Comorbidities and Mortality Impacts With Uncontrolled Gout
The persistently high sUA and chronic inflammation of uncontrolled gout can have an increased risk with other serious health conditions. Gout has also been associated with a higher risk of death from some diseases.1-3*
There Is an Increased Risk of Some Comorbidities Associated With Gout
In 1 claims database study, 95% of patients with urate crystal–confirmed gout had 2 or more comorbidities1,4*†:
Cardiovascular Disease
Patients with uncontrolled gout were 52% more likely to develop heart disease than those with controlled gout
Chronic Kidney Disease
Patients with uncontrolled gout were twice as likely to develop chronic kidney disease than those with controlled gout
Type 2 Diabetes
Gout is an independent risk factor for developing type 2 diabetes
*Patients with controlled gout were defined as having sUA <6.0 mg/dL and patients with uncontrolled gout with sUA ≥8.0 mg/dL.1
†Data from adult patients with gout and who had at least 90 days of continuous urate-lowering therapy (ULT) was collected from the Humana Research Database from 2007–2016. A total of 6831 patients were identified that met the inclusion criteria (5473 patients had controlled gout, and 1358 patients had uncontrolled gout).1
There is a bidirectional relationship between gout and some of its comorbidities, reflecting its systemic nature. The cycle and progression that patients with uncontrolled gout face may worsen comorbidities such as diabetes, metabolic syndrome, cardiovascular disease, and CKD, while some comorbidities may contribute to sustained elevated sUA levels.1,5
95% In 1 study, over 95% of patients with urate crystal-confirmed gout had 2 or more comorbidities6‡
‡The New York Department of Veterans Affairs electronic medical records were examined to allow an assessment of contraindications and comorbidities in patients with gout. Patients were required to have had a clinic or hospital visit during the review period (July 2007 to December 2008), and enrolled patients were identified based on any ICD-9 code for gout (Cohort I; N=575). Cohort II (n=478) was composed of patients in Cohort I meeting the American College of Rheumatology criteria for gout. Cohort III (n=41) was composed of patients in Cohort II with documented monosodium urate crystals in their synovial fluid or tophi. Comorbidities were identified by the presence of physician-assigned ICD-9-CM codes and confirmed by chart review.6
Too often, gout is dismissed as just flares in the toe. But what I see in practice is something much more serious. In reality, it is a progressive, systemic disease driven by persistently high serum uric acid levels and genetic factors.
Dr. John Albert, MD, Rheumatologist
Hear more on Dr. Albert’s review of gout and its impact on patients
Potential Mortality Impacts in Uncontrolled Gout
Gout can be associated with a higher risk of death from cardiovascular disease, renal disease, and diseases of the digestive system. Gout has been observed to be linked with cardiovascular and all-cause mortality.1,7,8§ People with gout disease duration <10 years have an increased risk of death.9||
Every 1 mg/dL increase in sUA was associated with a 24% increased risk in all-cause mortality10,11¶
The presence of subcutaneous tophi at baseline is an independent predictor of mortality from both cardiovascular and non-cardiovascular causes.9
People with visible tophi at diagnosis had a 185% higher risk of mortality from all causes compared to those without tophi9¶
§A multicenter, retrospective, observational study (N=22,714) collected data from several large population-based longitudinal studies in Italy. The study aimed to define the level of uricemia above which the independent risk of cardiovascular disease may increase. Patients were followed for ≥20 years up to July 31, 2017.10
||Prospective, observational study conducted in 295 people with gout disease duration of <10 years recruited from December 2006-January 2014. Study limitations include: (1) 26% of the cohort identified as Māori or Pacific Islander, and Māori or Pacific ethnicity was independently associated with death from all-causes and non-cardiovascular causes. Gout prevalence is higher and disease severity worse in Māori and Pacific people; thus, these results may not be internationally generalizable. (2) Although the inclusion criteria were broad, the convenience sampling scheme may have led to patients with more severe health problems volunteering to participate in a research study, potentially overestimating the standardized mortality rate compared with an analysis of people with gout in the general population. However, the baseline clinical characteristics of participants (including frequency of comorbidities) were similar to large population studies and clinical trials of people with gout. Further, this convenience sampling scheme should not have influenced the analysis of variables associated with mortality in the recruited group.9
¶Univariate Cox regression analysis.10
Watch Dr. Albert's Talk About the Impact of Gout
Dr. Albert, a rheumatologist who treats gout, discusses gout misunderstandings, the drivers of this progressive, systemic disease, associated comorbidities, and the impact gout can have on the body—along with a patient’s perspective.
Chapters
Chapter 1
Dr. Albert:
Gout is one of the oldest known diseases, yet it remains one of the most misunderstood.
Hi, my name is John Albert. I am a rheumatologist at the Rheumatic Disease Center in Milwaukee and Glendale, Wisconsin.
I've treated hundreds of patients with uncontrolled gout and have seen how deeply misunderstood this disease is.
Gout doesn't kill you, but it can make your life challenging. Like I always say, it's not your grandfather's gout.
