Transcript
WEBVTT
00:00:00.000 --> 00:00:02.209
Did you realise that Kidney Health Australia notes that 1.
00:00:02.209 --> 00:00:06.549
8 million Australians probably suffer from renal disease and don't know they have it?
00:00:07.028 --> 00:00:12.359
And also that the Indigenous population has twice the incidence of renal disease than the general population.
00:00:13.179 --> 00:00:19.710
Renal disease is a really important condition which we all need to know about and today we're going to hear more about it from Professor Stephen McDonald.
00:00:20.259 --> 00:00:27.879
He's a consultant nephrologist at the Royal Adelaide Hospital and his role includes care of the inpatients with all stages of kidney disease including those with dialysis.
00:00:28.314 --> 00:00:30.304
and also those who have had kidney transplants.
00:00:30.765 --> 00:00:37.304
He works in clinics around South Australia including a variety of settings in metropolitan Adelaide and regional and remote locations.
00:00:37.615 --> 00:00:47.844
He's actively engaged in research around the epidemiology of kidney disease and he leads the Australia and New Zealand Dialysis and Transplant Registry which is based at the South Australian Health and Medical Research Institute in Adelaide.
00:00:48.715 --> 00:00:56.405
G'day and welcome to Aussie Med Ed, the Australian medical education podcast, designed with a pragmatic approach to medical conditions by interviewing specialists in the medical field.
00:00:57.003 --> 00:01:07.474
I'm Gavin Nimon, an orthopaedic surgeon based in Adelaide, and I'm broadcasting from Kaurna I'd like to remind you that this podcast podcast players and is also available as a video version on YouTube.
00:01:08.155 --> 00:01:15.204
I'd also like to remind you that if you enjoy this podcast, please subscribe or leave a review or give us a thumbs up as I really appreciate the support and it helps the channel grow.
00:01:15.515 --> 00:01:24.515
I'd like to start the podcast by acknowledging the traditional owners of the land on which this podcast is produced, the Kaurna people, and pay my respects to the Elders both past, present and emerging.
00:01:29.114 --> 00:01:35.015
I'd like to remind you that all the information presented today is just one opinion and there are various ways of treating all medical conditions.
00:01:35.344 --> 00:01:39.254
Therefore, you should always seek the opinion from your health professionals in the area in which you live.
00:01:39.784 --> 00:01:48.625
Also, if you have any concerns about the information raised today, please speak to your general practitioner or seek advice from a health organisation such as Lifeline in Australia.
00:01:48.674 --> 00:01:53.105
.It's my pleasure now to introduce Professor Stephen MacDonald, a consultant nephrologist from the Royal Adelaide Hospital.
00:01:53.165 --> 00:01:53.944
Welcome Stephen.
00:01:53.944 --> 00:01:55.665
Thank you very much for coming on Aussie Med Ed.
00:01:56.665 --> 00:01:57.424
Thank you, Gavin.
00:01:57.424 --> 00:01:57.965
Thanks for having
00:01:58.034 --> 00:02:01.295
I'm really grateful for you , giving up your time, to be involved in this interview.
00:02:01.745 --> 00:02:04.924
So Stephen, can you tell me, first of all, how important is renal disease?
00:02:04.924 --> 00:02:05.795
How common is it?
00:02:06.125 --> 00:02:09.275
I believe there's a different incidence in the Indigenous population.
00:02:09.504 --> 00:02:11.835
Does it vary between other racial groups as well?
00:02:12.044 --> 00:02:12.294
Sure.
00:02:12.294 --> 00:02:12.594
Thanks.
00:02:12.594 --> 00:02:13.525
Great question, Gavin.
00:02:13.525 --> 00:02:19.724
And I'd like to start, of course, by acknowledging that I'm on the land of the Kaurna people and pay my respects to their elders past and present.
00:02:20.525 --> 00:02:31.189
So every year in Australia, about 3200, people actually start dialysis or have a Kidney transplant is their first form of kidney replacement therapy.
00:02:31.229 --> 00:02:44.639
So that's the very severe end of the spectrum that works out about 125, 130 people per million population per year, which puts us a little less than a lot of other comparable countries.
00:02:44.650 --> 00:02:47.900
So those rates are a little bit lower than most European countries.
00:02:48.689 --> 00:02:51.699
Of course, that's the most severe end of the spectrum.
00:02:51.699 --> 00:02:59.699
And there are many milder degrees of kidney disease, and the great majority of people, of course, don't have kidney disease of that severity.
