Prevalence and outcomes associated with hyperuricemia in hospitalized patients with COVID-19

Background: 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 proinflammatory cascade, and crystal deposition. Hyperuricemia in patients with COVID-19 may contribute to acute kidney injury and poor outcomes. Methods: We included 834 patients with COVID-19 who were >18 years old and hospitalized for >24 hours in the Mount Sinai Health System and had at least one measurement of serum UA. We examined the association between the first serum UA level and major adverse kidney events (MAKE, defined by a composite of all-cause in-hospital mortality or RRT 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 UA was 5.9 mg/dL (IQR 4.5-8.8). Overall, 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 MAKE (OR 2.5 per doubling, 95% CI 1.7-3.5) and in-hospital mortality (OR 1.7 per doubling, 95% CI 1.3-2.3) (Figure A & B). Serum UA levels were independently associated with a higher level of procalcitonin (β, 0.6;SE 0.2) and troponin (β, 1.2;SE 0.2) but was not associated with the serum ferritin, CRP, or IL-6 (Figure C). Conclusions: In patients admitted to the hospital for COVID-19, higher UA levels were independently associated with MAKE and mortality in a dose-dependent manner. In addition, hyperuricemia was associated with higher procalcitonin and troponin levels.