Today, I'm joined by someone who knows the realities of uncontrolled gout all too well. Paul, thanks for being here today. Please tell us a little about your journey with gout.
Paul:
Hi, I'm Paul Czajka. I've lived with gout for over 25 years. This disease reshaped my life in ways I never saw coming.
Dr. Albert:
Too often, gout is dismissed as just flares in the toe. But what I see in practice, and what Paul has lived through, is something much more serious.
In reality, it is a progressive, systemic disease driven by persistently high serum uric acid levels and genetic factors.
Even with current therapies, many patients continue to experience elevated uric acid, which can silently damage organs and can increase the risk of serious comorbidities.
Paul:
That was me. I didn't have flares in my toe, I had pain in my knees, hands, and ankles. For years, no one even looked for gout because my symptoms didn't match the textbook. Meanwhile, the disease was spreading.
I was in my 20s. Fit, active, running miles a week.
But the pain kept growing, until I couldn't walk upstairs, tie my shoes, or type with both hands.
Dr. Albert:
Here's what I always say, "Gout doesn't come looking for you. You have to go looking for it."
If we're only waiting for visible tophi or acute flares, we're missing a huge part of the disease.
Uric acid builds up silently; it doesn't just trigger flares. Uric acid can cause inflammation, joint erosion, kidney damage, and cardiovascular risk. And it doesn't stop building up when the flare ends.
Paul:
For a long time, I thought if I was not in pain, I was fine, but the disease was still active. By the time I understood uric acid buildup, I'd already had multiple surgeries for the removal of tophi and lost full motion in some fingers.
Dr. Albert:
I try to drive this home with my peers: "You're not just treating symptoms. You're managing a chronic, systemic, inflammatory process."
Absence of symptoms does not mean absence of disease activity.
Chapter 2
Paul:
I got used to pain. I lived with it quietly. But it made me irritable and disconnected. I missed time with my kids. And worse, some people assumed it was my fault.
When I was blamed for something I couldn't control, it was isolating. I started hiding my hands, my pain, my emotions.
I stopped drinking. Changed my diet. Took medications prescribed by my physicians. But I was still flaring, still hurting. At one point, I was told, "There's nothing else we can do." That was crushing.
Dr. Albert:
As you know, Paul, gout shaming is real. Patients are told it's a result of what they eat or how they live—but that's not always right.
We need to move beyond the flare. Beyond diet. Beyond wait and see.
Modifications to diet and lifestyle help but may not be enough. Especially in advanced disease, the body simply can't excrete enough uric acid. That is why sometimes, some patients, for example like Paul, may not benefit from these changes alone.
The real drivers are genetics, comorbidities, impaired uric acid excretion due to gut microbiome, and medications such as diuretics and low dose aspirin.
In my practice, I aim for a uric acid level of under 5 mg/dL, preferably closer to 2 or 3 mg/dL if we're trying to dissolve tophi. Lowering uric acid levels helps address an underlying cause, not just the symptoms.
Paul:
I didn't even know what my uric acid level meant. No one explained that to me until Dr. Albert did. If I had known what was really going on inside my body, I might have pushed for more, earlier.
Dr. Albert
And here's the irony: we check cholesterol and A1C, but we often skip uric acid. Why?
Paul:
If you're living with gout that isn't getting better, speak up and push for answers. You deserve to be listened to and to feel better.
Like you did for me.
Dr. Albert:
There are many different faces of gout; don't stop at symptom relief. This may be why a number of patients remain uncontrolled and undertreated.
As healthcare professionals, we must listen, challenge our assumptions, and do better for patients with uncontrolled gout.
Look at the full picture. Listen to your patients. And remember: the flare isn't the problem—it's the warning sign.
Paul, thank you for sharing your story. And thank you to everyone watching and for being part of this important conversation.
The more we listen, the more we know, the better we treat.
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The information provided on this website is intended for healthcare professionals (HCPs) for informational and educational purposes only. It is not intended to replace the independent clinical judgment of HCPs in diagnosing or treating individual patients.
References
1. Francis-Sedlak M, et al. Rheumatol Ther. 2021;8(1):183-197. 2. Shirvani-Rad S, et al. Front Med (Lausanne). 2023;10:1163778. 3. Vargas-Santos AB, et al. Arthritis Rheumatol. 2019;71(11):1935-1942. 4. Sandoval-Plata G, et al. Rheumatology (Oxford). 2021;60(7):3243-3251. 5. Afzal M, et al. Gout. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025. 6. Keenan RT, et al. Am J Med. 2011;124(2):155-163. 7. Perez-Ruiz F, et al. Ann Rheum Dis. 2014;73(1):177-182. 8. Singh JA, et al. Semin Arthritis Rheum. 2020;50(3S):S11-S16. 9. Vincent ZL, et al. J Rheumatol. 2017;44(3):368-373. 10. Virdis A, et al. Hypertension. 2020;75(2):302-308. 11. Zuo T, et al. BMC Cardiovasc Disord. 2016;16(1):207.