Serum and Urinary Biomarkers in COVID-19 Patients with or without Baseline Chronic Kidney Disease.

In a prospective, observational, non-interventional, single-center study, we assessed various plasma and urinary biomarkers of kidney injury (neutrophil gelatinase-associated Lipocain [NGAL], kidney-injury molecule-1 [KIM-1], and interleukin-18 [IL-18]); inflammation (IL-6, C-reactive protein [CRP]); plus angiotensin converting enzyme 2 (ACE2) in 120 COVID-19 patients (of whom 70 had chronic kidney disease (CKD) at emergency-department (ED) admission). Our aim was to correlate the biomarkers with the outcomes (death, acute kidney injury [AKI]). All patients had received a chest-CT scan at admission to calculate the severity score (0-5). Biomarkers were also assessed in healthy volunteers and non-COVID-19-CKD patients. These biomarkers statistically differed across subgroups, i.e., they were significantly increased in COVID-19 patients, except for urinary (u)KIM1 and uIL-18. Amongst the biomarkers, only IL-6 was independently associated with mortality, along with AKI and not using remdesivir. Regarding the prediction of AKI, only IL-6 and uKIM1 were significantly elevated in patients presenting with AKI. However, AKI could not be predicted. Having high baseline IL-6 levels was associated with subsequent ventilation requirement and death. The mortality rate was almost 90% when the chest CT-scan severity score was 3 or 4 vs. 6.8% when the severity score was 0-2 (p < 0.0001).

Renin-angiotensin-aldosterone system blockers in Bulgarian COVID-19 patients with or without chronic kidney disease.

When angiotensin-converting enzyme inhibitor/angiotensin receptor blocker-treated patients present with SARS-CoV-2 infection there is a debate to know whether renin-angiotensin-aldosterone (RAAS) blockers should be stopped or not. We conducted a prospective observational study in Bulgarian COVID-19-infected patients with or without chronic kidney disease (CKD) to assess whether maintenance RAAS blocker therapy has an impact on SARS-CoV-2 infection and its complications. We included 120 in-patient COVID-19 subjects, of whom 70 had CKD and 50 had normal renal function. A total of 30% of the patients (total number of 36 patients, 21 females) were receiving RAAS therapy at admission and it was maintained throughout hospitalization. The overall mortality was 19.2% (23 patients); there was no significant difference across the 2 groups (P-value = .21), except in RAAS blockers-treated hypertensive patients who had a significantly lower mortality as compared to non-RAAS-blockers-treated hypertensive patients (P = .04). Regarding subsequent intensive-care unit admission, there were 50% less patients in the RAAS group (4 out of 36, i.e., 11%) as compared to 19 out of 84 from the non-RAAS group, that is, 22.6% (P = .29). Overall, 37 patients developed acute kidney injury (any stage by KDIGO); of them 14 (37.8%) were receiving RAAS blockers. Acute kidney injury was not significantly associated with the use of RAAS blockers (P-value = .28). Likewise, both in non-CKD and in CKD patients the use of RAAS blockers did not have an impact on renal function recovery after SARS-CoV-2 infection. Finally, regarding RAAS blockers and the biological parameters outcome only D-dimers were significantly lower at the follow-up as compared to that in non-RAAS blocker treated patients. RAAS blockers benefited patients with hypertension by lowering mortality rate. Other than that, RAAS blocker therapy continuation during SARS-CoV-2 infection in CKD and non-CKD patients had no significant impact upon major outcomes.

COVID-19 Infection in Chronic Kidney Disease Patients in Bulgaria: Risk Factors for Death and Acute Kidney Injury.

Regarding COVID-19 infection, Bulgaria has one of the lowest rates of vaccination in Europe, and its COVID-19-related mortality rate has been one of the highest in the European Union. Chronic kidney disease (CKD)-COVID-19 patients are at higher risk of developing acute kidney injury (AKI) and death after hospital admission. This single-center prospective cohort study from Bulgaria included 120 in-patient COVID-19 subjects of whom 70 had CKD and 50 normal renal function. Diabetes mellitus, hypertension, obesity, and cardiovascular disease were statistically more prevalent in the CKD group as compared to the non-CKD group. At admission, D-dimer, creatinine, and urea levels were significantly higher in the CKD group, whereas estimated glomerular-filtration rate was significantly lower as compared to the non-CKD patients. During hospitalization, 23 patients (19.1%) died, of which 19 were in the CKD group (p-value = 0.0096); in addition, 38 developed AKI (31.6%), of which 31 were in the CKD group (p-value = 0.0006). Using binary logistic regression, being male, having experienced AKI, and not having been treated with remdesivir were independent risk factors for COVID-19-induced mortality. Regarding risk of AKI, having had COVID-19-related symptoms for more than 6 days before admission, having CKD at baseline, and having not received remdesivir therapy were independent predictive factors for developing AKI after admission.