Treatment of Acute Gout Flare in Chronic Kidney Disease
Low-dose oral corticosteroids (prednisone 30-40 mg daily for 5-7 days) are the safest first-line treatment for acute gout flares in patients with CKD, particularly in advanced stages (CKD 3-4), due to their high efficacy and avoidance of nephrotoxicity and drug interaction risks associated with NSAIDs and colchicine. 1
First-Line Treatment Options by CKD Stage
CKD Stage 3 (eGFR 30-59 mL/min)
Low-dose colchicine (1.2 mg followed by 0.6 mg one hour later, then 0.6 mg daily) is the preferred initial treatment when no contraindications exist, with dose reduction required in CKD. 2, 3
Glucocorticoids (oral or intra-articular) are equally appropriate first-line options, particularly when colchicine is contraindicated or not tolerated, with short courses of low-dose oral prednisone/prednisolone being effective and safe. 2
Avoid NSAIDs due to nephrotoxicity risk and potential for acute kidney injury. 2
CKD Stage 4 (eGFR 15-29 mL/min)
Low-dose oral corticosteroids (prednisone 30-40 mg daily for 5-7 days) are recommended as first-line therapy due to their high efficacy and tolerability in this population. 1
Intra-articular corticosteroid injection is equally effective for monoarticular or oligoarticular attacks and avoids systemic exposure, making it a suitable alternative. 1
NSAIDs are absolutely contraindicated in CKD stage 4 due to nephrotoxicity risk, potential for acute kidney injury, and cardiovascular complications. 1
Colchicine Dosing and Safety in CKD
Standard Acute Flare Dosing
The FDA-approved regimen for acute gout flares is 1.2 mg (two tablets) at the first sign of flare followed by 0.6 mg (one tablet) one hour later, with a maximum dose of 1.8 mg over one hour. 3
Higher doses have not been found to be more effective. 3
Critical Drug Interactions
Avoid concurrent use of strong CYP3A4 inhibitors (macrolides, diltiazem, verapamil, azole antifungals, cyclosporine, ritonavir/nirmatrelvir) with colchicine due to increased toxicity risk. 2
When colchicine must be used with strong CYP3A4 or P-gp inhibitors (clarithromycin, cyclosporine), reduce the acute flare dose to 0.6 mg × 1 dose, followed by 0.3 mg one hour later, with no repeat dosing for at least 3 days. 3
With moderate CYP3A4 inhibitors (diltiazem, verapamil, erythromycin), the acute flare dose should be 1.2 mg × 1 dose with no repeat for at least 3 days. 3
Toxicity Monitoring
The first symptom of colchicine poisoning is diarrhea; dosage must be reduced immediately if this occurs. 4
Colchicine toxicity is increased in patients with CKD, and dosage reduction is required based on level of kidney function. 5, 6
Alternative Treatments When First-Line Options Fail
- IL-1 inhibitors can be considered as a second-line option in case of failure, intolerance, or contraindication to colchicine, corticosteroids, and NSAIDs, though they are contraindicated in cases of infection and require neutrophil monitoring. 4
Initiating Urate-Lowering Therapy During Acute Flare
Consider starting allopurinol during or immediately after the acute flare rather than waiting for complete resolution, as delaying does not improve outcomes in patients with CKD. 1
Allopurinol remains the preferred first-line urate-lowering therapy even in CKD stage 4, and should be started at 50 mg daily (or every other day) and titrated every 2-5 weeks to achieve serum uric acid <6 mg/dL. 1, 7
When starting allopurinol, prescribe colchicine 0.5 mg daily (or every other day in CKD stage 4) for a minimum of 3-6 months to prevent acute flares. 1, 7
Common Pitfalls to Avoid
Do not use NSAIDs in CKD stage 3 or higher as they can exacerbate or cause acute kidney injury. 5, 6
Do not use standard colchicine dosing without checking for drug interactions, particularly with CYP3A4 and P-gp inhibitors, as fatal colchicine toxicity has been reported. 3
Do not delay treatment; the most important determinant of therapeutic success is how soon therapy is initiated, not which specific agent is chosen. 8
Do not forget flare prophylaxis when initiating urate-lowering therapy, as an increase in gout flares may occur after initiation due to mobilization of urate from tissue deposits. 3