Therapeutic Guidelines Kidney and Urinary

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Hi, and welcome to this Australian Prescriber Podcast. I'm Dr Justin Coleman, a GP in Brisbane at Inala Indigenous Health Service. And with me, I have another GP. One of my favourites, Dr Lee Fong, a GP in Newcastle, has been my guest on many a podcast. You seem to be the go-to person for all the latest Therapeutic Guidelines. Welcome back to the podcast, Lee.

Thank you for having me, Justin. Happy to be back.

Excellent. I look forward to plumbing the depths of your knowledge about kidneys and urinary tracts today, Lee. And in fact, this is the very first time. We haven't launched a new title for quite a while. Usually it's updates to old titles, but this is a brand-new guideline. There's lots of stuff, all the things you'd expect in the kidneys and urinary guidelines. We'll just run through about 5 or so.

The first is looking at chronic kidney disease diagnosis and screening. One of the expert group on the guideline came up with the concept of ABC screening, which is albuminuria. So that's doing a urine ACR [albumin-creatinine ratio]. Blood pressure, which of course we GPs are hopefully pretty good at. And C is for creatinine or really an estimated GFR. So those 3 things are important screening tools, the ACR, the blood pressure, and the eGFR (estimated glomerular filtration rate). How often should we measure these things, Lee?

A lot. So probably more frequently than what we are. I guess the context of that is chronic kidney disease is so common. It's more than twice as common as diabetes. So you're looking at 1 in 10 Australians with signs of CKD (chronic kidney disease) rising to 1 in 5 if we look at First Nations Australians. And it's something that unless you go looking for it, it'll get missed. And there's so many people with CKD who don't know that it's happening. So yes, proactive screening is essential. What we usually suggest and what we have in the Therapeutic Guidelines is just a one-off is fine. If you get to 60 years or older and you've got nothing else, you've got no other risk factors, then just doing a one-off is fine. But other than that, if you have got some risk factors, so for example, if you've got diabetes, you've got hypertension, you've got a single kidney, or you've got a history of acute kidney injury, then to do an annual screen would be the way to go.

With an acute kidney injury, we'd say for 3 years post the initial acute kidney injury, then for every 2 years after that. And there's some specific recommendations for First Nations as well.

And if you've had hypertension during pregnancy, they suggest ongoing and you're screening there as well. How do you go with screening your patients, Lee?

Yeah, this is kind of embarrassing. I thought, oh, I better check to see how I was doing, seeing as we've put out these guidelines. I had a quick look and did a little mini audit of patients over the age of 60 that I'd seen in the last 12 months. I just picked a sample of 10 and looked to see how many of them had ever had urine ACR done. And I got a fairly miserable 3 out of 10 for that one. And then I thought the other common group would be people that have hypertension. And so I had a quick look to see, again, another random sample of 10 to see how many of those I'd done a urine ACR on in the preceding 12 months. And they're also a fairly miserable 4 out of 10.

Well, Lee, that was a cheat question I prepared earlier because I happened to know I did better than you. So that's why I asked. To be fair, I do work in Aboriginal and Torres Strait Islander Health and clearly CKD is far more common. And also I probably have more people to help me screen the Aboriginal health workers and the nurses do that fairly routinely in my practice with spot ACR testing as well. I guess the point with the regular screening is not only that it occurs more commonly than we perhaps think, but also we can do something about it. And so early intervention does actually help with CKD, and not only the lifestyle things which we always knew helped, but also the medications. So in terms of medication regimens, a brief overall picture, Lee, what have we got?

We've got the things that probably most of us would be very familiar with. So we've got the ACE (angiotensin-converting enzyme) inhibitors, the A2RBs [angiotensin II receptor blockers]. Added to that, we've got the SGLT2 inhibitors. So with or without comorbid diabetes, we can throw those into the mix. And then there's a couple of specialist steps that could follow from that. So non-steroidal mineralocorticoid receptor antagonists and the GLP-1 (glucagon-like peptide-1) receptor agonists. So what that says is that there's quite a bit that we can do from a pharmacological perspective. And yeah, as you said, it does slow progression. And some estimates say that it could slow progression by 15 years or more. It can cut deterioration in kidney function by 50% or more. So very worthwhile to identify so we can get onto those things.

Yeah. So remembering that the emphasis is not merely to help protect the kidneys, but also really the fact that your kidneys are doing worse is usually a marker for cardiovascular disease. And in fact, people with chronic kidney disease are more likely to die from cardiovascular disease than they are to progress to kidney failure. So thanks for that. And that also reminds us about the every 2 year screening recommended in the book, which is if you do have established cardiovascular disease or a family history of kidney failure or obesity or in those who smoke or vape.

