(1) Experimental, descriptive study/ Level 5/n=not applicable(20).
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To identify the potential mechanism of AKI by COVID-19 by analysis of unicellular transcriptome in human kidney cells(20). |
The location of the genes angiotensin-converting enzyme 2 (ACE2) and transmembrane serine proteases (TMPRSS) showed relatively high co-expression in podocytes and proximal straight tubule cells. Candidate host cells for SARS-CoV-2 have been showed. TMPRSS2 enters host cells and is co-expressed with ACE2 in podocytes. There was no significant difference in the expression of TMPRSS and the ACE2 receptor in podocytes and cells in proximal straight tubules. Comparative analysis showed that co-expression of genes in renal cells was not inferior to that of the lung, esophagus, small intestine and colon, suggesting that the kidney may be an important target for this virus(20). |
Viral (SARS-CoV-2) cytopathic effect on podocytes and proximal straight tubules can cause AKI. The proposed mechanism for the pathophysiology of AKI during COVID-19 has yet to be validated in autopsies and in experiments on animals and cells(20). |
(2) Descriptive study/ Level 5/n=116(21). |
To explore the effects of SARS-CoV-2 infection on renal function by analyzing the clinical data of 116 hospitalized COVID-19 confirmed patients(21). |
Twelve (10.8%) showed a slight increase in blood urea nitrogen or SCr. Eight (7.2%) patients had a trace or 1+ albuminuria in patients without chronic kidney disease (CKD). All of these patients did not meet the AKI diagnostic criteria. During treatment, renal function indicators showed stable status in patients with CKD, without exacerbation of CKD, and pulmonary inflammation was gradually absorbed. SARS-CoV-2 RNA in the urine sediment was positive only in 4 patients out of 53 cases and 1 patient had a positive result in the SARS-CoV-2 open reading frame(21). |
AKI was unusual in COVID-19. SARS-CoV-2 infection does not result in AKI or worsens CKD in patients with COVID-19(21). |
(3) Retrospective cohort study/ Level 4/ n=113(26). |
To outline the clinical characteristics of patients with COVID-19 who died(26). |
Deceased patients, compared to recovered ones, were older (68 and 51 years old, respectively), male, with chronic hypertension and other cardiovascular comorbidities (54 [48%] and 16 [14%]). They had dyspnea, chest tightness and consciousness disorder (70 [62%], 55 [49%] and 25 [22%]). Leukocytosis was present in 56 (50%) of deceased patients and in 6 (4%) of those who recovered, and lymphopenia was present in 103 (91%) and 76 (47%) patients. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatinine, creatine kinase, lactate dehydrogenase, cardiac troponin I, N-terminal pro-brain natriuretic peptide and D-dimer levels were higher. The most common complications were acute respiratory distress syndrome (ARDS) (113; [100%]), type I respiratory failure (18/35; [51%]), sepsis (113 [100%]), acute cardiac injury (72/94; [77%]), alkalosis (14/35 [40%]) and AKI (28 [25%])(26). |
SARS-CoV-2 infection can cause pulmonary and systemic inflammation, leading to multiple organ dysfunction in high-risk patients. ARDS and respiratory failure, sepsis, acute cardiac injury and heart failure were the most common critical complications of COVID-19(26). |
(4) Retrospective control group study/Level 4/ n=964(27). |
To investigate the characteristics of dead patients and provide some ideas on COVID-19 treatment(27). |
The mean age was higher in the deceased group compared to recovered (P <0.001), underlying diseases (P <0.001), longer time from disease onset to hospitalization (Z = 3.216, P = 0.001). Upon admission, there was a greater proportion of dyspnea (χ = 60.905, P/<0.001) and sputum (χ = 13.250, P <0.001). The deceased group exhibited a lymphocyte count (Z = 8.037, P <0.00a1) and a lymphocyte/leukocyte proportion (Z = 10.315, P <0.001) that was lower at admission and hospitalization (Z = 5.242, P <0.001). ALT (Z = 2.592, P = 0.010), AST (Z = 7.308, P <0.001) and creatinine levels (Z = 6.478, P <0.001) were higher in the deceased group. C-reactive protein (CRP) were also higher (Z = 10.206, P <0.001). The deceased group had more ARDS (χ = 148.105, P <0.001), acute cardiac injury (χ = 93.222, P <0.001), AKI (χ = 23.257, P <0.001), and shock (χ = 14.618, P <0.001)(27). |
Compared to the recovered group, more patients in the deceased group exhibited characteristics of advanced age, pre-existing comorbidities, dyspnea, low oxygen saturation, increased leukocytes, decreased lymphocytes and elevated CRP levels. In addition, they presented ARDS, acute cardiac injury, AKI, shock, and IHD(27). |
(5) – Prospective cohort study, Level 4/n=701(19). |
To assess the association between abnormal renal function markers and death in patients with COVID-19(19). |
Upon admission, 43.9% of the 701 patients had proteinuria and 26.7% had hematuria. High SCr prevalence was 14.4%, high blood urea nitrogen was 13.1% and low glomerular filtration rate was 13.1%. AKI occurred in 5.1% of patients. High basal SCr (risk rate: 2.10, 1.36-3.26), high basal urea nitrogen (3.97, 2.57-6.14), AKI stage 1 (1.90, 0 , 76-4.76), stage 2 (3.51, 1.49-8.26), stage 3 (4.38, 2.31-8.31), proteinuria 1+ (1.80, 0, 81-4.00), 2 + ~3 + (4.84, 2.00-11.70) and hematuria 1+ (2.99, 1.39-6.42), 2 + ~3 + (5.56 , 2.58-12.01) were independent risk factors for death(19). |
Prevalence of kidney disease upon admission and development of AKI during hospitalization in patients with COVID-19 was high and is associated with hospital mortality(19). |
(6) Retrospective epidemiological study, Level 4/ n=52(28). |
To describe the clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia(28). |
The mean age of the 52 patients was 59.7 years old (SD 13.3), the majority 35 (67%) were men, 21 (40%) had chronic diseases and 51 (98%) had fever. Thirty-two (61.5%) patients died after 28 days of hospitalization and the median duration of admission to the intensive care unit (ICU) until death was 7 days (IQR 3-11). Compared to survivors, non-survivors were older (64.6 years old [11.2] vs 51.9 years old [12.9]). Twenty-six (81%) patients vs nine (45%) patients were more likely to develop ARDS and to receive mechanical ventilation (30 [94%] vs 7 [35%]). From clinical evolution, (35 [67%]) with ARDS, (15 [29%]) with AKI and (12 [23%]) with cardiac injury(28). |
The survival time of non-survivors is likely to be 1 to 2 weeks after admission to the ICU. Elderly patients (> 65 years) with comorbidities and ARDS are at increased risk of death(28). |