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1.
preprints.org; 2023.
Preprint in English | PREPRINT-PREPRINTS.ORG | ID: ppzbmed-10.20944.preprints202301.0195.v1

ABSTRACT

Systemic capillary leak syndrome (SCLS) is an uncommon, potentially life-threatening disorder defined as recurrent attacks of pseudo-shock. This syndrome occurs due to the disruption of endothelial cells, which leads to increased vascular permeability, causing intravascular fluid to leak into the extravascular space and albumin to be retained in the interstitial space. SCLS can lead to hypovolemia, peripheral hypoperfusion, and acute renal insufficiency. The syndrome is presented with fever, generalized edema, pleural effusions, dyspnea, hypovolemia, hemoconcentration, prerenal azotemia, shock, and syncope. After ruling out other causes of hypovolemic shock, the diagnosis of SCLS can be considered on the presence of the classical triad of hypotension, hemoconcentration, and hypoalbuminemia. Eliminating the precipitating factors is the cornerstone of SCLS management. It is advisable to be very cautious and weigh the risks and benefits of vaccination of people with a history of this condition. This review will discuss and compare different aspects of SLCS after SARS-CoV-2 infection and COVID-19 vaccination.


Subject(s)
Hypoalbuminemia , Syncope , Shock , Pleural Effusion , COVID-19 , Dyspnea , Hypovolemia , Fever , Acute Kidney Injury , Azotemia , Hypotension , Capillary Leak Syndrome , Edema
3.
J Am Soc Nephrol ; 33(2): 326-341, 2022 02.
Article in English | MEDLINE | ID: covidwho-2141035

ABSTRACT

BACKGROUND: Hereditary renal hypouricemia type 1 (RHUC1) is caused by URAT1/SLC22A12 dysfunction, resulting in urolithiasis and exercise-induced AKI (EIAKI). However, because there is no useful experimental RHUC1 animal model, the precise pathophysiologic mechanisms underlying EIAKI have yet to be elucidated. We established a high HPRT activity Urat1-Uox double knockout (DKO) mouse as a novel RHUC1 animal model for investigating the cause of EIAKI and the potential therapeutic effect of xanthine oxidoreductase inhibitors (XOIs). METHODS: The novel Urat1-Uox DKO mice were used in a forced swimming test as loading exercise to explore the onset mechanism of EIAKI and evaluate related purine metabolism and renal injury parameters. RESULTS: Urat1-Uox DKO mice had uricosuric effects and elevated levels of plasma creatinine and BUN as renal injury markers, and decreased creatinine clearance observed in a forced swimming test. In addition, Urat1-Uox DKO mice had increased NLRP3 inflammasome activity and downregulated levels of Na+-K+-ATPase protein in the kidney, as Western blot analysis showed. Finally, we demonstrated that topiroxostat and allopurinol, XOIs, improved renal injury and functional parameters of EIAKI. CONCLUSIONS: Urat1-Uox DKO mice are a useful experimental animal model for human RHUC1. The pathogenic mechanism of EIAKI was found to be due to increased levels of IL-1ß via NLRP3 inflammasome signaling and Na+-K+-ATPase dysfunction associated with excessive urinary urate excretion. In addition, XOIs appear to be a promising therapeutic agent for the treatment of EIAKI.


Subject(s)
Acute Kidney Injury/drug therapy , Hypoxanthine Phosphoribosyltransferase/metabolism , Organic Anion Transporters/deficiency , Urate Oxidase/deficiency , Xanthine Dehydrogenase/antagonists & inhibitors , Acute Kidney Injury/etiology , Acute Kidney Injury/metabolism , Allopurinol/pharmacology , Animals , Disease Models, Animal , Enzyme Inhibitors/pharmacology , Hypoxanthine Phosphoribosyltransferase/genetics , Kidney/drug effects , Kidney/metabolism , Kidney/pathology , Male , Mice , Mice, Inbred C57BL , Mice, Knockout , NLR Family, Pyrin Domain-Containing 3 Protein/metabolism , Nitriles/pharmacology , Organic Anion Transporters/genetics , Physical Exertion , Pyridines/pharmacology , Renal Tubular Transport, Inborn Errors/drug therapy , Renal Tubular Transport, Inborn Errors/etiology , Renal Tubular Transport, Inborn Errors/metabolism , Sodium-Potassium-Exchanging ATPase/metabolism , Urate Oxidase/genetics , Urinary Calculi/drug therapy , Urinary Calculi/etiology , Urinary Calculi/metabolism
4.
Front Immunol ; 13: 874426, 2022.
Article in English | MEDLINE | ID: covidwho-2141856

