text: Kidney in the net of acute and long haul coronavirus disease 2019 a potential role for lipid mediators in causing renal injury and fibrosis Severe COVID 19 disease is often complicated by acute kidney injury AKI which may transition to chronic kidney disease CKD Better understanding of underlying mechanisms is important in advancing therapeutic approaches SARS CoV 2 induced endothelial injury initiates platelet activation platelet neutrophil partnership and release of neutrophil extracellular traps The resulting thromboinflammation causes ischemia reperfusion I R injury to end organs Severe COVID 19 induces a lipid mediator storm with massive increases in thromboxane A2 TxA2 and PGD2 which promote thromboinflammation and apoptosis of renal tubular cells respectively and thereby enhance renal fibrosis COVID 19 associated AKI improves rapidly in the majority However 15 30 have protracted renal injury raising the specter of transition from AKI to CKD In COVID 19 the lipid mediator storm promotes thromboinflammation ischemia reperfusion injury and cytotoxicity The thromboxane A2 and PGD2 signaling presents a therapeutic target with potential to mitigate AKI and transition to CKD Ramatroban the only dual antagonist of the thromboxane A2 TPr and PGD2 DPr2 signaling could potentially mitigate renal injury in acute and long haul COVID Urgent studies targeting the lipid mediator storm are needed to potentially reduce the heavy burden of kidney disease emerging in the wake of the current pandemic 