The Rest is Kidneys

CKD Essentials: Your Top Questions Answered

• North West London Kidney Care • Season 1 • Episode 10

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The Rest is Kidneys podcast series is brought to you by Imperial College Healthcare NHS Trust and North West London Integrated Care Board (NWL NHS)

In this special Q&A episode, Prof Jeremy Levy, Dr Andrew Frankel, and specialist nurse Joana Teles tackle key CKD questions from primary care. They discuss CKD coding adjustments, NSAID safety, and the importance of optimising RAAS inhibitors and SGLT2 inhibitors. Practical guidance is given on prescribing, managing side effects, and using diuretics like furosemide effectively. 

The hosts emphasise that while lifestyle changes are crucial, medication remains key to slowing CKD progression and reducing cardiovascular risk.

Take-Home Messages:

CKD Coding – Adjust ACR coding as values improve; coding helps with safe prescribing.
NSAIDs & CKD – Generally avoid, but occasional short-term use may be safe in mild CKD.
RAASi & SGLT2 Inhibitors – Maximise doses; SGLT2 inhibitors are transformative for CKD and heart failure.
Managing Risks – Address side effects proactively but don’t let concerns block treatment.
Diuretics & Fluid Balance – Furosemide isn’t nephrotoxic; use it to relieve symptoms.
Hyperkalaemia – Potassium up to 6 mmol/L is usually safe; use binders before stopping RAASi.
Lifestyle & Medications – Diet and exercise help, but medication is often essential.

Effective CKD management balances accurate coding, lifestyle changes, and optimised medication use. While lifestyle adjustments help, RAAS and SGLT2 inhibitors are key to slowing progression and reducing cardiovascular risk. 

Primary care teams should confidently adjust treatment, manage side effects, and take a pragmatic approach to NSAIDs, diuretics, and hyperkalaemia. Proactive, evidence-based care ensures better long-term kidney health. 

The purpose of this podcast is to inform and educate health care professionals working in the primary care and community setting. The content is evidence based and consistent with NICE guidelines and North West Guidelines available at the time of publication.

The content of this podcast does not constitute medical advice and it is not intended to function as a substitute for a healthcare practitioner’s judgement.

Produced by award-winning media and marketing specialist Heather Pownall of Heather's Media Hub

The Rest is Kidneys makes kidney disease management easy.  The Rest is Kidneys is for primary care clinicians.  The Rest is Kidneys is NICE consistent, short and sweet. Welcome to the Restless Kidneys brought to you by the Northwest London NHS Kidney Care Team.

Jeremy: Hello, I'm Jeremy Levy. I'm a consultant nephrologist at Imperial College NHS Trust. 

Andrew: And I'm Andrew Frankel, a colleague of Jeremy, also a consultant nephrologist at Imperial College Healthcare NHS Trust. 

Joana: And I'm Joanna, kidney nurse, also at Imperial Hospital. This is very exciting. This is our 10th episode.

So firstly, I want to thank everyone that's been listening to the Rest is Kidney series and for the strong positive feedback. Over the past months, we've had a great deal of engagement with primary care and to celebrate this, we would like to reserve this 10th episode to answer some of the questions that so many of you have asked us.

We started this podcast at the end of last year, having had feedback that primary care colleagues wanted short, succinct advice about CKD, since this has become such an important issue in primary care, and you told us the podcast format would be ideal. So here we are. Then I persuaded my friends and colleagues, Andrew and Jeremy, to make this with me.

Jeremy: And yeah, we were persuaded and Joanna is very persuasive and Andrew, I should point out at this point, she's amazingly well organised and has been a brilliant leader of our merry gang. And we've been really excited and thrilled by the response. Today's January, mid-January 2025, and up to now, we've had 2,000 downloads of these podcasts, and in December alone, over 500 people listened, even with Christmas and New Year in the way.

Joanna really wanted us to reach the heady heights of Joe Rogan or Ricky Gervais, or even the rest is history. We're not quite there yet, but that's what we're aiming for. And, and we also should call out for our producer, Heather, who's been absolutely fantastic as well, are really happy with how these have gone.

And we really hope that you're finding them useful. And please do share them with your colleagues, your friends, your neighbours, and your dogs.  