ABSTRACT

Background: Several reports suggested that acute kidney injury (AKI) is a relatively common occurrence in hospitalized COVID-19 patients, but its prevalence is inconsistently reported across different populations. Moreover, it is unknown whether AKI results from a direct infection of the kidney by SARS-CoV-2 or it is a consequence of the physiologic disturbances and therapies used to treat COVID-19. We aimed to estimate the prevalence of AKI since it varies by geographical settings, time periods, and populations studied and to investigate whether clinical information and laboratory findings collected at hospital admission might influence AKI incidence (and mortality) in a particular point in time during hospitalization for COVID-19. Methods: Herein we conducted a prospective longitudinal study investigating the prevalence of AKI and associated factors in 997 COVID-19 patients admitted to the Baqiyatallah general hospital of Tehran (Iran), collecting both clinical information and several dates (of: birth; hospital admission; AKI onset; ICU admission; hospital discharge; death). In order to examine how the clinical factors influenced AKI incidence and all-cause mortality during hospitalization, survival analysis using the Cox proportional-hazard models was adopted. Two separate multiple Cox regression models were fitted for each outcome (AKI and death). Results: In this group of hospitalized COVID-19 patients, the prevalence of AKI was 28.5% and the mortality rate was 19.3%. AKI incidence was significantly enhanced by diabetes, hyperkalemia, higher levels of WBC count, and blood urea nitrogen (BUN). COVID-19 patients more likely to die over the course of their hospitalization were those presenting a joint association between ICU admission with either severe COVID-19 or even mild/moderate COVID-19, hypokalemia, and higher levels of BUN, WBC, and LDH measured at hospital admission. Diabetes and comorbidities did not increase the mortality risk among these hospitalized COVID-19 patients. Conclusions: Since the majority of patients developed AKI after ICU referral and 40% of them were admitted to ICU within 2 days since hospital admission, these patients may have been already in critical clinical conditions at admission, despite being affected by a mild/moderate form of COVID-19, suggesting the need of early monitoring of these patients for the onset of eventual systemic complications.


Subject(s)
Acute Kidney Injury , COVID-19 , Acute Kidney Injury/etiology , COVID-19/complications , Hospital Mortality , Humans , Iran/epidemiology , Longitudinal Studies , Prospective Studies , Retrospective Studies , Risk Factors , SARS-CoV-2
5.
J Am Soc Nephrol ; 33(3): 613-627, 2022 03.
Article in English | MEDLINE | ID: covidwho-2141043

ABSTRACT

BACKGROUND: The mechanisms underlying long-term sequelae after AKI remain unclear. Vessel instability, an early response to endothelial injury, may reflect a shared mechanism and early trigger for CKD and heart failure. METHODS: To investigate whether plasma angiopoietins, markers of vessel homeostasis, are associated with CKD progression and heart failure admissions after hospitalization in patients with and without AKI, we conducted a prospective cohort study to analyze the balance between angiopoietin-1 (Angpt-1), which maintains vessel stability, and angiopoietin-2 (Angpt-2), which increases vessel destabilization. Three months after discharge, we evaluated the associations between angiopoietins and development of the primary outcomes of CKD progression and heart failure and the secondary outcome of all-cause mortality 3 months after discharge or later. RESULTS: Median age for the 1503 participants was 65.8 years; 746 (50%) had AKI. Compared with the lowest quartile, the highest quartile of the Angpt-1:Angpt-2 ratio was associated with 72% lower risk of CKD progression (adjusted hazard ratio [aHR], 0.28; 95% confidence interval [CI], 0.15 to 0.51), 94% lower risk of heart failure (aHR, 0.06; 95% CI, 0.02 to 0.15), and 82% lower risk of mortality (aHR, 0.18; 95% CI, 0.09 to 0.35) for those with AKI. Among those without AKI, the highest quartile of Angpt-1:Angpt-2 ratio was associated with 71% lower risk of heart failure (aHR, 0.29; 95% CI, 0.12 to 0.69) and 68% less mortality (aHR, 0.32; 95% CI, 0.15 to 0.68). There were no associations with CKD progression. CONCLUSIONS: A higher Angpt-1:Angpt-2 ratio was strongly associated with less CKD progression, heart failure, and mortality in the setting of AKI.


