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1.
Acta Anaesthesiol Scand ; 2022 Nov 18.
Article in English | MEDLINE | ID: covidwho-2136573

ABSTRACT

OBJECTIVES: Estimations of glomerular filtration rate (eGFR) are based on analyses of creatinine and cystatin C, respectively. Coronavirus disease 2019 (COVID-19) patients in the intensive care unit (ICU) often have acute kidney injury (AKI) and are at increased risk of drug-induced kidney injury. The aim of this study was to compare creatinine-based eGFR equations to cystatin C-based eGFR in ICU patients with COVID-19. METHODS: After informed consent, we included 370 adult ICU patients with COVID-19. Creatinine and cystatin C were analyzed at admission to the ICU as part of the routine care. Creatinine-based eGFR (ml/min) was calculated using the following equations, developed in chronological order; the Cockcroft-Gault (C-G), Modified Diet in Renal Disease (MDRD)1999, MDRD 2006, Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI), and Lund-Malmö revised (LMR) equations, which were compared with eGFR calculated using the cystatin C-based Caucasian Asian Pediatric Adult (CAPA) equation. RESULTS: The median eGFR when determined by C-G was 99 ml/min and interquartile range (IQR: 67 ml/min). Corresponding estimations for MDRD1999 were 90 ml/min (IQR: 54); MDRD2006: 85 ml/min (IQR: 51); CKD-EPI: 91 ml/min (IQR: 47); and for LMR 83 ml/min (IQR: 41). eGFR was calculated using cystatin C and the CAPA equation value was 70 ml/min (IQR: 38). All differences between creatinine-based eGFR versus cystatin C-based eGFR were significant (p < .00001). CONCLUSIONS: Estimation of GFR based on various analyses of creatinine are higher when compared with a cystatin C-based equation. The C-G equation had the worst performance and should not be used in combination with modern creatinine analysis methods for determination of drug dosage in COVID-19 patients.

2.
Biomedicines ; 10(11)2022 Nov 17.
Article in English | MEDLINE | ID: covidwho-2116110

ABSTRACT

INTRODUCTION: Multisystem inflammatory syndrome in children (MIS-C) is a new clinical entity that has emerged in the context of the COVID-19 pandemic. Despite the less severe course of the disease, varying degrees of cardiovascular events may occur in MIS-C; however, data on vascular changes occurring in MIS-C are still lacking. Endothelial dysfunction (ED) is thought to be one of the key risk factors contributing to MIS-C. BACKGROUND: We conducted a prospective observational study. We investigated possible manifestations of cardiac and endothelial involvement in MIS-C after the treatment of the acute stage and potential predictive biomarkers in patients with MIS-C. METHODS: Twenty-seven consecutive pediatric subjects (≥9 years), at least three months post-treated MIS-C of varying severity, in a stable condition, and twenty-three age- and sex-matched healthy individuals (HI), were enrolled. A combined non-invasive diagnostic approach was used to assess endothelial function as well as markers of organ damage using cardiac examination and measurement of the reactive hyperemia index (RHI), by recording the post- to pre-occlusion pulsatile volume changes and biomarkers related to ED and cardiac disease. RESULTS: MIS-C patients exhibited a significantly lower RHI (indicative of more severe ED) than those in HI (1.32 vs. 1.80; p = 0.001). The cutoff of RHI ≤ 1.4 was independently associated with a higher cardiovascular risk. Age and biomarkers significantly correlated with RHI, while serum cystatin C (Cys C) levels were independently associated with a diminished RHI, suggesting Cys C as a surrogate marker of ED in MIS-C. CONCLUSIONS: Patients after MIS-C display evidence of ED, as shown by a diminished RHI and altered endothelial biomarkers. Cys C was identified as an independent indicator for the development of cardiovascular disease. The combination of these factors has the potential to better predict the cardiovascular consequences of MIS-C. Our study suggests that ED may be implicated in the pathophysiology of this disease.

3.
J Family Med Prim Care ; 11(7): 3971-3979, 2022 Jul.
Article in English | MEDLINE | ID: covidwho-2119686

ABSTRACT

Background: The COVID-19 pandemic has claimed millions of lives. A tool for early prediction of severity and mortality risk is desirable for better utilization of health care facilities. Several biomarkers like D-dimer, lactate dehydrogenase (LDH), C-reactive protein (CRP) and some recently explored biomarkers like serum cystatin C and serum calprotectin have been proposed as prognostic markers of COVID-19, but their role as prognostic markers is so far undefined. The present work attempted to investigate the possible role of serum cystatin C and serum calprotectin as prognostic tools to predict severity and outcome ahead of time. Material and Methods: This observational cohort study was carried out on 95 COVID-19 patients admitted to a dedicated COVID care facility from mid-October 2020 to January 2021. Serial estimations of serum cystatin C and serum calprotectin levels were done and assessed for significant difference between severe (NEWS 2 score ≥5) and non-severe (NEWS 2 score <5) groups, survivors and deceased and on the basis of comorbidities at each time points. Survival analysis was done based on the optimal thresholds for severity and mortality, calculated from the receiver operating characteristic (ROC). Result: The results showed that median cystatin C levels were significantly higher on the first day in the severe group (P < 0.001) and in patients with cardiovascular disease (P < 0.05), chronic lung disease (P = 0.009) and among patients who died (P < 0.05). It remained raised on day 3 in severe (P < 0.05) and deceased (P < 0.05) group. Serum calprotectin levels were significantly higher in patients with chronic lung disease (P = 0.008) and in those who died (P < 0.05). Conclusion: Serum cystatin C could be used as a tool for early prognosis and therapeutic decision-making for COVID-19 patients. Serum calprotectin seems to be a better marker of critical illness.