Joana: Quite. So, Andrew and Jeremy, we should do the work. I'll be asking you both some questions that we've collected over the last few weeks from Primary Care colleagues, hoping you can give us practical tips and feel free to agree or disagree.

You don't have to agree on everything. 

Jeremy: So, that's great. It's so good to be talking to you again. I will try very hard to disagree with Andrew. It is difficult because we generally say similar things, but I'm going to try and make him irritated today. 

Joana: So, here's our first question. We have been promoting CKD, so chronic kidney disease coding using urine albumin creatinine, so ACR codes as well as eGFR.

You'll all remember that the A code, A1 is if the urine ACR is less than 3 mg/mmol, A2 if the ACR is between 3-30, and A3 code if the urine ACR is greater than 30. So the question. If the urine ACR improves, for example, let's say 50 to 20, should the A code be changed from the A3 to A2?

Yes or no and why? 

Andrew: So, Joanna, the answer to that is yes, the code should be adjusted to reflect the patient's current condition. The proteinuria is lower, that is the ACR is lower, and that is better. This reflects the fact that the disease has improved, probably with the optimisation that's been undertaken.

And sometimes we can reduce the ACR quite significantly with treatment, and occasionally it can completely regress with the best treatments. And this, of course, has significant benefits for patients, including reduced risk of cardiovascular events and reduced risk of CKD itself progressing. So it's good for everyone, and it's important to reflect this properly in the coding.

Jeremy: So on this point, I can't disagree with Andrew at all. As you say, Joanna, this is an improvement in the urine proteinuria, and that's going to either reflect optimisation or better treatment or lifestyle changes such as weight loss. And it should be, and could be, encouraging for patients to see this improvement, you know, their kidneys are a bit better and that gives them better long term outcomes and less worse outcomes.

They're less likely to die early, have heart attacks and strokes or, (patients worry about this), ending up on dialysis, even if it's not the most important thing from our perspective. So yes, recode, but it's clearly not an emergency and doesn't need to be done at midnight. 

Joana: Now, it's great to start with the consensus, but let's move on slightly.

What about the very elderly or frail? Whilst we promote CKD coding to all, do we also need to be pragmatic and would we want to, for example, code, an 80 year old with significant frailty. 

Jeremy: So you're  absolutely right, Joanna. The addition of codes in a frail 80 year old, in my opinion, is not going to add huge amounts.

So an 80 year old with CKD stage 2, for example, or even 3A, let's say a GFR of 50 with no albuminuria, who's severely frail and may be housebound, is going to add absolutely nothing to their medical management. Because actually, A GFR of 50 might be completely normal for an 80 year old because kidneys definitely age.

So adding codes in that case may not be adding much value at all and certainly isn't going to be directing any treatments. 

Andrew: While I agree with a fair amount of what Jeremy has just said, there is an element that I do disagree with, and would want to always encourage primary care to code. You are absolutely right that it may not influence initial therapy or management. But there are other attributes to coding that are important in primary care because it labels a patient and it provides primary care with helpful reminders that may have relevance to safety.

For instance, ensuring that they recall the CKD level when making drug adjustments in medication reviews, avoiding non steroidals, and being careful with some painkillers, for example. So I agree, coding isn't everything. But it can still help practice, even in frail and elderly patients. 

Jeremy: So of course that's right, and I was really trying to deliberately rile Andrew a little bit, um, but this is the difference, isn't it?

The code is really helpful for thinking about other aspects of a person's care, even if a frail eighty year old doesn't necessarily need the addition of multiple new drugs to protect their kidneys, but it is an incredibly useful guide to making sure we're doing nothing else that causes harm. Yes, I agree with that, Andrew, of course I do.

Joana: In summary, CKD coding should reflect improvements and can be changed over time as EGFR or urine ACR changes. And even if the CKD code itself doesn't change medical treatment, it can be an important help with medication reviews and plans for ongoing management. This actually brings us nicely to our next question.

Non steroidal anti inflammatory drugs are widely used for analgesia, not just for chronic pain, but also for acute pain, like menstrual pain, gout, tooth pain. So in people with CKD, are we definitely saying no to NSAIDs? 

