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Saliba, F.; Mourad, O.; Mina, J.; Haddadin, F.; Aoun, L.; Almardini, S.; Abu-Baker, S.; Sangaraju, K.; Di Pietro, G.; Gaballa, D.; et al. Mechanisms Linking Hyperuricemia and Kidney Disease Progression. Encyclopedia. Available online: https://encyclopedia.pub/entry/56381 (accessed on 17 May 2024).
Saliba F, Mourad O, Mina J, Haddadin F, Aoun L, Almardini S, et al. Mechanisms Linking Hyperuricemia and Kidney Disease Progression. Encyclopedia. Available at: https://encyclopedia.pub/entry/56381. Accessed May 17, 2024.
Saliba, Fares, Omar Mourad, Jonathan Mina, Fadi Haddadin, Laurence Aoun, Shaza Almardini, Saif Abu-Baker, Koushik Sangaraju, Gaetano Di Pietro, Daniel Gaballa, et al. "Mechanisms Linking Hyperuricemia and Kidney Disease Progression" Encyclopedia, https://encyclopedia.pub/entry/56381 (accessed May 17, 2024).
Saliba, F., Mourad, O., Mina, J., Haddadin, F., Aoun, L., Almardini, S., Abu-Baker, S., Sangaraju, K., Di Pietro, G., Gaballa, D., & El-Sayegh, S. (2024, March 18). Mechanisms Linking Hyperuricemia and Kidney Disease Progression. In Encyclopedia. https://encyclopedia.pub/entry/56381
Saliba, Fares, et al. "Mechanisms Linking Hyperuricemia and Kidney Disease Progression." Encyclopedia. Web. 18 March, 2024.
Mechanisms Linking Hyperuricemia and Kidney Disease Progression
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This entry is adapted from the peer-reviewed paper 10.3390/rheumato4010005

Gout is highly prevalent in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD), owing to impaired uric acid excretion. However, treating gout in this population is challenging due to concerns about medication safety and efficacy with reduced kidney function. The 2020 American College of Rheumatology (ACR) guidelines recommend nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and systemic glucocorticoids to treat acute gout flares. These can also be used as prophylaxis when starting urate-lowering therapy (ULT) to prevent flares. For ULT drugs like allopurinol, febuxostat, probenecid, benzbromarone, lesinurad, and pegloticase, key efficacy outcomes per most guidelines include: achieving target serum urate levels (<6 or <5 mg/dL), resolving tophi, reducing gout flares over time, improving quality of life, and radiographic changes. 

gout chronic kidney disease hyperuricemia urate-lowering therapy acute gout flares hemodialysis

1. Introduction

Gout is one of the most common forms of inflammatory arthritis, resulting from elevated levels of serum uric acid (hyperuricemia), leading to the deposition of monosodium urate crystals in joints, soft tissues, and organs. It is characterized by recurrent acute flares of severe arthritis as well as chronic arthropathy if left untreated. In patients with end-stage renal disease (ESRD), gout is particularly prevalent, ranging from 15 to 30% [1]. The incidence of gout increases as kidney function declines, with rates as high as 11 per 100 person years in dialysis patients [2]. For instance, in a study of 1117 patients starting dialysis, the prevalence of gout was 29.5%: in men (32.8%) compared to women (24.7%) [3]. Factors associated with higher gout prevalence included male gender, white race, obesity, diabetes, diuretic use, and lower residual kidney function [4]. Multiple epidemiological studies have shown hyperuricemia as an independent risk factor for CKD onset and progression [5]. However, some investigators argue that uric acid is simply a marker of disease rather than playing a causal role [6]. Regardless, there appears to be a clear link between uncontrolled gout, hyperuricemia, and worsened kidney function. Small interventional trials of urate-lowering treatments have shown improved GFR and slowed CKD progression [7].
Hyperuricemia is the result of either increased production or inadequate excretion of uric acid, with the kidneys playing a major role in uric acid excretion by filtering and eliminating about two-thirds of circulating uric acid [8]. In CKD, the decline in glomerular filtration rate impairs uric acid excretion, leading to rising uric acid levels. National Health and Nutrition Examination Survey (NHANES) data shows that the prevalence of hyperuricemia increases substantially from 11 to 13% in early CKD to 64–78% in patients with eGFR 15–29 mL/min/1.73 m2 [9]. The presence of comorbidities such as hypertension and the use of diuretics may further reduce uric acid excretion in CKD patients [5].