4.
Int J Environ Res Public Health ; 19(21)2022 Nov 07.
Article in English | MEDLINE | ID: covidwho-2099560

ABSTRACT

Cystatin C is a specific biomarker of kidney function. We perform this meta-analysis to determine the association of Cystatin C with the COVID-19 severity. In this systematic review and meta-analysis, we searched PubMed, EMBASE, Cochrane library, and Web of Science for studies published until 2nd September 2022 that reported associations between Cystatin C levels and COVID-19 severity. The analysis was performed using a random-effects model to calculate pooled standard mean difference (SMD). Twenty-five studies were included in the meta-analysis. Pooled analysis showed statistically significant differences of Cystatin C levels among survive vs. decreased patients (0.998 ± 0.225 vs. 1.328 ± 0.475 mg/dL, respectively; SMD = -2.14; 95%CI: -3.28 to -1.01; p < 0.001). Cystatin C levels in COVID-19 severe vs. non-severe groups varied and amounted to 1.485 ± 1.191 vs. 1.014 ± 0.601 mg/dL, respectively (SMD = 1.81; 95%CI: 1.29 to 2.32; p < 0.001). Additionally, pooled analysis showed that Cystatin C levels in patients with acute kidney injury (AKI) was 1.562 ± 0.885 mg/dL, compared to 0.811 ± 0.108 mg/dL for patients without AKI (SMD = 4.56; 95%CI: 0.27 to 8.85; p = 0.04). Summing up, Cystatin C is a potentially very good marker to be used in the context of COVID-19 disease due to the prognosis of patients' serious condition, risk of AKI and mortality. In addition, Cystatin C could be used as a marker of renal complications in COVID-19 other than AKI due to the need to monitor patients even longer after leaving the hospital.


Subject(s)
Acute Kidney Injury , COVID-19 , Humans , Acute Kidney Injury/epidemiology , Acute Kidney Injury/etiology , Biomarkers , Cystatin C , Prognosis
5.
Biomedicines ; 10(11)2022 Oct 26.
Article in English | MEDLINE | ID: covidwho-2089994

ABSTRACT

COVID-19 is a systemic disease, frequently affecting kidney function. Dexamethasone is standard treatment in severe COVID-19 cases, and is considered to increase plasma levels of cystatin C. However, this has not been studied in COVID-19. Glomerular filtration rate (GFR) is a clinically important indicator of renal function, but often estimated using equations (eGFR) based on filtered metabolites. This study focuses on sources of bias for eGFRs (mL/min) using a creatinine-based equation (eGFRLMR) and a cystatin C-based equation (eGFRCAPA) in intensive-care-treated patients with COVID-19. This study was performed on 351 patients aged 18 years old or above with severe COVID-19 infections, admitted to the intensive care unit (ICU) in Uppsala University Hospital, a tertiary care hospital in Uppsala, Sweden, between 14 March 2020 and 10 March 2021. Dexamethasone treatment (6 mg for up to 10 days) was introduced 22 June 2020 (n = 232). Values are presented as medians (IQR). eGFRCAPA in dexamethasone-treated patients was 69 (37), and 74 (46) in patients not given dexamethasone (p = 0.01). eGFRLMR was not affected by dexamethasone. eGFRLMR in females was 94 (20), and 75 (38) in males (p = 0.00001). Age and maximal CRP correlated negatively to eGFRCAPA and eGFRLMR, whereas both eGFR equations correlated positively to BMI. In ICU patients with COVID-19, dexamethasone treatment was associated with reduced eGFRCAPA. This finding may be explained by corticosteroid-induced increases in plasma cystatin C. This observation is important from a clinical perspective since adequate interpretation of laboratory results is crucial.

