Dialysis-requiring acute urate nephropathy and mobilization gout flare in a patient with alcoholic ketoacidosis: a case report

Abstract Background Acute urate nephropathy (AUN) is a rare but potentially reversible cause of acute kidney injury (AKI), typically associated with tumor lysis syndrome. We present a non-malignancy-related case induced by excessive alcohol abuse, highlighting post-dialysis diagnostic challenges and the therapeutic dilemma of managing a gout flare in the setting of recovering AKI. Case presentation A 51-year-old male with chronic alcohol dependence was admitted with severe azotaemia, hyperkalaemia, severe oliguria, and decompensated metabolic acidosis. Despite intensive conservative medical management, the life-threatening hyperkalaemia and acidosis could not be resolved, necessitating the initiation of urgent haemodialysis (HD). After excluding alternative etiologies for the acute-on-chronic kidney injury, the diagnosis of acute urate nephropathy was established based on the presence of abundant uric acid crystalluria and extreme hyperuricaemia. Following HD and rasburicase administration, renal function rapidly improved; however, the rapid decline in serum uric acid provoked a classic mobilization gout attack. Due to impaired recovering renal function, NSAIDs and colchicine were contraindicated. The flare was safely and effectively managed with a standard-dose oral corticosteroid regimen. Conclusions Urgent haemodialysis can mask classic biochemical markers of AUN; thus, urine sediment analysis is essential. A rapid reduction in uric acid can trigger crystal mobilization and acute flares. In the vulnerable phase of AKI, corticosteroids represent the safest therapeutic option for acute gout.