Introduction: Hyperuricemia is related with several diseases, such as cardiovascular diseases, and renal disease. Fructose is a simple sugar that is present in fruits. Rapidly administration of fructose increase serum uric acid by increasing the degradation of purine nucleotides and synthesis of purine. Especially, in patients with renal dysfunction or gout, hyperuricemia related with excess fructose is easily developed. The severe hyperuricemia by fructose can be a cause of AKI which is abruptly developed. Case Report: A 58-year-old man visited due to abdominal discomfort and edema. He recently complained of oliguria. He had a gout and hypertension, and he also had a history of thyroid cancer. He is taking on ARB and turmeric for gout. He denied symptom such as diarrhea, a gouty attack was not recently developed. His serological data revealed followings: blood urea nitrogen, 101 mg/dL; creatinine, 14.46 mg/dL; uric acid, 30.0 mg/dL; bicarbonate, 14.3 mM/L. CT showed only several stones in both renal calyxes. He was treated with intravenous saline and bicarbonate for AKI and alkalization. Only several times of hemodialysis were required due to uremic symptoms. After six months later, his serum uric acid and creatinine levels returned to normal with only supportive treatment. Discussion: Intrinsic AKI is suspected but AKI caused by turmeric is rare. However, the patient took mixture of honey and turmeric 3 times daily for one year. The depletion of ATP related phosphorylation of fructose stimulates synthesis of uric acid. Thus, excessive fructose intake can be a cause of severe hyperuricemia. Hyperuricemia can lead to AKI by oxidative stress. We could not find cause of AKI except of excessive fructose and severe hyperuricemia. Therefore, the excess fructose in susceptible condition such as gout may easily result in AKI. Conclusively, fructose may clinically consider as a regulatory factor on the management of hyperuricemia.