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1.
Crit Care ; 26(1): 225, 2022 07 25.
Article in English | MEDLINE | ID: covidwho-1962881

ABSTRACT

BACKGROUND: Acute kidney injury (AKI) has been reported as a frequent complication of critical COVID-19. We aimed to evaluate the occurrence of AKI and use of kidney replacement therapy (KRT) in critical COVID-19, to assess patient and kidney outcomes and risk factors for AKI and differences in outcome when the diagnosis of AKI is based on urine output (UO) or on serum creatinine (sCr). METHODS: Multicenter, retrospective cohort analysis of patients with critical COVID-19 in seven large hospitals in Belgium. AKI was defined according to KDIGO within 21 days after ICU admission. Multivariable logistic regression analysis was used to explore the risk factors for developing AKI and to assess the association between AKI and ICU mortality. RESULTS: Of 1286 patients, 85.1% had AKI, and KRT was used in 9.8%. Older age, obesity, a higher APACHE II score and use of mechanical ventilation at day 1 of ICU stay were associated with an increased risk for AKI. After multivariable adjustment, all AKI stages were associated with ICU mortality. AKI was based on sCr in 40.1% and UO in 81.5% of patients. All AKI stages based on sCr and AKI stage 3 based on UO were associated with ICU mortality. Persistent AKI was present in 88.6% and acute kidney disease (AKD) in 87.6%. Rapid reversal of AKI yielded a better prognosis compared to persistent AKI and AKD. Kidney recovery was observed in 47.4% of surviving AKI patients. CONCLUSIONS: Over 80% of critically ill COVID-19 patients had AKI. This was driven by the high occurrence rate of AKI defined by UO criteria. All AKI stages were associated with mortality (NCT04997915).


Subject(s)
Acute Kidney Injury , COVID-19 , Acute Kidney Injury/diagnosis , Acute Kidney Injury/epidemiology , Acute Kidney Injury/etiology , Belgium/epidemiology , COVID-19/complications , Cohort Studies , Critical Illness , Hospitals , Humans , Intensive Care Units , Retrospective Studies
2.
Bratisl Lek Listy ; 123(5): 382-380, 2022.
Article in English | MEDLINE | ID: covidwho-1939235

ABSTRACT

BACKGROUND AND OBJECTIVE: SARS-CoV-2 as the newest member of Beta-Coronaviruses can cause a complicated disease called COVID-19. This virus is able to penetrate a broad range of human cells, such as liver, heart, and kidney cells via ACE2-associated endocytosis. Heart involvement can result in kidney injuries; it is now testified that kidney congestion occurs following the cardio-renal syndrome. Acute Kidney Injury is one of the most critical damages to the kidney in a wide range of COVID-19-caused kidney injuries (which includes proteinuria, hematuria, etc.). Examination of AKI risk factors in COVID-19 patients can assist physicians to prevent its incidence. The final aim of this systematic review was to collate the condition and risk factors of AKI and non-AKI COVID-19 patients and to investigate AKI incidence in high-risk patients. METHOD: A complete and comprehensive survey was performed by reviewing original articles and case reports indexed in various databases such as PubMed/Medline, Embase, and WoS to find appropriate articles. The eligible articles then were selected by two authors and entered into the evaluation process. This systematic review conforms PRISMA statement. RESULTS: After searching for potentially relevant articles, 14 out of the initial 463 articles from 6 countries were selected and evaluated. All of eligible articles have investigated the rate of AKI incidence and its physio-pathological consequences in COVID-19 patients in all conditions (not only patients in critical condition). First, the initial differences between AKI and non-AKI patients were compared. As an instance, our study revealed that mean of White Blood cells (WBC) was much higher in AKI patients which can be responsible for the severe conditions. Then, other variations like differences in laboratory and imaging findings were compared between these two groups. Our outcomes demonstrated that the presence of diabetes mellitus (DM), hypertension (HTN), and male sex can be three significant risk factors in AKI incidence in COVID-19 patients. Fatality rate and treatment methods were also compared among these two groups. CONCLUSION: As one of kidney damages, AKI can worsen COVID-19 patients' status by causing conditions such as acidosis. Our study shows the common symptoms in AKI COVID-19 patients were fever, cough, and malaise. The results of our study can help physicians to arrange COVID-19 with AKI patients' treatment strategy precisely (Tab. 8, Fig. 1, Ref. 48).


