Cardiorenal Metabolic Disease (15 Dec 2025)

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Dr Marilena Giannoudi (MG): Hello everyone, and welcome to another episode of Clinical Conversations, brought to you by the Royal College of Physicians of Edinburgh Trainee and Members Committee. My name is Doctor Marilena Giannoudi and I am the co-chair of the T&MC. And today I'm delighted to be joined by Doctor Andrew Frankel. We will be discussing the Cardiorenal Metabolic Syndrome, a beginner's Guide. Doctor Andrew Frankel is a consultant nephrologist at Imperial College. Over the last ten years, his passion has been working towards improving chronic kidney disease prevention and integrating with Cardiorenal metabolic management across his local network and London as a whole. So good morning and thank you so much for joining me.

Dr Andrew Frankel (AF): It's a real pleasure to be here. Marilena. Thank you for inviting me.

MG: I think the best place for us to start. For all our listeners, is to kind of quickly provide an overview of what chronic kidney disease is and why it's so important.

AF: So, the definition is very technical and very simple. It is an abnormality of kidney structure or function that is present for more than three months. By structure that could be ultrasound, by function it could be GFR. But evidence of damage could be identified by albuminuria or red blood cells in the urine. So, it's an abnormality of kidney function or structure, evidence of damage that last more than three months. Why it's important is the implications it carries for that individual patient. As your kidney function deteriorates, and particularly as protein leak increases, those individuals are at a dramatically increased risk of cardiovascular events. And by that, I mean all cardiovascular events, progression of chronic kidney disease and requiring end stage kidney failure treatment, and also of acute kidney injury. So as the implications that are much more important than the actual number, i.e. the GFR.

MG: And I think I speak on behalf of all doctors in training when we're clerking in patients, and we're looking frantically looking through GP records to see their past medical history. I think over half the people that I clock in will have CKD stage three and above, but it's very rare that you have the time to stop and think, well, why is that? So, what are the most common causes for chronic kidney disease?

AF: So of course, as a nephrologist and all your nephrology colleagues have been trained in specialist nephrology and we love to identify and manage and treat people who've got glomerulonephritis, inherited kidney diseases such as polycystic kidney disease. But the reality is that the most common cause of chronic kidney disease in the UK is actually kidney disease, in the context of diabetes and cardiovascular disease. And we used to talk about diabetic nephropathy. We used to talk about Cardiorenal syndrome. Renal artery stenosis. But we now recognize that this is essentially a single disorder cardiorenal metabolic disease. And it has slightly different phenotypes. But it is a common pathogenesis that's driving the cardiovascular disease and progression of kidney disease. And that's why you are seeing so many patients with kidney disease. And that's why the nephrology trainees, and if you go around the nephrology ward, are essentially seeing very large numbers of patients who essentially have cardiac disease. We are all looking after the same cohort of patients.

MG: And how should we be approaching managing these patients? Obviously, we need to be working in teams, and we need to be taking from each other's expertise. But what should our basic approach be? And certainly, as more junior trainees, if I can say that what should we be prioritising when we first come into contact with these patients?

AF: So, to some extent we say the same to primary care. You need to always look, and you describe the fact that you don't have the time to actually think about what's causing the CKD. But actually, a very quick sense check that this isn't acute kidney injury, that the patient has got a long history of diabetes or cardiovascular disease. And it's been long standing and considering whether or not a urinalysis shows blood as well as protein would be a good starting point to simply think I'm calling this cardiorenal metabolic. But could I be missing something more serious? So that's the first starting point. Once, if you identify something that's a concern rapidly changing kidney function, blood and protein, or a history that doesn't fit, that's when to ask your nephrological colleagues for help. But most patients will have cardiorenal metabolic disease. And the really good thing that's occurred in the last twenty years or fifteen years is that the management of the cardiac and the renal and the metabolic elements of cardiorenal metabolic disease are aligned. And you need to become expert in treating someone with cardiorenal metabolic disease and treating them from their renal as well as their cardiac perspective.