00:03:00.349 --> 00:03:19.439
Surveys have shown that about 10 to 11 percent of the overall population in Australia actually have some form of kidney disease, and that's usually one of the very much milder forms of kidney disease that might be manifest simply as an abnormal blood test, or a bit of blood and protein in the urine, or some form of abnormality of the kidneys or the bladder.
00:03:20.235 --> 00:03:25.413
In terms of the people that affect, so there is a steep age gradient.
00:03:25.424 --> 00:03:29.074
So the kidney disease is much more common among older people than younger people.
00:03:30.033 --> 00:03:39.524
You mentioned Aboriginal and Torres Strait Islander people and sadly kidney disease is much more common among people of Aboriginal and Torres Strait Islander background than in the general population.
00:03:39.954 --> 00:03:42.174
It's a bit more complex though than just ethnicity.
00:03:42.753 --> 00:03:49.463
It's about being of Aboriginal and Torres Strait Islander background and alsoif you are living remotely and you have a number of the other health challenges that go with that.
00:03:49.894 --> 00:03:59.324
Those factors all interact so that the rates become much, much higher if you're living in a remote environment than in a metropolitan environment.
00:03:59.324 --> 00:04:07.604
But overall, the rates of kidney disease are three and a half, four times higher among Aboriginal and Torres Strait Islander people than the general population.
00:04:08.454 --> 00:04:16.603
Again, there are some age differences and that, like many other chronic diseases, it tends to affect Aboriginal and Torres Strait Islander people at a younger age.
00:04:16.603 --> 00:04:20.843
And that's, of course, really important when you think about the impact on families and societies.
00:04:21.283 --> 00:04:21.874
right.
00:04:22.684 --> 00:04:24.944
Okay how do people actually present with it though?
00:04:24.944 --> 00:04:25.553
Yeah.
00:04:25.564 --> 00:04:36.134
So there's still a number of people, in fact, about one in five people who start dialysis actually present really in the last month or two before that.
00:04:36.153 --> 00:04:37.444
So they're so called late.
00:04:37.509 --> 00:04:38.709
presentations.
00:04:39.119 --> 00:04:47.249
And there are a number of factors that sometimes there's some form of catastrophic kidney disease that really is very rapidly progressive.
00:04:47.548 --> 00:04:54.033
But a lot of the time it really manifests the fact that the kidney disease can be, and often is just very slowly progressive.
00:04:54.033 --> 00:05:15.384
The signs and symptoms can be very mild, a little bit of fatigue or lethargy, or sometimes nothing at all until people go along to their doctor or they go along to the hospital and have a blood test done or whatever So there are that minority and that's a proportion that's been slowly declining over time, but it's still a really important factor.
00:05:15.793 --> 00:05:21.538
The great majority of people are picked up often through the routine general health care of people with chronic kidney disease.
00:05:21.538 --> 00:05:30.588
So about 40 percent of people who start dialysis actually have diabetes related kidney disease, and that's the most common form of kidney disease.
00:05:30.807 --> 00:05:35.278
And then on top of that, there's another 12 to 15 percent with vascular kidney disease.
00:05:35.517 --> 00:05:44.302
So more than half of people in that category, and they're a group of people that either are or should be having regular follow up and regular checks through their primary care networks.
00:05:44.302 --> 00:05:50.932
And those checks do include routinely screening for kidney disease on a six monthly basis, for example, if you have diabetes.
00:05:51.572 --> 00:05:53.562
So most people are picked up in that way.
00:05:53.583 --> 00:05:59.884
And then if the kidney disease progresses. They're referred on a lot of other people that picked up as part of other screens.
00:05:59.894 --> 00:06:08.545
For example people might've had a urine test, a dipstick to look for blood or protein in their urine as part of an employment medical or a superannuation medical or something like that.
00:06:08.595 --> 00:06:12.115
So there's a number of cases of kidney disease that are picked up like that.
00:06:13.045 --> 00:06:23.845
There's also a group of kidney diseases and about 30 percent of people with severe kidney disease have a form of glomerulonephritis and a number of those, are related to a systemic disease.
00:06:23.855 --> 00:06:26.035
So for example, lupus, it would be the most common one.
00:06:26.035 --> 00:06:29.314
And so there's that group of diseases as well.
00:06:29.564 --> 00:06:36.725
So A lot of them are actually associated with other conditions such that the attending physician is keeping an eye out for kidney disease.
00:06:36.975 --> 00:06:40.694
there a role for doing screening of the population like we do for faecal occult blood?
00:06:40.754 --> 00:06:43.564
Should we all be having urine dipsticks regularly at an older age?