Subject(s)
Acute Kidney Injury , COVID-19 , Acute Kidney Injury/diagnosis , Acute Kidney Injury/epidemiology , Acute Kidney Injury/etiology , COVID-19/complications , Female , Humans , Male , Proteinuria , Risk Factors , SARS-CoV-2
3.
Pediatr Crit Care Med ; 23(7): e361-e365, 2022 07 01.
Article in English | MEDLINE | ID: covidwho-1931962

ABSTRACT

OBJECTIVES: Multisystem inflammatory syndrome in children (MIS-C) manifests with heart dysfunction and respiratory failure some weeks after a severe acute respiratory syndrome coronavirus disease 2 infection. The aim of our study was to explore the prevalence, severity, timing, and duration of acute kidney injury (AKI) in MIS-C patients. Furthermore, we evaluated which clinical variables and outcomes are associated with AKI. DESIGN: Multicenter retrospective study. SETTING: Five tertiary hospital PICUs in Italy. Data were collected in the first 7 days of PICU admission and renal function was followed throughout the hospital stay. PATIENTS: Patients less than 18 years old admitted to the PICU for greater than 24 hours with MIS-C. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We collected the following data, including: demographic information, inflammatory biomarkers, lactate levels, Pa o2 /F io2 , ejection fraction, N-terminal pro-B-type natriuretic peptide (NT-proBNP), renal function (serum creatinine, urinary output, fluid balance, and percentage fluid accumulation), Vasoactive-Inotropic Score (VIS), pediatric Sequential Organ Failure Assessment (pSOFA), and Pediatric Index of Mortality 3. AKI was diagnosed in eight of 38 patients (21%) and severe AKI was present in four of eight patients. In all cases, AKI was present at PICU admission and its median (interquartile range) duration was 3.5 days (1.5-5.7 d). We did not identify differences between AKI and no-AKI patients when not making correction for multiple comparisons, for example, in weight, ejection fraction, pSOFA, Pa o2 /F io2 , and lactates. We failed to identify any difference in these groups in urine output and fluid balance. Exploratory analyses of serial data between no-AKI and AKI patients showed significant differences on lymphocyte count, NT-proBNP value, ejection fraction, pSOFA, Pa o2 /F io2 , and VIS. CONCLUSIONS: In this multicenter Italian PICU experience, MIS-C is associated with AKI in one-in-five cases. In general, AKI is characterized by an associated reduction in glomerular filtration rate with a self-limiting time course.


Subject(s)
Acute Kidney Injury , Acute Kidney Injury/diagnosis , Acute Kidney Injury/epidemiology , Acute Kidney Injury/etiology , Adolescent , COVID-19/complications , Child , Humans , Intensive Care Units, Pediatric , Prospective Studies , Retrospective Studies , Systemic Inflammatory Response Syndrome
4.
Front Cell Infect Microbiol ; 12: 838213, 2022.
Article in English | MEDLINE | ID: covidwho-1924077

ABSTRACT

The severe acute respiratory coronavirus 2 (SARS-CoV-2) has become a life-threatening pandemic. Clinical evidence suggests that kidney involvement is common and might lead to mild proteinuria and even advanced acute kidney injury (AKI). Moreover, AKI caused by coronavirus disease 2019 (COVID-19) has been reported in several countries and regions, resulting in high patient mortality. COVID-19-induced kidney injury is affected by several factors including direct kidney injury mediated by the combination of virus and angiotensin-converting enzyme 2, immune response dysregulation, cytokine storm driven by SARS-CoV-2 infection, organ interactions, hypercoagulable state, and endothelial dysfunction. In this review, we summarized the mechanism of AKI caused by SARS-CoV-2 infection through literature search and analysis.


