Research Article Kidney Blood Press Res Received: December 9, 2020 Accepted: March 7, 2021 DOI: 10.1159/000515714 Published online: June 7, 2021 COVID-19 in CKD Patients: Lessons from 553 CKD Patients with Biopsy-Proven Kidney Disease Juan León Román a Clara García-Carro a Irene Agraz a Nestor Toapanta a Ander Vergara a, b Alejandra Gabaldón c Irina Torres a Roxana Bury a Cinthia Baldallo a Daniel Serón a, b, d María José Soler a, b, d aDepartment of Nephrology, Vall d’Hebron University Hospital, Barcelona, Spain; bVall d’Hebron Research Institute (VHIR), Nephrology Department, Nephrology Research Group, Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain; cDepartment of Pathology, Vall d’Hebron University Hospital, Barcelona, Spain; dInstituto Carlos IIIFEDER, Red de Investigación Renal (REDINREN), Madrid, Spain Keywords in 26 patients; older (p = 0.01), hypertensive (p = 0.005), and Coronavirus · COVID-19 · Severe acute respiratory immunosuppressed (p = 0.01) patients, those using RAS- syndrome coronavirus 2 · Chronic kidney disease · blocking drugs (p = 0.04), and those with gastrointestinal Biopsy-proven kidney disease symptoms (p = 0.02) were more likely to be tested for CO­ VID-19. Twenty-two patients required hospitalization and 15.4% died. In bivariate analysis, mortality was associated Abstract with older age (p = 0.03), cardiovascular disease (p = 0.05), Introduction: Chronic kidney disease (CKD) patients infect- chronic obstructive pulmonary disease (p = 0.05), and low ed with COVID-19 are at risk of serious complications such as hemoglobin levels (p = 0.006). Adjusted Cox regression hospitalization and death. The prognosis and lethality of CO- showed that low hemoglobin levels at admission had 1.81 VID-19 infection in patients with established kidney disease greater risk of mortality. Conclusions: Patients with CO­ has not been widely studied. Methods: Data included pa- VID-19 infection and kidney disease confirmed by kidney bi- tients who underwent kidney biopsy at the Vall d’Hebron opsy presented a mortality of 15.4%. Swab test for COVID-19 Hospital between January 2013 and February 2020 with CO- was more likely to be performed in older, hypertensive, and VID-19 diagnosis during the period from March 1 to May 15, immunosuppressed patients, those using RAS-blocking 2020. Results: Thirty-nine (7%) patients were diagnosed drugs, and those with gastrointestinal symptoms. Low he- with COVID-19 infection. Mean age was 63 ± 15 years and moglobin is a risk factor for mortality. 48.7% were male. Hypertension was present in 79.5%, CKD © 2021 The Author(s) without renal replacement therapy in 76.9%, and cardiovas- Published by S. Karger AG, Basel cular disease in 64.1%. Nasopharyngeal swab was performed karger@karger.com © 2021 The Author(s) Correspondence to: www.karger.com/kbr Published by S. Karger AG, Basel María José Soler, mjsoler01 @ gmail.com This is an Open Access article licensed under the Creative Commons Attribution-NonCommercial-4.0 International License (CC BY-NC) (http://www.karger.com/Services/OpenAccessLicense), applicable to the online version of the article only. Usage and distribution for com- mercial purposes requires written permission. Introduction crease in CD3, CD4, and CD8 cells by immunosuppres- sive drugs for preventing graft rejection [9]. Severe acute respiratory syndrome coronavirus 2 There is limited scientific literature regarding CO­ (SARS-CoV-2) is a beta-coronavirus responsible for re- VID-19 infection and CKD, specifically in patients with spiratory infection with variable clinical expression, from glomerular and tubular kidney disease. The objective of its most frequent asymptomatic presentation to severe this study is to determine general characteristics, analyti- pneumonia complicated by acute respiratory distress cal studies, and clinical evolution of patients with CKD in syndrome (ARDS), multiple organ failure, and death [1, whom a percutaneous renal biopsy has been performed 2]. Transmission occurs through respiratory drops from at the Vall d’Hebron Hospital and who have presented person to person; even presymptomatic people are infec- COVID-19 infection and to identify risk factors