2. Treatment of Flares and Prophylactic Agents in Gout and CKD

The 2020 American College of Rheumatology (ACR) guidelines recommend nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and systemic glucocorticoids to treat acute gout flares. These can also be used as prophylaxis when starting urate-lowering therapy (ULT) to prevent flares. Interleukin-1 (IL-1) inhibitors like anakinra and canakinumab can be used for flares and prophylaxis too. However, there is a lack of consensus on proper dosing and monitoring of these medications in gout patients with chronic kidney disease (CKD) experiencing acute flares or needing prophylaxis when starting ULT. More evidence is needed to determine the optimal use of these agents for managing flares and preventing paradoxical flares when initiating ULT in the setting of CKD.
  • NSAIDs
Nonsteroidal anti-inflammatory drugs (NSAIDs) are typically contraindicated in patients with CKD due to the risk of renal-related side effects. The published literature on NSAIDs in gout has generally focused on demonstrating these potential adverse effects in CKD patients. Although the adverse effects of NSAIDs are well established, there is some evidence suggesting short-term NSAID use may be possible in end-stage renal disease. Patients with ESRD may be an exception for cautious use of NSAIDs, despite the high risk of side effects like gastrointestinal bleeding. Some evidence suggests short-term NSAID use in ESRD patients without residual kidney function may not affect blood pressure or electrolytes and could potentially be safer than alternative pain control options in this population. However, more research is still needed to definitively determine the safety of any NSAID use in CKD, particularly for the short-term treatment of acute gout flares. Current evidence indicates NSAIDs should generally be avoided but may potentially have a very limited role in certain CKD patients if used cautiously and under close monitoring [10].
Recommendations: In patients with creatinine clearance ≤30 mL/min, NSAIDs should be avoided due to the increased risk of acute kidney injury.
In patients on intermittent hemodialysis three times per week, NSAIDs are slightly dialyzable (20%) but should also be avoided. Hemodialysis patients with end-stage kidney disease may have greater risks of bleeding (e.g., GI), cardiovascular side effects, and loss of any residual kidney function with NSAID use [11].
Due to concerns about potentially exacerbating kidney dysfunction and other adverse events, NSAIDs are best avoided in patients with severe chronic kidney disease (CrCl ≤ 30 mL/min) or those receiving intermittent hemodialysis. The risks generally outweigh any potential benefits on these populations.
  • Colchicine
Colchicine, an anti-inflammatory drug that inhibits microtubule assembly and NLRP3 inflammasome activity, is commonly used for treating acute gout flares and as prophylaxis when starting urate-lowering therapy (ULT). As an anti-microtubule and anti-inflammatory agent, colchicine can help manage the pain and inflammation of acute gout attacks. It can also prevent paradoxical flares when initiating ULT due to its anti-inflammatory properties. Colchicine is one of the mainstay therapies for treating active flares and for prophylaxis against flares when starting long-term ULT. There are a few randomized controlled trials of colchicine for gout flare treatment, but none reported outcomes based on kidney function. Pharmacokinetic studies show colchicine clearance is reduced in severe kidney impairment (eGFR 15–29 mL/min/1.73 m2), and minimal clearance occurs with hemodialysis. Colchicine toxicity can be increased in patients with CKD due to reduced clearance, leading to adverse effects like rhabdomyolysis, neuromyopathy, and bone marrow suppression. Colchicine also has significant drug interactions with medications commonly used in CKD, like statins, cyclosporine for transplants, and macrolide antibiotics. These interactions are exacerbated by colchicine’s prolonged half-life in renal impairment. Therefore, colchicine requires very careful dosing and monitoring for toxicity in CKD patients, especially those on interacting medications [12].
Previous randomized trials of colchicine for gout did not report outcomes by kidney function, so evidence is lacking on its use in CKD. Case reports using varying colchicine doses and schedules in CKD had highly variable results—12 of 19 cases showed worsening kidney function, while 7 of those 19 were stable. Most case studies showed significant side effects or drug interactions, but it is unclear if colchicine was directly causal given the limitations. Ultimately, there is insufficient evidence to conclude on colchicine’s safety or efficacy in CKD [13]. Low-dose colchicine could be studied, as it is similarly effective in non-CKD patients. Based on experience, prophylactic dosing of 0.3–0.6 mg every other day or twice weekly, depending on CKD severity and interacting medications, may be reasonable. More research is needed, particularly on lower colchicine doses, to establish safe and effective use in CKD patients. Careful consideration of risks versus benefits is necessary, given concerns about potential toxicity and interactions.
Recommendations: In patients with creatinine clearance ≤30 mL/min, alternative therapies should be considered first if available and tolerated. If colchicine must be used, the following adjusted dosing is recommended: 1.2 mg at the first sign of a gout flare, followed by 0.6 mg 1 h later. Repeat dosing should not occur for at least 14 days. Alternatively, some experts suggest a single 0.3 mg dose at flare onset only, with repeat dosing no sooner than every 3–7 days.
Colchicine is typically avoided for gout flare treatment in patients undergoing hemodialysis. Since colchicine is not removed through dialysis, it can accumulate in these patients, increasing the risk of colchicine toxicity.
  • Corticosteroids
Corticosteroids are generally considered the safest option for treating gout flares in chronic kidney disease (CKD), though evidence is limited. They can be used to treat gout flares and, less ideally, as prophylaxis when starting urate-lowering therapy. However, a review found insufficient evidence to determine the effectiveness or safety of steroids for gout in chronic kidney disease (CKD). Most studies were case reports of severe, refractory gout, so the findings may not apply to the wider population. Clinicians are also concerned about comorbidities in gout-CKD patients, like hypertension, diabetes, and infection risk, that may preclude steroid use. More research is needed in the general gout-CKD population to establish steroid efficacy and safety. Caution is warranted given the potential side effects, especially with comorbid conditions. Steroids require an individual risk-benefit assessment for each patient. The current lack of strong evidence in CKD patients makes treatment decisions difficult when managing gout flares or prophylaxis.
Recommendations: For prednisone dosing in patients with creatinine clearance ≤30 mL/min or undergoing intermittent hemodialysis three times per week, no supplemental dose or dosage adjustment is necessary. Doses are 30 to 40 milligrams per day of the medication, either as a single daily dose or split into two doses, until the symptoms improve (which is usually within 2 to 5 days). Then, slowly taper the dosage as tolerated (typically over 7 to 10 days); a more gradual taper (for example, over 14 to 21 days) may be needed, especially in patients who have had multiple recent flare-ups of symptoms.
  • IL-1 Inhibitors
Interleukin-1 (IL-1) inhibitors like anakinra, canakinumab, and rilonacept have been used for gout flares and prophylaxis, but trials excluded advanced chronic kidney disease (CKD) patients and only reported pooled results. Case reports of anakinra and canakinumab in CKD showed limited kidney function decline [14][15], though some anakinra cases had non-fatal infections. Anakinra response was unaffected by CKD in hospitalized gout. Anakinra is renally cleared, so it requires extended dosing intervals in CKD due to its longer half-life. Overall, IL-1 inhibitors appear promising for gout in CKD, but larger, high-quality studies are needed reporting CKD-stratified outcomes to better define safety and optimal dosing. In researchers' experience, IL-1 inhibitors have been beneficial for difficult gout cases in CKD/ESRD lacking other options, but more evidence is needed to guide use in this population. Their potential should be explored further through research, specifically in patients with reduced kidney function.
Recommendations: For anakinra use in gout, it should be reserved for patients where first-line therapies are ineffective, contraindicated, or not tolerated. The recommended subcutaneous dosage in patients with creatinine clearance ≤30 mL/min or on hemodialysis is 100 mg every other day until symptom improvement, with a usual duration of 3 to 5 days [16].
For canakinumab and rilonacept, there are no specific dosage adjustments provided in the manufacturer’s labeling for patients with gout and chronic kidney disease (CKD). The use of canakinumab and rilonacept in CKD has not been adequately studied.