6.
Mol Genet Genomic Med ; 10(11): e2047, 2022 Nov.
Article in English | MEDLINE | ID: covidwho-2034932

ABSTRACT

BACKGROUND: Patients with impaired kidney function were found at a high risk of COVID-19 hospitalization and mortality in many observational, cross-sectional, and hospital-based studies, but evidence from large-scale prospective cohorts has been lacking. We aimed to examine the association of kidney function-related biomarkers and their genetic predisposition with the risk of developing severe COVID-19 in population-based data. METHODS: We analyzed data from UK Biobank to examine the prospective association of abnormal kidney function biomarkers with severe COVID-19, defined by laboratory-confirmed COVID-19 hospitalizations. Using genotype data, we constructed polygenic risk scores (PRS) to represent an individual's overall genetic risk for these biomarkers. We also identified tipping points where the risk of severe COVID-19 began to increase significantly for each biomarker. RESULTS: Of the 502,506 adults, 1650 (0.32%) were identified as severe COVID-19, before August 12, 2020. High levels of cystatin C (OR: 1.3; 95% CI: 1.2-1.5; FDR = 1.5 × 10-5 ), serum creatinine (OR: 1.7; 95% CI: 1.3-2.1; p = 3.5 × 10-4 ; FDR = 3.5 × 10-4 ), microalbuminuria (OR: 1.4; 95% CI: 1.2-1.6; FDR = 4 × 10-4 ), and UACR (urinary albumin creatinine ratio; OR: 1.4; 95% CI: 1.2-1.6; p = 3.5 × 10-4 ; FDR = 3.5 × 10-4 ) were found significantly associated with severe COVID-19. Individuals with top 10% of PRS for elevated cystatin C, urate, and microalbuminuria had 28% to 43% higher risks of severe COVID-19 than individuals with bottom 30% PRS (p < 0.05). Tipping-point analyses further supported that severe COVID-19 could occur even when the values of cystatin C, urate (male), and microalbuminuria were within their normal value ranges (OR >1.1, p < 0.05). CONCLUSIONS: Findings from this study might point to new directions for clinicians and policymakers in optimizing risk-stratification among patients based on polygenic risk estimation and tipping points of kidney function markers. Our results call for further investigation to develop a better strategy to prevent severe COVID-19 outcomes among patients with genetic predisposition to impaired kidney function. These findings could provide a new tool for clinicians and policymakers in the future especially if we need to live with COVID-19 for a long time.


Subject(s)
COVID-19 , Renal Insufficiency , Adult , Humans , Male , Cystatin C/urine , COVID-19/genetics , Genetic Predisposition to Disease , Cross-Sectional Studies , Uric Acid , Albuminuria/genetics , Biomarkers , Kidney
7.
Nephrology Dialysis Transplantation ; 37(SUPPL 3):i234-i235, 2022.
Article in English | EMBASE | ID: covidwho-1915704

ABSTRACT

BACKGROUND AND AIMS: One of the complications described in critically ill patients in intensive care units with severe COVID-19 was acute kidney injury (AKI). The pathophysiology of AKI in patients with COVID-19 is multifactorial. In addition to the direct virulence of SARS-CoV-2 in renal cells, the tissue inflammation and local immune cell infiltration, cytokine storm, secondary infections and nephrotoxicity associated drugs may contribute to AKI [1]. Mounting evidence throughout the pandemic suggests that patients with severe COVID-19 may have a cytokine storm syndrome, one of the possible causes of AKI in these patients [2]. The present prospective cohort study analysed the correlation between circulating cytokine profile and estimated glomerular filtration rate (eGFR) in patients with COVID-19. METHOD: After signing the informed consent, patients positive for SARS-CoV- 2 infection (n = 74) had blood samples (n = 139) collected at hospital admission until the day of the outcome. ELISA measured the cytokines IL-10, IL-4, L-6, TNF- α and IFN-γ , and the eGFR was calculated by the CKD-EPI Cystatin C equation. Statistics description: Continuous variables were checked for normality and presented as mean ± standard deviation or median and interquartile range. The association between continuous variables is shown in scatterplots, and a predicted response with 95% confidence interval (95% CI) is plotted using fractional polynomials. For linear correlations, we obtained P-values using Pearson's correlation coefficient. RESULTS: There is a more significant distribution of eGFR below 90 mL/min in the population studied, associated with older patients. Glomerular filtration rates were negatively correlated with age as expected (-0.60;P < 0.0001). Lower eGFR was correlated with levels of proinflammatory cytokines such as IL-6 (-0.33;P < .0007) and TNF- α (-0.21;P < .03);but without positive correlation with IL-10 (0.04;P < 0.68) or IFN-γ (-0.14;P < .16), even though higher IFN-γ levels have been linked to a worse prognosis in patients with severe COVID-19 [3]. Curiously, a positive correlation was observed between lower eGFR and IL-4 levels. CONCLUSION: These results demonstrate that a shift in the immune response profile, cytokines with a Th2 profile such as IL-4, and cytokines with systemic functions such as IL-6 and TNF-α can be related to renal failure. The elucidation of the potential pathophysiological mechanisms of AKI associated with COVID-19 as well as monitoring of cytokine levels can (a) help to identify patients with severe COVID-19 at risk of loss of renal function, (b) provide information on specific therapeutic strategies. (Figure Presented).