00:06:44.764 --> 00:07:27.456
So there have been a number of studies looking at whether that's effective and in particular whether that's cost effective and the answer is for people with defined risk factors, yes it is, and so it's incorporated into what is the routine standard of care for people with hypertension, for people with diabetes as part of the Standard health check for Aboriginal and Torres Strait Islander people that's incorporated in terms of the general population No, the current recommendation is not just to do a screening dipstick there is Discussion out there about dipsticks, which are very sensitive at finding blood and protein, but they also Take you down a path of false positives and it's quite common, in fact, about 10 percent of the population on any given day may have a trace of blood in the urine and, or a trace of protein.
00:07:27.985 --> 00:07:30.586
So there's then a process of follow up of that.
00:07:31.305 --> 00:07:40.326
I think the most important message though, is if there's any of those other associated risk factors, then that indicate screening and certainly if there's any other signs of kidney disease.
00:07:40.336 --> 00:07:47.572
So typically it'd be very early part of the workup if somebody presents with high blood pressure or an anemia, for example.
00:07:47.812 --> 00:07:48.423
Excellent.
00:07:49.132 --> 00:07:57.077
I might start off with a classification and how you tend to classify kidney disease and then go onto the workup that a GP or a medical student needs to be aware
00:07:57.077 --> 00:07:57.137
of.
00:07:57.137 --> 00:07:57.367
Sure.
00:07:57.788 --> 00:08:09.247
Yeah so I think there's a a number of ways you can look at this and I think one of the really early concepts to differentiate is between Chronic Kidney Disease and Acute Kidney Disease or Acute Kidney Injury as it's called now.
00:08:09.567 --> 00:08:14.218
And, the names I guess tell you what they're on and the causes and the workup of those are quite different.
00:08:14.398 --> 00:08:20.468
Different and acute kidney injuries, a really big and important topic, especially for people working in hospitals.
00:08:21.148 --> 00:08:25.677
the definition of chronic kidney disease is that it needs to be there for three months.
00:08:25.677 --> 00:08:27.382
So that's the technical definition.
00:08:27.992 --> 00:08:34.243
But in, in fact, of course, acute kidney injury tends to evolve over hours and days for both of those.
00:08:34.243 --> 00:08:41.567
The first way I start thinking about those is a really old fashioned way, but one that stood the test of time that is divided into renal, and post renal.
00:08:42.153 --> 00:08:58.802
And that's a good way to approach both chronic and acute kidney injury and what that means in practice is, making sure that there's no obstruction and at a practical level that means some form of imaging although just occasionally we still get people who come along typically males and a urinary catheter solves the whole problem.
00:08:58.898 --> 00:09:38.414
But some form of imaging to make sure that there's no obstruction of the lower tracts and then thinking through whether there's a pre renal cause And that's a more common way of thinking with acute kidney injury, but that's basically about optimizing blood pressure and fluid So once you've dealt with that, you're then left with situation of saying, okay the problem's not before the kidney, it's not after the kidney, it's related to the kidney, and then from there, there's a process of taking a good history and understanding whether there's any of those other factors we spoke about earlier on that might point you towards the cause of the kidney disease, what the rate of change of the kidneys and then physical examination is not that helpful for most times in terms of kidney disease.
00:09:38.725 --> 00:09:41.784
And then there's the usual process of investigation.
00:09:41.784 --> 00:09:48.160
Now, the key investigations for kidney disease are of course, blood tests, looking at serum creatinine and the calculated.
00:09:48.280 --> 00:10:07.471
Estimated Glomerular Filtration Rate, which is calculated from that, and the one that tends to get overlooked is often the urine and looking for the presence of blood and protein in urine and from there , like any other area of medicine, is often a form of pattern recognition saying, okay, is this a situation that is typical, say, of diabetic kidney disease?
00:10:07.480 --> 00:10:21.638
So somebody might have diabetes, slowly progressive kidney disease, some moderate degree of proteinuria, Or do they have no previous history of diseases some blood and protein in the urine and more rapidly progressive kidney disease.
00:10:22.248 --> 00:10:32.538
And so from there you need to form an an opinion about do you have enough information on the history and the examination and those investigations to be comfortable with a presumed diagnosis, or do you need.
00:10:33.092 --> 00:10:52.128
More information and if there's concern about an underlying renal parenchymal or intrinsic kidney disease, then the question of a kidney biopsy often comes up and that's typically the case if you don't have a good other explanation for kidney disease Or you're worried that there's something that's progressive that will need treatment.
00:10:52.418 --> 00:10:52.988
Okay.
00:10:53.077 --> 00:10:53.707
Excellent.
00:10:54.187 --> 00:10:57.908
So really then basically bloods urine test.
