Department of Pediatric Nephrology, Biocruces Bizkaia Health Research Institute, Cruces University Hospital, Barakaldo, Bizkaia, Spain.
Department of Pediatrics, Biocruces Bizkaia Health Research Institute, Cruces University Hospital, Barakaldo, Bizkaia, Spain.
Clin Exp Nephrol. 2024 Jan;28(1):13-22. doi: 10.1007/s10157-023-02394-2. Epub 2023 Sep 26.
Hyperuricemia contributes to decrease in kidney function and induces additional renal damage in children with acute kidney injury (AKI). Rasburicase oxidizes uric acid (UA), decreasing its serum quantities in less than 24 h.
This is a retrospective study involving hospitalized patients under 18 years of age with underlying pathology diagnosed with AKI and severe hyperuricemia treated with rasburicase over a 4-year period.
We describe 15 patients from 4 days of life to 18 years (median: 4.4 years). Seventy-three percent had known underlying pathologies. All presented worsening of basal renal function or AKI data. All received the usual medical treatment for AKI without response. Twenty percent received an extrarenal depuration technique. All had hyperuricemia with a mean (± SD) of 13.1 (± 2.19) mg/dl. After rasburicase administration UA levels fell to a mean (± SD) of 0.76 (± 0.62) mg/dl (p < 0.001) in less than 24 h. In parallel, a decrease in the mean plasma creatinine was observed (2.92 mg/dl to 1.93 mg/dl (p = 0.057)) together with a significant improvement of the mean glomerular filtration rate (16.3 ml/min/1.73 m to 78.6 ml/min/1.73 m) (p = 0.001)). No side effects were recorded. Kidney function normalized in all cases or returned to baseline levels.
Although the use of rasburicase is not routinely approved in pediatric patients with severe hyperuricemia and AKI, it has been used successfully without complications, and helped prevent progressive kidney damage. This study could serve as a basis for suggesting the off-label use of rasburicase for the management of complex pediatric patients in whom UA plays an important role in the development of AKI.
高尿酸血症可导致肾功能下降，并在儿童急性肾损伤（AKI）中诱发额外的肾脏损伤。尿酸氧化酶可将尿酸（UA）氧化，在不到 24 小时内降低其血清含量。
这是一项回顾性研究，纳入了在过去 4 年中因 AKI 和严重高尿酸血症而接受尿酸氧化酶治疗的 18 岁以下基础疾病诊断为 AKI 的住院患者。
我们描述了 15 名患者，年龄从 4 天到 18 岁（中位数：4.4 岁）。73%的患者有已知的基础疾病。所有患者的基础肾功能或 AKI 数据均恶化。所有患者均接受 AKI 的常规治疗，但均无反应。20%的患者接受了肾脏外清除技术。所有患者均有高尿酸血症，平均（±标准差）为 13.1（±2.19）mg/dl。尿酸氧化酶给药后，UA 水平在不到 24 小时内降至平均（±标准差）0.76（±0.62）mg/dl（p<0.001）。同时，观察到平均血浆肌酐水平下降（从 2.92mg/dl 降至 1.93mg/dl（p=0.057）），肾小球滤过率（GFR）的平均水平显著改善（从 16.3ml/min/1.73m 升至 78.6ml/min/1.73m）（p=0.001））。未记录到不良反应。所有患者的肾功能均恢复正常或恢复至基线水平。
尽管尿酸氧化酶在儿童严重高尿酸血症和 AKI 患者中并非常规批准使用，但它已成功用于无并发症，并有助于预防进行性肾损伤。本研究可为建议在 UA 在 AKI 发展中起重要作用的复杂儿科患者中应用尿酸氧化酶提供依据。
