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Kidney Week

Abstract: PO0216

Dietary Hyperuricemia Causes Nephropathy in a Cancer Patient

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology, Risk Factors, and Prevention

Authors

  • Ali, Aliasger Aun, The University of Texas Health Science Center at Houston John P and Katherine G McGovern Medical School, Houston, Texas, United States
  • Bejjanki, Harini, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States
  • Kala, Jaya, The University of Texas Health Science Center at Houston John P and Katherine G McGovern Medical School, Houston, Texas, United States

Group or Team Name

  • UT Houston/MD Anderson
Introduction

Hyperuricemia is associated with several diseases including kidney disease. Everyday drinks (sodas/juices) have very high fructose content, contributing to hyperuricemia through various mechanisms. Here we present a case of a cancer patient with Acute Kidney Injury (AKI) secondary to hyperuricemia in the setting of a sudden high intake in fructose rich drinks.

Case Description

A 49-year-old Asian man with history of myelofibrosis, coronary artery disease and chronic kidney disease stage 2, was admitted for AKI. He was recently admitted for septic shock due to scrotal abscess and discharged to a nursing home for wound care. He endorsed recent high intake of sodas and juices, due to dislike of food at the nursing home. His creatinine at previous admission was 1.1–1.4 mg/dl (similar to his baseline). His urinalysis (UA) routinely did not show uric acid crystals, and uric acid levels were within reference range. One week prior to admission, his creatinine was 1.97 mg/dl and UA showed occasional uric acid crystals. At current admission, creatinine was 3.02 mg/dl with uric acid level of 23.3 mg/dl, and UA showed uric acid crystals. He received 3 doses of 3 mg Rasburicase (9 mg total) the first day, after which uric acid level improved to 6.4 mg/dl, and creatinine dropped to 2.14 mg/dl. Three days later his creatine improved to 1.76 mg/dl, and repeat UA did not show uric acid crystals. A week after discharge, his creatinine was at baseline and uric acid level was normal. By the time visual examination of urine could be done, uric acid level had normalized.

Discussion

It is known that fructose is the only carbohydrate that increases uric acid levels. Fructose-induced hyperuricemia results from an increased degradation of purine ribonucleotides and causes increased purine synthesis. Hyperuricemia is common in patients with hematological malignancies with or without chemotherapy. Our patient had a hematological malignancy and endorsed drinking large amounts of soda and juice. Given many patients drink fructose rich drinks daily, it is imperative that the dangers of this dietary habit are highlighted, both to physicians and patients. Cancer patients can benefit from nutrition education and dietary modifications prior to and during chemotherapy to avoid hyperuricemia and renal failure. Dietary counselling can help avoid need for hospitalization as well as use of expensive uric acid lowering agents.