Table 1.

The association between acute kidney injury (AKI) and COVID-19 pneumonia

References	Type of the study	Findings
Xiao et al. [3]	A single-center retrospective observational study	The old age, male gender, sepsis, lymphopenia increase risk of AKI in COVID-19
Li et al. [7]	Retrospective study	Patients with COVID-19 pneumonia showed proteinuria (63%), elevated serum creatinine (19%), and high blood urea nitrogen (27%)
Wang et al. [8]	Prospective study	AKI is uncommon in COVID-19 pneumonia
Cheng et al. [9]	Cohort study	Proteinuria, hematuria, and high blood urea nitrogen are considered as independent risk factors for mortality in the hospitalized COVID-19 patients
Sharma et al. [12]	Case series	COVID-19-induced AKI through collapsing glomerulopathy, acute tubular injury, interstitial nephritis, and thrombotic microangiopathy
Pan et al. [16]	Single-cell transcriptome analysis	SARS-CoV-2-induced AKI through invasion of renal ACE2
Asselta et al. [19]	Systematic review	The frequency of AKI in COVID-19 was higher in occidental population
Shi et al. [23]	A retrospective cohort study	Suppression of IL-6 may be a prime therapeutic regimen in COVID-19
Bardaweel et al. [26]	Systematic review	DPP4 inhibitor sitagliptin attenuates COVID-19-induced AKI
Valencia et al. [27]	Systematic review	Higher expression of DPP4 is linked with development of AKI
Oussalah et al. [28]	Retrospective longitudinal cohort study	COVID-19 patients chronically treated by ACEIs or angiotensin II receptor blockers (ARBs) are at higher risk of AKI
Lee et al. [29]	A meta-analysis study	ACEI/ARB use is significantly linked with a higher incidence of AKI in hospitalized COVID-19 patients

DPP4, dipeptidyl peptidase 4; ACEIs, angiotensin-converting enzyme inhibitors; ARBs, angiotensin II receptor blockers