. 2020 Apr 28;45(8):100618. doi: 10.1016/j.cpcardiol.2020.100618

Table 7.

Summarized findings and interpretations of a systematic review of COVID-19 patients with renal dysfunction⁴⁸

	Results	General comments
Number of patients included (n = 193)	128 nonsevere 65 severe	55 (28%) developed AKI (used KDIGO criteria).
Alterations in renal function indicators on admission	BUN: 27 (14%) SCr: 20 (10%)	Suggests that renal dysfunction occurred before or at admission, indicating that viral replication of SARS-CoV-2 might play a role in the destruction of renal cells.
Exhibition of proteinuria and hematuria	Proteinuria: 88 (60%) Hematuria: 71 (48%)	Significant number of patients presented with these exhibitions, offering a potential time window for starting interventions to protect kidney function.
Exhibition of elevated level of BUN	59 (31%)	Median time from onset of admission to presence of BUN increase was 2 days.
Exhibition of elevated level of SCr	43 (22%)	Median time from onset of admission to presence of SCr increase was 5 days.
Exhibition of radiographic abnormalities of kidneys (N = 110)	106 (96%)	CT images of the 2 groups (severe and non-severe) are clearly distinguishable, suggesting a presence of renal dysfunction in COVID-19.
Difference in mortality risk of COVID-19 patients with and without AKI	Estimated hazard ratio indicates that the mortality risk of COVID-19 patients with AKI is ∼5.3x (P< 0.001) higher than the mortality risk of COVID-19 patients without AKI.
AKI, acute kidney injury; BUN, blood urea nitrogen; KDIGO, Kidney Disease Improving Global Outcomes; SCr, serum creatinine. Conclusions: BUN and SCr are key predictors of AKI and they were found to be significantly higher in non-severe cases of COVID-19 compared to other commonly known pneumonia. Both high levels of BUN and SCr were commonly observed in severe and deceased cases across the course of COVID-19. Unlike BUN, for other pneumonia cases, there were no reported elevated SCr levels. Occurrence of kidney dysfunction in COVID-19 patients could be due to kidney-lung crosstalk⁷⁶ for the following reasons: renal cells have the potential to be target sites for SARS-CoV-2 and inflammatory responses following lung impairments could damage the kidney, where this kidney-lung crosstalk could lead to a “cytokine storm” that acutely induces multi-organ failure and death. Furthermore, direct renal cellular damage is consistent with another report⁷⁷ which found acute renal tubular damage in 6 COVID-19 cases from the histological analysis of renal cell autopsies.