Subject(s)
Acute Kidney Injury , Heart Failure , Renal Insufficiency, Chronic , Acute Kidney Injury/complications , Aged , Angiopoietins , Female , Heart Failure/complications , Humans , Male , Prognosis , Prospective Studies , Renal Insufficiency, Chronic/complications , Risk Factors
6.
researchsquare; 2022.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-2391836.v1

ABSTRACT

Background COVID-19 infection is generally regarded as an acute self-limiting illness in children, but it can cause significant morbidity and mortality in both healthy and high-risk children. There are limited data on the outcomes of children with congenital heart disease (CHD) and COVID-19. This study aimed to examine the risks of mortality, in-hospital cardiovascular and non-cardiovascular complications in this patient population.Methods We analyzed data from hospitalized pediatric patients from 2020 using the nationally representative National Inpatient Sample (NIS). Children hospitalized for COVID-19 were included, and weighted data were used to compare in-hospital mortality and morbidities between children with and without CHD.Results Out of 33,220 children admitted with a diagnosis of COVID-19 infection(ICD-10 code:U07.1) during calendar year 2020, 875 (2.6%) had CHD. Compared to children without CHD, children with CHD had similar in-hospital mortality (1.2% vs 0.8%, p = 0.63), with adjusted OR (aOR) of 2.0 (95% CI: 0.5–8.3). Tachyarrhythmias and heart block were more likely in CHD children with an aOR of 4.9 (95% CI: 1.9–12.4) and aOR of 4.4 (95% CI: 2.0-9.7), respectively. Similarly, respiratory failure [aOR = 1.8 (1.2–2.9)], respiratory failure requiring non-invasive mechanical ventilation [aOR = 3.1 (1.5–6.2)] and invasive mechanical ventilation [aOR = 2.2 (1.2-4.0)], and acute kidney injury [aOR = 3.0 (1.8–4.9)] were all significantly higher among patients with CHD. Median length of hospital stay in children with CHD was longer than those without CHD [5 days (IQR: 2-9.3) vs. 3 days (IQR: 2–5), p = < 0.001].Conclusions Children with CHD hospitalized with COVID-19 infection were at increased risk of serious cardiovascular and non-cardiovascular adverse clinical outcomes. They were not at increased risk for death when compared to children without CHD but had increased length of hospital stay and utilization of healthcare resources.


Subject(s)
Heart Diseases , COVID-19 , Heart Block , Acute Kidney Injury , Respiratory Insufficiency , Death
7.
Int J Mol Sci ; 23(22)2022 Nov 17.
Article in English | MEDLINE | ID: covidwho-2116209

ABSTRACT

Since the outbreak of COVID-19 disease, a bidirectional interaction between kidney disease and the progression of COVID-19 has been demonstrated. Kidney disease is an independent risk factor for mortality of patients with COVID-19 as well as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection leading to the development of acute kidney injury (AKI) and chronic kidney disease (CKD) in patients with COVID-19. However, the detection of kidney damage in patients with COVID-19 may not occur until an advanced stage based on the current clinical blood and urinary examinations. Some studies have pointed out the development of subclinical acute kidney injury (subAKI) syndrome with COVID-19. This syndrome is characterized by significant tubule interstitial injury without changes in the estimated glomerular filtration rate. Despite the complexity of the mechanism(s) underlying the development of subAKI, the involvement of changes in the protein endocytosis machinery in proximal tubule (PT) epithelial cells (PTECs) has been proposed. This paper focuses on the data relating to subAKI and COVID-19 and the role of PTECs and their protein endocytosis machinery in its pathogenesis.


Subject(s)
Acute Kidney Injury , COVID-19 , Renal Insufficiency, Chronic , Humans , COVID-19/complications , SARS-CoV-2 , Acute Kidney Injury/metabolism , Renal Insufficiency, Chronic/metabolism , Kidney Tubules, Proximal/metabolism
8.
Crit Care Clin ; 38(3): 473-489, 2022 Jul.
Article in English | MEDLINE | ID: covidwho-2114478

ABSTRACT

Initial reporting suggested that kidney involvement following COVID-19 infection was uncommon but this is now known not to be the case. Acute kidney injury (AKI) may arise through several mechanisms and complicate up to a quarter of patients hospitalized with COVID-19 infection being associated with an increased risk for both morbidity and death. Mechanisms of injury include direct kidney damage predominantly through tubular injury, although glomerular injury has been reported; the consequences of the treatment of patients with severe hypoxic respiratory failure; secondary infection; and exposure to nephrotoxic drugs. The mainstay of treatment remains the prevention of worsening kidney damage and in some cases they need for renal replacement therapies (RRT). Although the use of other blood purification techniques has been proposed as potential treatments, results to-date have not been definitive.