Let's move on now to kidney cysts because with the rise of ultrasound, things like fatty liver and kidney cysts and thyroid nodules, these are all things we're seeing more and more of, just partly because we're doing more and more ultrasounds on people. The majority of cysts in the kidney are simple cysts and they're usually benign and don't require any further investigation or follow up. They're just noted on the ultrasounds or the CTs. But talk to me about if they're not simple cysts, what do we do there?

So if you've done the imaging and it's noted on the report that it's not a simple cyst, then there is a different pathway to follow. Basically, there's a radiological classification that you proceed along. It's all outlined in the guidelines. There's a beautiful flow chart which looks at the assessment and referral of adults with kidney cysts. It's pretty much a case of just following down that flow chart. The thing that I wasn't as aware of that was striking to me when it comes to polycystic kidney disease is seeing that for autosomal dominant polycystic kidney disease, there's actually a treatment available called tolvaptan, which is actually disease-modifying. So it can slow down eGFR decline. So very worthwhile both identifying and then referring early depending on what you find.

Thank you, Lee. Let's move on to lower urinary tract symptoms, which not surprisingly is extensively covered in these guidelines, all the varied causes of these things, overactive bladder, stress incontinence, benign prostatic obstruction, nocturnal polyuria, and various other things. Let's look at a couple in particular, which I've found interesting. So benign prostatic obstruction, which terminology wise, I grew up knowing it as BPH, benign prostatic hypertrophy, but I guess it's the obstruction that really matters. So it's a symptomatic diagnosis. So talk us through that in terms of where we start with benign prostatic obstruction.

So usually we start with alpha blocker therapy. So the things that we'd be very familiar with probably is prazosin in that regard because it's on the PBS (Pharmaceutical Benefits Scheme), but there's another alpha blocker that's not on the PBS called tamsulosin, which is also available. So usually you start with that, you give that a go for about a month, and then you consider adding a 5-alpha-reductase inhibitor if there's a bunch of criteria that are met. So they're most effective if you're looking at a prostate volume that's greater than 30 cubic centimetres, PSA (Prostate-Specific Antigen) higher than 1.4, and you need to make sure that the patient's well-informed about the potential adverse side effects. So there you're looking at things like say Avodart or Proscar, dutasteride, finasteride.

Looking at the side effects one at a time, so back to the alpha blockers, the tamsulosin and prazosin, a drop in blood pressure is certainly common, particularly early on. Postural hypotension and older people and those with kidney impairment are at higher risk of those. Any other significant side effects you look out for besides dizziness and postural symptoms?

Well, there's potential additive side effects, of course, if you're adding on to other antihypertensives. A little tip that one of the group noted was that in Asian populations, tamsulosin might have a greater effect. Maybe that's just because of lower body mass index. To the extent that in Asian countries, they often have a lower dose available of tamsulosin. We get the 400 micrograms dose availability on our shelves. In Asia, they have a 200 micrograms variant as well.

The other thing that I found really interesting and which I hadn't heard of is with cataract surgery. So there can be a very unpleasant sounding condition called floppy iris syndrome that can occur during cataract surgery, particularly if you're on tamsulosin. There's a description of that which sounds pretty horrific, which is that if you're on tamsulosin, you get the potential intraoperative problems, a billowing of floppiness of the iris, and this is in the context of the eye usually being irrigated during a lot of the surgery.

You can get iris prolapse towards a surgical incision and a progressively constricting pupil during the surgery. All of this can persist for weeks or months, even after tamsulosin has been ceased. So super important for the ophthalmologist to know that that's part of a patient's history.

Yeah, interesting. If the man does have a higher volume prostate, you might end up adding, as you said, the 5-ARIs of reductase inhibitors, finasteride, dutasteride. The main side effects there are reduced libido, erectile dysfunction, reduced ejaculatory volume. So it's certainly worth discussing those with younger men in particular or those for whom sexual activity is particularly important. PSA monitoring always a controversial topic. Talk us briefly through that if you're starting someone on a finasteride or dutasteride.

Typically, you would expect around a 50% drop in PSA within 6 to 12 months. So that's the expectation, and then it should flat line and pretty much stabilise at that low point. So the thinking here then is that you've kind of knocked out background BPH noise as far as PSA goes. So any deviation from that expected drop, so if you don't get to your 50% drop in 6 to 12 months, and then you get to a flat line, but then it starts to rise, does raise concerns about whether have you got a prostate cancer that's starting to take off. So there are some recommendations in the guidelines about monitoring PSA levels whilst a patient's on 5-ARI treatment.

All right. We'll leave people to look up those if they are starting that treatment. Overactive bladder is the other lower urinary tract symptom I wanted to talk about. So overactive bladder is where you get urinary frequency and urgency, nocturia, and urge incontinence, which can occur with overactive bladder, or that can also occur sometimes without it. So it's essentially a clinical diagnosis based on the history, and then you follow up with urodynamic studies. Talk to us about overactive bladder Lee.