Andrew: Joanna, there's always nuance, but I always start with the view that people who have CKD should avoid the use of non steroidal anti inflammatory drugs.

And that includes high strength topical non steroidal anti inflammatory drugs. Jeremy?

Jeremy: Yeah, this time I'm going to disagree with you a little bit, Andrew. Clearly just a little bit. And I quite enjoy that aspect of our conversations. So in my opinion, especially and essentially only in people with very mild early chronic kidney disease, such as of CKD 3A without proteinuria, and let's say a GFR of 52 ml/min.

If you needed two or three days of ibuprofen for a sprained ankle, period pain, or an episode of toothache, this is not going to cause significant harm. Similarly, even if somebody had slightly worse kidneys, let's say a eGFR of 30, and they've got bad arthritis. And they're already using paracetamol, and they say the only thing that allows them to go out and do their shopping is to take two doses of ibuprofen, and they do that once a week to go out shopping, then I think that would be perfectly acceptable.

Because what you need to remember is that where non steroidals cause harm in CKDs, almost always in the setting of another illness. So people who get volume depleted or dehydrated or febrile and then take a non steroidal in the setting of chronic kidney disease, then that combination of hits is very bad for the kidney.

Simply some long term chronic use of non steroidals, but often because people are also taking angiotensin blockade and then intercurrent illnesses occur. But two or three days of a standard dose of ibuprofen in early chronic kidney disease is very unlikely to be harmful. However, exactly as Andrew says, the nuance is important, so that in a short conversation with a patient, it is going to be much easier to say "These are drugs to avoid if at all possible", but if the patient then does want to say, "Surely doctor, can I take them just once a week if I'm going out shopping?"

Then you can have that conversation. That would be my view. 

Andrew: So Jeremy, we're definitely not going to fall out over this, despite your wish for us to have a debate and duel. And I just think it helped. It also reflects the answer to the first question about just being aware that the patient has CKD so that you can be vigilant about the use of nonsteroidals and, for instance, always consider the possibility that the patient is using this over the counter when they've had an unexpected drop in GFR, for instance.

Yes, be pragmatic. A general rule is to avoid. And what I always tell patients is try to avoid these drugs, please don't call an ambulance or go to A&E if you take one.

Joana: Thank you both. Now, let's move on slightly. When we talk about CKD treatment optimisation, the main groups of drugs that we are referring to are Converting Enzyme Inhibitors and, so ACE inhibitors, and Angiotensin Receptor Blockers as well, and SGLT2 inhibitors. Despite ACE and ARBs being around for decades, there is still a level of insecurity when prescribing it in chronic kidney disease.

We've had multiple questions, particularly on Ramipril, as the BNF states that it shouldn't be increased above 5 mg a day if the EGFR is lower than 30ml per minute. Now, in our guidelines, for maximal rapid RAASi dosing. And this would include Ramipril 10 mg for all levels of EGFR. Should people be switched to a different agent?

And should the dose be reduced if the EGFR falls down to 20? The BNF states it shouldn't be increased above the dose of 5 mg per day if the EGFR is lower than 30. Our guidelines, on the contrary, advise maximal rapid RAASi dosing, and this would include 10 milligrams for all levels of EGFR. So should people be switched to a different agent, and should the dose be reduced if the EGFR falls down to 20, for example? Jeremy?

Jeremy:  So the quick answer to those two questions, should you switch or should you reduce the dose, in my view, is no. And no, so no, don't change the formulation, the nature of the ACE inhibitor or the angiotensin blocker that the patient is on as GFR falls. All of these drugs we think are effective in protecting from cardiovascular events and progressive kidney disease, in chronic kidney disease, and no one agent seems to be better than any other. And the difficulty for the patient, the confusion to don't change the formulation of ACE or ARBs.

Maximum dose and dosing is a different issue, and the challenge here is that we're not using these drugs to lower blood pressure, we're using them to protect the kidneys, and we know that being on maximum doses has extra benefits over and above blood pressure lowering. And this is true at all levels of GFR. So people should remain on the maximum doses. And reducing Ramipril from 10 to 5 may therefore have less effect on ongoing progressive kidney dysfunction. So we would recommend staying on maximum doses, unless of course patients have problems with hyperkalaemia, high blood potassium, or low blood pressure.