MG: I think the next best question to go into is how do we treat these patients. But before we do that, I just want to take a step back. You mentioned, obviously, that we need to be considering the diabetic underlay of these patients and the chronicity of this, but I guess my question is what is more important? Is it the duration of a diagnosis of either metabolic syndrome or diabetes, or is it the extent of poor control?

AF: A really good question. And of course, poor control is known to have a worse outcome in terms of development of both cardiac and renal complications of diabetes. That poor control, though, is particularly in the first ten years after development. I say development, not diagnosis of diabetes. Once you've actually got cardiorenal metabolic disease, i.e. you've got a GFR of fifty-eight on the context of diabetes, or you have heart failure actually getting your hba1 C down from seventy seven to fifty five may be a good thing for some things. It's not going to slow down progression of cardiorenal metabolic disease. So, control is important in the first ten years. But duration will tell you a lot more about what's going on in terms of the underlying cardiorenal diagnosis.

MG: Thank you. I think that's really important to clarify. So, I will then go back to where we should have been before my little interlude. And that's to discuss treatment. You mentioned before that the treatment of cardiac and renal disease are very well aligned. So how should we be treating these patients? How can we really affect change for these patients?

AF: The tendency here is to jump into the pharmacotherapy. But I really can't do that without saying, first of all that unless you deal with lifestyle, unless you deal with patient education Activation and engagement. Unless you have the patient really understanding what's going on, nothing else will work. So, lifestyle and engagement are the fundamental principles for treatment of cardiorenal metabolic disease. And everyone who's training in cardiology and nephrology really needs to think, well, how do I upskill myself in relation to personalized care, health coaching and consultation skills? Because without that, you may think you're going to do a lot of good, but you won't achieve it. Then you do come to the pharmacotherapy, and we each now have we are both on an equal par and four pillars. I'm not going to say anything about the heart failure four pillars because I'm sure your listeners will know all about that. But what are the four pillars now that we have for kidney disease? Again, I think you'll recognize the commonality One. Ace inhibition. And by that, I mean maximal Ras inhibition. Getting them up to ramipril ten, losartan one hundred, and so forth, and maintaining that. Two SGLT2 inhibitors, anyone that you have to go with what the license and the nice indication is. Three this isn't really a pillar. Get the blood pressure right, and you need to do that after the other two, because blood pressure drops when you start the Ras and the SGLT2. I'm getting the blood pressure right to one hundred and ten to one hundred and thirty. In the majority of patients, particularly if they've got diabetes or proteinuria. Thinking about frailty, thinking about diabetes and potentially postural hypertension. Four if there's residual risk, i.e. you've got them on an Ace inhibitor and an SGLT2 and they still have Albuminuria the GFR is below sixty and they've got diabetes. Add in finerenone the new MRA and what will be coming out soon. In similar patients will be the addition of semaglutide. And I've got a feeling the GLP ones may become part of your armamentarium in the future as well. So those are our pillars. And whether you're a trainee in diabetes and cardiology or in nephrology, you need to feel confident and competent about prescribing those agents. If you'll forgive me for going on with one other point. The bit we have to learn from you is how we introduce those medicines. And we know in heart failure, the strong heart failure study and all the subsequent data that co-prescription and Co initiation is really actually quite important. And although we are building up a very layered approach in CKD, my prediction is that we are going to go for much more Co initiation in the coming years.

MG: I think that's what a lot of Europe is doing. But they have more combined pill therapy, which I think helps with that.

AF: Yes. Well, the UK has traditionally been very averse to combination therapies, and I hope I won't offend anyone who's doing clinical pharmacology as a specialty and listening in to this. But it was the clinical pharmacologist in the nineteen seventies and 80s who stalked Britain, adopting a lot of combination therapies. But they have fabulous combination therapies outside Europe and in the world. And actually, we will start to need those combination treatments.

