Review
Copyright ©The Author(s) 2020.
World J Nephrol. Nov 29, 2020; 9(2): 18-32
Published online Nov 29, 2020. doi: 10.5527/wjn.v9.i2.18
Table 1 Summary of acute kidney injury incidence in coronavirus disease 2019 patients
Ref.
Zhou et al[2]
Yang et al[8]
Guan et al[4]
Wan et al[16]
Arentz et al[6]
Cheng et al[10]
Italian data March 20, 2020[7]
Combined results without Italian data
Combined results with Italian data
Total patients1915210991352170147021219949220
Critically Ill1505255402173N/A291
ARDS59 (30.1%)35 (67%) 37 (3.4%)20 (14.8%)20 (95.2%)974 (13%)N/A268 (12.2%)
AKI28 (14.7%)15 (28.8%)6 (0.5%) 5 (3.7%)4 (19%) 36 (5.1%)N/A94 (4.2%)
RRT10 (5%)9 (17.3%)9 (0.85)5 (3.7%)N/AN/AN/A33 (1.5%)
Non survivors (NS)254 (28.3%)32 (61.5%)672 (6.1%)1 (0.7%)11 (52.4%)113 (16.1%)3200 (6.8%)278 (154)5 (12.6%)3478 (3354) (7%)
AKI in NS2,327 (50%)12 (37.5%)42 (6%)43 (10%)N/AN/A944 (29.5%)47 (30.5%) 991 (29.5%)
RRT in NS2,310 (18.5%)8 (25%)82 (11.9%)43 (10%)N/AN/AN/A30(19.5%)
Table 2 Summary of the mechanism of kidney injury in coronavirus disease 2019
Mechanism of kidney injury
Hypovolaemia
ARDS related AKI
Cytokine storm syndrome associated AKI
Direct viral invasion
Pre-renalFever causing insensible losses; Gastrointestinal volume losses Haemodynamic instability; High positive end expiratory pressure /intrathoracic pressure; Right heart failureHaemodynamic instability
Renal1Inflammation; Hypoxia/hypercapnia; Acid-base dysregulation; Tubular injuryInflammation; Possible glomerulopathy and TMA ( hypercoagulability)Inflammation; Possible Tubulopathy; Podocytopathy; Interstitial inflammation
Post renal