Subject(s)
Acute Kidney Injury , COVID-19 , Acute Kidney Injury/etiology , Acute Kidney Injury/therapy , COVID-19/complications , COVID-19/therapy , Humans , Renal Replacement Therapy , SARS-CoV-2
9.
Kidney360 ; 3(8): 1317-1322, 2022 08 25.
Article in English | MEDLINE | ID: covidwho-2111635

ABSTRACT

Background: Persistent hyperkalemia (hyperK) and hyperphosphatemia (hyperP) despite renal replacement therapy (RRT) was anecdotally reported in COVID-19 and acute kidney injury (AKI) requiring RRT (CoV-AKI-RRT). However, observation bias could have accounted for the reports. Thus, we systematically examined the rate and severity of hyperK and hyperP in patients with CoV-AKI-RRT in comparison with the pre-COVID-19 era. Methods: We identified patients with CoV-AKI-RRT treated with sustained low-efficiency dialysis (SLED) for ≥2 days in March-April 2020. As pre-COVID-19 control, we included patients with AKI treated with SLED in December 2019. We examined the rates of hyperK (serum potassium [sK] ≥5.5 mEq/L), severe hyperK (sK ≥6.5 mEq/L), hyperP (serum phosphate [sP] ≥4.5 mg/dl), and moderate or severe hyperP (sP ≥7-10 and >10 mg/dl, respectively) as %SLED-days with an event. Results: Along the duration of SLED, the incidence of hyperK was greater in CoV-AKI-RRT (n=64; mean 19%±2% versus 14%±3% SLED-days, P=0.002) compared with control (n=60). The proportion of patients with one or more event of severe hyperK was greater in CoV-AKI (33% versus 7%, P<0.001). The incidence of hyperP was similar between groups (mean 56%±4% versus 53%±5% SLED-days, P=0.49). However, the proportion of patients with one or more event of moderate and severe hyperP was greater in CoV-AKI-RRT (86% versus 60%, P=0.001, and 50% versus 18%, P<0.001, respectively). Among those with CoV-AKI-RRT, sK and sP correlated with lactate dehydrogenase (LDH; r=0.31, P=0.04, and r=0.31, P=0.04, respectively), whereas hyperP also correlated with shorter SLED runs (hours/run; r=-0.27, P=0.05). Conclusions: Refractory hyperK and hyperP were more frequent in CoV-AKI-RRT compared with the pre-COVID-19 era. Because of the correlation of sK and sP with higher LDH and sP with shorter SLED runs, intracellular ion release from cell injury due to cytokine storm and RRT interruptions may account for the findings.


Subject(s)
Acute Kidney Injury , COVID-19 , Hyperkalemia , Hyperphosphatemia , Acute Kidney Injury/epidemiology , COVID-19/complications , Humans , Hyperkalemia/epidemiology , Hyperphosphatemia/etiology , Lactate Dehydrogenases , Phosphates , Potassium , Renal Dialysis/adverse effects
10.
Anal Chem ; 94(47): 16290-16298, 2022 Nov 29.
Article in English | MEDLINE | ID: covidwho-2119298

ABSTRACT

One of the serious complications of COVID-19 is acute kidney injury (AKI), leading to a decrease in kidney function and even death. The concentration of ammonia (NH3) in the exhaled breath (EB) of COVID-19 patients suffering from AKI symptoms will be significantly increased. In this work, the detection of breath NH3 was performed at gold interdigital electrodes modified with a soluble polypyrrole microparticle and silver nanoparticle film (Au-IDEs/S-PPyMPs/AgNPs) as a noninvasive chemiresistor gas sensor. The response behavior of unmodified and modified gas sensors toward NH3 and other interfering compounds was studied. The Au-IDEs/S-PPyMPs/AgNPs exhibited NH3 detection in the linear dynamic range of 1.00-19.23 ppm, with a limit of detection of 0.12 ppm. Finally, the fabricated gas sensor was used to monitor the NH3 concentration in the EB of COVID-19 patients suffering from AKI symptoms. For this purpose, the gas sensor was validated in 19 EB samples (seven COVID-19-positive patients, four COVID-19-negative patients, and eight post-COVID-19 patients). The gas sensor was directly exposed to the EB samples, followed by recording the changes in electrical resistance via a low-cost digital multimeter. The sensing mechanism was explained as the interaction between breath NH3 and sensing materials. The breath NH3 concentrations have a desirable correlation (R2 = 0.8463) with the estimated glomerular filtration rate (eGFR) values in COVID-19-positive patients. The fabricated gas sensor can distinguish COVID-19-positive patients suffering from AKI symptoms from COVID-19-negative patients and post-COVID-19 patients. The present work can pave the way for the development of a simple and efficient analytical approach for COVID-19 patients with AKI without the need for sample pretreatment.