Subject(s)
Acute Kidney Injury , COVID-19 , Acute Kidney Injury/etiology , COVID-19/complications , Humans , Kidney , Peptidyl-Dipeptidase A , SARS-CoV-2
5.
Int J Mol Sci ; 23(13)2022 Jul 01.
Article in English | MEDLINE | ID: covidwho-1917525

ABSTRACT

Vitamin D has been described as an essential nutrient and hormone, which can cause nuclear, non-genomic, and mitochondrial effects. Vitamin D not only controls the transcription of thousands of genes, directly or indirectly through the modulation of calcium fluxes, but it also influences the cell metabolism and maintenance specific nuclear programs. Given its broad spectrum of activity and multiple molecular targets, a deficiency of vitamin D can be involved in many pathologies. Vitamin D deficiency also influences mortality and multiple outcomes in chronic kidney disease (CKD). Active and native vitamin D serum levels are also decreased in critically ill patients and are associated with acute kidney injury (AKI) and in-hospital mortality. In addition to regulating calcium and phosphate homeostasis, vitamin D-related mechanisms regulate adaptive and innate immunity. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections have a role in excessive proinflammatory cell recruitment and cytokine release, which contribute to alveolar and full-body endothelial damage. AKI is one of the most common extrapulmonary manifestations of severe coronavirus disease 2019 (COVID-19). There are also some correlations between the vitamin D level and COVID-19 severity via several pathways. Proper vitamin D supplementation may be an attractive therapeutic strategy for AKI and has the benefits of low cost and low risk of toxicity and side effects.


Subject(s)
Acute Kidney Injury , COVID-19 , Vitamin D Deficiency , Acute Kidney Injury/drug therapy , Acute Kidney Injury/etiology , COVID-19/complications , COVID-19/drug therapy , Calcium , Humans , SARS-CoV-2 , Vitamin D/metabolism , Vitamin D/therapeutic use , Vitamin D Deficiency/complications , Vitamin D Deficiency/drug therapy , Vitamins/therapeutic use
6.
Int J Mol Sci ; 23(13)2022 Jun 30.
Article in English | MEDLINE | ID: covidwho-1917517

ABSTRACT

Acute kidney injury (AKI) is a prevalent complication in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) positive inpatients, which is linked to an increased mortality rate compared to patients without AKI. Here we analysed the difference in kidney blood biomarkers in SARS-CoV-2 positive patients with non-fatal or fatal outcome, in order to develop a mortality prediction model for hospitalised SARS-CoV-2 positive patients. A retrospective cohort study including data from suspected SARS-CoV-2 positive patients admitted to a large National Health Service (NHS) Foundation Trust hospital in the Yorkshire and Humber regions, United Kingdom, between 1 March 2020 and 30 August 2020. Hospitalised adult patients (aged ≥ 18 years) with at least one confirmed positive RT-PCR test for SARS-CoV-2 and blood tests of kidney biomarkers within 36 h of the RT-PCR test were included. The main outcome measure was 90-day in-hospital mortality in SARS-CoV-2 infected patients. The logistic regression and random forest (RF) models incorporated six predictors including three routine kidney function tests (sodium, urea; creatinine only in RF), along with age, sex, and ethnicity. The mortality prediction performance of the logistic regression model achieved an area under receiver operating characteristic (AUROC) curve of 0.772 in the test dataset (95% CI: 0.694-0.823), while the RF model attained the AUROC of 0.820 in the same test cohort (95% CI: 0.740-0.870). The resulting validated prediction model is the first to focus on kidney biomarkers specifically on in-hospital mortality over a 90-day period.


