Gout is uric acid crystallizing in a joint. The attack is unmistakable — usually the big toe, exquisitely painful and swollen within hours, tender enough that a bedsheet is intolerable.
Most people with gout are never treated for gout. They are treated for the attacks.
The attacks are not the disease
Colchicine. Prednisone. An NSAID. The flare subsides in a few days and everyone moves on until the next one.
None of those drugs touch the uric acid, and the uric acid is the disease.
The crystals sit in your joints between attacks. They accumulate. Every flare is the immune system finding a deposit that was already there. Treating the flare and stopping is the equivalent of treating a fever and ignoring the infection.
If you have had gout for years and nobody has told you your uric acid number, you have never been treated for gout. You have been managed through attacks.
That is the majority of gout patients in this country. Not a minority. The majority.
What treating the disease actually means
Urate-lowering therapy — usually allopurinol — dissolves the crystal deposits over months. That is the treatment. Everything else is symptom control.
The target is a serum urate below 6 mg/dL, and below 5 when tophi are present. That number is measured, the dose is adjusted, and the number is measured again.
The second failure, for those who are on it
If you take allopurinol and still get attacks: you are probably underdosed, and probably nobody has rechecked your level.
Allopurinol gets started at 100 or 300 mg and left there. The urate never comes to target. Attacks continue. The patient concludes the drug does not work and stops it.
The drug works. The dose was never titrated to the number. If you have been on allopurinol for a year and cannot tell me your last uric acid level, that is the gap.
Why a nephrologist
About two-thirds of uric acid is cleared by the kidneys. Reduced kidney function raises uric acid, and gout is substantially more common in chronic kidney disease.
It runs both directions. Diuretics raise uric acid. Uric acid stones form in acidic urine. Chronic hyperuricemia may itself damage the kidney.
And nearly every gout medication requires dose adjustment when kidney function is reduced. NSAIDs should generally be avoided outright. Colchicine needs reduction and is dangerous at standard doses in advanced kidney disease.
Allopurinol dosing in kidney disease is where this compounds. It was historically capped low out of a caution the evidence does not support — which means patients with gout and reduced eGFR are the least likely to ever reach target, and the most likely to be told the drug failed them.
That combination is where the errors concentrate, and it is where a nephrologist belongs.
Treating an attack
Still necessary, and worth doing well. Colchicine, an NSAID, or a corticosteroid, chosen by what else is wrong with you. Steroids are frequently the right answer at a low eGFR. An injection into the joint works well when only one is involved.
Starting within hours matters. Waiting a day means a worse and longer attack.
But the attack ends either way. What happens after it decides whether you have another.
What starting urate-lowering therapy feels like
It can provoke a flare as deposits dissolve. This is expected and is not a reason to stop. It is, in fact, evidence the drug is working.
We cover that period with prophylaxis. Patients who stop the drug here — and many do, because nobody warned them — lose years.
What raises uric acid
Red meat, organ meat, shellfish. Beer and alcohol generally. Fructose, especially in sweetened drinks.
Diuretics. Low-dose aspirin. Chronic kidney disease. Obesity. Dehydration.
Diet is worth doing and is almost never enough. Most patients who need urate-lowering therapy need it regardless of what they eat, and being told to fix gout with diet alone delays the treatment that works while the deposits keep growing.
| Raises uric acid | Notes |
|---|---|
| Red meat and shellfish | High-purine foods |
| Alcohol, especially beer | Raises production and blocks clearance |
| Sugary drinks (fructose) | A major modern driver |
| Certain diuretics | Common and often overlooked |
| Reduced kidney function | Less uric acid is cleared |
Where this ends if nothing changes
Tophi — visible urate deposits in soft tissue that can ulcerate. Permanent joint destruction. Uric acid stones. Progression of kidney disease.
All of it preventable, over years, by a cheap generic pill and a blood test twice a year.
If you have had more than one gout attack and nobody has checked your uric acid, that is the appointment.