Subject(s)
Acute Kidney Injury , COVID-19 , Metal Nanoparticles , Humans , Silver , Ammonia , Polymers , Breath Tests , Pyrroles , COVID-19/complications , COVID-19/diagnosis , Acute Kidney Injury/diagnosis
11.
medrxiv; 2022.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2022.12.10.22283287

ABSTRACT

Convalescent plasma is a promising therapy for coronavirus disease 2019 (COVID-19), but its efficacy in intensive care unit (ICU) patients in a low and middle income country setting such as Suriname is unknown. Bedside plasma separation using the HemoClear device made convalescent plasma therapy accessible as treatment option in Suriname. Two hundred patients with severe SARS-CoV-2 infection requiring intensive care were recruited. Fifty eight patients (29%) received COVID-19 convalescent plasma (CCP) treatment in addition to standard of care (SOC). The CCP treatment and SOC groups were matched by age, sex, and disease severity scores. Mortality in the CCP treatment group was significantly lower than in the SOC group (21% versus 39%; Fisher's exact P = 0.0133). Multivariate analysis using ICU days showed that CCP treatment reduced mortality (hazard ratio [HR], 0.35; 95% CI, 0.18-0.66; P = 0.001), while complication of acute renal failure (creatinine levels >110 mol/L; HR, 4.45; 95%CI, 2.54-7.80; P < 0.0001) was independently associated with death. Decrease in chest X-ray score in the CCP treatment group (median -3 points, IQR -4 to -1) was significantly greater than in the SOC group (median -1 point, IQR -3 to 1, Mann Whitney P = 0.0004). Improvement in PaO2/FiOs ratio was also significantly greater in the CCP treatment group (median 83, IQR 8 to 140) than in the SOC group (median 35, IQR -3 to 92, Mann Whitney P = 0.0234). Further research is needed for HemoClear-produced CCP as therapy in SARS-CoV-2 infections together with adequately powered, randomized controlled trials.


Subject(s)
Schistosomiasis mansoni , COVID-19 , Severe Acute Respiratory Syndrome , Acute Kidney Injury , Death
12.
medrxiv; 2022.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2022.12.10.22283298

ABSTRACT

Objectives: This study was designed to assess the disproportionality analyses of adverse drug reactions (ADRs) related to hydroxychloroquine and remdesivir and how ADR reporting fluctuated during the COVID-19 pandemic. Methods: A retrospective observational study was conducted utilizing the Food and Drug Administrations Adverse Event Reporting System (FAERS) data between 2019 and 2021. The study was conducted in two phases. In the first phase, all reports associated with the drugs of interest were evaluated to assess all related adverse drug reactions. In the second phase, specific outcomes of interest (i.e., QT prolongation and renal and hepatic events) were determined to study their association with the drugs of interest. A descriptive analysis was conducted for all adverse reactions related to the drugs being studied. In addition, disproportionality analyses were conducted to compute the reporting odds ratio, the proportional reporting ratio, the information component, and the empirical Bayes geometric mean. All analyses were conducted using RStudio. Results: A total of 9,443 ADR reports related to hydroxychloroquine; 6,160 (71.49) patients were female, and higher percentage of patients of both sexes were over the age of 65 years. QT prolongation (1.48%), pain (1.38%), and arthralgia (1.25%) were most frequently reported ADRs during the COVID-19 pandemic. The association of QT prolongation with use of hydroxychloroquine was statistically significant (ROR 47.28 [95% CI 35.95-62.18]; PRR 42.41 [95% CI 32.25-55.78]; EBGM 16.08; IC 4.95) compared with fluoroquinolone. The outcome was serious medical events in 48.01% of ADR reports; 27.42% required hospitalization and 8.61% resulted in death. Of 6,673 ADR reports related to remdesivir, 3,928 (61.13%) patients were male. During 2020, the top three ADR reports were elevated liver function tests (17.26%), acute kidney injury (5.95%) and death (2.84%). Additionally, 42.71% of ADR reports indicated serious medical events; 19.69% resulted in death and 11.71% indicated hospitalization. The ROR and PRR of hepatic and renal events associated with remdesivir were statistically significant, (4.81 [95% CI 4.46-5.19] and 2.96 [95% CI 2.66-3.29], respectively. Conclusion: Our study showed that several serious ADRs were reported with the use of hydroxychloroquine, which resulted in hospitalization and death. Trends with the use of remdesivir were similar, but to a lesser extent. Therefore, this study showed us that off-label use should be based on thorough evidence-based evaluation. Keywords: COVID-19, hydroxychloroquine, remdesivir, QT prolongation, FAERS.