Subject(s)
Acute Kidney Injury , COVID-19 , Acute Kidney Injury/diagnosis , Acute Kidney Injury/etiology , Adult , Biomarkers , COVID-19/diagnosis , Hospital Mortality , Humans , Kidney , Retrospective Studies , SARS-CoV-2 , State Medicine
8.
Am J Case Rep ; 23: e936589, 2022 Jun 20.
Article in English | MEDLINE | ID: covidwho-1903898

ABSTRACT

BACKGROUND Rhabdomyolysis is a condition in which intracellular components are released into the blood and urine. Rhabdomyolysis can be caused by drug-related complications and COVID-19; however, the underlying mechanism is not clear. In this study, we report a case of rhabdomyolysis complicated by COVID-19, in which we presumed that the cause of rhabdomyolysis was related to prior administration of haloperidol by assessment of the drug history and progression of myopathy. CASE REPORT A 52-year-old man with schizophrenia experienced worsening insomnia 10 days before admission. Thus, haloperidol was increased from 1.5 mg to 3 mg once daily, and 2 to 3 days later, he developed hand tremors and weakness. One day prior to admission, the patient suddenly developed severe back pain. Based on the examination, the patient was diagnosed with COVID-19 complicated with rhabdomyolysis. Laboratory findings on admission were as follows: creatine phosphokinase: 41 539 IU/L; urinary myoglobin, 190×10³ ng/mL; and hematuria scale, grade 4. On day 1, he was started on saline infusion; therefore, haloperidol was discontinued. On day 2, the hematuria resolved. On day 5, the tremor, weakness, and back pain had resolved. On day 7, his creatine kinase level was 242 IU/L, and saline was administered. CONCLUSIONS It has been suggested that the onset of COVID-19 can exacerbate haloperidol-induced rhabdomyolysis. Therefore, if there is a complication of rhabdomyolysis and COVID-19, it is important to review the drug history, specifically that of haloperidol. We recommend hydration and discontinuation of haloperidol to avoid acute kidney injury, in addition to treating COVID-19.


Subject(s)
Acute Kidney Injury , COVID-19 , Rhabdomyolysis , Acute Kidney Injury/etiology , Haloperidol/adverse effects , Hematuria , Humans , Male , Middle Aged , Rhabdomyolysis/etiology
9.
BMJ Open ; 12(6): e059046, 2022 06 23.
Article in English | MEDLINE | ID: covidwho-1902007

ABSTRACT

OBJECTIVES: Acute kidney injury (AKI) is a frequent complication among critical ill patients with COVID-19, but the actual incidence is unknown as AKI-incidence varies from 25% to 89% in intensive care unit (ICU) populations. We aimed to describe the prevalence and risk factors of AKI in patients with COVID-19 admitted to ICU in Norway. DESIGN: Nation-wide observational study with data sampled from the Norwegian Intensive Care and Pandemic Registry (NIPaR) for the period between 10 March until 31 December 2020. SETTING: ICU patients with COVID-19 in Norway. NIPaR collects data on intensive care stays covering more than 90% of Norwegian ICU and 98% of ICU stays. PARTICIPANTS: Adult patients with COVID-19 admitted to Norwegian ICU were included in the study. Patients with chronic kidney disease (CKD) were excluded in order to avoid bias from CKD on the incidence of AKI. PRIMARY AND SECONDARY OUTCOME MEASURES: Primary outcome was AKI at ICU admission as defined by renal Simplified Acute Physiology Score in NIPaR. Secondary outcome measures included survival at 30 and 90 days after admission to hospital. RESULTS: A total number of 361 patients with COVID-19 were included in the analysis. AKI was present in 32.0% of the patients at ICU admission. The risk for AKI at ICU admission was related to acute circulatory failure at admission to hospital. Survival for the study population at 30 and 90 days was 82.5% and 77.6%, respectively. Cancer was a predictor of 30-day mortality. Age, acute circulatory failure at hospital admission and AKI at ICU admission were predictors of both 30-day and 90-day mortality. CONCLUSIONS: A high number of patients with COVID-19 had AKI at ICU admission. The study indicates that AKI at ICU admission was related to acute circulatory failure at hospital admission. Age, acute circulatory failure at hospital admission and AKI at ICU admission were associated with mortality.