00:10:58.634 --> 00:11:03.894
Imaging and ultrasound, is there any role for anything like an MRI or CT at any stage?
00:11:03.945 --> 00:11:58.126
Occasionally a CT, if you're worried about a blood flow, if you're concerned that there might Stenosis or renal vein thrombus or you're concerned that there might be a Malignancy, then they will be the particular roles in which you would go to a CT scan And you're going to need contrast with that CT scan MRI in terms of the diagnosis doesn't have a lot to offer the story of renal artery stenosis is an interesting one and I think most of the people I get referred to with that we end up not doing anything because one of the important changes in renal medicine in the last really 20 years has been the demonstration that Angioplasty or stenting of renal artery stenosis really doesn't make any difference in the great majority of cases, and there's good trial evidence to suggest that so when I was at medical school , there was quite a teaching about doing a nuclear medicine scan, find and then treat renal artery stenosis.
00:11:58.126 --> 00:12:04.606
And we tend not to go down those paths now unless there's a really, unique situation, a single functional kidney or something like that.
00:12:04.616 --> 00:12:12.043
What about drugs that may be impacting on the cause of renal disease, such as ACE inhibitors also non steroidal anti inflammatories and things?
00:12:12.043 --> 00:12:15.283
Yes, there are a number and they do actually change over time.
00:12:15.283 --> 00:12:19.192
They do vary a little bit depending on whether you're in a community of practice or hospital practice.
00:12:19.812 --> 00:12:46.878
There's a really important piece of history here as well and we were all taught in medical school about the role of Bex and Vincent's powders in Australia and that was one of the things that really Put Australian Nephrology on the map and that was a combination of aspirin and phenacetin which is a relative of paracetamol and they were all banned in Australia in the late 1970s But they had a very toxic role in causing papillary necrosis and kidney damage and also transitional cell carcinomas.
00:12:46.878 --> 00:13:01.633
And that the tail of that epidemic really did take another 25 years to die out total, I think in terms of the drugs you mentioned the at recommended doses in people with normal kidney function, there's no particular downside to taking non steroidals.
00:13:02.393 --> 00:13:05.600
Clearly there are other issues in terms of GI side effects and so on.
00:13:05.787 --> 00:13:13.059
The angiotensin receptor blockers and ACE and SGLT2 inhibitors, all actually have an effect.
00:13:13.600 --> 00:13:17.990
Reducing renal blood flow, but that's actually not nephrotoxic as such.
00:13:18.899 --> 00:13:25.373
It is part of their mechanism, and in the longer term, both of those groups do slow the progression of kidney disease.
00:13:25.893 --> 00:13:31.743
But, and this is where the but is, and it's true for both of those groups, in some settings, and in particular if people have volume depleted.
00:13:32.082 --> 00:13:38.643
Then you do set up a situation where you've artificially reduced renal perfusion and you can potentiate kidney injury.
00:13:38.643 --> 00:13:43.123
And that, that also applies if you've got non steroidal anti inflammatory drugs on board.
00:13:43.413 --> 00:13:59.368
And so that's, so typically we would give advice and I would hope most people would be given advice, particularly when they have SGLT2 inhibitors about what to do on a sick day, if people have got bad diarrhea or for whatever reason, they're becoming dehydrated, those drugs need to be stopped as does metformin, by the way.
00:13:59.868 --> 00:14:11.773
In terms of the drugs that cause toxicities to the kidneys, the good old fashioned ones of gentamycin is still around and we still see a little bit of of acute kidney injury related to that together with, vancomycin.
00:14:12.153 --> 00:14:27.177
There are a few drugs that can cause idiosyncratic or allergic toxicity, typically as an interstitial nephritis, and while that's rare on an individual basis, if you've got drugs that are used very commonly, it does Pop up from time to time.
00:14:27.177 --> 00:14:32.518
And the two classes I'm thinking of here are the proton pump inhibitors, so pantoprazole and so on.
00:14:32.768 --> 00:14:34.307
And the cephalosporins.
00:14:34.327 --> 00:14:42.317
And in both of those groups we do occasionally see people that present with an interstitial nephritis so an acute deterioration as we do occasionally with allopurinol.
00:14:42.317 --> 00:15:33.611
That's not a reason not to use those drugs, but it is a reason just to be aware that if people start developing acute kidney injury in the context of those drugs, you do need to be a little bit suspicious about that There is an interesting other effect of the PPIs, the proton pump inhibitors, they do tend to drop people's magnesium levels a bit and there is some evidence suggesting that they do put people at higher risk of getting acute kidney injury if there's other factors around about the place and the area where that's best Demonstrated is with the immune checkpoint inhibitors as a new class of drugs that have been very effective for a number of malignancies And themselves actually have a number of renal toxicities, but the combination of that does seem to be a synergistic that would be the main drug toxicities We would see together with I guess the other age old one would be amphotericin, which we still see a little bit of, but
00:15:33.711 --> 00:15:37.951
And of course the most common nephrotoxic drug would have to be sugar, with diabetes,
00:15:38.001 --> 00:15:38.991
absolutely.