for hos- tious [1]. The virus enters into human cells through the pitalization and mortality of those patients. angiotensin-converting enzyme receptor [1] and has a high tropism toward lung cells [2]. The first cases were described in Wuhan, China, and it was classified as an Materials and Methods international health emergency in March 2020 by the Medical records of 553 patients who underwent kidney biopsy WHO due to its high rate of infection and inherent com- at Vall d’Hebron Hospital between January 2013 and December plications [2]. Research has focused on preventing its 2019 were reviewed. In all biopsied patients, COVID-19 infection spread and trying to establish pharmacological treat- was assessed by reviewing clinical records and nasopharyngeal ments. There are studies with various drugs tested; until swabs for SARS-COV-2 from March 2020 to May 15, 2020. Clini- now, ventilatory support has been the fundamental basis cal and analytical data were collected from patients who had high clinical suspicion of COVID-19 infection as well as clinical course of treatment in severe cases that develop adult respiratory after infection (see online suppl. Fig. 1; for all online suppl. mate- distress syndrome [2]. rial, see www.karger.com/doi/10.1159/000515714). High clinical Several studies have focused on investigating the risk suspicion of COVID-19 infection in absence of a nasal swab was factors associated with developing ARDS [3]. Factors re- defined as the clinical diagnosis of those patients evaluated by a lated to increased risk of complications and death are age primary care physician who presented fever, gastrointestinal symptoms, and respiratory symptoms associated with contact with over 65 years, cardiovascular disease, lung disease, hyper- a patient diagnosed of COVID-19 infection. The Ethics Commit- tension, diabetes, and liver disease [3], as well as analytical tee of Vall d’Hebron University Hospital approved the study pro- alterations such as neutrophilia, elevation of acute phase tocol (PR [AG]5713/2020). reactants, and organic and coagulation dysfunction [4]. Demographics, clinical variables, and analytical results were Chronic kidney disease (CKD) is described as a risk obtained from the hospital computer system. The quantitative variables age, BMI, number of lymphocytes, platelets, and hemo- factor for both increased susceptibility to infection and globin presented a normal distribution. The normality of the vari- the development of serious complications [5]. The impact ables was assessed by the Kolmogorov-Smirnov test. of COVID-19 infection at renal level is poorly under- Qualitative variables are presented with their frequency distri- stood, and some authors have described acute kidney in- bution. Quantitative variables are presented with their mean with jury associated with COVID-19 infection evidencing in- standard deviation or median with interquartile range, 25–75%. First, we determined the distribution of the variables with the Kol- volvement in glomerular cells with quantification of viral mogorov-Smirnov test. The qualitative variables were analyzed genetic material in histological studies of deceased pa- with the χ2 test or Fisher’s exact coefficient. The relationship be- tients diagnosed with COVID-19 [6]. Among patients tween 2 quantitative variables was analyzed with the Spearman test with renal replacement therapy, the Goicoechea group and quantitative variables with the Student’s t test. Bivariate and [7] described a high mortality rate with 11 (30.5%) of 36 multivariate analyses were obtained with logistic regression. The Cox regression analysis was used to identify mortality risk factors patients with COVID-19 infection and ESRD on hemo- in patients with high suspicion of COVID-19 infection. Statistical dialysis. In addition, mortality was associated with ana- studies were processed with the SPSS version 20 program. lytical alterations such as elevation of lactate dehydroge- nase and C-reactive protein. Studying COVID-19, the Registry of the Spanish Society of Nephrology, Sánchez- Álvarez et al. [8] demonstrated higher mortality in hemo- Results dialysis patients compared to those with kidney trans- plantation