Background Kidney disease accompanying coronavirus disease 2019 (COVID-19) is not well understood, and information about the presentation of acute kidney injury (AKI), its risk factors, and outcomes is scarce, particularly in Bahrain and the Gulf region. In this study, we aimed to determine the rate of AKI among patients hospitalized with COVID-19 pneumonia at a tertiary hospital in Bahrain and to describe the various aspects of AKI in these patients, including its relationship with respiratory failure and in-hospital mortality. Methods This retrospective observational cohort study of patients admitted with COVID-19 pneumonia from April 1 to May 31, 2020, excluded those aged less than 18 years, those with end-stage renal disease, and those with renal transplants. Clinical and laboratory patient data were collected. The Kidney Disease: Improving Global Outcomes (KDIGO) criteria were used to define AKI. Results The mean age across the 73 included patients was approximately 54 years; about 60% were men, and nearly 58% were Bahraini nationals. Of the patients, 39.7% (29) developed AKI during hospitalization, out of which 11.0% reached stage 1, 15.1% reached stage 2, and 13.7% reached stage 3. Of all patients, seven (9.6%) required hemodialysis. Chronic kidney disease conferred an increased risk for AKI (P = 0.003) as did critical COVID-19 status (P < 0.001) and the necessity for mechanical ventilation or intensive care admission (P < 0.001 for both). Additionally, AKI was significantly associated with a lower PaO 2 /FiO 2 (partial pressure of arterial oxygen/percentage of inspired oxygen) ratio (P < 0.001) and a greater number of medications for COVID-19 pneumonia (P = 0.003). Finally, in-hospital death tolls were remarkably higher in patients with AKI (P < 0.001). No association was found between AKI and each of the following therapies: angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, tocilizumab, and convalescent plasma. Conclusions The rate of AKI in patients hospitalized with COVID-19 pneumonia at our institution is relatively high and is strongly associated with disease severity, respiratory failure, and in-hospital mortality. Awareness of kidney disease in COVID-19 patients is crucial and of vital importance.

Aim: COVID-19 pandemic continues and dearth of information remains considering the utility of various inflammatory biomarkers. We carried out the present study to delineate the roles of these biomarkers in various strata of patients with coronavirus infection. Materials & methods: A retrospective study was carried out after obtaining approval from the relevant Ethics Committee. Patients established with COVID-19 infection as shown by positive real-time quantitative PCR test were included. Details on their demographics, diagnosis, whether they received tocilizumab, and the values of the following biomarkers were obtained: IL-6, C-reactive protein (CRP), serum ferritin, D-dimer, procalcitonin, fibrinogen, lactate dehydrogenase and creatinine kinase. Receiver operating characteristic curves were plotted and correlation of biomarkers with IL-6 were estimated. Results: One-hundred and three patients were recruited. We observed that serum ferritin followed by D-dimer had better predictive accuracy in identifying patients with pneumonia compared with asymptomatic; and CRP in addition to the earlier markers had better accuracy for predicting severe illness compared with mild–moderate. Serum IL-6 levels were significantly higher in patients with severe illness admitted in intensive care unit. Significantly, higher levels of IL-6 and serum ferritin were observed in patients receiving tocilizumab. A trend of increased IL-6 levels was observed immediately following the initiation of tocilizumab therapy followed by a drop thereafter. Conclusion: We observed serum ferritin, D-dimer and CRP to accurately predict patients developing severe COVID-19 infections as well as those at risk of developing COVID pneumonia. A trend in IL-6 levels was observed in patients on tocilizumab therapy.

Background: Contradictory evidence exists regarding the association between serum vitamin D levels and the severity and outcomes in coronavirus 2019 (COVID-19) infected patients. We undertook the present study to evaluate the serum vitamin D levels with the other laboratory biomarkers, and the outcomes in our critically ill patients. Methods: A retrospective observational study was carried out in 58 critically ill adults. Details on their demographics, laboratory parameters such as 25-hydroxy vitamin D [25(OH)D] levels, interleukin-6, serum ferritin, lactate dehydrogenase, creatine kinase (CK), D-dimer, C-reactive protein, fibrinogen, procalcitonin, and erythrocyte sedimentation rate were retrieved. Serum 25(OH)D levels were categorized as follows: ≥50 nmol/L – normal; 30–49 – insufficient; and &lt;30 nmol/L – deficient. Post-hoc, we also compared the outcomes between those with 25(OH)D levels of 80 nmol/L and above, with those of &lt;80 nmol/L. Results: Fifty-eight patients were recruited of which 31 (53.4%) died. Mean ± SD serum 25(OH)D levels amongst the study participants were 48.5 ± 27.7 nmol/L. Twenty-two (37.9%) individuals had insufficient 25(OH)D levels, and 15 (25.9%) were deficient. Eight (13.8%) participants had their serum 25(OH)D levels ≥80 nmol/L. Median (range) 25(OH)D levels were not significantly different between those who died compared to those alive [41 (20–162) vs. 41 (17–86) nmol/L; p = 0.8]. Significantly higher D-dimer levels were observed amongst those with &lt;80 nmol/L serum 25(OH)D levels. No significant differences were observed between 25(OH)D and other laboratory biomarkers except for elevated CK in patients with insufficient 25(OH)D levels. Conclusion: We did not observe any significant differences in the serum 25(OH)D levels amongst our critically ill adults who died and who were alive at the time of their admission.

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