3. Urate-Lowering Therapy (ULT)

The appropriate use of urate-lowering therapy (ULT) in gout patients with chronic kidney disease (CKD) is controversial. Guidelines from the American College of Rheumatology (ACR), the European League Against Rheumatism (EULAR), and the British Society for Rheumatology differ on important aspects like allopurinol dosing in CKD [17]. For ULT drugs like allopurinol, febuxostat, probenecid, benzbromarone, lesinurad, and pegloticase, key efficacy outcomes per most guidelines include: achieving target serum urate levels (<6 or <5 mg/dL), resolving tophi, reducing gout flares over time, improving quality of life, and radiographic changes. However, clinical trials of these therapies have largely excluded or underrepresented patients with advanced CKD [18]. This has resulted in limited evidence to guide ULT use in gout patients with significant kidney impairment. Differing expert opinions have led to conflicting guideline recommendations, causing confusion on optimal ULT dosing and monitoring in this population. More research focused on ULT efficacy and safety outcomes, specifically in CKD, is critically needed to inform guidelines and clinical practice.
  • Allopurinol
The American College of Rheumatology (ACR) guidelines strongly recommend allopurinol as first-line urate-lowering therapy (ULT) for gout, including in CKD. Studies show allopurinol can safely reduce serum urate in CKD. However, starting at low doses (<100 mg/day) is strongly advised in moderate-to-severe CKD to prevent allopurinol hypersensitivity syndrome. Renal impairment, especially with higher starting doses and/or concomitant diuretics, increases the risk of allopurinol hypersensitivity syndrome (AHS)—a rare but potentially life-threatening reaction. Kidney dysfunction reduces allopurinol clearance, leading to higher oxipurinol levels, which is thought to increase susceptibility to AHS. The HLA-B5801 allele also raises the risk of severe allopurinol skin reactions; those of Korean, Han Chinese, or Thai descent are more likely to have this allele. Allopurinol should be avoided in patients testing positive for HLA-B5801, given the heightened risk of adverse cutaneous reactions. HLA-B*5801 testing allows the exclusion of patients genetically predisposed to allopurinol hypersensitivity [18].
In practice, allopurinol doses are often limited in CKD due to toxicity concerns, causing under-treatment. However, allopurinol can be safely up-titrated in CKD based on evidence. The VA STOP-GOUT study of 351 gout patients with stage 3 CKD showed a treat-to-target strategy starting at 100 mg allopurinol and up-titrating achieved urate targets without increased toxicity or worsening kidney function in most [19]. Other studies confirm allopurinol can be escalated safely even in CrCl <30 mL/min to reach goal urate [20]. Higher allopurinol doses may be needed in CKD patients who are heavier or on diuretics [21]. Ultimately, CKD patients may require ≥300 mg/day to reach urate targets [22].
Recommendations: For allopurinol dosing in kidney impairment [23]:
-
Creatinine clearance (CrCl) >15 to 30 mL/min: Suggested initial dose is 50 mg every other day.
-
CrCl 5 to 15 mL/min: Recommended initial dose is 50 mg twice weekly.
-
CrCl <5 mL/min: Recommended initial dose is 50 mg once weekly.
-
For patients on intermittent hemodialysis three times per week, allopurinol is dialyzable with oxypurinol clearance of approximately 39–50%. The recommended initial allopurinol dose in this population is 100 mg three times weekly, administered after each dialysis session.
For allopurinol titration and maintenance dosing in patients with CrCl ≤30 mL/min:
Gradually increase the dose in increments of ≤100 mg/day every 2–4 weeks. Using smaller increments (≤50 mg/day) and longer intervals (≥4 weeks) may be preferred. Some experts delay the initial increase for 1–2 months until after the peak risk period for allopurinol hypersensitivity syndrome has passed. Titrate to the minimum daily dose needed to achieve the goal urate-lowering effect. Doses >300 mg daily can be considered with appropriate patient education and monitoring for potential toxicity like rash, itching, and elevated liver enzymes. If the desired serum uric acid level cannot be achieved, switching to an alternative agent can be considered [24].
For allopurinol titration and maintenance dosing in hemodialysis:
