SARS-CoV-2 infection and diabetes: Pathophysiological mechanism of multi-system organ failure

Figure 3 Possible mechanism of diabetes and severe acute respiratory syndrome coronavirus 2-induced renal dysfunction. Hyperglycemia in diabetes is associated with increased oxidative stress mediated endothelial cell (EC) dysfunction, hypovolemia, and diabetic ketoacidosis that subsequently induces renal dysfunction. Likewise, inflammation in diabetes is associated with increased oxidative stress mediated EC dysfunction and hypercoagulability mediated cardiac dysfunction that subsequently leads to renal dysfunction. On the other hand, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection reduces the availability of angiotensin converting enzyme-2 numbers, which results in elevated serum angiotensin II and subsequent kidney injury and fibrosis due to hypertension. Additionally, hypovolemia in SARS-CoV-2 infection induces renal dysfunction. Finally, inflammation in SARS-CoV-2 infection is associated with cytokine storm mediated endothelial cell dysfunction and upregulation of damage-associated molecular patterns, hypercoagulability mediated cardiac dysfunction results in renal dysfunction. EC: Endothelial cell; Ang II: Angiotensin II; ACE2: Angiotensin converting enzyme-2; DAMPs: Damage-associated molecular patterns; SARS-CoV-2: Severe acute respiratory syndrome coronavirus 2.