00:15:39.121 --> 00:15:42.475
And that's, there's no doubt about that.
00:15:42.524 --> 00:15:47.595
Diabetes has, as I said earlier on, become the number one cause of kidney failure.
00:15:47.875 --> 00:15:49.134
That's true in Australia.
00:15:49.134 --> 00:15:50.365
It's true all over the world.
00:15:50.384 --> 00:15:55.304
The rates of kidney disease in Malaysia are now higher than they are in Australia.
00:15:55.304 --> 00:15:56.855
That's driven by diabetes.
00:15:56.965 --> 00:16:01.100
Taiwan has the highest national rate of kidney disease in the world.
00:16:01.120 --> 00:16:04.059
And that again is driven by diabetes and carbohydrates.
00:16:05.519 --> 00:16:19.269
One of the things that people have asked is it the fact, are we getting better or worse at treating diabetes or preventing kidney disease and The answer to that, in Australia at least, is that if you've already got diabetes, the risk of getting kidney disease hasn't increased over time.
00:16:19.269 --> 00:16:25.519
In fact, that's trickled down a bit, which is what you'd expect with the introduction of ACE inhibitors and Sgf2 inhibitors and so on.
00:16:25.830 --> 00:16:31.990
What's changing, though, is of course the number of people with diabetes and the duration of which they have diabetes for.
00:16:31.990 --> 00:16:34.750
And that's a really important predictor of kidney disease.
00:16:35.309 --> 00:16:51.919
It's a good thing that people are surviving longer and reflects the better treatment of All of the other comorbidities that go with having diabetes, but the reality is at the end of the day, there are more people in the population with diabetes, and so that does drive more people with kidney disease related to diabetes.
00:16:52.019 --> 00:17:00.289
The target hemoglobin A1c, if you've got diabetes, is the same whether you do or don't have kidney disease There's not a separate target.
00:17:00.289 --> 00:17:03.750
What does have separate targets is blood pressure.
00:17:03.750 --> 00:17:24.732
So if you have even mild levels of kidney disease or a bit of albuminuria, proteinuria or mildly abnormal kidney disease Then there is evidence to try and get blood pressure down to 130 on 80 as an average rather than the usual targets and that benefit is both in the slowing of the rate of progression of kidney disease as well as the risk of the usual vascular complications
00:17:26.238 --> 00:17:30.468
So Stephen, you know my passion for trying to divide things up into groups of three or four.
00:17:30.788 --> 00:17:34.708
Can interstitial renal disease be subclassified into three or four different subgroups?
00:17:34.847 --> 00:17:36.357
Is that a good way of thinking about it?
00:17:37.188 --> 00:17:38.087
I think so.
00:17:38.087 --> 00:17:43.738
You could divide it into glomerular disease, interstitial disease and tubular disease.
00:17:43.907 --> 00:17:45.057
That would be one way to do it.
00:17:45.067 --> 00:17:49.468
It's not a great fit because the other important group of kidney diseases are the inherited diseases.
00:17:49.468 --> 00:17:53.022
So there's having talked about diabetes and glomerular nephritis.
00:17:53.123 --> 00:18:00.252
The, one of the things that's changed a lot in kidney disease in the last five years or so has been the genetic element of that.
00:18:00.762 --> 00:18:06.192
So for traditionally polycystic kidney disease is in fact the most common inherited condition.
00:18:06.192 --> 00:18:09.512
And that's about 15 percent of all people that start dialysis.
00:18:09.512 --> 00:18:11.202
And there's about half that number.
00:18:11.222 --> 00:18:14.952
So six to 8 percent or so people with Alport syndrome, which is.
00:18:15.663 --> 00:18:22.123
Classically taught as an X linked disease with kidney diseases associated with hearing loss and some eye abnormalities and so on.
00:18:23.073 --> 00:18:34.202
What were now understanding with the availability of better genomic technology and the ability to massively sequence things is that firstly that the inheritance and the genetic.
00:18:34.313 --> 00:18:59.458
Basis of both of those is much more complex than we thought previously Rather than just having one or two diseases for polycystic kidney disease There's now a series of more minor disease sites has been identified There has been the development the understanding of what they just Gene codes for the polycystin protein and what that gene does and now the development of a specific Intervention for polycystic kidney disease something called Tovaptin.