Gradually increase the dose in increments of ≤50 mg/day (e.g., 150 mg three times weekly) every 2–5 weeks. Some experts delay the initial increase for 1–2 months until after the peak risk period for allopurinol hypersensitivity syndrome. Titrate to the minimum dose necessary to achieve the goal of urate lowering. Doses >300 mg daily can be considered with appropriate patient education and monitoring for potential toxicity like rash, itching, and elevated liver enzymes. [18] Doses up to ~400 mg daily have been reported [25].
  • Febuxostat
Febuxostat is a novel non-purine selective xanthine oxidase inhibitor (XOi) mainly metabolized by the liver and excreted renally and fecally, reducing the burden on the kidneys. The American College of Rheumatology strongly recommends using a low starting dose of febuxostat (<40 mg/day) with ongoing titration rather than higher initial doses in chronic kidney disease patients. Smaller studies have shown febuxostat benefits over allopurinol in slowing kidney disease progression and delaying dialysis in moderate-to-severe CKD if uric acid levels ≤7 mg/dL are achieved. However, recent studies disagree on mortality risk with febuxostat versus allopurinol. The CARES trial found higher cardiovascular and all-cause mortality with febuxostat versus allopurinol in gout patients with cardiovascular disease, leading to a black box warning for febuxostat. However, CARES did not stratify outcomes by kidney function [26]. The subsequent FAST trial in gout patients with cardiovascular risk factors found no increased cardiovascular mortality with febuxostat versus allopurinol and lower all-cause mortality with febuxostat, but excluded advanced CKD [27]. The cardiovascular and mortality risks of febuxostat, specifically in advanced chronic kidney disease, remain unclear. Further studies in patients with significant renal dysfunction are needed to clarify if cardiovascular concerns exist with febuxostat use in this population. A retrospective cohort study by Chung-te Liu found patients with a severely reduced estimated glomerular filtration rate (eGFR) had a higher risk of myopathy with febuxostat treatment. This suggests regular monitoring of creatine kinase levels for early detection of febuxostat-associated myopathy may be warranted, especially in chronic kidney disease (CKD) patients [28].
Recommendations: For febuxostat dosing in kidney impairment:
Creatinine clearance <30 mL/min: Recommended initial dose is 20–40 mg once daily. Observational studies have reported safety of 60 and 80 mg/day in hyperuricemia; careful titration can be considered in patients unresponsive to standard doses [29].
Intermittent hemodialysis (thrice weekly): Unlikely to be dialyzed due to high protein binding. The recommended initial dose is 20–40 mg once daily without supplemental dosing. A small observational study reported doses up to 80 mg/day were safe in hyperuricemia; careful titration may be done if unresponsive to standard doses [30].
  • Uricosurics
Uricosurics like probenecid, benzbromarone, and lesinurad promote uric acid excretion and are another urate-lowering therapy class. Probenecid is generally avoided with creatinine clearance <50 mL/min as it is thought ineffective [30]. Thus, the ACR guidelines strongly recommend allopurinol or febuxostat over probenecid in stage ≥3 chronic kidney disease. Benzbromarone has shown efficacy for creatinine clearance <25 mL/min but has been removed from many markets due to hepatotoxicity concerns [31]. Lesinurad is now withdrawn after a manufacturer decision and was contraindicated in creatinine clearance <45 mL/min [32]. In summary, uricosurics like probenecid and lesinurad have limited utility in advanced CKD due to renal clearance requirements. Benzbromarone may be effective, but it has toxicity concerns. Xanthine oxidase inhibitors like allopurinol or febuxostat are generally preferred over uricosurics for urate lowering in moderate-to-severe kidney disease. Combination therapy with a xanthine oxidase inhibitor (XOi) and a uricosuric can be very effective for lowering urate. If uricosuric toxicity results from high intratubular urate levels, then combination therapy could theoretically reduce this risk. However, uricosurics are usually avoided in advanced chronic kidney disease (CKD), so this approach is largely untested in this population.