Subject(s)
Acute Kidney Injury , COVID-19 , Renal Insufficiency, Chronic , Acute Kidney Injury/etiology , Adult , COVID-19/complications , Critical Illness , Hospital Mortality , Humans , Intensive Care Units , Renal Insufficiency, Chronic/complications , Renal Insufficiency, Chronic/epidemiology , Retrospective Studies , Risk Factors
10.
PLoS One ; 17(6): e0264510, 2022.
Article in English | MEDLINE | ID: covidwho-1887002

ABSTRACT

INTRODUCTION: The SARS-CoV-2 pandemic is a major challenge for patients, healthcare professionals, and populations worldwide. While initial reporting focused mainly on lung involvement, the ongoing pandemic showed that multiple organs can be involved, and prognosis is largely influenced by multi-organ involvement. Our aim was to obtain nationwide retrospective population-based data on hospitalizations with COVID-19 and AKI in Germany. MATERIALS & METHODS: We performed a query of G-DRG data for the year 2020 via the Institute for the hospital remuneration system (Institut für das Entgeltsystem im Krankenhaus GmbH, InEK) data portal and therefore included hospitalizations with a secondary diagnosis of RT-PCR proven COVID-19 infection, aged over 15 years. We included hospitalizations with acute kidney injury (AKI) stages 1 to 3. Age-specific and age-standardized hospitalization and in-hospital mortality rates (ASR) per 100.000 person years were calculated, with the German population of 2011 as the standard. RESULTS: In 2020, there were 16.776.845 hospitalizations in German hospitals. We detected 154.170 hospitalizations with RT-PCR proven COVID-19 diagnosis. The age-standardized hospitalization rate for COVID-19 in Germany was 232,8 per 100.000 person years (95% CI 231,6-233,9). The highest proportion of hospitalizations associated with COVID-19 were in the age group over 80 years. AKI was diagnosed in 16.773 (10.9%) of the hospitalizations with COVID-19. The relative risk of AKI for males was 1,49 (95%CI 1,44-1,53) compared to females. Renal replacement therapy (RRT) was performed in 3.443 hospitalizations, 20.5% of the hospitalizations with AKI. For all hospitalizations with COVID-19, the in-hospital mortality amounted to 19.7% (n = 30.300). The relative risk for in-hospital mortality was 3,87 (95%CI 3,80-3,94) when AKI occurred. The age-standardized hospitalization rates for COVID-19 took a bimodal course during the observation period. The first peak occurred in April (ASR 23,95 per 100.000 person years (95%CI 23,58-24,33)), hospitalizations peaked again in November 2020 (72,82 per 100.000 person years (95%CI 72,17-73,48)). The standardized rate ratios (SRR) for AKI and AKI-related mortality with the overall ASR for COVID-19 hospitalizations in the denominator, decreased throughout the observation period and remained lower in autumn than they were in spring. In contrast to all COVID-19 hospitalizations, the SRR for overall mortality in COVID-19 hospitalizations diverged from hospitalizations with AKI in autumn 2020. DISCUSSION: Our study for the first time provides nationwide data on COVID-19 related hospitalizations and acute kidney injury in Germany in 2020. AKI was a relevant complication and associated with high mortality. We observed a less pronounced increase in the ASR for AKI-related mortality during autumn 2020. The proportion of AKI-related mortality in comparison to the overall mortality decreased throughout the course of the pandemic.


Subject(s)
Acute Kidney Injury , COVID-19 , Acute Kidney Injury/etiology , Aged , Aged, 80 and over , COVID-19/epidemiology , COVID-19 Testing , Female , Hospital Mortality , Hospitalization , Hospitals , Humans , Male , Retrospective Studies , Risk Factors , SARS-CoV-2
12.
J Am Soc Nephrol ; 33(3): 565-582, 2022 03.
Article in English | MEDLINE | ID: covidwho-1883777