Subject(s)
COVID-19 , Pain , Long QT Syndrome , Death , Learning Disabilities , Acute Kidney Injury , Arthralgia
13.
researchsquare; 2022.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-2346684.v1

ABSTRACT

Background: The national spread of safety interventions has been slow and difficult. While it is widely known that hospital contextual features and implementation factors impact spread of evidence-based interventions, there is little prospective research on modifiable factors that impact implementation at multiple sites. Nephrotoxic Injury Negated by Just-in-Time Action (NINJA) is a system-level patient safety intervention that led to a sustained reduction in nephrotoxic medication–associated acute kidney injury (NTMx-AKI) at one hospital. Our objective was to prospectively characterize the association between context and implementation factors and reduction of NTMx-AKI at nine hospitals implementing NINJA, using mixed methods. Methods: Grounded in i-PARIHS, we used qualitative comparative analysis (QCA) to assess the association between context and implementation factors, measured quarterly by survey, and reduction of NTMx-AKI, measured using statistical process control and ARIMA modeling. Interviews provided an understanding of causal processes underlying associations identified in QCA. Qualitative and quantitative data were collected and analyzed concurrently and then merged. Results: Five hospitals reduced AKI, four did not. Overall, the collaborative reduced NTMx- AKI by 8 cases per 1000 patient-days per month (95% CI: 14.6-1.4; p=0.018). QCA analysis revealed that hospitals needed to have a baseline AKI rate > 1.0 to reduce NTMx-AKI (Ncon 1.0, Ncov 0.83). In addition, hospitals that reduced NTMx-AKI had either (a) a pharmacist champion and > 2 pharmacists working on NINJA (Scon 1.0, Scov 0.8) or (b) No other organizational priorities causing implementation delays (Scon 1.0, Scov 0.2). Involving quality improvement coordinators or data analysts did not influence success. Qualitative interviews supported these findings and underscored the importance of how the NINJA implementation team integrated with frontline staff. Conclusions: We identified two different pathways to successful reduction in NTMx-AKI when implementing NINJA. These findings have implications for the future spread of NINJA and suggest an approach to study spread and scale of safety interventions more broadly.


Subject(s)
Ataxia , Kidney Diseases , Acute Kidney Injury
14.
arxiv; 2022.
Preprint in English | PREPRINT-ARXIV | ID: ppzbmed-2212.01067v1

ABSTRACT

Background: The COVID-19 pandemic has had a profound impact on health, everyday life and economics around the world. An important complication that can arise in connection with a COVID-19 infection is acute kidney injury. A recent observational cohort study of COVID-19 patients treated at multiple sites of a tertiary care center in Berlin, Germany identified risk factors for the development of (severe) acute kidney injury. Since inferring results from a single study can be tricky, we validate these findings and potentially adjust results by including external information from other studies on acute kidney injury and COVID-19. Methods: We synthesize the results of the main study with other trials via a Bayesian meta-analysis. The external information is used to construct a predictive distribution and to derive posterior estimates for the study of interest. We focus on various important potential risk factors for acute kidney injury development such as mechanical ventilation, use of vasopressors, hypertension, obesity, diabetes, gender and smoking. Results: Our results show that depending on the degree of heterogeneity in the data the estimated effect sizes may be refined considerably with inclusion of external data. Our findings confirm that mechanical ventilation and use of vasopressors are important risk factors for the development of acute kidney injury in COVID-19 patients. Hypertension also appears to be a risk factor that should not be ignored. Shrinkage weights depended to a large extent on the estimated heterogeneity in the model. Conclusions: Our work shows how external information can be used to adjust the results from a primary study, using a Bayesian meta-analytic approach. How much information is borrowed from external studies will depend on the degree of heterogeneity present in the model.