So it's titrating the drugs really against the patient and any effects and trying to keep them on the maximum dose, which will provide maximum kidney benefit. 

Andrew: So Jeremy, on this we agree, and I think the key points that have come out of this are that RAASi, that is the ACE inhibitors or the angiotensin 2 blockers, provide additional benefits to people with CKD over and above their blood pressure effects.

Those benefits are seen at maximal level when the dose is at maximal level and we should be aiming to give people that benefit as speedily as possible. So not titrating over years, but titrating up to maximal dose over weeks. And the regime that's recommended is delineated in the Northwest London CKD guidelines. And that is to, if the patient is robust, because of course, if they are frail, you need to do it more cautiously. But if they're robust, give them five milligrams, check their kidney function and potassium after two to three weeks and if all is okay and the blood pressure is okay get them up to 10 milligrams of Ramipril, or the equivalent in any other ACE or ARBs.

And we do not stop RASi as GFR falls and we remind people while they are on these treatments, always to use good sick day guidance to temporarily omit the RASi if they are acutely unwell, but then resume this once they have recovered. 

Joana: Brilliant. Now, still in this topic, NICE only recommends RAASi therapy, so again, ACE inhibitors or ARBs, if the ACR is greater than 30.

And of course, our local guidelines are consistent with this, but is there any context that you would initiate this sooner? Our guidance only recommends this if the ACR is greater than 30 in the absence of diabetes, but in this context, are there any patients that you would consider initiating this sooner with a lower ACR?

Jeremy: So again, very common question, as you say, Joana. So the absolute benefit of the RAASi group of drugs in protecting kidneys, is actually only evident in people with Proteinuria. If you don't have proteinuria, then lowering blood pressure seems to be very important. We know that. But the class of drug that you use does not seem to matter.

And proteinuria as a marker essentially of glomerular damage or glomerular hyperfiltration is where the angiotensin blocking drugs are most beneficial. But having said that, these drugs are incredibly well tolerated, very rarely cause side effects, and so they're often used first line for the treatment of hypertension, aren't they? And most hypertension guidelines have RASi as first line choice. The  benefits for kidneys are minimal in the absence of proteinuria, but they are often used. And it is crucial to treat blood pressure properly and to treat it aggressively in anybody with CKD, and these drugs are very effective.

Andrew: Slightly beyond the question. There is another thing to consider in people without diabetes, without hypertension, and who do not have proteinuria, and therefore in whom RAASi are not indicated. They may still have an indication for an SGLT2 inhibitor, such as Empagliflozin. And we describe this in our guidelines, particularly if the GFR is between 20 and 45.

And in that situation, you should be able to still consider Initiating SGLT2 inhibitors in these patients, even if they are not on RAASi, as this still shows that drugs have benefit both for progression of CKD and reducing cardiovascular events. Although, of course, the vast majority of the patients that are seen in primary care will require both RASi and SGLT2 inhibitors.

Jeremy: So that point, Andrew, that's relatively new, isn't it? That's the use particularly of Empagliflozin, but SGLT2 inhibitors in people with really moderately advanced CKD and no proteinuria that these drugs have benefit for cardiovascular and renal protection. But that's all been come out really in the last less than a year almost, isn't it?

Andrew: Correct, Jeremy. Absolutely. 

Joana: So this is really helpful. So RAASi therapy should be optimised to maximal dose independent of the EGFR. When we talking about earlier CKD management, so in the absence of albuminuria, then aggressive hypertension management is really key to treat these patients. Andrew, you started talking about SGLT2 and so did Jeremy, which is another hot topic.

But before we just go into that, I'd like to take us back to diagnosis. If we have a 40 year old patient, let's say with EGFR greater than 90, so absolutely preserved function and the urinary ACR that is mildly positive, around 15, has been repeated and consistently between 10 and 20. So CKD stage G1 A2 without diabetes.

What would be our expectation for our primary care colleagues to do, coding and monitoring yearly or something else? 

Andrew: So we have actually considered diagnosis in one of our other podcasts. This is not a completely rare situation. It is still important, I'll remind people of some of the general principles for primary care to do a urine dip, to look for any blood.