ABSTRACT

BACKGROUND: Endothelial cell injury is a common nidus of renal injury in patients and consistent with the high prevalence of AKI reported during the coronavirus disease 2019 pandemic. This cell type expresses integrin α5 (ITGA5), which is essential to the Tie2 signaling pathway. The microRNA miR-218-5p is upregulated in endothelial progenitor cells (EPCs) after hypoxia, but microRNA regulation of Tie2 in the EPC lineage is unclear. METHODS: We isolated human kidney-derived EPCs (hkEPCs) and surveyed microRNA target transcripts. A preclinical model of ischemic kidney injury was used to evaluate the effect of hkEPCs on capillary repair. We used a genetic knockout model to evaluate the effect of deleting endogenous expression of miR-218 specifically in angioblasts. RESULTS: After ischemic in vitro preconditioning, miR-218-5p was elevated in hkEPCs. We found miR-218-5p bound to ITGA5 mRNA transcript and decreased ITGA5 protein expression. Phosphorylation of 42/44 MAPK decreased by 73.6% in hkEPCs treated with miR-218-5p. Cells supplemented with miR-218-5p downregulated ITGA5 synthesis and decreased 42/44 MAPK phosphorylation. In a CD309-Cre/miR-218-2-LoxP mammalian model (a conditional knockout mouse model designed to delete pre-miR-218-2 exclusively in CD309+ cells), homozygotes at e18.5 contained avascular glomeruli, whereas heterozygote adults showed susceptibility to kidney injury. Isolated EPCs from the mouse kidney contained high amounts of ITGA5 and showed decreased migratory capacity in three-dimensional cell culture. CONCLUSIONS: These results demonstrate the critical regulatory role of miR-218-5p in kidney EPC migration, a finding that may inform efforts to treat microvascular kidney injury via therapeutic cell delivery.


Subject(s)
Acute Kidney Injury/etiology , Acute Kidney Injury/metabolism , Endothelial Progenitor Cells/metabolism , Endothelial Progenitor Cells/pathology , Integrin alpha5/metabolism , MicroRNAs/physiology , Acute Kidney Injury/pathology , Animals , Disease Models, Animal , Humans , Mice , Mice, Inbred C57BL , Mice, Knockout , Receptor, TIE-2/physiology , Signal Transduction/physiology
13.
Crit Care Clin ; 38(3): 473-489, 2022 Jul.
Article in English | MEDLINE | ID: covidwho-1878083

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
15.
Curr Opin Anaesthesiol ; 35(2): 215-223, 2022 Apr 01.
Article in English | MEDLINE | ID: covidwho-1860920

ABSTRACT

PURPOSE OF REVIEW: Acute kidney injury (AKI) is common in hospitalized patients and is a major risk factor for increased length of stay, morbidity, and mortality in postoperative patients. There are multiple barriers to reducing perioperative AKI - the etiology is multi-factorial and the diagnosis is fraught with issues. We review the recent literature on perioperative AKI and some considerations for anesthesiologists that examine the far-reaching effects of AKI on multiple organ systems. RECENT FINDINGS: This review will discuss recent literature that addresses the epidemiology, use of novel biomarkers in risk stratification, and therapeutic modalities for AKI in burn, pediatrics, sepsis, trauma, cardiac, and liver disease, contrast-induced AKI, as well as the evidence assessing goal-directed fluid therapy. SUMMARY: Recent studies address the use of risk stratification models and biomarkers, more sensitive than creatinine, in the preoperative identification of patients at risk for AKI. Although exciting, these scores and models need validation. There is a need for research assessing whether early AKI detection improves outcomes. Enhanced recovery after surgery utilizing goal-directed fluid therapy has not been shown to make an appreciable difference in the incidence of AKI. Reducing perioperative AKI requires a multi-pronged and possibly disease-specific approach.