after COVID-19 infection. Interestingly, kid- Thirty-nine of the 553 patients have been diagnosed ney transplant patients with COVID-19 infection with COVID-19 infection (either by swab confirmation presented rapid clinical progression associated with de- or high clinical suspicion) since March 2020. The average 2 Kidney Blood Press Res Román et al. DOI: 10.1159/000515714 Table 1. Demographic and clinical characteristics of the 39 patients Variable Total Survivors Nonsurvivors p value (n = 33) (n = 6) Age, years 63±15 61±14.9 75±9.3 0.03 Male 19 (48.7) 15 (45.5) 4 (66.7) 0.34 Ethnicity Caucasian 32 (82.1) 26 (78.8) 6 (100) Latin 6 (15.4) 6 (18.2) 0 (0) 0.46 Asian 1 (2.6) 1 (3.0) 0 (0) BMI, kg/m2* 28.8±6.5 29.2±6.8 25.6±4.0 0.23 Tobacco 13 (33.3) 10 (30.3) 3 (50.0) 0.35 Hypertension 31 (79.5) 25 (75.8) 6 (100) 0.18 Diabetes 19 (48.7) 17 (51.5) 2 (33.3) 0.41 Cardiovascular disease 25 (64.1) 19 (57.6) 6 (100) 0.05 Chronic obstructive pulmonary disease 8 (20.5) 5 (15.2) 3 (50.0) 0.05 Rheumatologic disease 8 (20.5) 6 (18.2) 2 (33.3) 0.44 Use of RAS-blocking drugs 18 (46.2) 18 (54.5) 0 (0) 0.01 CKD not on RRT 30 (76.9) 25 (75.8) 5 (83.3) 0.69 Kidney replace therapy 9 (23.1) 8 (20.5) 1 (2.6) 0.69 Dialysis 4 (10.3) 3 (9.1) 1 (16.7) 0.57 Kidney transplant 5 (12.8) 5 (12.8) 0 (0) 0.31 Immunosuppression 17 (43.6) Prednisone 15 (38.5) Mycophenolate 7 (17.9) Tacrolimus 6 (15.4) 13 (39.4) 4 (66.7) 0.22 Rituximab 1 (2.6) Omalizumab 1 (2.6) Everolimus 1 (2.6) SARS-CoV-2 swab test 26 (66.7) 20 (60.6) 6 (100) 0.06 Symptoms Fever 26 (66.7) 22 (66.7) 4 (66.7) 1.00 Myalgia 18 (46.2) 17 (51.5) 1 (16.7) 0.12 Diarrhea, nausea/vomiting 9 (23.1) 7 (21.2) 2 (33.3) 0.52 Image-proven pneumonia 19 (48.7) 33 (100) 6 (100) 0.34 Hospitalization 22 (56.4) 17 (51.5) 5 (83.3) 0.15 Treatment Hydroxychloroquine 20 (51.3) 17 (51.5) 3 (50.0) 0.95 Lopinavir/ritonavir 15 (38.5) 12 (36.4) 3 (50.0) 0.53 Azithromycin 23 (59.0) 19 (57.6) 4 (66.7) 0.68 Tocilizumab 6 (15.4) 4 (12.1) 2 (33.3) 0.19 High-dose corticosteroids 9 (23.1) 6 (18.2) 3 (50.0) 0.09 Variables with normal distribution are expressed as mean ± standard deviation. Qualitative variables are ex- pressed as n (%). Bold indicates significant p values of ≤0.05. * BMI in 32 of 39 patients. BMI, body mass index; RAS, renin-angiotensin system; CKD, chronic kidney disease; RRT, renal replacement therapy. age was 63 ± 15 years and 48.7% were male. Demograph- 51.3% received hydroxychloroquine, 38.5% lopinavir/ ic and clinical characteristics are shown in Table 1 in the ritonavir, 59.0% azithromycin, 15.4% tocilizumab, and total studied subjects, survivors, and nonsurvivors. In 23.1% high-dose corticosteroids. In our studied patients, brief, hypertension was present in 79.5% of patients, CKD 11.4% (4/31) of lupus nephritis, 3.3% (2/59) of IgAN, and without renal replacement therapy in 76.9%, and cardio- none of (0/31) membranous patients were diagnosed of vascular disease in 64.1%. The most frequent symptoms COVID-19 infection. Membranous nephropathy pa- were fever (66.7%) and myalgias (46.2%). Twenty-two tients seem to be protected against COVID-19 infection; percent of patients required hospital admission, of which however, statistical differences among groups were not COVID-19 in CKD Patients Kidney Blood Press Res 3 DOI: 10.1159/000515714 Color version available online Fig. 1. Histological diagnoses of the renal biopsies of the 39 patients. IgA, IgA nephropathy; GN, glomerulone- phritis; FSGS, Focal Segmental Glomerulosclerosis. detected (p = 0.07). Of all studied subjects, 15 patients with the rest of comorbidities and clinical manifestations (38.5%) with CKD without KRT and 7 (17.9%) patients (Table 2). with KRT were admitted to the hospital. There were no Analytical results of patients with hospital admission significant differences regarding the risk of hospitaliza- are depicted in Table 3. The mortality rate was 15.4%. In tion and death between CKD patients with and without the actuarial survival analysis, chronic obstructive pul- KRT (p = 0.14 and p = 0.69, respectively). In addition, monary disease (COPD) was significantly increased in there was no significant difference in mortality between nonsurvivors