Although respiratory failure and hypoxaemia are the main manifestations of COVID-19, kidney involvement is also common. Available evidence supports a number of potential pathophysiological pathways through which acute kidney injury (AKI) can develop in the context of SARS-CoV-2 infection. Histopathological findings have highlighted both similarities and differences between AKI in patients with COVID-19 and in those with AKI in non-COVID-related sepsis. Acute tubular injury is common, although it is often mild, despite markedly reduced kidney function. Systemic haemodynamic instability very likely contributes to tubular injury. Despite descriptions of COVID-19 as a cytokine storm syndrome, levels of circulating cytokines are often lower in patients with COVID-19 than in patients with acute respiratory distress syndrome with causes other than COVID-19. Tissue inflammation and local immune cell infiltration have been repeatedly observed and might have a critical role in kidney injury, as might endothelial injury and microvascular thrombi. Findings of high viral load in patients who have died with AKI suggest a contribution of viral invasion in the kidneys, although the issue of renal tropism remains controversial. An impaired type I interferon response has also been reported in patients with severe COVID-19. In light of these observations, the potential pathophysiological mechanisms of COVID-19-associated AKI may provide insights into therapeutic strategies.

尽管呼吸衰竭和低氧血症是COVID-19的主要表现，但肾脏受累也很常见。现有证据支持在 SARS-CoV-2 感染背景下发生急性肾损伤 (AKI) 的许多潜在病理生理学途径。组织病理学结果强调了 COVID-19 患者 AKI 与非 COVID 相关脓毒症患者 AKI 之间的相似性和差异。急性肾小管损伤很常见，尽管肾功能明显下降，但通常很轻微。全身血流动力学不稳定很可能导致肾小管损伤。尽管将 COVID-19 描述为细胞因子风暴综合征，但 COVID-19 患者的循环细胞因子水平通常低于因 COVID-19 以外原因引起的急性呼吸窘迫综合征患者。组织炎症和局部免疫细胞浸润已被反复观察到，并且可能在肾损伤中发挥关键作用，内皮损伤和微血管血栓也可能如此。死于 AKI 的患者的高病毒载量结果表明病毒侵入肾脏，尽管肾向性问题仍然存在争议。据报道，重症 COVID-19 患者的 I 型干扰素反应受损。根据这些观察结果，COVID-19 相关 AKI 的潜在病理生理机制可能为治疗策略提供见解。