Subject(s)
Acute Kidney Injury , Acute Kidney Injury/diagnosis , Acute Kidney Injury/epidemiology , Acute Kidney Injury/etiology , Biomarkers , Child , Creatinine , Humans , Incidence , Postoperative Complications/diagnosis , Postoperative Complications/epidemiology , Postoperative Complications/etiology , Risk Factors
16.
Sci Rep ; 12(1): 8650, 2022 05 23.
Article in English | MEDLINE | ID: covidwho-1860396

ABSTRACT

COVID-19 is strongly influenced by age and comorbidities. Acute kidney injury (AKI) is a frequent finding in COVID-19 patients and seems to be associated to mortality and severity. On the other hand, the role of kidney dysfunction in COVID-19 is still debated. We performed a retrospective study in a cohort of 174 hospitalized COVID-19 patients in Italy from March 3rd to May 21st 2020, to investigate the role of kidney dysfunction on COVID-19 severity and mortality. Moreover, we examined in depth the relationship between kidney function, age, and progression of COVID-19, also using different equations to estimate the glomerular filtration rate (GFR). We performed logistic regressions, while a predictive analysis was made through a machine learning approach. AKI and death occurred respectively in 10.2% and 19.5%, in our population. The major risk factors for mortality in our cohort were age [adjusted HR, 6.2; 95% confidence interval (CI) 1.8-21.4] and AKI [3.36 (1.44-7.87)], while, in these relationships, GFR at baseline mitigated the role of age. The occurrence of AKI was influenced by baseline kidney function, D-dimer, procalcitonin and hypertension. Our predictive analysis for AKI and mortality reached an accuracy of ≥ 94% and ≥ 91%, respectively. Our study scales down the role of kidney function impairment on hospital admission , especially in elderly patients. BIS-1 formula demonstrated a worse performance to predict the outcomes in COVID-19 patients when compared with MDRD and CKD-EPI.


Subject(s)
Acute Kidney Injury , COVID-19 , Acute Kidney Injury/epidemiology , Acute Kidney Injury/etiology , Aged , COVID-19/complications , Glomerular Filtration Rate , Humans , Kidney , Retrospective Studies , Risk Factors , SARS-CoV-2
17.
BMJ Case Rep ; 15(5)2022 May 19.
Article in English | MEDLINE | ID: covidwho-1854257

ABSTRACT

A woman in her 70s presented to the hospital being generally unwell 8 days following the first dose of the AstraZeneca COVID-19 vaccination. She was in stage III acute kidney injury (AKI) with hyperkalaemia and metabolic acidosis. Urinalysis showed haematoproteinuria. Renal immunology screen was negative. She subsequently underwent two renal biopsies. The second biopsy showed features consistent with acute tubulointerstitial nephritis. She was commenced on oral steroids, which led to marked improvement of her renal function.There are reasons why AKI can occur post vaccination such as prerenal AKI from reduced oral intake postvaccination due to feeling unwell or developing vomiting or diarrhoea. Intravenous fluids were given to this patient but with no meaningful improvement in renal function. She developed a possible reaction to the AstraZeneca COVID-19 vaccine, which led to AKI as supported by the interstitial inflammation and presence of eosinophils on renal biopsy.


Subject(s)
Acute Kidney Injury , COVID-19 , Nephritis, Interstitial , Acute Kidney Injury/etiology , Acute Kidney Injury/pathology , COVID-19/prevention & control , COVID-19 Vaccines/adverse effects , Female , Humans , Nephritis, Interstitial/chemically induced , Nephritis, Interstitial/pathology , Vaccination
18.
J Korean Med Sci ; 37(19): e154, 2022 May 16.
Article in English | MEDLINE | ID: covidwho-1847143

ABSTRACT

Coronavirus disease 2019 (COVID-19) is one of the most widespread viral infections in human history. As a breakthrough against infection, vaccines have been developed to achieve herd immunity. Here, we report the first case of microscopic polyangiitis (MPA) following BNT162b2 vaccination in Korea. A 42-year-old man presented to the emergency room with general weakness, dyspnea, and edema after the second BNT162b2 vaccination. He had no medical history other than being treated for tuberculosis last year. Although his renal function was normal at last year, acute kidney injury was confirmed at the time of admission to the emergency room. His serum creatinine was 3.05 mg/dL. Routine urinalysis revealed proteinuria (3+) and hematuria. When additional tests were performed for suspected glomerulonephritis, the elevation of myeloperoxidase (MPO) antibody (38.6 IU/mL) was confirmed. Renal biopsy confirmed pauci-immune anti-neutrophil cytoplasmic antibody (ANCA)-related glomerulonephritis and MPA was diagnosed finally. As an induction therapy, a combination of glucocorticoid and rituximab was administered, and plasmapheresis was performed twice. He was discharged after the induction therapy and admitted to the outpatient clinic 34 days after induction therapy. During outpatient examination, his renal function had improved with serum creatinine 1.51 mg/dL. We suggest that MPA needs to be considered if patients have acute kidney injury, proteinuria, and hematuria after vaccination.


