This research mainly analyzed SARS-CoV-2-induced renal dysfunction, its risk factors and prognosis in two weeks after discharge. Our results indicate that male elderly COVID-19 patients with hypertension were more prone to renal dysfunction. In addition, SARS-CoV-2-evoked renal dysfunction were not fully recovered in two weeks after discharge.
Increasing data have confirmed that SARS-CoV-2 induced multiple organ injuries, mainly including liver dysfunction, myocardial injury, lymphocyte reduction and even respiratory failure [7–10]. In this research, the levels of serum uric acid, urea nitrogen, creatinine, cystatin C and eGFR were detected and renal function was evaluated among COVID-19 patients on admission and discharge. Our results indicated that creatinine and cystatin C were increased, eGFR was decreased in severe COVID-19 patients. There was no difference of uric acid, urea nitrogen and cystatin C between mild and severe COVID-19 patients. Furthermore, the number of COVID-19 patients with renal dysfunction was more in severe patients than those in mild patients. Renal dysfunction was more pervasive in severe patients with COVID-19. Our data indicate that renal dysfunction on admission is positively correlated with the severity of COVID-19 patients.
Earlier studies have confirmed that older age elevated the risk of death in COVID-19 patients [11, 12]. Several comorbidities aggravated the severity of COVID-19 patients [13, 14]. In this research, the influences of demographic characteristics on renal dysfunction were evaluated. No difference was observed in urea nitrogen between female and male patients. Uric acid and cystatin C were decreased, eGFR was increased in females. Additionally, we found that the levels of uric acid, urea nitrogen, creatinine and cystatin C were higher and the level of eGFR was lower in the older patients than those in younger patients. Of 154 COVID-19 patients, there were 22 (14.3%) patients with hypertension, 8 (5.19%) patients with diabetes and 12 (7.79%) patients with other chronic diseases. Furthermore, the influences of basic complications on renal dysfunction were analyzed. Our results indicated that the levels of urea nitrogen and cystatin C were increased in COVID-19 patients with hypertension. Further analysis found that uric acid, urea nitrogen, creatinine and cystatin C were increased and eGFR was decreased in COVID-19 patients with diabetes. Furthermore, we also found that eGFR was decreased in COVID-19 patients with other chronic diseases. These results indicate that male, older age and basic comorbidities with hypertension and diabetes may aggravate the risk of renal dysfunction in COVID-19 patients. For the sake of analyzing the risk factors of renal dysfunction among COVID-19 patients, the multivariate logistic regression was performed. These results suggested that male, older age and hypertension were three independent risk factors of renal dysfunction among COVID-19 patients. Generally speaking, male elderly COVID-19 patients with hypertension are more prone to renal dysfunction.
The prognosis of renal dysfunction in COVID-19 patients remained obscure. This is an urgent problem which is worthy of researching whether renal dysfunction recovers during a short-term after discharge. In the present project, 150 cases with COVID-19 were followed up and renal function were measured via blood routine tests. Every renal marker and the rate of renal dysfunction were compared between on admission and in two weeks after discharge among COVID-19 patients. Although, no significant difference of urea nitrogen, creatinine, cystatin C and eGFR were observed before and after discharge. However, the levels of uric acid were slightly increased in two weeks after discharge compared with COVID-19 patients on admission. Moreover, the abnormal number of patients with creatinine, cystatin C and eGFR were similar between on admission and in two weeks after discharge. Interestingly, a few patients with serum creatinine, cystatin C and eGFR were still out of the normal range in two weeks after discharge. These data suggest that renal function indexes of 3.33% cases with COVID-19 were not fully recovered in two weeks after discharge. Hence, whether SARS-CoV-2 evokes a long-time renal dysfunction is needed to be researched in the next therapeutic methods.
The mechanism of which SARS-CoV-2 evokes renal dysfunction is still unknown. More and more reports have revealed that SARS-CoV-2 plays a pathogenetic role in COVID-19 patients through the receptor of angiotension converting enzyme (ACE)2 [15, 16]. At present, several researches demonstrated that ACE2 is also expressed in renal tubular epithelium . Therefore, we speculate that SARS-CoV-2 may directly damage kidney tissue through binding to the ACE2 receptor. Besides, earlier studies found that inflammatory cytokines were dramatically elevated in patients with COVID-19 [18–20]. It is generally known that cytokine storm was associated with the severity and the levels of IL-6 and CRP can predict the severity and prognosis of COVID-19 patients [21, 22]. IL-6 is a multifunctional cytokine that transmits cell signaling and regulates immune cells . CRP is an acute-phase proinflammatory cytokine and a sensitive biomarker of infection and tissue damage . High levels of CRP or IL-6 always induces cytokine storm and impairs multiple organs function. In the present study, we found that IL-6 and CRP were positively associated with renal dysfunction. Therefore, these results indicated that SARS-CoV-2-induced cytokine storm may be one of the mechanisms of renal dysfunction.
There are several weaknesses in this study. Firstly, this was only a single center research, all patients were from the Fuyang City in Anhui Province which caused selection bias. All patients with COVID-19 were timely found and treated in the Fuyang City, so COVID-19 patients only were mild and severe cases in the Fuyang City, the prevalence was very low and severity of renal dysfunction was modest. Secondly, renal dysfunction was evaluated only through the linear determination of biomarkers and not in an accepted and comparable way (AKIN, KADIG, etc), more assessment methods are needed to evaluate the renal dysfunction in the next project. Thirdly, because of minor specimen, a larger sample size is needed to perform. Fourthly, this current study was only a hospital-based prospective cohort study, the mechanism by which SARS-CoV-2 induced renal dysfunction in COVID-19 patients was unclear, more animal studies and in vivo experiment are needed in the future research.