00:18:59.748 --> 00:19:19.205
So for families now with polycystic kidney disease for people with Early stage disease that is progressing there is now a treatment that we can offer that will slow down the rate of progression , our understanding of All port syndrome and the the related conditions that affect glomerular basement membrane has changed dramatically.
00:19:19.205 --> 00:19:25.336
And we now know that's really part of a broader spectrum of inherited glomerular basement membrane disorders.
00:19:25.665 --> 00:19:32.280
And that many of those are not just x-linked in, inherited their inherited via variety of different ways.
00:19:32.671 --> 00:19:38.161
Now they're the sort of conditions, if you like, with a nice, simple, almost monogenic inheritance.
00:19:39.330 --> 00:19:50.790
One of the things over the years is there's always been this group of people, maybe 10 -15 percent overall, that have had kidney disease where we haven't been able to assign a clear cause.
00:19:50.840 --> 00:19:58.667
They've turned up, they've progressed and they've ended up going all the way through to starting dialysis without a good cause being defined.
00:19:59.048 --> 00:20:08.144
Biopsies might just show diffuse scarring and so on and that's an area where The genetic side of things is now uncovering a whole variety of candidate genes.
00:20:08.335 --> 00:20:17.375
We're not yet at a stage where we can link them to specific interventions, but it is clearly an area that's going to evolve over the next 10 15 years or so.
00:20:17.884 --> 00:20:20.751
So obviously that's a significant cause areas
00:20:20.751 --> 00:20:29.942
yeah, and then it does get more complex because genes don't exist in isolation, and then there's this area of the interaction between genetics and the environmental influences.
00:20:30.273 --> 00:20:40.508
In some respects that's true even of diabetes, I mean there's a substantial inherited tendency to get diabetes, but that's not the thing, the genes haven't changed over the last 50 years, what's changed is the environment.
00:20:41.403 --> 00:20:46.222
These treatments you're talking about for let's say polycystic kidney disease, how do these treatments work?
00:20:46.272 --> 00:20:46.573
Sure.
00:20:46.792 --> 00:20:55.064
The tolvaptan is something that, that specifically blocks the transporter pump that causes the development and the enlargement of the cysts in the kidney.
00:20:55.833 --> 00:21:01.973
And it is an aqua retic or a vasopressin agonist and causes people to have a, a diuresis effectively.
00:21:02.144 --> 00:21:12.763
The evidence base around that is fairly targeted so that if people are losing more than five mils per minute per year of EGFR then that's been shown to be a benefit.
00:21:12.983 --> 00:21:19.114
It's not a simple treatment in the sense that you're talking about tablets twice a day, but in particular, it pushes the your urine output up over.
00:21:19.344 --> 00:21:22.644
3 litres and you're then drinking and then going to the toilet a fair bit.
00:21:22.644 --> 00:21:29.564
But for people who have progressive kidney disease, that's, that's a discussion we have and say, okay, look, that's the side effects of treatment.
00:21:29.804 --> 00:21:36.173
The beneficial effects of treatment are, it slows the progression by around about 30 to 40 percent and you can actually work that out.
00:21:36.203 --> 00:21:39.064
That equates to a number of years of deferral of dialysis.
00:21:39.094 --> 00:21:43.824
So that's that's clearly a decision that many people would go down the path
00:21:43.864 --> 00:21:50.388
So is this something you'd start at a young age, even before you've got symptoms of or even signs of polycystic disease?
00:21:50.388 --> 00:21:53.278
Is there any genetic test to start it off and then start this treatment?
00:21:54.272 --> 00:22:06.863
Sure so typically people with polycystic kidney disease we would often end up screening family members and then if you followed them for a year or two, that's when you would have that discussion, even in the absence of any symptoms.
00:22:07.242 --> 00:22:36.803
Most, the great majority, well over 90 percent of cases of polycystic kidney disease are among people with known families and there are a couple of reasons, often people end up having some form of abdominal imaging for whatever reason, tends to happen more often in women than men because of period related abdominal pains and so on and so you would often Have a diagnosis made that way, but often people do want to just find out, particularly when they get into their early to mid twenties and start thinking about their own families.
00:22:37.482 --> 00:22:45.242
At the moment I mentioned that there's a number of different genes that drive and there's within those, there's a number of different mutations that drive.
00:22:45.337 --> 00:22:55.164
Polycystic Kidney Disease and so that unfortunately is not currently available a single genetic test that I can Order for somebody who comes to see me to say have I got polycystic kidney disease?
