Hyperuricemia hastens the decline of renal function in chronic kidney disease and activates the pro-inflammatory Nlrp3 inflammasome. Studies from the 1970s posited that high rates of hyperuricemia seen in sickle cell anemia (SCA) patients were due to high nucleotide production resulting from a chronic ischemia activated bone marrow. As such, serum uric acid (UA) levels may vary between states of vaso-occlusion. It is currently unknown whether serum UA is variable over time, nor the effect of hyperuricemia on renal injury and inflammation in SCA. In this prospective study, we measured serum and urine UA, renal injury and inflammation biomarkers among patients with SCA hospitalized for a vaso-occlusive crisis (VOC) and again at a time of baseline state of health without acute pain (steady state). We found no difference in the mean serum UA between VOC and steady state (mean difference = 0.01 SE 0.32, p = 0.5151). We found at VOC that renal excretion of UA was positively correlated with C Reactive Protein (CRP) (R 2 = 0.77, p = 0.0097), urine Interleukin-18 (IL-18; R 2 = 0.51, p = 0.0463), and urine Kidney Injury Molecule-1 (KIM-1; R 2 = 0.81, p = 0.0025). At steady state, we found negative correlations with renal excretion of UA and KIM-1 (R 2 = 0.86, p = 0.001) and N-acetyl-β-D-glucosaminidase (NAG; R 2 = 0.66, p = 0.0146). Our study is the first to describe lack of variation in serum UA between VOC and steady state. Future studies should be planned to determine mechanism of hyperuricemia development, and whether hyperuricemia is associated with sickle cell renal injury and inflammation.