MG: Yeah, if it's okay with you, I think it would be very useful for us to just discuss some of these medications in a little bit more detail, because I will speak for myself. I'm terrified of kidney disease, and I'd like to think I'm not the only one. And we have lots of listeners that are actually quite scared of the kidneys. And I think one of the biggest concerns that we. I speak on behalf of everyone here that trainees could possibly have is, yes, okay. We know to prescribe these medications, especially Ace inhibitors and so on. But what do we do when the kidney function isn't optimal? And at what point do we need to be scared? And at what point do we really need to push? Because actually we know that this is going to create long term benefit despite an EGFR number that we see that makes us wonder, are we doing the right thing or not?

AF: That's a really important question. And I was having a discussion today with the new chairman of the British Heart Failure Society about just this issue and heart failure. Nurses are getting more confident in this area, and I hope you specialty trainees will do so too. Part of the most important Messages is for nephrologists to stop frightening you. You have a job to do. Your job is to optimize people with heart failure. And you need to do that because that will save lives and stop these people coming up to hospital. Changes in GFR are numbers, and we bandy around the word acute kidney injury inappropriately. You should be aware that the ESC guidelines suggest that actually you can accept much larger drops in GFR than we do in people without heart failure. If you're giving an ace arb for heart failure. So, you need to feel more confident. What you need to do, though, is to make sure you're doing the right thing, and the patient is appropriately optimised. Get the patient on maximal rest but do look at their other treatments. Ensure that they're not taking non-steroidals if their blood pressure is going to drop and they're on doxazosin, I know that's less likely in a heart failure environment. Drop the doxazosin because you don't want the blood pressure to drop too far. Diuretics are brilliant to offload, but make sure they're not being overused, and the patient isn't actually being volume depleted. Then you've got that patient at baseline. Go ahead and do your job. The GFR will drop. And what you often see is it drops. And then it reaches a new baseline. And you're able to maintain the patient in that new baseline. If it drops and it continues to drop, then obviously you need to think again and get the help of your friendly nephrologist. And I think it's about us liberalizing and really freeing you from the spectre of you put this patient into acute kidney injury. That's going to be really important in improving the management of people with heart failure and indeed, CKD.

MG: And how long should we be waiting before saying, okay, we either stop or this is a new baseline and we continue. Is it two weeks, six weeks or is it just very individualized?

AF: I would say you're going to do your test in two to three weeks. And in fact, this is in most of the guidelines. If your GFR is dropped what ten fifteen percent. Fine. Next test is when they have their next routine blood test. Don't need an additional monitor if it's dropped forty percent. But you think this patient has heart failure. They really need this drug, and you've checked all the things I've said. Repeat the blood test in another month. Make sure they're well. And if it's around the same, then say this is probably their new baseline. And if they're benefiting from it, then you say good you're getting the benefit from this treatment.

MG: Great. And you obviously mentioned one of the I guess it's not really new anymore, but the SGLT2 therapies, which we're seeing being increasingly used from a kidney point of view. Is there a medication that you would prefer, or is any SGLT2 on board better than no SGLT2? They are all the same in terms of kidney protection, but they have different evidence bases and different nice guidance. So primary care is limited. You will never make a mistake by prescribing whichever one you prescribe. As you know, Canna is only really licenced to be used in diabetes, but actually its cardiorenal protection is just as powerful as the other drugs. We don't know what it's like non-diabetes, but it's just as powerful. However, that being said, if they've not got diabetes, Empa or Dapa are going to be the drugs of choice. I know we touched on this briefly, but I think it would be quite good for our listeners at what point we should be considering referring to nephrologists, because I think a lot of these patients that we're seeing are actually being treated in the community, either by primary care or, as you mentioned, by the community heart failure team. They may be on cardiology wards. They may be on the acute medical wards. So, at what point do we need to be phoning nephrology for advice?