As if there is blood with this small amount of protein, it does mean that the patient may require referral to a kidney clinic, even with normal GFR. If there is no blood, but just this low level of protein with an ACR of around 15, then it is unlikely that more than just kidney health monitoring will be required.

Jeremy, would you like to elaborate on that? 

Jeremy: Yeah, and I agree with what you said. So that dipstick's important to make sure there isn't blood and protein in the urine. But then if we're left with this person who does not have diabetes, has got a normal GFR, but this low level albuminuria, proteinuria, and ACR of say 15, we're almost never going to undertake a kidney biopsy, which in the end might be the only definitive way to make a proper diagnosis.

But there are some other things to be very careful about. I would certainly be asking questions about a family history of kidney failure, because if there's a family history and then you've got somebody who's younger with proteinuria, that's really important to know about and there might be further tests we would do.

I'll be asking them to make sure there are no features of systemic disease that might be leading to kidney involvement, such as lupus, and clearly in the general population this is uncommon, but there are groups of people, younger women for example, where this may be more relevant. You should certainly be checking the blood pressure in anybody with proteinuria because that would need treating and would be a very important indication, and then you certainly should review.

So in this person with normal GFR, low level proteinuria, and no other features. I'd be wanting them reviewed in six months time. And if nothing's changed, then yes, an annual check of the urine ACR, the blood pressure, and the blood for an EGFR may be absolutely fine and continue to be done, in primary care.

But if there were any other features from that brief history or from that exam, then a referral may well be indicated. And you can then give the person advice about maintaining their kidney health. The advice we talked about for lifestyle, for diet, for exercise and reinforcing that annual check. Kidney disease is silent. So if you've got this early proteinuria, having it checked once a year is going to be very important to make sure nothing is changing over time. 

Joana: Excellent. So we really are exploring the land of early CKD detection and optimisation, so CKD coding G1 and G2. And in this context, then a yearly kidney health check would be mostly appropriate.

Let's not forget treatment optimisation when appropriate, including aggressive blood pressure management if needed. However, when there is uncertainty of the cause or particularly when we have other red flags such as blood in the urine, then a nephrology referral may be important to consider. Now, let's move on to the hot topic, SGLT2 inhibitors, also known as glyphosates.

These drugs were developed initially for diabetes, but rapidly expanded into treating CKD and heart failure. So they significantly reduced mortality, they reduced the risk of heart failure hospitalisations. as well as reducing the rate of CKD decline and the risk of kidney failure. So they have an intrarenal effect.

Would you say this has been the major landmark in CKD management in your careers? 

Andrew: Maybe in my career, perhaps no, as I go back many years, but certainly in the 21st century, yes. We have a huge evidence base now for these drugs with multiple trials across a range of levels of CKD that have shown significant benefits in relation to reduction in adverse outcomes for people with or without diabetes.

Furthermore, these are remarkably well tolerated drugs with very few overall side effects. It does remain important to give individuals on an SGLT2 inhibitor good sick day guidance and to be warned about the small risk of urine infection and genital fungal infection. And they should not be used In people with type 1 diabetes, or any patient prone to ketosis, but the vast majority of people with type 2 diabetes, or those with CKD and no diabetes, can, and should, be offered them.

Jeremy: So Andrew clearly wants to add them to the drinking water, to Greg's sandwiches, to Marks and Spencer's prawn cocktails, and I agree with him essentially. These have been fantastic drugs. He also implied that he's really ancient, and I know you can't see him on the podcast, but Andrew really isn't that old.

But these have been fantastic drugs, and this range of indications has widened and widened with really high quality trials, lower levels of GFR, and this presence of kidney disease even without proteinuria. Yeah, we're not going to disagree on this either, Joana. 

Joana: So we all recognise how life changing these drugs are, but we actually need to support our colleagues to safely prescribe them.

So let's unpick some of the side effects that you already started to mention. Andrew, diabetic ketoacidosis. Could it happen? in people without diabetes. 

Andrew: So just to help the audience understand why we get this disorder, SGLT2 inhibitors have an effect on the liver that increases ketone production. It's analogous to making the body believe it is in a starved state.