00:22:55.200 --> 00:23:26.701
The so that the screening is very much based on imaging, on ultrasound, and the reliability, or in particular the specificity of that, because that's the key thing we're looking at here, how confidently can you exclude that you've inherited polycystic kidney disease, and unfortunately, because there's always a few people that It's not really until you're around about 30 years of age that you can be confident that a clean ultrasound or an ultrasound with the absence of cysts would mean that you're not going to develop polycystic kidney disease later in life.
00:23:26.965 --> 00:23:27.435
Okay.
00:23:28.266 --> 00:23:33.046
The other scenario where that often becomes important is when people are thinking about donating kidneys.
00:23:33.105 --> 00:23:42.050
So by definition, often family members are often thinking about donating kidneys to other family members or relatives who may already have polycystic kidney disease.
00:23:42.145 --> 00:23:42.586
Okay.
00:23:43.596 --> 00:23:47.998
What about the other issue of the vesico-ureteric reflux causing kidney damage.
00:23:48.367 --> 00:23:52.788
That's obviously a post renal type condition, but that can lead to chronic kidney disease as well.
00:23:52.788 --> 00:23:56.137
Is that still common or is that less of an issue nowadays with better detection?
00:23:57.522 --> 00:24:02.573
look, I think it's incidence is neither high or lower than it has been for some time.
00:24:02.863 --> 00:24:11.413
I think there've been a number of trials and the pediatricians over the years have tried various approaches to treatment of urinary tract infections and treatment of surgery.
00:24:11.413 --> 00:24:18.173
And More broadly though, that category is now tends to be called ca, KUT, congenital abnormalities of the kidney and the urinary tract.
00:24:18.843 --> 00:24:27.343
and that's an area where the early detection and the early treatment more broadly, not just specifically of vesico-ureteric, has made a difference.
00:24:27.647 --> 00:24:30.988
, the other comment to make about that is that's an area where.
00:24:32.048 --> 00:24:35.988
The impact of genetics is really very substantial, as has now been demonstrated.
00:24:35.988 --> 00:24:38.667
There are strong genetic drivers for a number of those conditions.
00:24:39.508 --> 00:24:44.778
As an adult nephrologist, I guess I don't actually see or really get involved in the diagnosis of that.
00:24:44.978 --> 00:24:50.030
We do see people who have chronic kidney disease as they shift from the pediatric to the adult environment.
00:24:50.621 --> 00:24:55.421
But happily, from my perspective, that's something that my colleagues at the Children's Hospital tend to take care of.
00:24:55.675 --> 00:25:01.625
And what sort of level of functional deterioration can you have in a kidney before you actually start getting abnormalities in the numbers?
00:25:01.675 --> 00:25:04.415
Does it deteriorate right at the end or is it a slow deterioration?
00:25:05.776 --> 00:25:25.496
So typically, so if typically we would talk about the estimated glomerular filtration rate, which is calculated using some standard formulas from somebody's serum creatinine, so if a normal EGFR 80 to 110 or so, people would often talk about EGFR as percent of normal kidney function, which is the shorthand.
00:25:26.155 --> 00:25:37.104
And Technically stage 3 kidney disease, which is the first one that's defined just on the basis of Blood tests is less than 60 really from 60 down to about 30 or so Which is stage 3.
00:25:37.374 --> 00:26:05.425
People wouldn't I wouldn't expect them to feel a lot if any in the way of symptoms and secondly, it's not going to have much of an effect on the other electrolytes, for example, nor would you expect, it would be unusual to see an anemia or other specific renal complications as you start getting down into stage 4 chronic kidney disease, so an EGFR of less than 30 That's very much where you start to see a lot of the other metabolic complications of kidney disease.
00:26:05.675 --> 00:26:11.435
So you start to see phosphates rise initially because your kidneys are not excreting phosphates.
00:26:11.445 --> 00:26:13.726
That leads to some hyperparathyroidism.
00:26:14.500 --> 00:26:25.932
Of renal anemia starts to come into play, and that's quite a complex area because there's a relative lack of erythropoietin reduction, but there are also changes in how we absorb iron in the setting of chronic kidney disease.
00:26:26.272 --> 00:26:29.573
And then there are some changes to vitamin D at.
00:26:29.688 --> 00:26:32.387
Activation and the development of a metabolic acidosis.
00:26:32.387 --> 00:26:33.597
So they're broadly speaking.
00:26:33.597 --> 00:26:46.182
That's the metabolic changes that you see with an EGFR from 30, 25 down to 20 and there's also the range in which you would often expect people to develop some form of symptoms.
00:26:46.182 --> 00:26:53.307
Many people would not but, those symptoms would typically be and Nonspecific lethargy and fatigue and so on.
