The Management of Patients With Gout in a Nephrology Setting
In this video, James Matera, DO, discusses the current standard of care in the management of a patient with gout in a nephrology setting, managing a patient to avoid symptoms and minimize gout flares, and the common agents used to manage patients with gout, including xanthine oxidase inhibitors and uricosuric agents. This is part one of a three-part video series.
For more gout content, visit the disease state hub.
Watch part two of this three-part series here.
Watch part three of this three-part series here.
TRANSCRIPTION:
James Matera, DO: Good afternoon. This is Dr. James Matera here. I'm the Senior Vice President for Medical Affairs and Chief Medical Officer at CentraState Medical Center in Freehold, New Jersey. And I'm happy to be talking a little bit about gout and hyperuricemia today for our audience. So when we talk about gout, a lot of information comes out as to who is best suited to manage gout. Is it the primary care physician, the rheumatologist, or the nephrologist? I really feel that the treatment of gout as well as asymptomatic hyperuricemia, which we'll talk about in a little bit, should be a team-based approach. And this needs to incorporate the primary care physician who's often going to be that person getting the call for an acute flare on the nights or weekends. But we also have to include the rheumatologists because a lot of our guidelines come from their societies. And certainly, the Nephrologists because the impact that uric acid has on the skeletal system as well as the kidneys is very important.
So when we use shared decision-making tools with the patient, we must clearly outline our goals of care making that one of the utmost critical thinking points for us, and that will help us ensure compliance with therapy and then eventually reduce adverse effects. As a nephrologist, I often pay a lot of attention to the effects of uric acid on CKD. So in this regard, we know that if we want to treat and ultimately prevent gouty arthropathy, we have a lot more that we have to do. So when we define hyperuricemia, and again we're not talking about whether it's gout or not but just hyperuricemia, that equates to a serum uric acid level of greater than seven equivalents, I'm sorry, milligrams per deciliter in males and six milligrams per deciliter in females. This is often found as a comorbid condition in patients who have more common diseases that we see, such as hypertension and type 2 diabetes.
These also, as we know, along with uric acid itself, but those diseases present risk factors for the progression of CKD. So if we couple those two things with the overall excretion of uric acid and CKD, we can see that hyperuricemia increases dramatically as CKD progresses. With normal renal function and normal uric acid excretion. The incidence and the prevalence of gout is only about 1-2% of the population, but we increase that to almost a third of all patients who have CKD stage four, which is defined as an estimated GFR of less than 30, and that can be a very important comorbid condition. When we discuss hyperuricemia independent of gout or gout flares, the prevalence in the general population with normal renal function is about 10%, but that can increase to as high as 80% in CKD patients and those with end-stage renal disease.
This makes you ask one question: Does hyperuricemia with or without gout play a role in chronic kidney disease? And I think that's still an important factor to look at, and I'll talk about a couple of studies as we go along. One of the things we all want for our gout patients, and one thing that they want for sure is to avoid symptoms. So when we look at that, the gout patient is often in a lot of pain. So we want to look at that, whether they have acute or chronic gouty arthropathy, and we'll talk about a little bit of a progression as we go along. These patients may benefit from urate-lowering therapy simply to avoid these symptoms which can be debilitating, and then also contribute to significant joint mortality and morbidity. So treatment should be rendered if there's no contraindication. If a patient has had two or more documented gout flares within a year, or if they have tophi, which is kind of the end stage of gout and gouty arthropathy, or they have clear radiographic signs of joint erosion or damage, those are patients that really should be considered for urate-lowering therapy.
When we use shared decision-making, the team-based approach that we just talked about, I think this really becomes critical. So even though we can use the guidelines for treatment that I mentioned, if the patient has other conditions, particularly CKD stage three or higher or uric acid kidney stones, you may not want to wait until they've had two gout flares. You may want to intervene a little bit earlier with urate-lowering therapy. When we talk about asymptomatic patients, that's a little more controversial. Studies really have not borne out that treating asymptomatic hyperuricemia is beneficial in this class. However, if there is some positive impact on long-term, then it is something that we want to talk about in our shared decision-making. So how do we minimize gout flares? Well, anyone who's suffered a flare of gout will surely want to undertake the measures to prevent that from happening.
This requires a really good working knowledge of the provider and clinician to understand some of the therapies that we use and how they work to lessen gout flares. So when we talk about medications, I like to break it down into two basic parts, although now there are some studies looking at other areas, and we'll talk about that in a future video. The most common agents that we look at are basically divided into two classes. Those that are xanthine oxidase inhibitors, the classical allopurinol and febuxostat. Or the uricosuric agents would cause you to increase your excretion of uric acid. And of those, we'll talk about a couple of agents, although there are certainly others and many more in development. When we look at the xanthine oxidase inhibitors, the ones we're most commonly familiar with, they help block the conversion of hypoxanthine to uric acid in the purine metabolism pathway.
That's why it's also critical for these patients to have a good education, usually from a dietician, on how to reduce purines in general in their diet. Allopurinol is the oldest, that's the most common, and that really should remain as our first-line therapy for almost all patients starting on urate-lowering therapy. Here, I would start with about 100 milligrams per day, I may go less if I have advanced chronic kidney disease, and then titrate up in a dose-related fashion. Febuxostat, which is another agent initially was touted for being very good or beneficial to use on chronic kidney disease. But some other studies through the years have shown that allopurinol may as safe as well. So when I use febuxostat though, I use 40 milligrams and then can titrate up to a dose of 80. There have been some adverse cardiovascular events, and I'll talk about those in a separate video, associated with febuxostat.
And I'll try to show the two studies that really looked at that. When we deem Uricosuric agents, the ones that are going to help us excrete, the classic ones that come to mind are Probenecid, which has been out there for a long time and can be used at 100 milligrams BID. And again, titrated up. But we also have a newer agent that falls into this, an injectable agent called Pegloticase. That's given every two weeks, and it would certainly not be my first-line therapy, but I will tell you a case a little later where we did have to use that for various reasons for the inability to tolerate any other medications. But I don't recommend that as a first-line agent.
So that's my classic overview of gout right now. Thank you for watching this video. As we go into the other two, we'll get a little more specific on some of the reasons for gout, the differential between acute and chronic gout, and talk a little bit more about some of the adverse effects of medications. Please stay tuned for those.