disease patients, not all but most usually have a low to low normal calcium.You do occasionally, get the ones with high so those ones would certainly be less likely to get that flip.
Let's say like calcium deposition, secondary to that high blood calcium but that's an indicator or a mark of a whole different condition which we can discuss.Now or later, which is secondary renal hyperparathyroidism my brain just exploded there because that kind of stuff, I had to go read it.
Okay.It's like it is it is very complex, but I think it can cut really, simply often be broken down to just phosphate levels.Like, phosphate levels for me with, like, Ike, I'm really kind of particular with phosphate levels when it comes to chronic kidney disease, patients, and and the tricky thing is your standard blood reference range is not the guide.
You want to be using for phosphate levels.When you've got chronic kidney disease patients, Iris, have their own reference range Target for phosphate level.And a lot of those targets fall within the standard, blood reference rates, you might have a printout of a blood.That's got normal, phosphate in inverted commas, but for that level of Iris kidney disease.
That hot plate levels way too high for that patient.And so you may not Institute treatment like a phosphate binder, if it's already on a renal diet but you really should okay, as this dogs and cats equally or Don't think at yeah, yeah, absolutely.
So I think the standard reference right for phosphate, correct me if I'm wrong, but it's like .82 2.2 or something like that.And Iris recommend, depending on the stage like the more advanced stage 2 I guess you could.Let's say the higher the phosphate can because you know, you've got more significant kidney disease but two stages, three and four.
I think it's 1.9 off the stage for its 1.9.It has, it should be under and that's still within the reference range.The stage 3, it's 1 point 6 into stages. 1.2 it should be under 1.54, they're all reference range, but they're all also possibly hire for that stages of disease.
So that's only if you have a renal disease that that correct chronic chronic, chronic kidney.Wow, that is really cool.That's new.That's awesome again.Can we dig again?I'm sure we learn to somewhere.But so why do we care so much about the phosphate in kidney disease?
How does it come into play with secondary?Renal hyperparathyroidism?Yeah.Like phosphate kind of if we go way back into the seventies when they did some of the first studies on dogs, they did nephrectomies and dogs, you know, with great ethics approval.I'm sure what that both.
Get wait, take both your kidneys out.Well, I took while they took one because I needed to study the folks of that one remaining on and then they compared, let's say a phosphate restrictive is non phosphate restricted diet and this wasn't even protein.Restricted.This was just simply phosphate restricted like the two-year survival rate was well over double or 75% to your survival rate in those fed.
Phosphate restricted diet with 33% said, non phosphate restricted and we know like phosphate is one of the earliest markers that will rise really early with reduction in GFR.And then this whole Cascade of events basically happens where we get an increase in the fiber, growth factor, F, DF 23.
We get Klein and calcitriol or calcitriol levels basically vitamin D, which in part is secreted from the kidney.So is our kidneys, are dying, have less cellular capability of secreting, vitamin D.And then we start to get a reduction in ionized calcium.
And then that triggers an increase in pth level because that pth of parathyroid hormone is going to try and bring that calcium back up into normal reference range.Okay.And then we get all the deleterious effects of parathyroid hormone, including osteoclast Iqbal.And resorption and various issues around the body.
So phosphate to me kind of underpinning.This whole calcium, phosphate, parathyroid, calcitriol into play.And we really, I think Advance.We really need to be quite aggressive in our phosphate control.Okay, cool.
Just don't have time to summarize that whole cycle.So kidneys I said, kidneys, don't make the hormones that help you regulate your calcium.The parathyroid says, oh, there's not enough calcium.Let's pump out more hormone to get some more calcium in the body says, well, yeah, let's get some calcium out of your bones and and that's when you can get calcium being deposited in the renal coaches as well.
Oh my misunderstanding, it probably more just to normalize blood.Calcium levels.Okay, I'm yeah.Okay cool.So, is that calcium?Well kind of then we kind of have the option to do.We supplement with Kelsey Trail, do we add in something, like Vitamin B or there's another drug and not sure not many people have heard of Sinner Celts it which is another drug as well that kind of plays into this whole secondary renal hyperparathyroidism dilemma.
And so basically in terms of management from that perspective, first thing is we want to aggressively manage her, phosphate level to renal died, donkey phosphate restricted, so that our first sort of line therapy and then if that's not enough, then a phosphate binder, and then Want to monitor, phosphate levels and get it to that Iris tag at reference range.
And once we've done that, then we want to read this calcium and see what calcium's are and ideally an ionized calcium.And then if ionized calcium still low despite aggressive phosphate management.That's the situational.You probably want to introduce some calcitriol, some vitamin D, just to help the body up, that calcium level into the normal range, and reduce that exit parathyroid secretion, and it's kind of on the flip side of that.
At that point, when phosphate is normal, if calcium's High, then we want to introduce that drug called similar culture, which basically does the opposite.It kind of tricks.The parathyroid into thinking.There's more calcium in the body, and it lowers the calcium levels.Okay.And reduces the parathyroid secretion all right, that makes sense.
Gee, you look stunned now, I do sadly.When we get to this current chronic kidney disease management inside.I used to do it a lot, General.It's an emergency like oh okay back to your GPS and you guys.
Yeah.Robo specialist level, you know, not, not many GPS would go to this level.
Well, I hope they wouldn't Do.But most kind of, you know, cap out at this point and referred on, okay?It's just even though you might not do it yourself, I still find it really useful to know when you should be referring to knowing about these sort of things to go.
All right, this remember Glenn said that, think about it, this is like behind me or if you're going to go see a specialist.There you go, kidneys in a nutshell.Hope you enjoyed it.Hope you learned something.
Hope it didn't scare you too much.We've got a lot more.Give me stuff over on the clinical podcast last week.We recorded an epic episode about acute kidney injury with PCC specialist, dr.Rob Webster, go to Vivian supercars.com, free two week trial.
And again, if you need the notes on these, they really going to help you.I use them all the time.Go to The V12 that calm and we'll have a link updating to get access to the Charlotte.Enjoy have a great week.

Prof Jill Maddison

Dr Rosanne Jepson

Dr Clint Yudelman