Management of acute kidney injury in patients with COVID-19

Abstract

The outbreak of coronavirus disease 2019 (COVID-19) has rapidly evolved into a global pandemic. Most patients with COVID-19 have mild symptoms, but about 5% develop severe symptoms, which can include acute respiratory distress syndrome, septic shock, and multiple organ failure. Kidney involvement is frequent, with clinical presentation ranging from mild proteinuria to progressive acute kidney injury (AKI) necessitating renal replacement therapy (RRT). An understanding of the pathophysiology and mechanisms of kidney damage and AKI in the setting of critical illness and COVID-19 is emerging, although further research is needed to identify patients at risk of AKI and to guide management strategies. As no specific treatment options exist for AKI secondary to COVID-19, intensive care is largely supportive. Current approaches to prevention and management of AKI, and identification of potential indications for use of RRT and sequential extracorporeal therapies, are based mainly on clinical experience, and AKI strategies are adapted empirically to patients with COVID-19. International collaborative and cross-disciplinary research is needed to obtain adequate evidence to support current clinical approaches and to develop new approaches to management.

Figure 1

Acute kidney injury in COVID-19 Multiple dependent pathways in the setting of COVID-19 increase the risk of acute kidney injury. The possible haemodynamic, proinflammatory, and proapoptotic consequences of lung inflammation, cytokine release syndrome, and hypercoagulability on renal function, and potential organ support options, are shown. ARDS=acute respiratory distress syndrome. COVID-19=coronavirus disease 2019. DAMPS=damage-associated molecular patterns. ECMO=extracorporeal membrane oxygenation. IL=interleukin. SARS-CoV-2=severe acute respiratory syndrome coronavirus 2. TNF=tumour necrosis factor.

Figure 2

Management of acute kidney injury necessitating renal replacement therapy in patients with COVID-19 Management recommendations focus on AKI in COVID-19 rather than usual practice for AKI, and are based largely on our clinical experience. All therapeutic options need to be tested in rigorous studies and ideally randomised trials in the context of COVID-19. In the absence of specific therapies, all options should be considered according to each patient's needs. The extracorporeal therapies included in the figure for consideration can be complementary to pharmacological support. The activity targets for anticoagulant therapy are indicative only and should be tailored to each patient's characteristics and clinical condition. The general principle is that maximal anticoagulation should be achieved in the extracorporeal circuit with minimal systemic effects; if systemic anticoagulation is indicated, an integrated prescription should be considered. *These treatments might be indicated in special cases in which immunodysregulation is evident, inflammatory parameters or cytokines are elevated, and other supportive therapies are failing or insufficient; haemadsorption can be achieved with haemoperfusion or CRRT with membranes with high adsorption properties. AKI=acute kidney injury. Anti-Xa=anti-factor Xa. aPTT=activated partial thromboplastin time. Ca²⁺=ionised calcium. COVID-19=coronavirus disease 2019. CRRT=continuous renal replacement therapy. CVVHD=continuous veno-venous haemodialysis. CVVHDF=continuous veno-venous haemodiafiltration. ECCO₂R=extracorporeal carbon dioxide removal. ECMO=extracorporeal membrane oxygenation. HCO=high cutoff. LMWH=low-molecular-weight heparin. MCO=medium cutoff. RCA=regional citrate anticoagulation. RCTs=randomised controlled trials. RRT=renal replacement therapy. UFH=unfractionated heparin.