Acute Kidney Injury In COVID-19 Patients Research Articles

Klotho-derived peptide KP1 ameliorates SARS-CoV-2-associated acute kidney injury.

Introduction: The severe cases of COVID-19, a disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), often present with acute kidney injury (AKI). Although old age and preexisting medical conditions have been identified as principal risk factors for COVID-19-associated AKI, the molecular basis behind such a connection remains unknown. In this study, we investigated the pathogenic role of Klotho deficiency in COVID-19-associated AKI and explored the therapeutic potential of Klotho-derived peptide 1 (KP1). Methods: We assessed the susceptibility of Klotho deficient Kl/Kl mice to developing AKI after expression of SARS-CoV-2 N protein. The role of KP1 in ameliorating tubular injury was investigated by using cultured proximal tubular cells (HK-2) in vitro and mouse model of ischemia-reperfusion injury (IRI) in vivo. Results: Renal Klotho expression was markedly downregulated in various chronic kidney disease (CKD) models and in aged mice. Compared to wild-type counterparts, mutant KL/KL mice were susceptible to overexpression of SARS-CoV-2 N protein and developed kidney lesions resembling AKI. In vitro, expression of N protein alone induced HK-2 cells to express markers of tubular injury, cellular senescence, apoptosis and epithelial-mesenchymal transition, whereas both KP1 and Klotho abolished these lesions. Furthermore, KP1 mitigated kidney dysfunction, alleviated tubular injury and inhibited apoptosis in AKI model induced by IRI and N protein. Conclusion: These findings suggest that Klotho deficiency is a key determinant of developing COVID-19-associated AKI. As such, KP1, a small peptide recapitulating Klotho function, could be an effective therapeutic for alleviating AKI in COVID-19 patients.

Acute kidney injury in children with moderate-severe COVID-19 and multisystem inflammatory syndrome in children: a referral center experience.

Data on the characteristics of acute kidney injury (AKI) in pediatric COVID-19 and MIS-C are limited. We aimed to define the frequency, associated factors and early outcome of AKI in moderate, severe or critical COVID-19 and MIS-C; and to present a tertiary referral center experience from Türkiye. Hospitalized patients ≤ 18years of age with confirmed COVID-19 or MIS-C at İhsan Doğramacı Children's Hospital, Hacettepe University, between March 2020-December 2021 were enrolled. The characteristics of AKI in the COVID-19 group were investigated in moderate, severe and critically ill patients; patients with mild COVID-19 were excluded. The median (Q1-Q3) age in theCOVID-19 (n = 66) and MIS-C (n = 111) groups was 10.7years (3.9-15.2) and 8.7years (4.5-12.7), respectively. The frequency of AKI was 22.7% (15/66) in COVID-19 and 15.3% (17/111) in MIS-C; all MIS-C patients with AKI and 73.3% (11/15) of COVID-19 patients with AKI had AKI at the time of admission. Multivariate analyses revealed need for vasoactive/inotropic agents [Odds ratio (OR) 19.233, p = 0.002] and presence of vomiting and/or diarrhea (OR 4.465, p = 0.036) as independent risk factors of AKI in COVID-19 patients; and need for vasoactive/inotropic agents (OR 22.542, p = 0.020), procalcitonin and ferritin levels as independent risk factors of AKI in theMIS-C group. Age was correlated with lymphocyte count (r = -0.513, p < 0.001) and troponin level (r = 0.518, p < 0.001) in MIS-C patients. Length of hospital stay was significantly longer in both groups with AKI, compared to those without AKI. Mortality was 9.1% in theCOVID-19 group; and was associated with AKI (p = 0.021). There was no mortality in MIS-C patients. AKI recovery at discharge was 63.6% in COVID-19 survivors and 100% in MIS-C patients. Independent risk factors for AKI were need for vasoactive/inotropic agents and vomiting/diarrhea in moderate, severe or critical COVID-19 patients; and need for vasoactive/inotropic agents and severe inflammation in MIS-C patients. Our findings suggest that inflammation and cardiac dysfunction are associated with AKI in MIS-C patients; and the association with age in this group merits further studies in larger groups. Early outcome is favorable; long-term follow-up for kidney functions is needed.