Subject(s)
COVID-19 , Hypertension , Kidney Diseases , Acute Kidney Injury , Obesity , Diabetes Mellitus
15.
Crit Care Nurs Clin North Am ; 34(4): 481-490, 2022 Dec.
Article in English | MEDLINE | ID: covidwho-2104621

ABSTRACT

The COVID-19 pandemic disproportionately affected individuals with kidney disease causing significant morbidity and mortality worldwide. Sars-coV-2 infection has been linked to the development of acute kidney injury and worsening of underlying kidney function. Multiple challenges were encountered during the COVID-19 pandemic resulting in valuable lessons learned for future pandemics, public health emergencies, and disasters related to the care of individuals with kidney disease. The COVID-19 pandemic has further exposed the extensive need for more nurses to be knowledgeable about the care of kidney disease and able to provide specialized nephrology care.


Subject(s)
Acute Kidney Injury , COVID-19 , Humans , Pandemics , SARS-CoV-2
16.
Physiol Rep ; 10(20): e15507, 2022 10.
Article in English | MEDLINE | ID: covidwho-2100495

ABSTRACT

Acute kidney injury (AKI) is a common event, occurring in ~5% and ~35% of hospitalized and ICU patients, respectively. The development of AKI portends an increased risk of morbidity, mortality, prolonged hospitalization, and subsequent development of chronic kidney disease (CKD). Given these facts, a multitude of experimental studies have addressed potential methods for inducing AKI prevention in high-risk patients. However, successful clinical translation of promising experimental data has remained elusive. Over the past decade, our laboratory has focused on developing a method for safely triggering AKI protection by inducing "kidney preconditioning" in mice by the intravenous administration of a combination of Fe sucrose (FeS) + tin protoporphyrin (SnPP). These agents induce mild, but short lived, 'oxidant stress' which synergistically activate a number of kidney 'self-defense' pathways (e.g., Nrf2, ferritin, IL-10). Within 18-24 h of Fe/SnPP administration, marked protection against diverse forms of experimental toxic and ischemic AKI results. FeS/SnPP-mediated reductions in kidney injury can also indirectly decrease injury in other organs by mitigating the so called "organ cross talk" phenomenon. Given these promising experimental data, three phase 1b clinical trials were undertaken in healthy subjects and patients with stage 3 or 4 CKD. These studies demonstrated that FeS/SnPP were well tolerated and that they up-regulated the cytoprotective Nrf2, ferritin, and IL-10 pathways. Two subsequent phase 2 trials, conducted in patients undergoing 'on-pump' cardiovascular surgery or in patients hospitalized with COVID 19, confirmed FeS/SnPP safety. Furthermore, interim data analyses revealed statistically significant improvements in several clinical parameters. The goals of this review are to: (i) briefly discuss the historical background of renal "preconditioning"; (ii) present the experimental data that support the concept of FeS/SnPP- induced organ protection; and (iii) discuss the initial results of clinical trials that suggest the potential clinical utility of an 'oxidant preconditioning' strategy.


Subject(s)
Acute Kidney Injury , COVID-19 , Renal Insufficiency, Chronic , Mice , Animals , NF-E2-Related Factor 2/metabolism , Interleukin-10/metabolism , Oxidants/pharmacology , Kidney/metabolism , Acute Kidney Injury/prevention & control , Acute Kidney Injury/metabolism , Renal Insufficiency, Chronic/prevention & control , Renal Insufficiency, Chronic/metabolism , Ferritins
17.
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
18.
Turk J Med Sci ; 52(5): 1495-1503, 2022 Oct.
Article in English | MEDLINE | ID: covidwho-2091803

ABSTRACT

BACKGROUND: Acute kidney injury is strongly associated with mortality in critically ill patients with coronavirus disease 2019 (COVID-19); however, age-related risk factors for acute kidney injury are not clear yet. In this study, it was aimed to evaluate the effects of clinical factors on acute kidney injury development in an elderly COVID-19 patients. METHODS: Critically ill patients (≥65years) with COVID-19 admitted to the intensive care unit were included in the study. Primary outcome of the study was the rate of acute kidney injury, and secondary outcome was to define the effect of frailty and other risk factors on acute kidney injury development and mortality. RESULTS: A total of 132 patients (median age 76 years, 68.2% male) were assessed. Patients were divided into two groups as follows: acute kidney injury (n = 84) and nonacute kidney injury (n = 48). Frailty incidence (48.8% vs. 8.3%, p < 0.01) was higher in the acute kidney injury group. In multivariate analysis, frailty (OR, 3.32, 95% CI, 1.67-6.56), the use of vasopressors (OR, 3.06 95% CI, 1.16-8.08), and the increase in respiratory support therapy (OR, 2.60, 95% CI, 1.01-6.6) were determined to be independent risk factors for acute kidney injury development. The mortality rate was found to be 97.6% in patients with acute kidney injury. DISCUSSION: Frailty is a risk factor for acute kidney injury in geriatric patients with severe COVID-19. The evaluation of geriatric patients based on a frailty scale before intensive care unit admission may improve outcomes.