as compared with survivors, and use of RAS CKD stages 1–3 and CKD stages 4–5 (p = 0.53). Histo- blockade drugs was significantly increased in survivors as logical diagnosis of kidney biopsies was as follows: dia- compared with nonsurvivors (online suppl. Fig. 2–5). betic kidney disease (20.5%), lupus nephropathy (10.3%), The Cox regression analysis suggested that nonsurviving minimal change disease, allergic interstitial nephritis, and COVID-19 patients had a lower hemoglobin levels at ad- secondary FSGS (7.7%), and vasculitis (7.7%) (see Fig. 1). mission as compared to surviving COVID-19 patients Of note, 17 patients received immunosuppression at CO- (Table 4). Low hemoglobin did not statistically correlate VID-19 diagnosis, 12 for their underlying glomerular dis- with other laboratory parameters such as D-dimer, C-re- ease and 5 of them to prevent allograft kidney rejection. active protein, and IL-6 (p = 0.23, p = −0.27, and p = 0.33, There were no significant differences in mortality be- respectively). tween patients with and without immunosuppression. Swab was performed in 26 patients (66.7%) with CO­ VID-19 suspicion. In the bivariate analysis, older age (p = Discussion/Conclusions 0.01), hypertensive (p = 0.005), and immunosuppressed (p = 0.01) patients, those using RAS-blocking drugs (p = Our study evaluates the prevalence, clinical character- 0.04), and those with gastrointestinal symptoms (p = istics, and prognosis of patients followed after kidney bi- 0.02) were more likely be tested for COVID-19 than those opsy in our outpatient consult with high suspicion or in- 4 Kidney Blood Press Res Román et al. DOI: 10.1159/000515714 Table 2. Clinical characteristics of patients with and without SARS-CoV-2 swab test Variable Without SARS-CoV-2 p value SARS-CoV-2 swab positive swab (n = 13) (n = 26) Age, years 55±17 68±12 0.01 Male 6 (46.2) 13 (50.0) 0.82 BMI, kg/m2* 27.1±7.1 29.1±6.34 0.41 Tobacco 3 (23.1) 10 (38.5) 0.34 Hypertension 7 (53.8) 24 (92.3) 0.005 Diabetes 4 (30.8) 15 (57.7) 0.11 Cardiovascular disease 6 (46.2) 19 (73.1) 0.09 Chronic obstructive pulmonary disease 2 (15.4) 6 (23.1) 0.58 Rheumatologic disease 0 (0) 8 (30.1) 0.22 Use of RAS-blocking drugs 9 (69.2) 9 (34.6) 0.04 CKD without RRT 12 (92.3) 18 (69.2) 0.11 Dialysis 0 (0) 4 (15.4) 0.14 Kidney transplant 1 (7.7) 5 (19.2) 0.35 Dead 0 (0) 6 (23.1) 0.06 Immunosuppression 2 (15.4) 15 (57.7) 0.01 Symptoms Fever 7 (53.8) 19 (73.1) 0.23 Myalgia 6 (46.2) 12 (46.2) 1.00 Diarrhea, nausea/vomiting 0 (0) 9 (34.6) 0.02 * BMI in 32 of 39 patients. BMI, body mass index. Bold indicates significant p values of ≤0.05. Table 3. Comparison of analytical results of the 22 patients hospitalized for COVID-19 Variable Total Survivors Nonsurvivors p value Leukocytes × 109/L 7.84 (4.46–9.23) 7.40 (3.85–9.55) 8.43 (6.35–10.36) 0.48 Neutrophils × 109/L 5.80 (2.70–7.90) 5.40 (2.25–8.39) 6.20 (4.10–9.50) 0.49 Lymphocytes × 109/L 0.89±0.55 0.82±0.49 1.16±0.72 0.23 Platelets × 109/L 175.36±61.0 176.47±62.84 171.60±61.03 0.88 Creatinine, mg/dL 1.99 (1.32–3.78) 2.04 (1.25–3.68) 1.73 (1.23–4.48) 0.97 Hemoglobin, g/dL 11.76±1.60 12.25±1.17 10.12±1.89 0.006 D-dimer, ng/mL 395.50 (157.50–623.50) 406.0 (181.0–619.0) 1,024.33 (169.99–1,521.50) 0.71 C-reactive protein, mg/dL 5.75 (2.86–15.58) 5.07 (2.72–15.48) 11.85 (9.51–13.72) 0.31 Interleukin, 6 pg/mL 38.60 (22.62–85.34) 37.45 (21.06–69.88) 1,475.16 (68.32–2882.0) 0.10 Ferritin, ng/mL 718 (561.50–1,292.75) 718.0 (576.50–1,193.75) 926.50 (506.0–1,347.0) 0.87 Lactate dehydrogenase, UI/L 318.50 (220.25–443.0) 304.0 (224.50–411.50) 370.50 (266.0–510.50) 0.60 Leukocytes n = 22 (17 survivors and 5 nonsurvivors), platelets n = 22 (17 survivors and 5 nonsurvivors), hemoglobin n = 22 (17 sur- vivors and 5 nonsurvivors), D-dimer n = 20 (17 survivors and 3 nonsurvivors), CRP n = 19 (16 survivors and 3 nonsurvivors), IL-6 n = 17 (15 survivors and 2 nonsurvivors), ferritin n = 16 (14 survivors and 2 nonsurvivors), and LDH n = 20 (16 survivors and 4 nonsurvi- vors). Bold indicates significant p values of ≤0.05. Variables with normal distribution are expressed as mean±standard deviation. Vari- ables with abnormal distribution are presented in median (IQ25%–IQ75%). fection