Fig. 1

Pulmonary–renal damage patterns of COVID-19. Clinical and histopathological data of COVID-19-associated ARDS and AKI indicate common etiological factors, including direct virus-mediated cell damage, endothelial damage and thrombo-inflammation, dysregulation of the immune response and hyperinflammation, and dysregulation of the renin–angiotensin–aldosterone system. In addition, use of mechanical ventilation, hemodynamic instability, volume overload, superimposed sepsis, and collapsing glomerulopathy have all been implicated in glomerular disease and tubular damage in COVID-19. In contrast to bronchoalveolar lavage fluid, urine is accessible at any time point for non-invasive assessment of organ involvement. The urinary tubuloglomerular pattern may mirror the bronchoalveolar damage pattern and, thus, allow characterization and assessment of the stage of the pulmonary disease by means of serial urine analysis. The table summarizes potential candidate urinary markers that could inform lung injury in the setting of COVID-19-associated ARDS. However, it is unclear which marker is most accurate for this purpose and what cut-offs are needed, and this requires further investigation. The left histopathological image shows diffuse alveolar damage with hyaline membranes at the alveolar walls as morphologic correlate of ARDS. The right histopathological image shows acute tubular injury with flattened brush borders and cytoplasm of the epithelial cells in dilated tubules as morphologic correlate of AKI. ACE2 angiotensin-converting enzyme 2, AKI acute kidney injury, ARDS acute respiratory distress syndrome, COVID-19 coronavirus disease 2019, IGFBP7 insulin-like growth factor-binding protein 7, IL interleukin, PAI-1 plasminogen activator inhibitor-1, NGAL neutrophil gelatinase-associated lipocalin, RAAS renin–angiotensin–aldosterone system, SARS-CoV-2 severe acute respiratory syndrome coronavirus type 2, TIMP-2 tissue inhibitor of metalloproteinases-2, TNFR tumor necrosis factor receptor