Table 2 Patterns and associated mechanisms of acute kidney injury in patients with COVID-19

Viral cytopathic effect

Proteins critical for mediating cellular SARS-CoV-2 infection– ACE2, TMPRSS2, and CTSL–are highly expressed in kidney [18, 36,37,38,39]. Expression is mainly localized to the apical brush border of proximal tubular cells and podocytes [36]. Viral protein and RNA have been demonstrated at the cellular level in kidney tissue, supporting a potential role for direct viral infection in the pathogenesis of AKI [18, 38,39,40,41]. Studies have demonstrated presence of mRNA in post mortem kidney tissues and its presence may correlate with clinical outcomes [42]. However, the specificity of these reports have been questioned, and the actual presence of replicating virus in renal epithelium remains controversial [43,44,45], as nucleic acid tests and immunohistochemistry failed to detect the virus in kidney tissues [23].

Hemodynamic compromise

AKI is more common in patients requiring mechanical ventilation and vasopressor support [7, 10]. Inadequate volume resuscitation and tissue hypoperfusion may lead to AKI. Hemodynamic compromise from pulmonary embolism, right ventricular dysfunction, and myocardial injury may contribute [46, 47].

The ARDS-AKI axis

AKI is the most common extra-pulmonary organ injury in ARDS via mechanisms including hypoxemia, reduced cardiac output, and systemic inflammation [48, 49]. Moreover, AKI-induced lung injury may further propagate severity of disease [50]. 10/20/2020 7:10:00 PM10/20/2020 7:10:00 PM

Glomerular injury

Possible direct viral effect and/or cytokine induced podocyte injury, along with a genetic predisposition, may result in collapsing glomerulopathy [9, 51,52,53,54,55,56].

Rhabdomyolysis

Rhabdomyolysis with histologic evidence of pigment deposition in renal tubules has been demonstrated [22, 40, 52, 57, 58].