Nephrologists can play a key role in the diagnosis and treatment of gout in patients with CKD
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When an individual has an excess of uric acid in the blood, it can crystallize in the joints and cause gout, the most common form of inflammatory arthritis in the United States.
While impaired renal function can directly lead to increased blood levels of uric acid, many nephrologists are unaware of the high prevalence of gout among patients with chronic kidney disease.
As nephrologists, we see first-hand the many challenges that people face when living with CKD. Comorbidities like cardiovascular disease, hypertension, diabetes, anemia and hyperlipidemia are well known and understood to be part of CKD care. Gout must become part of that focus as well.
Gout flares
The challenge is that gout has traditionally been looked at as a nuisance of intermittent painful episodes – a condition that exists when the patient is experiencing the acute inflammation of a gout flare.
In truth, however, gout is a chronic, progressive disease. Uric acid crystal deposits remain after a flare-up and build up in patients, even during the intercritical periods between these symptomatic flares.
Two studies presented at the National Kidney Foundation Spring Clinicals Meeting earlier this year analyzed the prevalence, risk factors and health outcomes related to gout in patients who have advanced CKD and in patients undergoing chronic dialysis. In the first study, data from patients with CKD treated by 111 nephrologists across the United States showed that 23.2% of patients met the study criteria for gout.
More concerning was that 36% of patients who met gout criteria based on their medications or clinical symptoms never received a formal gout diagnosis.
In addition, among patients who did have a formal gout diagnosis, more than 36.3% were not on any uric acid-lowering therapy.1
Chronic inflammation
The longer gout remains untreated, the more uric acid crystals will build up and deposit, which leads to more severe and more frequent gout flares, as well as chronic erosive joint damage. Even when symptoms subside following a flare-up, inflammatory biomarker research demonstrates that low-grade chronic inflammation remains. This not only means that more severe gouty arthritis will ensue, but there may also be a greater risk to develop or worsen other comorbidities, such as cardiovascular disease.
Risk of mortality
A second study analyzed data from the United States Renal Data System on patients with end-stage kidney disease. Data showed a 13.5% prevalence of gout in patients with ESKD on dialysis. Multivariate comparison of patients with gout vs. patients without gout on dialysis demonstrated gout to be an independent risk factor for both mortality and cardiovascular disease-related hospitalizations.2 Furthermore, patients on dialysis with gout were also found to require higher doses of erythropoietin stimulating agents and a higher risk for red blood cell transfusions, which provides further evidence of the chronic inflammatory state that gout can cause.2
Options for patients with CKD
While treatments for gout are available, not all of these are entirely effective or appropriate for patients with CKD. For instance, non-steroidal anti-inflammatory medications are a common treatment for gout flares, but these are not safe to use in many patients with CKD. Steroids, like prednisone, can be extremely effective but come with notable adverse events. Regardless, while both treatments can help treat inflammation, these only address the symptomatic effects of gout rather than its underlying source.
To do that, it is critical to reduce the levels of uric acid in the bloodstream and stop the accumulation of uric acid crystals. While several treatments exist that serve this function, sometimes these treatments are underused or ineffective, particularly in patients with CKD.
The first line of defense against gout is making dietary changes that may help moderately reduce uric acid levels. However, most patients will need pharmaceutical support to lower these levels to a point that would stop the progression of gout. In patients with gout and no signs of CKD, an initial pharmaceutical option could be a uricosuric agent that causes the kidneys to excrete more uric acid. For patients with CKD, however, this is generally not an option as the reduced kidney function makes these drugs less effective and confer a higher risk of renal injury and kidney stones.
Another class of medications called xanthine oxidase inhibitors decrease uric acid levels by preventing its production from precursor molecules. These medications can be effective for many patients but many times are started too late or at an ineffective dose so uric acid accumulates despite use. When these therapies do not work, it is important to consider a uricase medication that metabolizes the uric acid itself and can remove years or even decades of accumulated uric acid burden for these patients.
Gout is more prevalent and more severe in how it affects patients with CKD. When left undertreated, it can continue to reduce quality of life and worsen health outcomes. But the good news is that gout is a highly treatable disease in the right hands. As nephrologists, our experience and expertise in managing the multiple complications and comorbidities that challenge our patients with CKD makes us best suited to alleviate the suffering caused by progressive uric acid deposition and gout.
- References:
- 1. Stern L, et al. Poster #205. Presented at: National Kidney Foundation Spring Clinical Meetings; April 6-10, 2022; Boston.
- 2. Bleyer A, et al. Poster #206. Presented at: National Kidney Foundation Spring Clinical Meetings; April 6-10, 2022; Boston.
- For more information:
- Brad Marder, MD, is the medical director of nephrology in medical affairs at Horizon Therapeutics. He can be reached at bmarder@horizontherapeutics.com.
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