So you are having an increased level of ketones in the body, you have ketosis if you're on SGLT2 inhibitor. The problem comes if you then have a second stimulating factor, and that could include a person going on to a ketogenic diet, for instance. Or a person with diabetes who's on insulin, where there is a dramatic reduction in insulin, or indeed if the insulin is stopped. Or, if the person then develops an infection or dehydration. So as long as you are careful in your choice of patients. Avoiding people with type 1 diabetes or type 2 diabetes with low insulin secretion phenotype. Give them good sick day guidance and advice to avoid ketogenic diets. The risk of ketoacidosis caused by these drugs is rare in people with diabetes and vanishingly rare in the absence of diabetes.

Joana: Andrew, tell us about hypoglycaemia. We know the way these drugs work is by increasing glucose excretion in the urine. So, is there a risk of hypoglycaemia? How do we minimise this risk in people without type 2 diabetes? 

Andrew: So, Joanna, SGLT2 inhibitors on their own should not cause hypoglycaemia. However, if they are used in conjunction with insulin or sulfonylurea, they can aggravate the tendency that these drugs have to cause hypoglycaemia.

But, this will really only occur if the GFR is preserved. And this is an important point that the glycaemic effect of SGLT2 inhibitors, wanes as the GFR declines and reduces significantly by the time the GFR is below 45, and completely disappears at a GFR of 30. That glycaemic benefit is quite different from the cardiorenal benefits of these drugs that persist down to very low GFRs.

Therefore, if you are starting an SGLT2 inhibitor in a person with diabetes on insulin or sulfonylurea, you only need to make adjustments to the insulin or sulfonylurea in people who have preserved GFR, above 45, and who have HbA1c's that are already well controlled, i.e. less than 58. And in this situation, we recommend a 20 percent reduction in insulin, but never stopping the insulin. And if they're on Sulfonylurea, a 50 percent reduction in those drugs. 

Joana: That's reassuring. So there is a risk of hypoglycaemia, but this is really only in people with other glucose lowering drugs. So only in diabetes and even in diabetes, only when we have relatively preserved function, particularly EGFR greater than 45. So that's reassuring.

So Jeremy, Another hot topic is UTIs and genital thrush. So do we stop SGLT2s after a single UTI episode or after genital thrush? 

Jeremy: No. Clearly for the patients, it's disturbing and uncomfortable and needs to be treated. But after a single episode, a urinary infection or episode of thrush, you should of course pause the gliflozin for a few days so that the urine doesn't become sugary, and that will help you treat the infection. But then you should try and restart the gliflozin.

Clearly if somebody is getting recurrent or second episodes, then they can't tolerate these medicines and they should stop them because you can't have people having recurrent episodes of perineal fungal infections or urinary infections. But actually recurrent episodes are very uncommon.

So after a first episode, no, pause the drug and then re challenge. But recurrent episodes, yes. 

Joana: That's very clear. Andrew, following up on this, let's talk about the risk of forniers gangrene. Our primary care colleagues gave us feedback on multiple occasions that the requirement to tell people about the risk of this condition in writing becomes a blocker for SGLT2 initiation in primary care.

Have you ever seen this condition and what would be your recommendations to our colleagues? 

Andrew: This is really unfortunate, and actually I believe not appropriate, but understand primary care have to currently deal with this according to CQC requirements. Fourniers gangrene is a polymicrobial, rapidly progressive disorder that has a very adverse outcome.

It's a very dangerous disorder. I have seen this, but not in the context of SGLT2 inhibitors. There is no real evidence at all that SGLT2 inhibitors increase the incidence of Fourniers gangrene. The issue is that people who get Fourniers gangrene are people who have poor diabetes control and poor genital hygiene. It's that combination that causes the risk. And SGLT2 inhibitors do not, there's no evidence that they will increase that risk.

What I always do is to tell people to differentiate between genital infections, which is thrush and itchiness, which requires non urgent treatment, to a situation where they feel pain or tenderness or see redness in their groin or genital area, and particularly if they develop fever.

This situation requires more urgent attention and attendance in A&E. It is exceedingly unusual, and thrush is much more common and simple thrush is not painful, not red and not tender.

