ABSTRACT
Infections may directly invade kidney or cause immune mediated injury, antigens of microorganisms' form circulating immune-complexes what is seen in post infectious glomerulonephritis. Renal injury may occur in multi-organ failure as is the case in systemic infammatory response syndrome (SIRS) or altered cytokine expression, hemodynamic instabilities, hemolysis, rhabdomyolysis, and cardio or hepatorenal syndrome. Nearly all viral infections can induce kidney injury by various mechanisms including direct cytopathic effects to immune complex mediated GN and vasculitis as well. Hepatitis B, hepatitis C, human immunodefciency virus, hantavirus and coronavirus disease 2019 (COVID-19) infections can induce glomerulopathy. Many of the viral infections such as parvovirus, Epstein-Barr virus and cytomegalovirus have been associated with very severe injury in the form of collapsing focal segmental glomerulosclerosis. Clinicopathological manifestations of viral infections include;Acute kidney injury (AKI) which is the most common presentation and can be de novo or acute on chronic kidney disease, acute and chronic glomerulonephritis syndrome, nephrotic syndrome, nephritic-nephrotic syndrome, acute or chronic tubulointerstitial nephritis, and rapidly progressive glomerulonephritis. Up to forty percent of patients who recover AKI may develop chronic kidney disease (CKD). Renal involvement is common in patients with COVID-19 infections;patients can present with proteinuria and hematuria even in moderately involved patients and at hospital admission, but AKI frequently develops in critically ill patients and is a marker of multiple organ dysfunction and ominous outcome. Fluid resuscitation at emergency department and lung-protective measures lowers the risk of AKI by obviating ventilator-induced hemodynamic disturbances and cytokine storm effects on the kidneys.