Subject(s)
Acute Kidney Injury , COVID-19 , Frailty , Humans , Male , Aged , Female , Critical Illness/epidemiology , Frailty/complications , Frailty/epidemiology , COVID-19/complications , COVID-19/epidemiology , Acute Kidney Injury/therapy , Intensive Care Units
19.
Viruses ; 14(11)2022 Oct 30.
Article in English | MEDLINE | ID: covidwho-2090371

ABSTRACT

BACKGROUND: COVID-19 severity is determined by cardiometabolic risk factors, which can be further aggravated by chronic immunosuppression in kidney transplant recipients (KTRs). We aimed to verify the main risk factors related to hypertension (HTN) that contribute to COVID-19 progression and mortality in that population. METHODS: Retrospective analysis of 300 KTRs from March 2020 to August 2020 in a single center. We compared the main outcomes between HTN (n = 225) and non-HTN (n = 75), including admission to the intensive care unit (ICU), development of acute kidney injury (AKI), need for invasive mechanical ventilation or oxygen, and mortality. RESULTS: Of the patients in the study, 57.3% were male, 61.3% were white, the mean age was 52.5 years, and 75% had HTN. Pre-existing HTN was independently associated with higher rates of mortality (32.9%, OR = 1.96, p = 0.036), transfer to the ICU (50.7%, OR = 1.94, p = 0.017), and AKI with hemodialysis (HD) requirement (40.4%, OR = 2.15, p = 0.011). In the hypertensive group, age, diabetes mellitus, heart disease, smoking, glycemic control before admission, C-reactive protein, lactate dehydrogenase, lymphocytes, and D-dimer were significantly associated with COVID-19 progression and mortality. Both lower basal and previous estimated glomerular filtration rates posed KTRs with HTN at greater risk for HD requirement. CONCLUSIONS: Therefore, the early identification of factors that predict COVID-19 progression and mortality in KTRs affected by COVID-19 contributes to therapeutic decisions, patient flow management, and allocation of resources.


Subject(s)
Acute Kidney Injury , COVID-19 , Hypertension , Kidney Transplantation , Humans , Male , Middle Aged , Female , Kidney Transplantation/adverse effects , Retrospective Studies , Transplant Recipients , Hypertension/epidemiology , Hypertension/etiology , Risk Factors , Cohort Studies
20.
researchsquare; 2022.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-2266933.v1

ABSTRACT

Background: Patients with COVID-19 have a high incidence of acute kidney injury (AKI), which is associated with mortality. The objective of the study was to determine the factors associated with AKI in patients with COVID-19. Methodology: A retrospective cohort was established in two university hospitals in Bogotá, Colombia. Adults hospitalized for more than 48 hours from March 6, 2020, to March 31, 2021, with confirmed COVID-19 were included. The main outcome was the incidence of AKI during the 28 days following hospital admission. Results: A total of 1584 patients were included: 60.4% were men, 738 (46.5%) developed AKI, 23.6% were classified as KDIGO 3, and 11.1% had renal replacement therapy. The risk factors for developing AKI during hospitalization were male sex (OR 2.27, 95% CI 1.73-2.99), age older than 65 years (1.02, 1.01-1.03), HTN (OR 6.16, 1.98-19.2), the use of vancomycin (1.59, 1.06-2.39), piperacillin/tazobactam (OR 1.65, 1.19-2.28), and vasopressor support (2.36, 1.51-3.69). The gross hospital mortality for AKI was 45.5% versus 11.7% without AKI. Conclusions: This cohort showed that male sex, age, history of hypertension and chronic kidney disease (CKD), presentation with elevated qSOFA, in-hospital use of nephrotoxic drugs and the requirement for vasopressor support were the main risk factors for developing AKI in patients hospitalized for COVID-19.


Subject(s)
Renal Insufficiency, Chronic , COVID-19 , Hypertension , Kidney Diseases , Acute Kidney Injury
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