8.
Am J Med Sci ; 364(6): 706-713, 2022 Dec.
Article in English | MEDLINE | ID: covidwho-1914122

ABSTRACT

BACKGROUND: In Japan, during the coronavirus disease 2019 (COVID-19) pandemic, patients with non-hypoxia are recommended to recuperate at home or in pre-hospital facilities. However, it was observed that unexpected hypoxia may occur and become severe subsequently in patients whose symptoms were initially expected to improve naturally. The aim of this study is to validate biomarkers that can predict at an early stage the emergence of hypoxia in COVID-19 patients without hypoxia. METHODS: We retrospectively enrolled 193 patients with COVID-19, excluding patients with hypoxia and severe disease from the onset. Participants were classified into two groups according to the emergence of hypoxia during the clinical course, and the laboratory data were compared to identify biomarkers that could predict early the emergence of hypoxia. RESULTS: The areas under the curve for serum cystatin C (CysC) and C-reactive protein (CRP) levels for the emergence of hypoxia during the clinical course were higher than those for other biomarkers (CysC, 0.84 and CRP, 0.83). Multivariate analysis showed that high serum CysC and CRP levels were associated with the emergence of hypoxia during the clinical course. CONCLUSIONS: Elevated serum CysC and CRP levels were associated with the emergence of hypoxia during the clinical course in COVID-19 patients without hypoxia. These findings may help determine the need for hospitalization in initially non-hypoxic COVID-19 patients.


Subject(s)
COVID-19 , Cystatin C , Humans , C-Reactive Protein , Retrospective Studies , Predictive Value of Tests , Biomarkers
9.
Exp Biol Med (Maywood) ; 247(17): 1570-1576, 2022 Sep.
Article in English | MEDLINE | ID: covidwho-1896295

ABSTRACT

D-dimer is an established biomarker of thromboembolism and severity in COVID-19. We and others have recently reported the dysregulation of tissue factor pathway inhibitor (TFPI), FXIII, fibrinolytic pathway, inflammatory markers, and tissue injury markers, particularly in severe COVID-19. However, association of these markers with thromboembolism in COVID-19 remains elusive. The correlation analyses between these markers in patients with moderate (non-ICU) and severe COVID-19 (ICU) were performed to delineate the potential pathomechanisms and impact of thromboembolism. We observe a negative correlation of plasma TFPI (r2 = 0.148, P = 0.035), FXIII (r2 = 0.242, P = 0.006), and plasminogen (r2 = 0.27, P = 0.003) with D-dimer, a biomarker of thromboembolism, levels in these patients. Further analysis revealed a strong positive correlation between fibrinolytic markers tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) (r2 = 0.584, P < 0.0001). Interestingly, a significant positive correlation of PAI-1, but not tPA, was observed with platelets and endothelial cells dysfunction markers P-selectin (r2 = 0.184, P = 0.01) and soluble CD40 ligand (sCD40 L) (r2 = 0.163, P = 0.02). Moreover, calprotectin (S100A8/A9) and cystatin C (CST3), previously linked with thromboembolism, exhibited positive correlations with each other (r2 = 0.339, P = 0.0007) and with the level of D-dimer independently in COVID-19. Finally, the tissue injury marker myoglobin demonstrated a strong positive correlation with D-dimer (r2 = 0.408, P = 0.0001). Taken together, inverse correlations of TFPI and FXIII with D-dimer suggest the TF pathway activation and aberrant fibrin polymerization in COVID-19 patients. The elevated level of PAI-1 is potentially contributed by activated platelets and endothelial cells. S100A8/A9 may also play roles in impaired fibrinolysis and thromboembolism, in part, through regulating the CST3. These findings strengthen the understanding of thromboembolism and tissue injury and may help in better management of thromboembolic complications in COVID-19 patients.


Subject(s)
COVID-19 , Thromboembolism , Biomarkers , CD40 Ligand/metabolism , Cystatin C/metabolism , Endothelial Cells/metabolism , Fibrin Fibrinogen Degradation Products/metabolism , Fibrinolysis/physiology , Humans , Leukocyte L1 Antigen Complex , Lipoproteins , Myoglobin/metabolism , P-Selectin/metabolism , Plasminogen/metabolism , Plasminogen Activator Inhibitor 1 , Tissue Plasminogen Activator/metabolism
10.
Braz J Infect Dis ; 26(3): 102365, 2022.
Article in English | MEDLINE | ID: covidwho-1821152