4. In Hemodialysis Patients

Treating acute gout flares in patients on renal replacement therapy (RRT) can be challenging given the limitations of therapeutic options for this population with renal impairment. Glucocorticoids preferably administered intra-articularly, or interleukin-1 (IL-1) inhibitors are generally preferred for acute flare management over colchicine and NSAIDs, which have higher risks of side effects in the setting of limited kidney function [33].
For prophylaxis against paradoxical flares when initiating urate-lowering therapy (ULT), systemic glucocorticoids are often used due to concerns about adverse events with other prophylactic agents. However, chronic steroid exposure has known risks that must be weighed. Approaches using very low initial ULT doses without prophylaxis have demonstrated some success and could represent an option for flare prevention in this population [34].
Whether to continue ULT after the initiation of dialysis has been debated. Some data suggest that gout improves once dialysis is started. However, the overall prevalence of gout in the dialysis population remains substantial. Evidence on continuing ULT in patients on renal replacement therapy is limited, consisting mostly of case reports and series [35].

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Subjects: Rheumatology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Fares Saliba
,
Omar Mourad
,
Jonathan Mina
,
Fadi Haddadin
,
Laurence Aoun
,
Shaza Almardini
,
Saif Abu-baker
,
Koushik Sangaraju
,
Gaetano Di Pietro
,
Daniel Gaballa
,
Suzanne El-sayegh
View Times: 84
Revisions: 2 times (View History)
Update Date: 19 Mar 2024
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