confirmed by COVID-19. Data from the literature may be ascribed in part to the fact that the majority of pa- in this population are scarce. In our cohort, the preva- tients were kidney disease patients without ESRD. Recent lence of COVID-19 was 7.05% (39 out of 553 patients), publications from Williamson et al. [10] indicate that di- and the mortality rate was 15.4%. In comparison with alysis or ESRD highly increases mortality (HR 3.69) of other series, our mortality rate was low [7, 8], and this COVID-19-infected patients. In concordance with COVID-19 in CKD Patients Kidney Blood Press Res 5 DOI: 10.1159/000515714 Table 4. Adjustment of variables and Cox regression of characteristics with significant differences associated with mortality Variable Unadjusted risk Adjusted risk Adjusted risk Adjusted risk cardiovascular (95% CI, p value) cardiovascular disease cardiovascular disease, disease, COPD, RAS blockers (95% CI, p value) COPD (95% CI, p value) (95% CI, p value) Hemoglobin, 10.12±1.89 g/dL 1.88 (1.16–3.03; 0.01) 1.75 (1.08–2.85; 0.02) 2.04 (1.12–3.57; 0.02) 1.81 (1.04–3.13; 0.04) CI, confidence interval; COPD, chronic obstructive pulmonary disease; RAS, renin-angiotensin system. Bold indicates significant p values of ≤0.05. Goicoehea et al. [7] and Sánchez et al. [8], there were no acting on the RAAS was not associated with a higher risk significant differences in mortality between gender. Wu of testing positive for COVID-19 or higher risk of severe et al. [4] described in their cohort study of 201 patients COVID-19. Our study also suggests in part the nondele- that those who developed ARDS secondary to COVID-19 terious effect of RAS blockade in renal patients in the new infection were older patients and had hypertension and COVID-19 pandemic era. diabetes as comorbidities. In our bivariate analysis, age Fever was presented in 66.7%, myalgia in 46.2%, gas- >65 years, cardiovascular disease, and chronic obstruc- trointestinal symptoms in 23.1%, and 48.7% presented tive pulmonary disease were identified as risk factors for pneumonia evidenced by radiography and/or chest to- mortality in our COVID-19 patients. mography. In addition, according to the WHO classifica- Interestingly, nasopharyngeal PCR of COVID-19 was tion, 48.7% of patients presented mild clinical symptoms only performed in 26 patients (66.7%), which may be re- and 17.9%, critical disease with septic shock. Our findings lated to the overwhelming and containment period of the were similar to those of other authors regarding the high pandemic disease. Among them, older age, male sex, prevalence of fever and myalgias [7, 8]. One of the limita- COPD, hypertension, diabetes, and hypercholesterol- tions of this study is that we had only collected data on emia have been identified as risk factors of worse clinical fever, myalgia, and gastrointestinal symptoms as clinical prognosis and the need of intensive care unit admission expressions of COVID-19, so we cannot compare other as Grasselli et al. [11] defined in their cohort study of symptoms and signs such as oxygen desaturation, cough, 3,988 patients admitted in the intensive care unit. Our and time of evolution of the clinical condition. Wu et al. results suggest that patients at risk for severe disease are [4] also described analytical risk factors to the develop- admitted and subsequently tested in hospitals [12]. As ex- ment of ARDS, and progression from ARDS to death in- pected, none of our COVID-19 infection suspicion pa- cluded neutrophilia and organ and coagulation dysfunc- tients without swab diagnosis died, reinforcing again the tion (higher LDH and D-dimer); by contrast, our study idea that the nonswab patients were patients with low risk only found low hemoglobin levels as a risk factor for in- of severe disease. creased mortality. Interestingly, this result has not been The beneficial/deleterious effects of RAS blockade widely observed in other series [18]. have been under discussion since the COVID-19 out- There is no consensus on the optimal treatment in pa- break [13–15]. However, Fan et al. [16] supported the del- tients with COVID-19 infection; likewise, the treatment eterious effect of RAS blockade