Based on the existing literature, we speculate that the sudden increase in UA after living donation might result in the poor recovery of renal function through endothelial dysfunction, [9] inflammation, vasoconstriction, [10, 11] and increased COX-2 expression [12], which may eventually lead to hypertension, [51, 52] hyperglycemia, and dyslipidemia [53, 54]. The gene discussed is PTGS2; the disease is metabolic syndrome.