What are the consequences of not taking allopurinol in a patient with gout?

Medical Advisory BoardAll articles are reviewed for accuracy by our Medical Advisory Board
Educational purpose only • Exercise caution as content is pending human review
Article Review Status
Submitted
Under Review
Approved

Last updated: April 24, 2026 • View editorial policy

Have a follow-up question?

Our Medical A.I. is used by practicing medical doctors at top research institutions around the world. Ask any follow up question and get world-class guideline-backed answers instantly.

What Happens When You Have Gout and Don't Take Allopurinol?

If you have gout and don't take allopurinol (or another urate-lowering therapy), you will experience recurrent, painful gout flares and progressive joint damage from ongoing monosodium urate crystal deposition in your joints and soft tissues, potentially leading to chronic gouty arthropathy, tophi formation, and kidney complications.

The Natural Course of Untreated Gout

Without urate-lowering therapy like allopurinol, gout follows a predictable and damaging trajectory:

Progressive Joint Damage and Flares

  • Recurrent acute attacks: You'll continue having painful gout flares with increasing frequency over time. The inflammatory attacks cause severe joint pain, swelling, and disability during each episode 1.
  • Chronic tophaceous gout: Persistent hyperuricemia leads to progressive deposition of monosodium urate crystals in joints and soft tissues, forming tophi (visible lumps of urate crystals). This represents irreversible tissue damage 1.
  • Chronic gouty arthropathy: Long-term crystal deposition causes permanent joint destruction, chronic pain, and functional impairment that significantly impacts quality of life 1.

Kidney Complications

  • Urolithiasis: Elevated uric acid increases risk of kidney stone formation 1.
  • Acute kidney injury: Patients with untreated gout face higher risk of acute kidney injury, particularly when using NSAIDs to treat recurrent flares 2. Interestingly, allopurinol use was associated with lower risk of acute kidney injury in gout patients 2.
  • Progressive renal damage: Chronic hyperuricemia and urate crystal deposition can contribute to kidney damage over time 1.

Why Allopurinol Is Essential

The 2020 American College of Rheumatology guidelines strongly recommend allopurinol as the preferred first-line agent for all gout patients requiring urate-lowering therapy 3. Here's the mechanistic rationale:

How Allopurinol Works

Allopurinol inhibits xanthine oxidase, the enzyme that converts hypoxanthine to uric acid. This reduces both serum and urinary uric acid levels, typically achieving measurable reductions within 2-3 days 1. The goal is to lower serum urate below the saturation point (typically <0.36 mmol/L or <6 mg/dL) to:

  • Prevent new crystal formation
  • Dissolve existing crystal deposits
  • Stop the cycle of recurrent flares

The Critical Difference

Unlike uricosuric drugs that increase urinary uric acid excretion (potentially worsening kidney problems), allopurinol reduces uric acid production, making it safer for patients with renal impairment 1.

When Treatment Is Indicated

The guidelines provide clear direction on who needs allopurinol:

Strong Indications for Starting Allopurinol

  • Recurrent gout attacks (≥2 episodes per year) 4
  • Presence of tophi 4
  • Chronic kidney disease 4
  • Urolithiasis 4
  • Chronic gouty arthropathy

When You Might Defer Treatment

The 2017 American College of Physicians guideline suggests you can consider not starting long-term urate-lowering therapy after a first gout attack or with infrequent attacks (<2 per year), as not all patients will have frequent recurrences 4. However, this is a shared decision requiring discussion of individual risk factors.

Important caveat: Even patients with higher serum urate levels (>9 mg/dL) have only a 20% chance of developing gout within 5 years, so asymptomatic hyperuricemia alone is not an indication for allopurinol 3.

The Adherence Problem

A major challenge is that compliance with allopurinol is notoriously poor:

  • Only 18% of patients remain compliant throughout treatment 5
  • Patients are compliant only 56% of the time on average 5
  • 10.4% discontinue after just one prescription 5

Why Patients Stop Taking Allopurinol

The most common reasons patients give for not taking allopurinol include 6:

  • Wanting to lead a normal life (23%)
  • Testing if they really need it (22%)
  • Wanting to think of themselves as healthy (20%)

This is problematic because untreated gouty arthritis leads to serious adverse outcomes that are usually avoidable with proper urate-lowering therapy 5.

Clinical Outcomes Without Treatment

Quality of Life Impact

Without allopurinol, you face:

  • Recurrent episodes of severe joint pain requiring treatment with NSAIDs or colchicine
  • Progressive functional impairment from chronic joint damage
  • Visible tophi causing cosmetic concerns and mechanical joint problems
  • Increased healthcare utilization for acute flare management

Mortality Considerations

While allopurinol shows a neutral effect on all-cause mortality in gout patients 7, the real benefit is in preventing the morbidity associated with recurrent flares and chronic joint damage. The medication's value lies in preventing disability and improving quality of life, not necessarily extending lifespan.

The Bottom Line

Without allopurinol or alternative urate-lowering therapy, gout will progress from episodic painful attacks to chronic, disabling arthropathy with permanent joint damage and potential kidney complications. The 2020 ACR guidelines strongly recommend starting allopurinol (beginning at low doses ≤100 mg/day with gradual titration) for patients with recurrent gout attacks, tophi, or other complications 3. The key is achieving and maintaining serum urate below 0.36 mmol/L (6 mg/dL) to prevent crystal deposition and allow existing deposits to dissolve 1.

Related Questions

A patient had a serum uric acid level of 8 mg/dL last month and was started on allopurinol 100 mg daily and colchicine. When should the uric acid level be rechecked, and at what point should the allopurinol dose be increased?
Do gouty tophi shrink or resolve with effective allopurinol therapy, or are they permanent?
What are the recommendations for using allopurinol in patients with mild Acute Kidney Injury (AKI)?
When should allopurinol be initiated in a patient experiencing an acute gout flare?
Can increasing the dose of allopurinol precipitate acute gout attacks?
What is the conversion of vitamin D 50 micrograms to international units (IU)?
How much normal saline should be mixed with a 500 mg Rocephin (ceftriaxone) for intramuscular administration?
What is the significance of an early precordial transition on an otherwise normal sinus rhythm electrocardiogram?
In peritoneal dialysis, how does icodextrin (7.5% high‑molecular‑weight glucose polymer) achieve better ultrafiltration than conventional dextrose solutions (1.5‑2.5%)?
In a 75‑year‑old patient with chronic kidney disease (glomerular filtration rate ≈30 mL/min) receiving metronidazole 500 mg three times daily IV and azithromycin 500 mg daily IV for a persistent upper respiratory infection, with resolved diarrhea, mild AST elevation, serum potassium 5 mmol/L, and Ringer’s lactate 60 mL/h, how should the antimicrobial dosing, potassium management, and fluid therapy be adjusted?
What non‑pharmacologic treatments are recommended for managing gout?

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.