Abstract
PurposeThe ongoing pandemic caused by the novel severe acute respiratory coronavirus 2 (SARS-CoV-2) has stressed health systems worldwide. Patients with chronic kidney disease (CKD) seem to be more prone to a severe course of coronavirus disease (COVID-19) due to comorbidities and an altered immune system. The study’s aim was to identify factors predicting mortality among SARS-CoV-2-infected patients with CKD.MethodsWe analyzed 2817 SARS-CoV-2-infected patients enrolled in the Lean European Open Survey on SARS-CoV-2-infected patients and identified 426 patients with pre-existing CKD. Group comparisons were performed via Chi-squared test. Using univariate and multivariable logistic regression, predictive factors for mortality were identified.ResultsComparative analyses to patients without CKD revealed a higher mortality (140/426, 32.9% versus 354/2391, 14.8%). Higher age could be confirmed as a demographic predictor for mortality in CKD patients (> 85 years compared to 15–65 years, adjusted odds ratio (aOR) 6.49, 95% CI 1.27–33.20, p = 0.025). We further identified markedly elevated lactate dehydrogenase (> 2 × upper limit of normal, aOR 23.21, 95% CI 3.66–147.11, p < 0.001), thrombocytopenia (< 120,000/µl, aOR 11.66, 95% CI 2.49–54.70, p = 0.002), anemia (Hb < 10 g/dl, aOR 3.21, 95% CI 1.17–8.82, p = 0.024), and C-reactive protein (≥ 30 mg/l, aOR 3.44, 95% CI 1.13–10.45, p = 0.029) as predictors, while renal replacement therapy was not related to mortality (aOR 1.15, 95% CI 0.68–1.93, p = 0.611).ConclusionThe identified predictors include routinely measured and universally available parameters. Their assessment might facilitate risk stratification in this highly vulnerable cohort as early as at initial medical evaluation for SARS-CoV-2.
Highlights
In late 2019, SARS-CoV-2 broke out in China and subsequently expanded to a worldwide public health crisis with more several millions infected and more than 1 millionLisa Pilgram and Lukas Eberwein have contributed .Lukas Tometten and Sebastian Dolff have contributed .Members of the Lean European Open Survey on SARS-CoV-2-infected patients (LEOSS) Study group are listed in the Acknowledgement section.Extended author information available on the last page of the article deaths so far
A total of 2817 SARS-CoV-2-infected patients from 105 registered study sites were enrolled in LEOSS between March 16, 2020 and August 06, 2020 and considered valid for analysis
We identified 426/2817 (15.2%) patients with pre-existing chronic kidney disease (CKD). 2391/2817 (84.9%) SARS-CoV-2-infected patients without underlying CKD were considered as referential population
Summary
In late 2019, SARS-CoV-2 broke out in China and subsequently expanded to a worldwide public health crisis with more several millions infected and more than 1 millionLisa Pilgram and Lukas Eberwein have contributed .Lukas Tometten and Sebastian Dolff have contributed .Members of the LEOSS Study group are listed in the Acknowledgement section.Extended author information available on the last page of the article deaths so far. In late 2019, SARS-CoV-2 broke out in China and subsequently expanded to a worldwide public health crisis with more several millions infected and more than 1 million. Lisa Pilgram and Lukas Eberwein have contributed . Lukas Tometten and Sebastian Dolff have contributed . Kidney disease seems to be accompanied by worse outcome in COVID-19. SARS-CoV-2 interacts with the transmembrane protein angiotensin-converting enzyme 2 (ACE-2), best known for its role in the renin–angiotensin–aldosterone system (RAAS). ACE-2 is expressed in alveolar cells in the lung, as well as in the kidney, most abundant in proximal tubular cells and podocytes [2]. ACE-2 was first reported as a functional viral receptor after the SARS epidemic in 2003 [4]. SARS-CoV-2 might cause direct tubular injury via direct viral toxicity which is supported by the
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