Baseline characteristics and exposures
A total of 379 patients diagnosed as COVID–19 were enrolled during the study period. Among them 11 had underlying kidney disease, 19 patients had elevated Scr upon admission, and 7 patients had a history of cancer. Data from the remaining 342 patients became the sample of this retrospective cohort study. The median age of enrolled patients was 56 years (IQR 39–68 years), 49.1% were male. More than half of the patients admitted had comobidities (60.2%, n = 206) with cardiac disease being the most common comorbidity (27%, n = 95). As all patients enrolled were SARS-CoV–2 RNA positive, antiviral treatment was administered in all enrolled patients. In addition, antibiotics was also used among majority of patients (86.3%, n = 295). Corticosteroid and intravenous immunoglobin was administered in almost half of the enrolled patients. The estimated average onset time from the development of the first symptom to hospitalization was 9 days (IQR 6–12 days). Upon admission, 52.6% (n = 180) were assessed to be non-severe cases compared to 47.4% (n = 162) were considered cases with severe pneumonia according to the guidelines published by the Chinese Health Authorities (see table 2 for further details).
Development of AKI
AKI at any stage was identified in 13.4% (n = 46) of the cases in this study by 7 days after admission. 7.0% (n = 24) were stage 1, and 6.43 % (n = 22) were assessed to be stage 2–3. Compared with patients without AKI (i.e., AKI-), age, percentage of being a male, comorbidity of cardiac disease, severity of pneumonia were significantly higher in patients with AKI (i.e., AKI+). The AKI+ group also had an higher leukocyte and lower lymphocyte counts, higher leverls of C-reactive protein, procalcitonin, and aspartate aminotransferase.
Elevated biomarkers of myocardial dysfunction such as B-type natriuretic peptide and cardiac troponin I were much higher in the AKI+ group. In addition, dysfunction of coagulation system was observed with significantly higher Fibrinogen and D-dimer in the AKI+ group. Bilateral penumonia was more commonly seen in the AKI+ group, and corticosteroids was more often used in AKI+ group. There was no significant difference in terms of antibiotic use and pre-hospitalization days between groups (see table 3 for details).
In bivariate logisitic analysis, the following factors were significantly associated with the development of AKI: age (p<0.001), male (p<0.001), history of cardiovascular disease (p<0.001), leukocytes count (p<0.001), C-reactive protein (p<0.001), albumin (p<0.001), cardiac troponin I (p<0.001), fibrinogen (p<0.001), D-dimer (p = 0.005), use of corticosteroids (p = 0.01), and severity of pneunonia at admission (p<0.001). In the multi-logistic regression model, several factors were independently associated with the development of AKI: age increase (OR = 1.12,95% CI:1.05–1.25); with a past medical history of cardiac disease (OR = 2.17, 95% CI:1.33–4.22); elevated leukocytes (OR = 1.36, 95%CI:1.11–1.66); higher levels of C-reactive protein (OR = 1.03, 95%CI:1.01–1.05), increased fibrinogen (OR = 1.08, 95%CI:1.02–1.13, p = 0.004), and severity of pneumonia on admission (OR = 2.65, 95%CI:1.11–3.88, p<0.001). The model was statistically significant x2 = 76.4 and can explain 55.8% (R2) of the variance in AKI development.
Mortality
Overall mortality was 26.9% (92/342) in this study. Mortality was significantly higher in those with AKI (AKI+ versus AKI-: 19.3% (57/298) compared to 76.1% (35/44). Through stratification, we found a mortality rate for stage 1 AKI patients of 62.5% (i.e., 15/24). This dramatically rose to 90.9% (i.e., 20/22) for stage 2 - 3 AKI patients. The median number of in-hospital survival days was significantly shorter for AKI+ group compared to AKI- group (AKI+ 21days vs. AKI- 18 days; p < 0.001). In the final model AKI was significanlty assocaited with mortality (log-rank test, x2 = 80.1, p<0.001). Please see Figure 1 for complete data.
Covariate-adjusted hazards analyses for death are shown in table 4, a diagnosis of AKI at any stage was associated with significantly higher hazard ratio (HR) of death during hospital stay (HR = 1.90, 95%CI:1.20–3.00, p = 0.006) compared to those without AKI. Furthermore, severity of AKI was also independently associated with a greater hazard ratio for death after covariate - adjustment (Stage 1 AKI vs. Non-AKI, HR = 1.4; 95%CI 0.77–2.55; p<0.001; Stage 2 - 3 AKI vs. no AKI HR = 2.56; 95%CI 1.50–4.39; p<0.001).