Gout is the most common form of inflammatory arthritis affecting 1.5 % of the UK population. Various clinical presentations exist with an underlying common pathophysiology of urate crystal deposition within tissues causing inflammation and tissue damage. The key risk factor is hyperuricaemia.

A raised serum urate is common in chronic kidney disease, predominantly from a combination of impaired clearance and diuretic use. Although many patients with hyperuricaemia remain asymptomatic, some will present with an acute attack of gout. Less commonly, acute kidney injury due to uric acid nephropathy may be seen as part of the acute tumour lysis syndrome in patients undergoing chemotherapy or radiation therapy for the treatment of malignancies with rapid cell turnover, such as leukemia and lymphoma.

In much the same way as you would diagnose gout in a patient who does not have renal disease, namely with pain, inflammation and often immobility of a single joint. Eighty percent of presentations involve the lower limb. Important clues to the diagnosis are involvement of the first MTP joint and the presence of gouty tophi, but gout should be considered in a differential diagnosis of any kidney patient with monoarthritis. The demonstration of negatively birefringent uric acid crystals in joint fluid is pathognomonic for acute gout though it is frequently not possible to obtain a sample of joint fluid, for example if the first MTP joint is the only joint involved.

The most important is probably septic arthritis. Leucocytosis and fever may be present in both. The only certain way to distinguish septic arthritis from acute gout is by aspiration and culture of joint fluid. The distinction is critical because the treatment of gout is with anti-inflammatory drugs and the treatment of septic arthritis is with a prolonged course of antibiotic. Pseudogout, which often presents as a hot swollen knee in elderly with OA, is another important differential. Patients with pseudogout have chondrocalcinosis on x-ray & rhomboid crystals of calcium pyrophosphate in synovial fluid.

Serum uric acid is not helpful in diagnosis but is an important target for prevention. Not every patient with hyperuricaemia will develop gout and serum uric acid may fall during an acute attack, becoming falsely negative. Serum uric acid is an important target for prevention of gout with drugs that inhibit its production, the doses of which should be increased until the serum uric acid falls below 0.30 mmol/l, if tolerated.

Treat as soon as possible with NSAIDs, colchicine or steroids. NSAIDs should be given in full doses. There is no evidence to suggest that any one NSAID is better than any other. The starting dose of colchicine for acute gout in patients with normal renal function is 1 mg stat then 0.5 mg tds until the attack resolves or gastrointestinal side effects develop. Prednisolone 40 mg once daily for 5–10 days is an effective alternative if NSAIDs or colchicine are contraindicated or poorly tolerated. Allopurinol should not be started during an acute attack but in patients already established on allopurinol, it should be continued and the acute attack treated conventionally. Opiate analgesics can be used as adjuncts. Rest, cold packs and splintage can be helpful.

The options are the same but NSAIDs and colchicine are relatively contraindicated. NSAIDs may cause a reversible decline in renal function. This might be acceptable if given for a few days to patients whose renal function is only mildly impaired but generally they are best avoided. The impact on renal function is less relevant on regular dialysis although the use of NSAIDs is often then limited by hyperkalaemia and GI upset. Colchicine is cleared by the kidney. Some patients can abort an acute attack of gout by taking 0.5–1 mg at the very first twinge but higher doses are not recommended when GFR <60 ml/min and for this reason a short course of prednisolone may be the best option.

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