To date, only two studies have been published from the DRC examining patients admitted with COVID-19 (17, 18). Both these studies were limited by a lack of robust analysis of biological and laboratory parameters that might predict hospital mortality in COVID-19 (5, 18). Our retrospective cohort study, carried out in the DRC, aims to add comprehensive data about mortality risk factors for COVID-19. The findings demonstrate that an age greater than 65 years old, AKI stage 3 and a raised serum PCT and CRP level on admission were significant predictors of mortality in COVID-19 patients. Additionally, increasing levels of creatinine during hospital admission were associated with an increased mortality.
Globally, the hospital COVID-19 mortality rates varies between 4 and 70% (19–25).This disparity is partially explained by differences in the epidemiology of the study populations as well as in their hospital management. For example, Du et al demonstrated that older patients with pre-existent co-morbidities had a higher risk of mortality than a younger healthier person (25). Ciceri et al. reported 23% mortality in patients presenting less severe forms on admission (a median oxygen saturation of 93%) (26). In comparison, our study revealed a mortality of 32.0% of whom only 24.5% had an age > 65 years, and had few comorbidities and upon admission had a less severe form of the disease (mean PaO2 62.62 ± 14.0 mmHg). In contrast to international studies demonstrating that being male is associated with an increased risk of mortality (27), our findings did not demonstrate any significant gender difference in risk.
As in several previous studies (25–29), in our study an advanced age was associated with increased mortality from COVID-19. This vulnerability amongst the elderly is often explained by immunoscenescence that is accompanied by a decrease in the production of native T and B cells as well as a decrease in the function of immune cells participating in innate immunity (28). These changes reduce the effective viral clearance and increase the likelihood of triggering a deregulated immune response in which cytokines are largely released from activated immune cells causing a cytokine storm (28). In addition to immune senescence, there are several other age-related factors such as comorbidities resulting in higher morbidity and mortality 28). In our cohort, the number of comorbidities also increased with age.
Viral infections are not usually associated with a raised serum PCT, a finding supported in current COVID-19 research (30). Procalcitonin, which is the 116-amino acid precursor of the hormone calcitonin, is normally synthetized and released by thyroid parafollicular C cells (30). It can also be synthetized in many extrathyroid tissues during bacterial infection which is mediated by increased concentration of tumor necrosis factor alpha (TNFα) and interleukin 6 (30). Worldwide, the average PCT level on admission is less than 0.25 ug/L in COVID-19 patients (31). During admission for COVID-19, an increased PCT is explained either by a bacterial hospital acquired co-infection or by a general deterioration of the patient (32). Several studies have reported that elevated PCT is positively associated with the severity of COVID-19 (33–36). Hu et al. describe bacterial co-infection rates, defined by a positive blood culture in 20% of those who were severely unwell and in 50% who were critically unwell. Yet, in 50% of those with severe COVID-19 and in 80% of those critically unwell the PCT was raised (30). In our study, 12/81 (14.8%) of admission blood cultures were positive yet the PCT was raised in 29.5% of those patients. Our study demonstrated that during infection with COVID-19 a progressive elevation of PCT served as a marker for a poor prognosis. This funding was supported by a study by Lippi et al. (37).
Acute Kidney Injury (AKI) affects approximatively 20–40% of COVID-19 patients admitted to intensive care (38). It is considered as a marker of disease severity and a negative prognostic factor for survival (38, 39). AKI can lead to impaired acid-base, fluid, and electrolyte homeostasis, all of which may contribute to worse outcomes for patients with COVID-19 (39).In our cohort the incidence of AKI was 16.2%. A progressive elevation of creatinine was noted as a marker for poor prognosis, yet, only AKI stage 3 was found to be an independent risk factor associated with mortality. AKI is a well-recognised factor of poor prognosis but during the SARS Cov-2 pandemic few studies have found a significant association between AKI and death (38).This might be explained by the findings of Cheng et al. who demonstrated that only AKI Stages 2 or 3 are associated with a high risk of mortality (40).