We appreciate the letters by Dr. Bhaskar et al.  and by Dr. Silver et al. .
In their letters, they put forward some views and comments on our article “Coronavirus
Disease 19 Infection Does Not Result in Acute Kidney Injury: An Analysis of 116 Hospitalized
Patients from Wuhan, China” . All of the issues raised by them are very important
and deserve our attention and considerations. Here, we would like to respond to their
comments in the letters and explain their questions about the observations in our
paper. We hope that our responses could relieve them of some concerns.
As regards Dr. Bhaskar et al.'s concern about the roles of ACE2 expression in SARS-CoV-2
infection, a recent study shows that the cells with ACE2 expression may act as target
cells and be susceptible to SARS-CoV-2 infection, such as type II alveolar cells in
the lung . It should be noted that the ACE2 protein has been proved to have an
abundant expression in many kinds of cells, including renal tubular epithelial cells.
Therefore, it is reasonable to speculate that SARS-CoV-2 may also invade kidney and
lead to AKI. However, the information regarding the pathological findings in COVID-19
is limited at present. The reports showed that there were main histological changes
in the lung [5, 6]. Until now, there are no data and evidence showing that SARS-CoV-2
infection might directly impair the kidney, although SARS-CoV-2 RNA could be detected
from urine, including our results . Therefore, in addition to the lung, whether
the kidney is the main target organ of SARS-CoV-2 and it causes an obvious AKI need
more pathological and virological evidence in the future study. Moreover, data on
ACE inhibitor application in COVID-19 are important in this setting and should also
As regards Dr. Bhaskar et al.'s concern about mortality in our study, we included
116 patients with COVID-19 hospitalized in the Department of Infectious Diseases.
Eleven (11/116, 9.5%) patients were with acute respiratory distress syndrome (ARDS)
and were transferred to ICU. Seven out of 11 ARDS patients transferred to ICU died
of respiratory failure. As a result, the overall mortality rate of COVID-19 was 6.03%
(7/116), while the mortality rate of ARDS patients with COVID-19 in ICU was 63.6%
(7/11). There is indeed a high mortality, which is in agreement with the results of
the study by Wu et al. .
As regards Dr. Silver et al.'s concern about the incidence of AKI in patients with
COVID-19, our explanations and answers are as follows. Our department started to treat
patients with COVID-19 from the middle of January 2020. Previously, these patients
were consultant in “fever clinic,” which serves as an outpatient department, and were
diagnosed as “unknown origin viral pneumonia” for admission. They were confirmed the
diagnosis as COVID-19 by the SARS-CoV-2 RNA test immediately, when PCR detection was
available. In that time, our wards were specialized for isolation and treatment of
these patients. Thirty out of 116 cases with other diseases already hospitalized at
the time of their COVID-19 were diagnosed. The others were newly admitted from “fever
clinic.” All hospitalized patients in our wards were at the acute phase of their illness.
The patients clinical categories and comorbidities are presented in table 1 of our
paper. The judgment of patients' condition and clinical type is mainly based on the
degree of hypoxemia and lung damage .
In our paper, AKI was identified according to Kidney Disease: Improving Global Outcomes
(KDIGO) . However, few patients without CKD could accurately provide the baseline
levels of SCr. When baseline SCr was not available, SCrGFR-75 as surrogate for the
baseline SCr was used to diagnose AKI . Renal function and urine were tested weekly
in all patients during the treatment of COVID-19. Although the weekly test may not
have been sufficiently frequent in certain instances for finding AKI, the high frequency
of examination is useful, especially in critical patients.
In this study, 5 patients with ESKD received regular dialysis. The serum creatinine,
blood urea, electrolytes, and urine analysis were used to evaluate whether kidney
deterioration occurs in them. The symptoms, physical examination results, hemodynamic
stability (e.g., blood pressure) were closely monitored as well.
Although AKI is currently reported in critical cases of COVID-19, especially in dead
cases as high as 23–32% [11, 12], it may be related to severe hypoxemia and/or multiple
organ dysfunction syndrome (MODS) induced by inflammatory storm or to high comorbidities.
Whether this renal injury is directly caused by SARS-CoV-2 infection is still unclear.
In our paper, we did not find a significant AKI in these 11 ARDS cases, including
7 dead patients with ARDS. The critical patients in our study were in small number.
Therefore, the differences on kidney impairment from available studies in COVID-19
may associate with the severity of illness.
Many early studies suggested a lower incidence (3–9%) of AKI in those with COVID-19
infection [13, 14, 15]. As an early report, our study showed clinical data of 116
hospitalized COVID-19 patients analyzed over 4 weeks for correlation with renal injury.
Approximately 10.8% of patients with no prior kidney disease showed elevations in
blood urea or creatinine, and 7.2% of patients with no prior kidney disease showed
albuminuria. All these patients did not meet the diagnostic criteria of AKI. From
these results, we concluded that AKI was uncommon in general population with COVID-19.
Based on the study from SARS-CoV infection in SARS patients in 2003 , the data
showed that AKI was uncommon, but the mortality was formidably high (91.7%, 33 of
36 cases). Our results were similar and consistent with the presentation of renal
injury in SARS. Moreover, in the present study, we also found that unlike a high mortality
in SARS complicated with renal injury, none of 5 patients with CKD died from SARS-CoV-2
Actually, our study showed that a mild renal injury was present rather than AKI in
general population with COVID-19. We also suggested that regular monitoring of renal
function in COVID-19 patients is necessary, especially in patients with elevated plasma
creatinine levels. In the event of signs of AKI, potential interventions, including
CRRT, should be used as early as possible.
Finally, our study is a preliminary and retrospective analysis, which had several
limitations. Whether SARS-CoV-2 infection results in serious kidney impairment remains
to be explored further. It will be crucial to comprehensively characterize larger
datasets of COVID-19 patients across hospitals (meta-analyses) to demonstrate if the
kidney function is actively impaired due to the viral infection and SARS-CoV-2 could
easily lead to kidney damage and if renal diseases are a major high risk factor for
aggravating COVID-19 consequences.
We declare no competing interests.