therapy in the COVID in patients with glomerular and tubular diseases is estab- pandemic era in terms of increased infection and severity lished under general protocols and adjusted renal func- of the disease; Sparks et al. [17] in agreement with several tion of each patient. Treatments administered in our pa- scientific societies recommended to continue RAS block- tients were based on the protocol designed by the Infec- ade in front of the absence of evidence to support its dis- tious Diseases team at the Vall d’Hebron Hospital. In the continuation [16, 17]. After that, several studies come out first pandemic wave, COVID-19 treatment in case of analysing the RAS effect on COVID-19 patients or pa- pneumonia without severity criteria included lopinavir/ tients at risk for COVID-19. Liu et al. [14] showed a pos- ritonavir, hydroxychloroquine, and azithromycin; tocili- sible RAS blockade benefit in terms of protecting against zumab was reserved for those patients with pneumonia, acute distress syndrome in patients older than 65 years adult respiratory distress syndrome, interleukin-6 levels and hypertension. In concordance, Reynolds et al. [15] >40 pg/mL, and/or D-dimer >1,500 ng/mL. Treatment demonstrated that previous treatment with medications with high doses of intravenous corticosteroids was re- 6 Kidney Blood Press Res Román et al. DOI: 10.1159/000515714 served for patients with severe respiratory failure and ab- Statement of Ethics sence of response to tocilizumab. The study protocol was approved by the Ethics Committee of Our study has some limitations. First, the retrospective Vall d’Hebron University Hospital and was conducted in full ac- character of the study does not allow us to establish cau- cordance with the principles of the Declaration of Helsinki PR sality. Second, interpretation of our results is limited by (AG) 5713/2020. Informed consent for renal biopsy was signed for the small sample size. Third, risk factors between ana- each patient. Consent for this retrospective study was not needed. lytical results could not be accurately analyzed due to the absence of D-dimer, IL-6, ferritin, and LDH in all patient Conflict of Interest Statement outcomes. Despite this, we were able to create a model that exposes risk or protective factors and mortality. M.J.S. reports conflicts of interest with fees from NovoNordisk, In conclusion, our study showed a decreased mortality personal fees from Janssen, grants and nonfinancial support from compared to other series with more advanced CKD and Boehringer, nonfinancial support from Eli Lilly, personal fees from AstraZeneca, nonfinancial support from Esteve, personal fees COVID-19 infection where dialysis or ESRD highly in- from Fresenius, personal fees from Mundipharma, personal fees creased the mortality rate. Swab test for COVID-19 was from Pfizer, personal fees from Bayer, and personal fees from Vi- more likely to be performed in older, hypertensive, and for, outside the submitted work. The results presented in this ar- immunosuppressed patients and those with gastrointes- ticle have not been published previously in whole or part, except tinal symptoms. In addition, it is important to mention in abstract format. that nonswab patients with COVID-19 disease presented a milder disease without any case of death. In our study, Funding Sources low hemoglobin levels at admission were identified as risk factors for mortality in COVID-19 patients with kidney The authors are current recipients of research grants from the disease. Fondo de Investigación Sanitaria-Feder (FI17/00257 and EIN2020- 1123381) and Redinren (RD16/0009/0030). Acknowledgment Author Contributions The article is dedicated to all health care personnel who have J.L., C.G., I.A., R.B., and C.B. analyzed the current literature, contributed to the investigation and treatment of COVID-19 in- provided critical feedback, and helped to draft the manuscript. fection, as well as in honor of all patients who died fighting the N.T., A.V., and I.T. reviewed the database and designed the tables pandemic. and figures. A.G. provided kidney biopsies feedback. 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DOI: 10.1159/000515714