So if you look at in the context of it mostly being about instability or overactivity, the first line management tends to focus on rehabilitation. So strategies to try and retrain the bladder, improve your control, inhibit your detrusor contractions, and look at what your contributing factors are and modify them. So typically for a lot of patients, the bladder rehab by itself can improve the symptoms, and then hopefully you don't need to go onto any further interventions. But if you've got severe or you've got symptoms that are really bothering them, then a combination of bladder rehabilitation and drug therapy would generally be embarked upon.

So when it comes to drug therapy options, there's an option called the beta-3 agonists, so mirabegron. Some people would've come across that as Betmiga, and there's anticholinergic medications. So between the 2 of them, the Beta-3 agonists pretty much have similar efficacy where compared to the anticholinergic drugs. The typical starting dose of mirabegron is 50 mg daily. And so that's worthwhile knowing. Just be a little bit cautious there as far as potential for side effects, especially as far as blood pressure goes. You do want to make sure that the patient doesn't have severe or poorly controlled hypertension, a blood pressure over say 180/110 or above.

When it comes to anticholinergic drug therapy, generally speaking, probably want to avoid using regular anticholinergics in somebody that's over the age of 65, so probably preferable to push towards the beta3 agonists in that context. And also in the context of, say, menopause, for example, worthwhile having a think about considering intravaginal oestrogen in those patients who have got overactive bladder and vaginal atrophy. And so you can combine intravaginal oestrogen, for example, with the bladder rehab and the other drug therapies if it's needed.

Too many other sections to cover, one being management of long-term urinary catheters. If you have a patient with that, there's certainly great information in Therapeutic Guidelines. But I thought we'd finish now with wetting in children, and it is a very common thing we see in general practice, and it upsets families and kids, perhaps more than we realise. It can be a very socially significant symptom. Children over the age of 5 with ongoing wetting do need a proper assessment. Many of them do grow out of it, but after the age of 5, it's a bit hard to predict who will and who won't. Let's look at daytime wetting first, and we tend to start with non-drug management for daytime wetting.

Yeah, that's right. So it's educating families about bladder function, normalising voiding habits, looking at other potentially contributing factors like fluid intake and constipation. So many children improve with just those conservative measures alone. So that's worthwhile saying because for most children, when we start on this journey, medications aren't actually needed.

And so that's talking about bladder function, normalising voiding habits and looking at fluid intake and constipation, which I must say I find quite a lot as a contributing factor in general practice. If and when we do use medications, we have to select carefully those with them possibly in conjunction with the paediatrician if you feel the need. And that would be, again, anticholinergics, which I must say I've very rarely used in children or certainly very rarely commence them myself.

Yeah, I think there's a lot of hesitation and it's fair about using anticholinergics in children. I guess most of us have long heard messages about trying to avoid anticholinergics in the older adult population. Though apparently the evidence doesn't show the same sort of cognitive risks in children, so they are an option. I guess I would probably personally push towards having a specialist involved at that stage. Certainly there are, for example, oxybutynin patches available that a specialist could help initiate. There's also other options as well. So mirabegron is also potentially an option that might be initiated by a specialist. Having said that, it is private script and off-label.

Nighttime wetting in some ways I'm more familiar with treating and the bell and pad alarm I think is still a tried and true. It can actually cost a bit of money to hire, and often there's a nurse involved as well, but I think it's an excellent first line measure.

And if that doesn't work out, then desmopressin is still an option. One thing that was news to me was that intranasal desmopressin, even though it's still available and still listed as an indication as far as nighttime wetting goes, it's actually, it's not recommended when there are actually other options available. I think there's a wafer as well as a tablet. And that's because intranasal absorption of desmopressin is pretty unpredictable. And that means you might end up with higher doses than you're anticipating, which can in turn lead to hypernatremia, which if you're very unlucky, you could then end up with seizures. And so in some other jurisdictions, they've removed nighttime wetting as an indication of intranasal desmopressin. So something worth keeping in mind.

Interesting. I did not know that. And then I guess the bottom line with kids with ongoing daytime or nighttime wetting at some point you can refer. I tend to refer perhaps a bit early. Those who are very experienced in it might refer a bit later, but certainly there's other difficulties as well if they're having trouble voiding when they do micturate or have sleep apnoea or significant constipation, faecal incontinence, that sort of thing you would tend to refer to someone cleverer than yourself.

I would certainly do that.

Dr Lee Fong, it has been a pleasure as always to have you on the podcast. You seem to be on more expert groups than one could poke a stick at. I look forward to the next Therapeutic Guidelines update with you whenever that may be.

Looking forward to it as well. Thank you, Justin.

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My guests' views are their own and don't represent Australian Prescriber, and my views are certainly all mine.

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