In the absence of kidney disease, the treatment of an acute attack of gout involves the use of a nonsteroidal anti-inflammatory drug (NSAID) (see Chapter 19) or an adrenocortical steroid taken in pill form, or drugs that promote the urinary excretion of uric acid. None of these treatments is safe in people with chronic kidney disease. However, doctors do prescribe allopurinol, which inhibits the production of uric acid whether kidney disease is present or not. Unfortunately, dietary restrictions are of little value in reducing attacks of gout.
When gout occurs in the course of renal failure, patients should avoid NSAIDs, steroids, and drugs that promote uric acid excretion, because all may adversely affect kidney function. Colchicine, a drug that does not injure the kidneys, is available, but it may cause other problems, as detailed below. This drug inhibits the formation of the microcrystals of uric acid that form in joints and give rise to the symptoms of gout. It is given hourly, in doses of 0.65 mg, until diarrhea occurs. By this time the symptoms of gout disappear. In fact, this response is so characteristic that it is used as a diagnostic test for gout. If colchicine does not work, hot soaks of the affected joint may help. In severe cases, it may be necessary to inject cortisol into the affected joint.
Sodium bicarbonate (see Chapter 10) alkalinizes the urine, preventing the formation of uric acid stones, and also may help prevent further kidney damage.
A daily dose of one or two colchicine tablets is also very effective in preventing future attacks, but occasionally such treatment leads to serious or even fatal toxicity. French researchers have described patients with chronic renal failure given 1 mg per day of colchicine (a small dose) who developed severe neuromyopathy (weakness, neuralgia, and muscle dissolution) within a week; two of them died. Clearly, colchicine should not be prescribed long term for patients with chronic renal failure.
Patients with elevated serum uric acid concentrations (whether they have kidney disease or not) should be prescribed daily allopurinol, which specifically blocks the synthesis of uric acid. The dose of allopurinol should be sharply reduced in patients with severe renal failure, because their bodies metabolize it more slowly; 50 mg per day or even as little as 25 mg per day may be about right. Some patients show allergic reactions to allopurinol; they may be treated effectively with oxypurinol instead.
Occasional patients exhibit low uric acid levels, reflecting a hereditary defect. This has nothing to do with chronic renal failure, except that such people tend to form kidney stones composed of uric acid and may develop acute kidney failure after exercise. Treatment of uric acid stone-formers is simple: daily doses of sodium bicarbonate. As noted in Chapter 10, this makes uric acid more soluble.
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