00:26:53.347 --> 00:27:12.241
As people's kidney disease progresses and it gets down to that more severe phase, now we're talking EGFR is around about 15 or so, then that's where people would start to see more severe manifestation of those symptoms and depending on the type of kidney disease there of course can be other symptoms, classically fluid retention may well be an issue and so on.
00:27:13.259 --> 00:27:22.962
does raise the question about what happens next and where do you start and when do you start thinking about dialysis, kidney transplantation and all those sorts of options.
00:27:23.673 --> 00:27:39.363
And so typically that point around EGFRs of 15 to 20 would be where you would be, if somebody's having kidney disease that's slowly progressing or rapidly progressing, you would be having conversations around what are the treatment options in your situation?
00:27:39.867 --> 00:28:00.048
Is is dialysis something that's going to be appropriate and if so, what type of dialysis is kidney transplantation an option, bearing in mind that for people that have a, an available living donor then so called preemptive transplantation or transplant more or less at the time at which you would otherwise start dialysis is the ideal form of kidney replacement therapy.
00:28:00.048 --> 00:28:17.897
For And there are some people, quite a few people, particularly elderly people in whom dialysis really doesn't offer any particular benefits and in that group we'd be going down a path, a conservative path of supportive care but not necessarily providing dialysis.
00:28:18.702 --> 00:28:29.613
You've touched upon the various treatment options then, so if we go through them you've obviously got dialysis the first option, or there's other medications you can use to help pre dialysis or is it purely just dialysis?
00:28:29.623 --> 00:28:32.053
And what about the old peritoneal dialysis?
00:28:32.353 --> 00:28:33.603
I presume that's not done anymore,
00:28:33.603 --> 00:28:41.073
No still very much so I guess nephrologists, like everybody we're pretty clever and we can do multiple things.
00:28:41.083 --> 00:28:44.472
So as you taking care of somebody with deteriorating kidney disease.
00:28:44.488 --> 00:28:46.778
There's at least three get back to your rule of threes.
00:28:46.778 --> 00:28:52.448
There's at least three lines of thinking and talking to, to patients that you're doing.
00:28:52.498 --> 00:28:57.907
One is making sure that you've got all of the various measures in place to slow the progression of kidney disease.
00:28:58.048 --> 00:28:59.228
So blood pressure control.
00:29:00.117 --> 00:29:02.458
Blood sugar control for people with diabetes and so on.
00:29:03.097 --> 00:29:13.204
The second is making sure that you have particularly in those more severe stages of kidney disease, detected and have treated the complications of kidney disease and a lot of those can be easily treated.
00:29:13.204 --> 00:29:19.589
So I mentioned the anemia that might involve some erythropoietin injections and so on and that's really important in terms of keeping people well and so on.
00:29:20.410 --> 00:29:38.651
Now, having said that, the third line of discussion is really one of them saying, okay, in an ideal world, you are well, your rate of progression is still slow, but if it's still progressing, then there's going to come a time at which you're.
00:29:33.976 --> 00:29:42.881
You will reach a stage of so called you do nothing, you're going to get sick of kidney failure and potentially even go on and die of kidney failure.
00:29:43.171 --> 00:29:47.621
So that's the situation in which dialysis and kidney transplantation become options.
00:29:47.820 --> 00:29:50.421
Dialysis doesn't make people walk differently.
00:29:50.421 --> 00:29:52.191
It doesn't make people smarter or faster.
00:29:52.191 --> 00:29:56.040
It just simply replaces the kidney function to stop you dying of kidney failure.
00:29:56.810 --> 00:30:02.474
There is very, one of the things that Australia contributed to nephrology is to.
00:30:02.535 --> 00:30:09.404
Provide the definitive trial that says, okay, there's no gain on starting dialysis before really the development of symptoms.
00:30:09.404 --> 00:30:18.059
There were some suggestions that starting at an EGFR of, 12 to 15 might prevent or might lead to reduced mortality and better outcomes.
00:30:18.109 --> 00:30:19.220
That's not the case.
00:30:19.480 --> 00:30:25.450
So typically dialysis would be started around an EGFR of 7 to 8 or so.
00:30:26.750 --> 00:30:36.291
Having said that you mentioned Peritoneal dialysis there are two main forms of dialysis hemodialysis and peritoneal dialysis from a nephrological perspective.
00:30:36.382 --> 00:30:50.557
They both do the job They both do it equally as well and so that the decision of one versus the other is really one of horses for courses for an individual patient Across Australia, depending on where you are, somewhere between a quarter and a third of people are doing peritoneal dialysis.