ABSTRACT

BACKGROUND: Patients infected with SARS-CoV-2 can develop acute kidney injury (AKI), associated with adverse clinical outcomes. In Mexico, an AKI incidence of 60.7% was reported in patients with COVID-19. Serum cystatin C is a well-known marker for AKI. It has been postulated as a marker for mortality in Chinese patients with COVID-19. Information regarding levels of cystatin C in COVID-19-infected patients is nonexistent among Mexican or Latin American populations. AIM: This work aimed to assess the level of cystatin C as an indicator of AKI and mortality among COVID-19 patients from Mexico. METHODS: A cross-sectional study among 38 adults was performed in the Regional High Specialty Hospital of the Yucatan Peninsula in Merida, Yucatan, Mexico. Baseline characteristics and clinical and biomechanical parameters were collected, and serum levels of cystatin C were measured by ELISA. RESULTS: A total of 71% (27 patients) with COVID-19 developed AKI; 78% were men, and 22% were women. In addition, 60% of individuals (16 men; 7 women) died due to COVID-19 complications. Serum levels of cystatin C were higher in those individuals who developed AKI (p = 0.001). A logistic regression model indicated that individuals with serum levels of cystatin C above 0.84 ng/mL had a 23-fold increased risk of developing AKI (OR, 23.7, 95% CI, 2.59-217.00, p = 0.005). However, increased cystatin C was not independently associated with mortality in the Mexican population (HR, 1.01, 95% CI, 0.66-1.56, p = 0.959). CONCLUSION: The results suggest that serum levels of cystatin C indicate AKI in COVID-19 patients. Although we recommend caution when using serum cystatin C levels as an indicator of mortality among the Mexican population, it is essential to note that cystatin C elevates earlier than creatinine, which is an advantage for timely clinical interventions.


Subject(s)
Acute Kidney Injury , COVID-19 , Cystatin C , Acute Kidney Injury/diagnosis , Acute Kidney Injury/virology , Adult , Biomarkers , COVID-19/diagnosis , COVID-19/mortality , Cross-Sectional Studies , Female , Humans , Male , Mexico/epidemiology , Prospective Studies , SARS-CoV-2
11.
Exp Biol Med (Maywood) ; 247(14): 1205-1213, 2022 07.
Article in English | MEDLINE | ID: covidwho-1808181

ABSTRACT

Severe coronavirus (SARS-COV-2) infection often leads to systemic inflammation accompanied by cardiovascular complications including venous thromboembolism (VTE). However, it is largely undefined if inflammatory markers such as lipocalin-2 (LNC2), calprotectin (S100A8/A9), and cystatin C (CST3), previously linked with VTE, play roles in cardiovascular complications and advancement of COVID-19 severity. To investigate the same, hospitalized moderate and severe (presented pneumonia and required intensive care) COVID-19 patients were recruited. The levels of plasma LNC2, S100A8/A9, CST3, myoglobin, and cardiac Troponin I (cTnI) were assessed through enzyme-linked immunosorbent assay (ELISA). The investigation revealed a significantly upregulated level of plasma LNC2 at the moderate stage of SARS-CoV-2 infection. In contrast, the levels of S100A8/A9 and CST3 in moderate patients were comparable to healthy controls; however, a profound induction was observed only in severe COVID-19 patients. The tissue injury marker myoglobin was unchanged in moderate patients; however, a significantly elevated level was observed in the critically ill COVID-19 patients. In contrast, cTnI level was unchanged both in moderate and severe patients. Analysis revealed a positive correlation between the levels of S100A8/A9 and CST3 with myoglobin in COVID-19. In silico analysis predicted interactions of S100A8/A9 with toll-like receptor 4 (TLR-4), MyD88 LY96, and LCN2 with several other inflammatory mediators including MMP2, MMP9, TIMP1, and interleukins (IL-6, IL-17A, and IL-10). In summary, early induction of LCN2 likely plays a role in advancing the COVID-19 severity. A positive correlation of S100A8/A9 and CST3 with myoglobin suggests that these proteins may serve as predictive biomarkers for thromboembolism and tissue injury in COVID-19.


Subject(s)
COVID-19 , Venous Thromboembolism , Biomarkers , COVID-19/complications , Calgranulin A/metabolism , Calgranulin B/metabolism , Cystatin C/metabolism , Humans , Lipocalin-2 , Myoglobin/metabolism , SARS-CoV-2
12.
Journal of Cellular and Molecular Anesthesia ; 7(1):32-39, 2022.
Article in English | EMBASE | ID: covidwho-1772041

ABSTRACT

Background: Prediction and early diagnosis of acute kidney injury (AKI) in critically ill Coronavirus disease 2019 (COVID-19) patients are of great importance. Therefore, using promising renal biomarkers such as cystatin C and neutrophil gelatinase-associated lipocalin (NGAL) to identify the risk of future AKI is crucial. Materials and Methods: A total of 89 adult patients with COVID-19 were included in this study. Serum cystatin C and NGAL concentration were assessed on intensive care unit (ICU) admission then repeated after 48 hours. Serum creatinine was followed for 7 days to report the development of AKI. Results: Among the COVID-19 patients, 28.1% developed AKI. Although admission serum creatinine was not significantly different between the AKI group and the non-AKI group (p=0.375), admission Cystatin C (p=0.018), and NGAL (p<0.001) were significantly different between both groups. After 48 hours, a change in Cystatin C level (p<0.001) but not NGAL (p=0.4) was a predictor for AKI. Logistic regression model including age (p=0.031), Cystatin C on 48 hrs (p=0.003) and NGAL on admission (p=0.015) could predict AKI in COVID-19 patients. Conclusion: Serum Cystatin C and NGAL in ICU could be used to predict AKI in COVID-19 patients. A logistic regression model including age, Cystatin C on 48hrs, and NGAL on admission might be a tool for individualized risk estimation of AKI in COVID-19 patients.