Joana: Jeremy, what about hyperkalaemia? Is this a common side effect? Since people are peeing out sugar in essence, this will increase the water secretion. So how worried do we need to be about this? 

Jeremy: So no, this isn't really a significant issue either. When people start these medicines, I do warn them that they will notice increased urine output for a couple of weeks.

Many patients actually say they don't notice this, but it resolves usually within two to three weeks of starting the medicines. And so clearly during this time, it is important that they don't get dehydrated and they keep drinking, but people don't need to increase their fluid intake or change what they're doing.

And I've not actually ever seen it causing a problem. But again, Partly why it's important to remind people about sick day guidance with all of these medicines, inhibitors, ACE inhibitors and blockers, and that if they get fever, diarrhoea, vomiting, then they need to pause the drugs for a few days. So no, not a major issue.

Andrew: The other issue to add to this is that we know these drugs, SGLT2 inhibitors, are also effective treatments for CKD and heart failure, and fluid overload can be a complication in both these conditions. That means that this extra diuresis effect can actually be beneficial in some cases in helping to relieve fluid overload.

Joana: That's actually very good. It's not a massive problem but even when it happens in a lot of cases would actually be beneficial to help relieve fluid overload in some of the patients, particularly those with CKD and heart failure. And since we start touching on diuresis, we can't close this episode without touching on Furosemide.

We had multiple questions around this. Furosemide increases creatinine and reduces EGFR. And because of that, it can be quite challenging for clinicians in primary care and hospitals as well, to be fair, who get worried about Furosemide being nephrotoxic or causing kidney failure.

This is a very common question. Also from our Heart Failures team, so should we avoid Furosemide in CKD? Should the dose be reduced? Should we stop it? Can we increase the dose if people have worsening peripheral pulmonary edema? 

Jeremy: So Joana, you said we're ending, but you've just given me four questions in one sentence, so that's very unfair.

But the bottom line is that using diuretics is for symptomatic relief, and they can be very helpful, and they don't need to be stopped. They're not nephrotoxic in CKD. Of course, there are times when Furosemide can be nephrotoxic, but actually this is a rare problem, as with lots of drugs, where it might cause interstitial nephritis. But that's not common.

What most healthcare professionals are describing is that the creatinine goes up a bit, the GFR falls as you diuresis somebody. And that's predictable. You're making somebody slightly volume depleted and that will cause the creatinine to go up, but that's not a problem in itself. It's not nephrotoxicity. And what you're treating is volume or fluid overload, and that can be very helpful for patients. If people have got badly swollen legs or pulmonary edema. They need to get rid of salt and water and using Furosemide is helpful. So the drugs don't need to be stopped. They're not nephrotoxic. You just need to be using them carefully. And in heart failure, especially, we know that the creatinine will go up and the GFR will fall often in combination with aces And we're happy to accept falls of GFR in this setting of heart failure of often up to 25%, because patients are feeling better.

Now these drugs are not protective long term. They're not reducing mortality, but they are making people feel much better. And often we do use really quite high doses in people with advanced chronic kidney disease. And again, that's not harmful, but they are being used for symptom control predominantly. 

Andrew: I would also add here that particularly in people with heart failure and CKD, we are not aiming for them to have slim or ballerina's ankles and we might need to accept a small amount of Ankle edema, is a situation that patients have, where the ideal balance lies.

The key symptom that needs to be considered is the breathlessness and the quality of life, that's what you need to use the Furosemide to manage and not necessarily to completely clear the patient of peripheral edema. 

Joana: So diuresis can and should be done particularly when patients are symptomatic, knowing that we, the main thing is monitoring and we shouldn't over diurese, and ensure the patient doesn't get too dry. So that's really helpful. We're almost at the end, but there, there is a common question from pharmacists. What do they do when patients have a serum potassium levels around 5. 5 to 5. 8 after treatment optimisation that has been reshaped, has not worsened, but has not improved below 5. 5? Is this acceptable?

This takes us back to our most viewed episode on hyperkalemia, 'Bananas are not a problem'. Jeremy, do you mind reminding our listeners of the potassium thresholds first? 