AF: So, as we've said right at the beginning, you're going to be seeing loads of patients due to the fact that fifty percent of the patients you see may have CKD. That doesn't surprise me at all. Please don't refer them all to us. Otherwise, we'll refer them. Otherwise, we'll refer all our heart failure patients to you. But it's if something isn't right, i.e. the change doesn't match the treatment. Urine analysis shows blood. There's something about the story that isn't right. Please feel free. Or if the patient is reaching a point where they may need to consider renal replacement therapy. But most units now in our unit at Imperial have a dialogue. We cross talk about patients. And one of the things that I try and really bang on about is that dialogue doesn't have to be a traditional. You write a letter to me, I arrange to see the patient in outpatients, see the patients. They miss the first two appointments and then write back to you. It can be a simple email e advice. Some of them are linked to electronic hospital systems. We just talk to each other. We presented each other's MDTs or present at certain MDTs. And that dialogue, I think, helps.

MG: Perfect. And I guess the only question as a consequence of that is you've obviously mentioned the importance of blood tests and monitoring those and the importance of urinalysis. Is there an indication for kidney ultrasounds in these patients?

AF: So, if you've got someone with CKD, they generally would have had an ultrasound in primary care or secondary care. If you've got someone with long standing CKD, I don't think it's the cardiologist's job to do the ultrasound, but you do need to watch out for patients who are having changing GFR to make sure you're not missing obstruction. So I don't think I would put that on your plate, but I do think you need to bear in mind that most patients with CKD should have had an ultrasound to determine kidney size, structure, and making sure we're not missing another disorder, such as polycystic or obstructive uropathy.

MG: Thank you. I think that's actually been a very thorough overview of Cardiorenal metabolic syndrome. I can't think of any questions myself of where we go from here. And I'm just wondering if there is any kind of last bits of advice you'd like to give to any of the medical trainees that listen to us about how we kind of go forward in treating these patients because as we keep saying, we're just going to keep seeing them wherever we work.

AF: So, I want to mention two things before I come to your last bit of advice. One is getting people optimized on heart failure and CKD treatments is going to save lives. Maintaining them on maximal rests is going to save lives. Getting them on to mineralocorticoid receptor antagonists is going to save lives. You do need to be aware when you start these treatments that hyperkalaemia is an anticipated event in these patients. Predict it. Try and reduce the chances of this occurring. Have good dialogues with your emergency medicine acute medicine teams so they don't stop these treatments if the patient develops hyperkalaemia because there's lots of ways this can be managed. I just want to really get that message in terms of the other key message. I think we've all got to educate each other and embed the educational Cardiorenal metabolic disease within our programs. I think you should feel as confident about managing RASi in people with CKD as I do. I think you should be as confident and competent in using GLP one receptor antagonists. Then that's probably coming down the line for you as I do, or as the Diabetologist does. And those are the things that we need to do. We need to look at our education programs and have a bit more emphasis on this disorder, CRM.

That's great. Thank you. And I guess the last little thing that we should probably tell our listeners is about your podcast, For Kidney Sake. Any plugs that you want to give us? Oh, please.

AF: So, this is a series of bite size, fifteen to twenty minute podcasts designed for primary care but covering every aspect of CKD management. And I'm absolutely certain among the list of subjects, there will be many that specialty trainees. Not just nephrology, but in cardiology, diabetes and anyone who deals with CRM will find very useful because indeed there are some CRM focused podcasts. So, it's called for kidneys sake. Just Google that or Google Northwest London CKD and you'll find the link there. And happy to have you all aboard.

MG: Perfect. What I'll do is I'll also put it in the footnotes of our podcast today. In the footnotes, you'll also find a link to the guidelines that you mentioned to our listeners. Thank you for listening to us. We hope you've found this podcast useful. For more CKD episodes, you can listen back on other Clinical conversations podcasts and certainly listen to the full Kidney Speak podcast as well. And Andrew, thank you so much for joining me today. I know I've learned a lot, and I'm sure that all our listeners will love as well.

AF: Thank you so much for inviting me. Pleasure.

MG: Thank you. 

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