Subject(s)
Acute Kidney Injury , COVID-19 , Glomerulonephritis , Microscopic Polyangiitis , Acute Kidney Injury/diagnosis , Acute Kidney Injury/etiology , Adult , Antibodies, Antineutrophil Cytoplasmic , BNT162 Vaccine , COVID-19 Vaccines/adverse effects , Creatinine , Female , Glomerulonephritis/pathology , Hematuria/etiology , Humans , Male , Microscopic Polyangiitis/diagnosis , Microscopic Polyangiitis/drug therapy , Microscopic Polyangiitis/etiology , Proteinuria/etiology , RNA, Messenger , Vaccination
19.
Saudi J Kidney Dis Transpl ; 32(5): 1220-1234, 2021.
Article in English | MEDLINE | ID: covidwho-1835075

ABSTRACT

Coronaviruses are ubiquitous pathogens and have caused epidemics in the recent past. Coupled with globalization, they have the potential to transform into the pandemic, as is the case of coronavirus disease 2019 (COVID-19). Primarily to start as a respiratory illness, they are known to cause systemic disease and affect many organ systems. Due to the lack of, universally proven, specific anti-viral therapy, the mainstay of treatment is "supportive care" and some of the patients afflicted with it, require intensive care and organ support for lungs and/or kidneys. Patients with the diseases of the kidney, particularly those on dialysis and kidney transplant recipients, are predisposed to the worst outcomes with COVID-19. It also leads to acute kidney injury, which is an important and independent determinant of prognosis in these patients. It also creates a huge demand for the delivery of renal replacement therapy. COVID-19 is an emerging and evolving disease, and so, it is important to understand the mechanism and management of kidney diseases in COVID-19.


Subject(s)
Acute Kidney Injury , COVID-19 , Acute Kidney Injury/diagnosis , Acute Kidney Injury/epidemiology , Acute Kidney Injury/etiology , Female , Humans , Kidney , Male , Pandemics , SARS-CoV-2
20.
Iran J Kidney Dis ; 16(2): 147-151, 2022 03.
Article in English | MEDLINE | ID: covidwho-1823867

ABSTRACT

Acute kidney injury (AKI) , proteinuria in the nephrotic or subnephrotic range and hematuria might be seen in patients with coronavirus disease 2019 (COVID-19) infection. In this case study we present a 59 years old manwho was diagnosed with immune-complex glomerulonephritis after development of rapidly progressive kidney failure accompanied by pulmonary hemorrhage, 2 months after COVID-19 infection. The patient was hospitalised with the diagnosis of acute kidney injury and nephrotic syndrome. Hemodialysis was performed due to uremic symptoms. Cyclophosphamide, methylprednisolone and plasmapheresis were started. Pathologic examination of kidney biopsy revealed features compatible with immune complex-related acute glomerulonephritis. Cyclophosphamide and plasmapheresis were discontinued , and treatment with 1 mg/kg/day methylprednisolone was continued. Immune-complex glomerulonephritis can be seen following COVID-19 infection. It is important to diagnose this disease entity as soon as possible . Steroidtherapy and other supportive modalities might be sufficient in the treatment.  DOI: 10.52547/ijkd.6527.


Subject(s)
Acute Kidney Injury , COVID-19 , Glomerulonephritis , Acute Kidney Injury/diagnosis , Acute Kidney Injury/etiology , Acute Kidney Injury/therapy , Cyclophosphamide , Female , Glomerulonephritis/diagnosis , Glomerulonephritis/drug therapy , Humans , Male , Methylprednisolone/therapeutic use , Middle Aged
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