Prevalence and Outcomes Associated with Hyperuricemia in Hospitalized Patients with COVID-19.

IF 5.5 3区 材料科学 Q2 CHEMISTRY, PHYSICAL ACS Applied Energy Materials Pub Date : 2022-01-01 Epub Date: 2021-12-09 DOI:10.1159/000520355
Kinsuk Chauhan, Pattharawin Pattharanitima, Federica Piani, Richard J Johnson, Jaime Uribarri, Lili Chan, Steven G Coca
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Abstract

Introduction: Coronavirus 2019 (COVID-19) can increase catabolism and result in hyperuricemia. Uric acid (UA) potentially causes kidney damage by alteration of renal autoregulation, inhibition of endothelial cell proliferation, cell apoptosis, activation of the pro-inflammatory cascade, and crystal deposition. Hyperuricemia in patients with COVID-19 may contribute to acute kidney injury (AKI) and poor outcomes.

Methods: We included 834 patients with COVID-19 who were >18 years old and hospitalized for >24 h in the Mount Sinai Health System and had at least 1 measurement of serum UA. We examined the association between the first serum UA level and development of acute kidney injury (AKI, defined by KDIGO criteria), major adverse kidney events (MAKE, defined by a composite of all-cause in-hospital mortality or dialysis or 100% increase in serum creatinine from baseline), as well as markers of inflammation and cardiac injury.

Results: Among the 834 patients, the median age was 66 years, 42% were women, and the median first serum UA was 5.9 mg/dL (interquartile range 4.5-8.8). Overall, 60% experienced AKI, 52% experienced MAKE, and 32% died during hospitalization. After adjusting for demographics, comorbidities, and laboratory values, a doubling in serum UA was associated with increased AKI (odds ratio [OR] 2.8, 95% confidence interval [CI] 1.9-4.1), MAKE (OR 2.5, 95% CI 1.7-3.5), and in-hospital mortality (OR 1.7, 95% CI 1.3-2.3). Higher serum UA levels were independently associated with a higher level of procalcitonin (β, 0.6; SE 0.2) and troponin I (β, 1.2; SE 0.2) but were not associated with serum ferritin, C-reactive protein, and interleukin-6.

Conclusion: In patients admitted to the hospital for COVID-19, higher serum UA levels were independently associated with AKI, MAKE, and in-hospital mortality in a dose-dependent manner. In addition, hyperuricemia was associated with higher procalcitonin and troponin I levels.

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COVID-19 住院患者中高尿酸血症的患病率和相关结果
导言冠状病毒 2019(COVID-19)可增加分解代谢,导致高尿酸血症。尿酸(UA)可通过改变肾脏自动调节、抑制内皮细胞增殖、细胞凋亡、激活促炎症级联反应和晶体沉积而造成肾脏损伤。COVID-19 患者的高尿酸血症可能导致急性肾损伤(AKI)和不良预后:我们纳入了 834 例 COVID-19 患者,这些患者年龄大于 18 岁,在西奈山医疗系统住院超过 24 小时,至少测量过一次血清 UA。我们研究了首次血清 UA 水平与急性肾损伤(AKI,根据 KDIGO 标准定义)、主要肾脏不良事件(MAKE,根据院内全因死亡率或透析或血清肌酐比基线增加 100% 的复合定义)以及炎症和心脏损伤标志物之间的关系:在 834 名患者中,中位年龄为 66 岁,42% 为女性,首次血清尿酸中位数为 5.9 mg/dL(四分位数范围为 4.5-8.8)。总体而言,60%的患者出现了 AKI,52%的患者出现了 MAKE,32%的患者在住院期间死亡。在对人口统计学、合并症和实验室值进行调整后,血清 UA 增高一倍与 AKI(比值比 [OR] 2.8,95% 置信区间 [CI] 1.9-4.1)、MAKE(比值比 2.5,95% 置信区间 [CI] 1.7-3.5)和院内死亡率(比值比 1.7,95% 置信区间 [CI] 1.3-2.3)增加有关。较高的血清 UA 水平与较高的降钙素原(β,0.6;SE 0.2)和肌钙蛋白 I(β,1.2;SE 0.2)水平独立相关,但与血清铁蛋白、C 反应蛋白和白细胞介素-6 无关:结论:在因 COVID-19 入院的患者中,较高的血清 UA 水平与 AKI、MAKE 和院内死亡率呈剂量依赖关系。此外,高尿酸血症还与降钙素原和肌钙蛋白 I 水平升高有关。
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来源期刊
ACS Applied Energy Materials
ACS Applied Energy Materials Materials Science-Materials Chemistry
CiteScore
10.30
自引率
6.20%
发文量
1368
期刊介绍: ACS Applied Energy Materials is an interdisciplinary journal publishing original research covering all aspects of materials, engineering, chemistry, physics and biology relevant to energy conversion and storage. The journal is devoted to reports of new and original experimental and theoretical research of an applied nature that integrate knowledge in the areas of materials, engineering, physics, bioscience, and chemistry into important energy applications.
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