Gout, Tophi and the Kidneys (PRA 2011 Presentation Part 2)

Depending on the stage of the disease, treatment goals for gout may vary. These usually include:
  • Terminating attacks of gout as soon as possible
  • Preventing the recurrence of flares
  • Preventing and reversing complications
In patients with chronic kidney disease, achieving these treatment goals become difficult due to the potential complications arising from available therapies. When treating gout in a patient with chronic kidney disease, only colchicine, steroids, and some urate lowering drugs can still be used.
Steroids. Steroids are the most effective drugs to use when treating acute flares of gout – whether ina patient with uncomplicated or complicated forms. It’s use as a prophylactic agent is controversial as even patients receiving high doses of the drug for other medical indications still develop flares. Literature have cited use ofPrednisone from 20-50 mg/day for a mean duration of 10 days. Used properly, a dramatic response would be expected within 48 hours. Most of the time, a poor response is observed if steroids are immediately tapered off before clinical improvement. It would then be reasonable to maintain a high initialdose for 3 days  before tapering.Most would agree that cosyntrophin or ACTH is effective in treating acute gout due to its action of stimulating endogenous steroid production. However, recent literature cite its ability to stimulate peripheral melanocortin 3 receptors which would help suppress the ongoing inflammatory process. Some would believe that this make the drug more effective than steroids. The prescribed dose is 25 IU IM for monoarticular flares and 40 IU IM for polyarticular flares. For most patients, a second injection given 24-48 hours after the first one may be needed to completely terminate a gout attack.

Colchicine. Colchicine is effective in terminating an acute attack if administered within 12 hours of symptom onset. However, it is an even better prophylactic agent against gout flares. A recent randomized controlled trial had compared the efficacy of low-dose colchicine (1.8 mg/day) versus the more popularly used high-dose colchicine (4.8 mg/day – given as a 1.2 mg initial dose followed by 0.6 mg every 2 hours until either the attack stops or the patient develops toxicity to diarrhea). The study found that the low-dose schedule is as effective as the high dose administration of the drug but with a safety profile comparable to placebo. This should discourage doctors from using high-doses of colchicine since, most of the time, patients develop toxicity (diarrhea in particular) before the arthritis gets better. For prophylaxis, standard doses of the drug are within the 0.6 – 1.8 mg/day range.

No dose adjustments in colchicine is warranted if Creatinine Clearance (Cr Cl) is >50ml/min. However, the maximum dose of colchicine is 0.6 mg/day if CrCl is 35-49ml/min and 0.6mg every 2-3 days if CrCl is 10-34ml/min, Colchicine should be avoided in patients with CrCl <10ml/min and in patients undergoing hemodialysis. The drug is non-dialyzable and continued use predisposes to toxicity. Other contra-indications  are significant liver disease and combined liver and renal  Some authors recommend monitoring muscle enzymes if we decide to give colchicine in patients with CrCl<50 ml/min.

We should also be careful when co-administering colchicine with the following drugs: macrolides (i.e. clarithromycin), statins (i.e. pravastatin), ketoconazole and cyclosporin. There have been case reports of significant toxicity when colchicine is given together with these drugs in patients with renal disease.

Reference: El-Zawawy H, Mandell B. Managing gout: How is it different in patients with chronic kidney disease. Cleveland Clinic J Med 2019; 77 (12): 919-28.


Author: Sids Manahan MD 🇵🇭

Rheumatology. Internal Medicine. Educating Patients and Colleagues. Curating Rheumatology. Bloggero-Wanabe.

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