Acute Kidney Injury in COVID-19 Patients

Acute Kidney Injury (AKI) has emerged as a significant complication of COVID-19, affecting up to 30% of hospitalised patients and disproportionately severe in those requiring intensive care. The pathogenesis of COVID-19-associated AKI is multifactorial, involving direct viral invasion, dysregulated immune responses, endothelial dysfunction, and perturbations in coagulation. Evidence from autopsy studies reveals viral particles in renal tubular epithelial cells and activation of complement pathways. Clinically, AKI in COVID-19 manifests as abrupt increases in serum creatinine, proteinuria and haematuria, often necessitating renal replacement therapy and correlating with increased mortality. Geographic variability in incidence and outcomes highlights the influence of resource availability and patient comorbidities. Recognition of AKI risk factors—older age, hypertension, diabetes and pre‐existing chronic kidney disease—underpins preventive strategies and close monitoring in at‐risk cohorts, with implications for long-term renal prognosis.

Research from Nature Portfolio

Recent studies have identified soluble urokinase-type plasminogen activator receptor (suPAR) as a mediator of COVID-19-associated proteinuria and glomerular injury. Elevated suPAR levels correlate with disease severity and variant-specific responses, as animal models and patient cohorts demonstrate podocyte dysfunction that can be mitigated by suPAR blockade or vaccination. A consensus report on COVID-19-associated AKI delineates a framework for diagnosis, prevention and management, emphasising standardisation of acute kidney injury staging, judicious fluid management and contingency planning for renal replacement therapy in resource-limited settings. Foundational work has demonstrated direct viral tropism for renal tubular cells via angiotensin-converting enzyme 2, inducing tubular damage, hypoxia-related molecule expression and complement deposition, thus solidifying the mechanistic basis for AKI in COVID-19.

Acute Kidney Injury in COVID-19 Patients publication trend

The graph below shows the total number of articles in acute kidney injury in covid-19 patients across all publications each year (not limited to Nature Index journals).

Technical terms

Acute Kidney Injury (AKI): Rapid decline in renal function, defined by increases in serum creatinine or reduced urine output.

Renal Replacement Therapy (RRT): Extracorporeal procedures, such as haemodialysis, used to substitute kidney function in severe AKI.

suPAR: Soluble urokinase-type plasminogen activator receptor, a circulating biomarker linked to podocyte activation and proteinuria.

Podocyte: Specialized epithelial cell in the glomerulus essential for filtration barrier integrity.

ARDS: Acute respiratory distress syndrome, a form of severe respiratory failure often associated with multi-organ injury including AKI.

References

1. SuPAR mediates viral response proteinuria by rapidly changing podocyte function. Nature Communications (2023).
2. COVID-19-associated acute kidney injury: consensus report of the 25th Acute Disease Quality Initiative (ADQI) Workgroup. Nature Reviews Nephrology (2020).
3. Human kidney is a target for novel severe acute respiratory syndrome coronavirus 2 infection. Nature Communications (2021).
4. Epidemiology and outcomes of early-onset AKI in COVID-19-related ARDS in comparison with non-COVID-19-related ARDS: insights from two prospective global cohort studies. Critical Care (2023).
5. Renal implications of coronavirus disease 2019: insights into viral tropism and clinical outcomes. Current Opinion in Microbiology (2024).
6. Acute kidney injury in patients hospitalized with COVID-19 from the ISARIC WHO CCP-UK Study: a prospective, multicentre cohort study. Nephrology Dialysis Transplantation (2021).