A Man With Severe Tophaceous Gout, Stage 3 Chronic Kidney Disease
In this video, Monica Richey, MSN, ANP-BC/GNP, discusses the clinical challenges and strategies in managing a patient with severe tophaceous gout and stage 3 chronic kidney disease, including urate-lowering therapy and diet counseling. This is part two of a two-part case presentation series on patients with gout.
Watch part one of this two-part case presentation series on patients with gout here.
For more gout content, visit the disease state hub.
TRANSCRIPTION:
Monica Richey: My name is Monica Richey. I'm a nurse practitioner working in rheumatology for over 20 years. I currently work at Northwell Health on Long Island, New York.
All right, so now we dive into case number two. We have a 65-year-old Hispanic gentleman, Mr Leon.
He's retired and has a history of hypertension and chronic kidney disease stage 3. He reports uncontrollable gout for many, many years.
He has severe swelling, chronically of hands, elbows, and feet. He reports that a lot of his joints have those little bumps and he cannot completely move his hands. He has a documented history of gout for many years.
He tells us that he's non-compliant with his medications and that he has failed allopurinol and febuxostat. He has multiple gout flares, and his symptoms are only getting worse. He was diagnosed with gout over 10 years ago.
The other medications that he's taking are amlodipine 10/mg/d, his creatinine clearance is about 55 mL/min, and has no history of cardiovascular disease. His mother had gout, but it was controlled by diet.
He does not smoke, consumes alcohol frequently, and has a sedentary lifestyle. His vital signs are normal.
He's very uncomfortable. He comes in with his wife. When you start to examine him and you will see pictures in a minute, you will see large, multiple tophi affecting almost every joint, including the hands, feet, knees, ankles, and as well as the shoulders. When we do the laboratory testing, he is uric acid is 10.5.
His serum creatine is 1.8 mg/dL. And his complete blood count is within normal limits. And again, I'm thinking ahead of time so I can do all the blood work on my own.
He's not of Asian descent, so I don't need to use an HLA-B58-01. But because of the load of the tophi and because he failed taking oral medications, I know that I have to treat this patient a little bit more aggressively than if it was a different case. So, I ordered what we call a G6PD and that is specifically for the pegloticase case medication because he has such a large load of tophi.
Figure 1. The patient has multiple tophi affecting almost every joint, including the hands, feet, knees, ankles, and the shoulders.
To put this whole history together, he's non-compliant with oral medication. He tells you that he drinks almost every day. He has a chronic disease, and he has a very large load of tophi.
What we decided to put him on is the IV pegloticase because that is the only way to control his uric acid… not only to control his uric acid but also lower or get rid of the tophi. Pegloticase is a medication that is specifically engineered to get uric acid out of the body through the urine. So, it transforms uric acid into a form that is treated by the kidneys.
He's in a lot of pain. His creatinine is 1.8 mg/dL. So, colchicine here wasn't the best thing for him. I put him on a very high dose of prednisone. So, I started him on 40mgs/d just to relieve some of his pain and discomfort.
And then we start the process to get him onto the pegloticase, which is a complicated order. Usually, only rheumatologists or nephrologists will order that medication.
You have to check for the G6PD, making sure the patient is not deficient in G6PD enzyme. He was not, so he was fine to get the pegloticase.
His uric acid was very high, and it's accepted standard therapy now to start the patient also on a medication called methotrexate, which is a medication for rheumatoid arthritis. However because pegloticase causes a lot of infusion reactions, the standard therapy now is to put patients on methotrexate to decrease the risk of reaction. Once the patient is on pegloticase, you must check the uric acid every 2 weeks before the next infusion to make sure that the uric acid is decreasing. If the uric acid either stalls or starts to increase, that means that the patient is developing antibodies to the medication and he is probably going to react when he sits in a chair. So, every day, one day before the infusion, they'll sit, they will check the uric acid, and if the uric acid is going down, and I've seen uric acid zero for over six months with this particular medication, you continue to give the medication. Any indication that the uric acid is going up, you stop that medication.
In his case, we started him first methotrexate for about a month, 15/mg once a week with folic acid. And then after a month, he was started on pegloticase.
And he completed about six months of the medication. And he was able to get rid of at least 50. And we opted to continue for another six months to make sure all the tophi was done. He had no reactions after the pegloticase.
So, the take-away message in this particular case are if everything else fails, pegloticase is an option for you, particularly if there is a lot of tophi. This patient was completely disabled before coming in, and after, he was able to resume a normal life.
You have to check the uric acid. Therapy should be continued for at least 6 months, and then if there is still tophi, you can continue for over a year.
You must maintain patients on prednisone for the time that you are on medication. So, in his case, he was maintained on prednisone 5/mgs after the initial load of 40.
For dietary counseling, patients must quit drinking, and the patient must change their diet.
All the lifestyle modifications that we spoke about before are mandatory to continue with any medication for gout. We must emphasize hydration. We must emphasize diet.
A little bit of exercise goes a long way, and patients must maintain a healthy weight.