13.
Biosens Bioelectron ; 208: 114234, 2022 Jul 15.
Article in English | MEDLINE | ID: covidwho-1767930

ABSTRACT

Chronic kidney disease (CKD) is the most neglected chronic disease affecting over 750 million persons in the world. Currently, many patients with cancers or other chronic diseases (i.e., CKD) struggle to receive clinical treatment or examination due to hospitals cancelling or delaying in the COVID-19 pandemic, which may increase the risk of death. Cystatin C (Cys C) has been proposed as a potential glomerular filtration rate (GFR) marker for the early detection of acute kidney injury and CKD. However, most traditional methods for Cys C detection are immunoassays using serum as a sample and are tedious to perform and economically burdensome. To diagnose the disease in the early stage and carry out daily management during the current pandemic, we developed an integration of hydrogel microneedle patch (HMNP) and lateral flow cassette (LFC) to rapidly detect Cys C in skin interstitial fluid (ISF) in 25 min for blood-free CKD management anytime and anywhere by the naked eye that can reduce the impact of an individual's quality of life and life expectancy. Conceivably, this strategy presents a wide scope in the application of numerous other diseases if corresponding analytes are available in skin ISF.


Subject(s)
Biosensing Techniques , COVID-19 , Renal Insufficiency, Chronic , COVID-19/diagnosis , Creatinine , Female , Humans , Male , Pandemics , Point-of-Care Testing , Quality of Life , Renal Insufficiency, Chronic/diagnosis
14.
Diagnostics (Basel) ; 12(1)2022 Jan 04.
Article in English | MEDLINE | ID: covidwho-1637531

ABSTRACT

The aim of our study was to evaluate the influence of asymptomatic infection and the occurrence of symptomatic COVID-19 on specific biochemical, renal, and immune parameters-renalase, neutrophil gelatinase-associated lipocalin (NGAL) cystatin C (CysC), and creatinine-and their weekly fluctuations during a one-month observation period in COVID-19 patients admitted to hospital. The study involved 86 individuals: 30 patients with diagnosed COVID-19, 28 people with asymptomatic infection confirmed with IgG antibodies-the IG(+) group-and 28 individuals without any (IgG, IgE) anti-SARS-CoV-2 antibodies-the IG(-) group. In the COVID-19 group, blood was drawn four times: (1) on day 0/1 after admission to hospital (C1 group), (2) 7 days later (C7 group), (3) 14 days later (C14 group), and (4) 28 days later (C28 group). In the IG(-) and IG(+) groups, blood was drawn once. There were no significant differences in creatinine, Cys C, and uric acid between any of the analyzed groups. NGAL levels were significantly higher in IG(+) and at all time-points in the COVID-19 groups than in controls. A similar observation was made for renalase at the C7, C14, and C28 time-points. Plasma renalase, NGAL, and CysC are unrelated to kidney function in non-critically ill COVID-19 patients and those with asymptomatic infection. Renalase and NGAL are most likely related to the activation of the immune system rather than kidney function. Asymptomatic SARS-CoV-2 infection causes a rise in plasma NGAL levels similar to those observed in symptomatic COVID-19 patients. Therefore, more attention should be paid to tracking and monitoring the health of these people.

15.
Critical Care Medicine ; 50:75-75, 2022.
Article in English | Academic Search Complete | ID: covidwho-1595251

ABSTRACT

Proximity extension assays measured plasma renin, ACE2, and renin-receptor, as well as >40 markers of endothelial, alveolar, cardiac, and renal injury. Over time, critically ill patients develop higher RAS markers that are associated with non-pulmonary organ injury and worse 28-day outcome. B Introduction: b The renin-angiotensin system (RAS) is not well characterized over the course of severe COVID-19 illness. [Extracted from the article] Copyright of Critical Care Medicine is the property of Lippincott Williams & Wilkins and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)