Jeremy: Uh, yeah, of course, Joana, but listeners should go and listen to that whole episode, shouldn't they? But yes, so the bottom line is that actually we're comfortable with patients having serum potassiums in the setting of CKD, of up to 6 millimoles per litre. We are worried if the potassium is more than 6. 5 millimoles per litre, which definitely needs urgent action, and that may be via an emergency department. Between 6 and 6. 5 certainly needs rechecking, but that can be within 24 hours and is not a middle of the night emergency. And up to 6, does need a review and a check, to make sure the patient's not doing other funny things, not having an extreme diet, but is not an emergency. Potassium's a 5. 5 to 5. 8 while people are taking RASi drugs are really quite common and are acceptable in the setting of chronic kidney disease. 

Joana: And, Andrew, what about if the potassium is 5.8? Should RASi therapy be reduced, so the ACE inhibitors or ARB? 

Andrew: Jeremy has succinctly already described the fantastic detail he's given in our hyperkalemia podcast and I agree with him. If the potassium is 5. 8 and stable, it is reasonable to continue the RASi. However, you might need to think about other contributing factors to high potassium and just check them as Jeremy has described.

And remember that the addition of a potassium binder such as Lokelma or Veltasa will allow the safer continuation of RASi in the longer term and allow the patients to achieve all of its benefits of RASi. 

Joana: So in summary it is safe, and the priority is let's continue the maximum dose of RASi therapy and of course we can always introduce potassium binders if the limit is slightly at the upper threshold.

So thank you both. I now have a last final question and this is actually the final one. Perhaps a more challenging one. We have covered most questions around coding, but most of it has been about pharmacological interventions. But we actually know that the foundation of CKD management relies on healthy lifestyle as it does the management of most long term conditions.

So if a patient is newly diagnosed with chronic kidney disease, completely averse to taking medication and willing to change their lifestyle first, what would be your approach? Is it possible to manage CKD with lifestyle alone? Yes or no? 

Andrew: Um, my answer to that is no. Now I need to be really clear that the lifestyle intervention and management is really important in people with chronic kidney disease and particularly in relation to prevention of cardiovascular disease. But, if we are trying to preserve GFR and avoid the need for renal replacement therapy in a person's lifetime, and of course this is even more important as the person is younger at diagnosis, we mustn't fool ourselves because it is really extremely likely that this can only be achieved with the addition of medications such as ACE inhibitors, ARBs, blood pressure control, and SGLT2 inhibitors.

Jeremy: So I really want to be argumentative given we're about to finish Joanna and say yes, you could control CKD only with lifestyle changes, but that's clearly not going to be correct. But engaging patients is really important. So this conversation may well start out by absolutely supporting the patient in trying to make the really important lifestyle changes that will make a difference before you start to talk to them about medications.

So we can engage them and activate them, make sure they think about their lifestyle, their diet, their salt intake, their protein intake, their lack of exercise, the fact that they're overweight, because significant weight loss, undertaking exercise, changing your diet can reverse diabetes in the early stages and can improve GFR and reduce proteinuria.

So in somebody who doesn't have severe problems, has early chronic kidney disease, these are going to be really important benefits and encouraging the patients around that. We're all seeing people drinking litres of fizzy carbonated drinks with terrible diets who weigh a hundred kilograms, and tackling all of that will make a significant difference.

So this is absolutely a critical first approach. And for some people may on its own have major benefits. But most people are going to need additional factors, but certainly that's how we should start. 

Joana: Fantastic. Thank you both so much for joining me here today and answering all these questions from our Primary Care colleagues.

I hope this podcast and all our previous ones have been useful and do share them with all of your colleagues as Jeremy alluded when we started. I hope you like this and please review our podcast. Thank you both so much for joining me today and in answering all these questions that our primary care colleagues have asked us. And if you like this, of course, do review the podcast so more people can find it. 

Jeremy: Thanks, Joanna. And Andrew, it's been a pleasure as always chatting with you.

I think we should do another 10 or 20 podcasts about chronic kidney disease. It's clearly the most important healthcare topic there is at the moment. 

Andrew: Jeremy, we'll finish definitely by agreeing. Um, absolutely. I've really enjoyed this. There's a lot more still to talk about and I'd be delighted to do that.

But thank you so much for inviting me on this podcast.