Severe Polyarticular gout mimicking sepsis after acute kidney injury: a case report

Severe gout flares may rarely present as systemic inflammatory syndromes, closely mimicking sepsis. Milk-of-urate bullae are an uncommon manifestation of extensive crystal burden and are typically described in chronic tophaceous gout. The combination of polyarticular involvement, extreme inflammatory markers, acute kidney injury (AKI), and bullous lesions represents a diagnostic challenge.

A 69-year-old man presented with generalized weakness and incapacitating migratory joint pain after lying on the floor for three days. Laboratory evaluation revealed acute prerenal kidney injury and a fulminant inflammatory response (CRP 47.7 mg/dl, leukocytes 16.8 × 10³/μl, procalcitonin 4.05 ng/ml), prompting a sepsis work-up and empiric broad-spectrum antibiotics. No infectious focus was identified. 18F-FDG PET-CT demonstrated intense tracer uptake in multiple finger and toe joints, particularly in both first metatarsophalangeal joints. Over subsequent days, the patient developed erythema, swelling, and painful limitation of these joints, followed by bullous skin lesions containing milky fluid. Serum uric acid was elevated at 9.61 mg/dl. Polyarticular gout was diagnosed. After partial renal recovery, anti-inflammatory therapy with naproxen and colchicine was initiated, resulting in rapid clinical improvement and spontaneous ulceration of the urate bullae. Inflammatory markers normalized. Urate-lowering therapy with allopurinol was started prior to discharge.

This case illustrates how severe polyarticular gout can mimic fulminant sepsis with extreme inflammatory markers and FDG-PET hypermetabolism. Acute kidney injury acted as a trigger for catastrophic crystal inflammation. Milk-of-urate bullae reflected extensive systemic urate burden. Recognition of this pattern is essential to avoid diagnostic delay and unnecessary antimicrobial therapy.