2.1 COVID-19 infection and acute kidney
injury
Progressive acute kidney injury (AKI) is common among hospitalized
COVID-19 patients, and is an independent risk factor for mortality. It
has been reported that AKI was one of the complications observed in
hospitalized COVID-19 patients with its occurrence ranging between 0.5%
and 80% (Ng et al., 2020a). The mechanisms underlying
COVID-19–associated AKI are unknown. However, proposed mechanisms of
kidney injury range from direct viral infection to effects on the
renin-angiotensin-aldosterone system, hemodynamic instability,
coagulopathy, and cytokine storm. In a systematic review and
meta-analysis of outcomes for patients with COVID-19 and AKI among 20
cohorts covering 13,137 hospitalized COVID-19 patients, prevalence of
AKI was found to be 17%, out of which 77% experienced severe COVID-19
infection and 52% died (Robbins-Juarez et al., 2020). AKI was
associated with increased odds of death among COVID-19 patients (pooled
odds ratio 15.27, 95% CI 4.82-48.36), although there was considerable
heterogeneity across studies and among different regions in the world.
About 5% of all patients in the study required the use of kidney
replacement therapy. The study concluded that kidney dysfunction was
common among patients with COVID-19, and patients who develop AKI have
inferior outcomes (Robbins-Juarez et al., 2020).
Proteinuria and hematuria were common features observed in about 40% of
COVID-19 patients on hospital admission (Perico et al., 2020). In one
observational study of 5,449 hospitalized patients, the incidence of AKI
was 36.6% with 14.3% of patients requiring dialysis and this was even
higher in patients admitted at the intensive care unit (Benedetti et
al., 2020). Autopsy reports from kidneys of COVID-19 deceased patients
revealed acute tubular injury and collapsing glomerulopathy as the most
prominent damage to the kidneys (Cheruiyot et al., 2020; Su et al.,
2020). Electron microscopy of kidney biopsies revealed viral-like
particles in the glomeruli and renal tubules although the particles were
not conclusively that of SARS-CoV-2 (Perico et al., 2020; Su et al.,
2020). The incidence of AKI in COVID-19 patients was also highlighted in
15 separate studies, with an odds ratio (OR) of 18.5% based on COVID-19
severity (Cheruiyot et al., 2020). The OR for COVID-19 patients with
AKI-associated mortality was reported to be as high as 23.95%. In some
710 COVID-19 patients who reported to the hospital, prevalence of
elevated markers of renal function such as serum creatinine and blood
urea nitrogen (BUN) was 15.5% and 14.1%
respectively,
with 26.9% of these patients coming in with microscopic hematuria and
44% having proteinuria although the incidence of AKI in these patients
was reported as 3.2% (Swai et al., 2020). According to this and other
supporting data, AKI is likely associated with worse prognosis in
COVID-19 patients and increases their mortality rates (Izzedine and
Jhaveri 2021; Taher et al., 2020). In a related retrospective analysis
of medical records from 85 COVID-19-positive patients in Wuhan from
January 17 to March 3, 2020, 27.06% of the patients developed AKI
especially among the elderly (59-92 years old) (Diao et al., 2021).
During this study, varying degrees of tubular necrosis, luminal brush
border sloughing and vacuole degeneration was observed in a Hematoxylin
and Eosin staining of 6 kidney samples as well as the presence of
CD68+ macrophages, CD8+ T cells,
CD4+ T cells and CD56+ natural
killer cells from deceased COVID-19 patients (Diao et al., 2021). In
conclusion, COVID-19 infection likely accelerates the development of
AKI, especially among elderly patients.