Table 2 Potential management strategies for COVID-19 AKI
Therapy | Rationale | Recommendation |
|---|---|---|
Standard measures | ||
Standard measures based on AKI risk and stage | Prevention and management depend on the risk and stage of AKI | Strategies based on KDIGO and other relevant guidelines are appropriate for risk- and stage-based prevention and management of COVID-19 AKI (ungraded) |
Measurement of kidney function | The measurement of kidney function is necessary for precise clinical assessment of risk and stage of AKI. Serum creatinine and urine output are the current gold standards for the evaluation of kidney function, although neither is kidney specific or sensitive for detection of early kidney injury | We recommend monitoring kidney function using a minimum serum creatinine and urine output with careful consideration of the limitations of both (evidence level: 1B) |
Haemodynamic optimization | Hypovolaemia, hypotension, and vasoplegia may occur in patients with COVID-19. Fluid and vasopressor resuscitation using dynamic assessment of cardiovascular status may reduce the risk of renal injury and respiratory failure | We recommend individualized fluid and haemodynamic management based on dynamic assessment of cardiovascular status (evidence level: 1B) |
Fluid management | The composition of crystalloids for volume expansion is important. Individual trials in non-COVID patients have shown reduced risk of AKI with use of balanced fluids for initial volume expansion, especially in sepsis | We recommend using balanced crystalloids as initial management for expansion of intravascular volume in patients at risk of or with COVID-19 AKI unless an indication for other fluids exists (evidence level: 1A) |
Glucose management | Insulin resistance and a hypercatabolic state are common in COVID-19 and contribute to hyperglycaemia | We suggest monitoring for hyperglycaemia and use of intensive glucose-lowering strategies in high-risk patients (evidence level: 2C) |
Nephrotoxin management | Nephrotoxins are frequently prescribed in patients with COVID-19. The risks and benefits of these medications and their alternatives need to be closely and frequently assessed. This includes assessment of NSAID use | We recommend limiting nephrotoxic drug exposure where possible and with careful monitoring when nephrotoxins are required (evidence level: 1B) |
Use of contrast media | Some studies have challenged the relevance of contrast media toxicity in critically ill patients; furthermore, sodium bicarbonate and N-acetylcysteine have not been shown to prevent contrast-media-associated AKI | We recommend optimization of intravascular volume status as the only specific intervention to prevent contrast-media-associated AKI (evidence level: 1A) |
Experimental strategies | ||
Antivirals | Some evidence suggests that direct viral infiltration of tubular cells and podocytes has an impact on tubule function and glomerular filtration | Evidence that antivirals may reduce the risk of COVID-19 AKI is indirect and limited |
Immunomodulatory agents (e.g. hydroxychloroquine, corticosteroids, tocilizumab, sarilumab, anakinra, imatinib, dasatinib, ciclosporin, immunoglobulins, baricitinib) | SARS-CoV-2 infection can induce the release of IL-1, IL-6, TNF and other cytokines, as well as secondary HLH. Immunomodulatory agents have the potential to attenuate cytokine production or block cytokine-receptor activation and inhibit autophagy and lysosomal activity to modulate inflammation in host cells | Existing data on immunomodulation in COVID-19 do not show an impact on the development or progression of AKI |
Systemic anticoagulation | Thrombi in the renal microcirculation may contribute to the development of AKI | No data are available to show that anticoagulation strategies reduce the risk of AKI or mitigate AKI progression. Systemic anticoagulation may be needed to maintain filter patency during RRT |
Statins | Statins inhibit the production of pro-inflammatory cytokines (e.g. TNF, IL-10, IL-6 and IL-8) and the activation and proliferation of T cells, potentially leading to immunomodulation | No data are available to show that statins reduce the risk of AKI or mitigate progression |
ACE-I and/or ARBs | ACE-I and ARBs increase ACE2 levels and may rescue cellular ACE2 activity | The impact of RAAS inhibitors on the development or prevention of COVID-19 AKI is uncertain |
NSAIDs | Anti-inflammatory properties | Effect unknown |
Recombinant ACE2 | Potential to neutralize the SARS-CoV-2 and rescue cellular ACE2 activity | Under investigation |
Serine inhibitors | Blockage of transmembrane protease serine 2 activity and prevention of viral infiltration | Under investigation |