16.
Wiadomosci Lekarskie ; 74(10 cz 2):2640-2645, 2021.
Article in English | MEDLINE | ID: covidwho-1589773

ABSTRACT

OBJECTIVE: The aim: To examine the diagnostic possibilities of determining the level of cystatin C in the blood serum in order to ascertain the functional status of the kidneys in patients with type 2 diabetes (those who recovered from COVID-19 infection) depending on the presence or absence of non-alcoholic fatty liver disease (further - NAFLD) and malnutrition. PATIENTS AND METHODS: Materials and methods: We investigated 18 patients with type 2 DM, who were included in the first group of the patients examined;group 2 consisted of 20 patients with type 2 DM and non-alcoholic fatty liver disease (NAFLD), namely with non-alcoholic steatohepatitis;and group 3 of the patients examined consisted of 30 patients with type 2 DM and obesity. RESULTS: Results: Renal damage in patients with metabolically associated diseases in the background of respiratory disease due to COVID-19 infection was also indicated by changes in urine test indicators, and namely - proteinuria and erythrocyturia, leukocyturia in urine sediment. The examination of cystatin C (Cys C) level indicates its statistically significant increase in patients of all examined groups, with the highest levels established in group 3 patients (with its increase up to 2.58 +/- 0.11 mg/L, compared with the norm of 0.75 +/- 0.04 mg/L in the control group - p < 0.01). The examination of GFR by calculation, where the Cys C index in serum was used, revealed a significant decrease in this parameter in all the examined groups of patients. At the same time, the maximum values were found in group 1 patients (65.7 +/- 1.4 ml/min per 1.73 m2 of the body surface), and the minimum values - in group 3 patients (48.3 +/- 2.7 ml/min per 1.73 m2 of the body surface). CONCLUSION: Conclusions: An increase in serum cystatin C levels was determined in type 2 diabetes patients, with the lowest level in group 1 patients (1.24 +/- 0.07 mg/L - p < 0.05), and the highest level in patients suffering from type 2 diabetes combined with NAFLD and obesity (2.58 +/- 0.11 mg/L - p < 0.01). A moderate to severe course of COVID-19 infection in patients with type 2 diabetes as well as with its combination with NAFLD and obesity contributes to the development of renal functional disorders in these patients. Moreover, an increase in serum Cys C levels is a more sensitive and earlier marker of renal damage development in comorbid pathology.

17.
J Nephrol ; 35(1): 59-68, 2022 Jan.
Article in English | MEDLINE | ID: covidwho-1356092

ABSTRACT

BACKGROUND: Combined markers of renal dysfunction and inflammation, e.g., cystatin C, might assist with risk stratification and clinical decisions in patients with coronavirus disease 19 (COVID-19). We conducted a systematic review and meta-analysis with meta-regression of serum cystatin C in COVID-19. METHODS: We searched PubMed, Web of Science and Scopus, between January 2020 and February 2021, for studies reporting serum cystatin C concentrations, measures of clinical severity and survival outcomes in hospitalized COVID-19 patients (PROSPERO registration number: CRD42021245295). RESULTS: Thirteen studies in 2510 COVID-19 patients, 1972 with low severity or survivor status and 538 with high severity or non-survivor status during follow up, were included in the meta-analysis. The pooled results showed that serum cystatin C concentrations were higher in patients with high disease severity or non-survivor status (standard mean deviation, SMD, 1.71, 95% CI 0.95 to 2.46, p < 0.001). Extreme between-study heterogeneity was observed (I2 = 97.5%, p < 0.001). Sensitivity analysis, performed by sequentially removing each study and re-assessing the pooled estimates, showed that the magnitude and direction of the effect size was not substantially modified. The Begg's and Egger's t tests did not show publication bias. In meta-regression, the SMD of serum cystatin C was not associated with age, proportion of males, C-reactive protein, neutrophils, lymphocytes, aspartate aminotransferase, alanine aminotransferase, albumin, creatinine, creatine kinase-MB, lactate dehydrogenase, and proportion of patients with diabetes or hypertension. CONCLUSIONS: Higher concentrations of serum cystatin C were associated with higher COVID-19 severity and mortality.


Subject(s)
COVID-19 , Cystatin C/blood , C-Reactive Protein , COVID-19/diagnosis , COVID-19/mortality , Humans , Severity of Illness Index
18.
Front Endocrinol (Lausanne) ; 12: 642452, 2021.
Article in English | MEDLINE | ID: covidwho-1302108

ABSTRACT

Background: We investigated if the concentration and "rangeability" of cystatin C (CysC) influenced the prognosis of coronavirus disease 2019 (COVID-19) in patients suffering from, or not suffering from, type 2 diabetes mellitus (T2DM). Methods: A total of 675 T2DM patients and 572 non-T2DM patients were divided into "low" and "high" CysC groups and low and high CysC-rangeability groups according to serum CysC level and range of change of CysC level, respectively. Demographic characteristics, clinical data, and laboratory results of the four groups were analyzed. Results: COVID-19 patients with a high level and rangeability of CysC had more organ damage and a higher risk of death compared with those with a low level or low rangeability of CysC. Patients with a higher level and rangeability of CysC had more blood lymphocytes and higher levels of C-reactive protein, alanine aminotransferase, and aspartate aminotransferase. After adjustment for possible confounders, multivariate analysis revealed that CysC >0.93 mg/dL was significantly associated with the risk of heart failure (OR = 2.231, 95% CI: 1.125-5.312) and all-cause death (2.694, 1.161-6.252). CysC rangeability >0 was significantly associated with all-cause death (OR = 4.217, 95% CI: 1.953-9.106). These associations were stronger in patients suffering from T2DM than in those not suffering from T2DM. Conclusions: The level and rangeability of CysC may influence the prognosis of COVID-19. Special care and appropriate intervention should be undertaken in COVID-19 patients with an increased CysC level during hospitalization and follow-up, especially for those with T2DM.


