Proposed mechanisms include direct viral-induced tubular or glomerular injury, altered renin-angiotensin-aldosterone (RAAS) regulation, rhabdomyolysis, and thrombotic disease [8,9]. Kidney biopsy findings include acute tubular necrosis [10], glomerular fibrin thrombi, pigmented tubular casts, and collapsing focal segmental glomerulosclerosis [9]. Here, REN is linked to focal segmental glomerulosclerosis.