Subject(s)
Biomarkers/blood , COVID-19/diagnosis , COVID-19/mortality , Cystatin C/blood , Diabetes Mellitus, Type 2/physiopathology , SARS-CoV-2/isolation & purification , Aged , COVID-19/blood , COVID-19/virology , Case-Control Studies , Female , Humans , Male , Middle Aged , Prognosis , Retrospective Studies , Risk Factors
19.
Front Pharmacol ; 12: 587816, 2021.
Article in English | MEDLINE | ID: covidwho-1172974

ABSTRACT

Background: Coronavirus disease- (COVID-19-) related renal function abnormality is associated with poor prognosis. However, the clinical significance of dynamic changes in renal function indicators has not been studied, and no studies have evaluated the renal function in COVID-19 patients by cystatin C. Objective: This study aimed to evaluate the effect of abnormal renal function on admission on prognosis of COVID-19 patients and the prognostic value of various renal function indicators. Methods: A total of 1,764 COVID-19 patients without a history of chronic kidney disease were categorized into two groups, an elevated cystatin C group and a normal cystatin C group, based on the results of renal function tests on admission. The clinical characteristics were compared between the two groups, and logistic or Cox regression analyses were performed to explore the associations between elevated cystatin C/serum creatinine levels and disease severity and survival. We also performed receiver operating characteristic (ROC) curve, Kaplan-Meier survival, and curve fitting analyses. Results: When adjusted for several significant clinical variables, elevated cystatin C levels on admission were independent predictors of disease severity (p < 0.001), and elevated creatinine levels were independent predictors of death (p = 0.020). Additionally, the ROC curve analysis shows that elevated cystatin C levels [area under the curve (AUC): 0.656] have a better predictive value for disease severity than elevated creatinine levels (AUC: 0.540). The survival curves of patients with elevated cystatin C/creatinine levels show a sharper decline than those of patients with normal cystatin C/creatinine levels (p < 0.001). The curve fitting analysis revealed that, compared to the flat curves of cystatin C and creatinine levels for patients who survived, the curves for patients who died kept rising, and cystatin C levels rose above the normal range earlier than creatinine. Conclusions: Elevated cystatin C, which occurs earlier than serum creatinine, is useful for the early detection of renal function abnormality and might have better predictive value for disease severity in COVID-19 patients, while elevated serum creatinine may have a better predictive value for risks of death.

20.
Nephrology (Carlton) ; 26(6): 513-521, 2021 Jun.
Article in English | MEDLINE | ID: covidwho-1050365

ABSTRACT

AIM: This study aims to determine the frequency of COVID-19 related AKI and to identify the early predictors of AKI. METHODS: This study is a single-center, retrospective, observational study. Hospitalized COVID-19 patients between 24/03/2020 and 31/05/2020 were included in the study. All patients were evaluated for renal dysfunctions with urine dipstick, protein/creatinine ratio, albumin/creatinine ratio in spot urine, serum cystatin C, serum creatinine level on hospital admission, and 28th day of hospital admission. To assess the utility of these parameters to predict AKI, a receiver-operating characteristic curve was generated and the area under the curve (AUC) was calculated. RESULTS: 348 patients were included. The average incidence of AKI was 4.9% (n = 17). The incidence of AKI in mild, moderate and severe COVID-19 cases was 1.3% (n = 4), 9.0% (n = 3) and 76.9% (n = 10), respectively. Proteinuria was detected in 7.8% (n = 27) of patients with a urine dipstick test. In spot urine analysis, proteinuria was found in 20.1% (n = 70) of patients. The frequency of persistent proteinuria was 5.2% (n = 18). The AUC alue of serum cystatin C, D-dimer and albumin/creatinine ratio to predict COVID-19 related AKI were 0.96 (0.90 to 1.0), 0.94 (0.89-0.98), and 0.95 (0.91-0.98). CONCLUSION: In COVID-19 patients with normal serum creatinine levels on hospital admission, albuminuria, serum cystatin C and D-dimer levels may be an early predictor of COVID-19 related AKI and these patients should be monitored closely for AKI. Since the sample size in the AKI group was small, our study results should be confirmed with larger cohort studies.


Subject(s)
Acute Kidney Injury/etiology , COVID-19/complications , SARS-CoV-2 , Acute Kidney Injury/blood , Acute Kidney Injury/epidemiology , Adult , Aged , Creatinine/blood , Cystatin C/blood , Female , Fibrin Fibrinogen Degradation Products/analysis , Humans , Male , Middle Aged , Retrospective Studies
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