#3750 SERUM AMYLOID A AS PROGNOSTIC MARKER FOR CKD AND NON-CKD COVID-19 PATIENTS ADMITTED TO THE EMERGENCY ROOM

Abstract Background and Aims Patients with chronic kidney disease (CKD) and a SARS-CoV-2 infection are at higher risk of developing acute kidney injury (AKI) and of mortality after hospital admission. Herein, we assessed whether serum amyloid A (SAA) was associated with outcomes (AKI and/or death). Method The study group included 160 patients: 70 Covid-19-positive CKD patients (eGFR &amp;lt;60 mL/min), 50 Covid-19-positive patients with no history of kidney disease, 20 Covid-19-negative CKD patients, and 20 healthy controls. We collected data on patients’ gender, age, co-morbidities, and laboratory results from blood and urine samples taken at admission into the ER, and from healthy volunteers. All participants gave their informed consent for trial with protocol №12/31.05.2022 approved by the ethical committee KENIMUS of the Medical University of Sofia, Bulgaria. Laboratory values included calculated eGFR (by the CKD-EPI 2021 formula), highly sensitive inflammatory markers, D-dimer, blood-cell counts, and changes in urine parameters. Co-morbidities included hypertension, obesity, diabetes mellitus, vascular disease, and CKD. All patients had been treated by the official protocol of the Republic of Bulgaria for SARS-CoV-2. We determined the levels of SAA across the four groups to assess if this biomarker could predict AKI, risk of mortality, and if there was a significant difference between the CKD and non-CKD patients. Results Overall, median age of Covid-19 patients was 56.4 years; gender ratio was 50% M/F in all groups. Median duration of symptoms before hospitalization was 6 days. Of the 160 patients, 30% were febrile with temperatures &amp;gt;38oC. Overall, creatinine level on admission was elevated in 40% of cases; eGFR was &amp;lt;60 mL/min/1.73 m2 in 37.5% of patients. Mean value of eGFR on admission was 82.3 mL/min/1.73 m2 for the non-CKD Covid-19-positive group, 49.5 mL/min/1.73 m2 for the CKD Covid-19-positive group, 62.3 mL/min/1.73 m2 for the CKD patients without COVID-19, and 111.1 mL/min/1.73 m2 for the healthy control group. In total, three Covid-19 patients needed renal-replacement therapy: two patients from the CKD group and one from the non-CKD group. AKI occurred in 38 Covid-19 patients (23.7%). Of these, 31 had CKD (44.3% of the Covid-19 positive CKD patients). Overall, within our cohort of 160 patients, in-hospital mortality was 14.3% (23 patients): of these, 82.6% had AKI (19 patients). Overall, 100% of patients that did not survive Covid-19 also had CKD. We analyzed the levels of SAA across the groups. The reference limits considered for negative results were &amp;lt;7 pg/mL; the ELISA could measure values up to 300 pg/mL. Of the 23 patients that died, 19 had levels &amp;gt;300 pg/ml (82.6%), whilst the remainder had results &amp;gt;250 pg/mL. The other patients who survived the infection in our cohort had levels well below 200 pg/ml. When the patients with AKI and without AKI were compared on the basis of SAA, patients with AKI had significantly higher biomarker values (p- = 0.02). When compared across the four groups, no significant differences were found except when comparing the healthy control group with the other three groups, where there was significance of p&amp;lt;0.0001 in each comparison. Conclusion We confirm that SAA was a reliable biomarker for predicting AKI in Covid-19 patients. It also acted as a predictor for a fatal outcome in patients with severely Covid-19 infection. In conclusion, SAA is a reliable marker, highly informative in the emergency department setting, enabling us to have an early prognosis for the outcome of the Covid-19 infection for the patients in our cohort.

#4208 CRP EXACERBATES SARS-COV-2-NUCLEOCAPSID PROTEIN-INDUCED ACUTE KIDNEY INJURY

Abstract Background and Aims COVID-19, caused by severe acute respiratory syndrome coronavirus (SARS-CoV-2), is a progressive viral pneumonia with a broad spectrum of clinical manifestations involving multiple organs. Acute kidney injury (AKI) is common in COVID-19, especially the critically ill patients. Our previous study proved that kidney-specifically overexpressing SARS-CoV-2 N protein induces AKI, which become worsen in mice under ischemic condition. Clinically, CRP is a risk factor for AKI in COVID-19 patients. Recent clinical study showed that CRP Apheresis is able to effectively remove the plasma CRP and thus improve the clinical outcome in critically ill COVID-19 patients. We thus hypothesize that CRP may not only be a biomarker or risk factor, but also a potential mediator or novel therapeutic target for COVID-19 AKI. Method The role of CRP in COVID-19 AKI was investigated in a mouse model of AKI induced by ultrasound-microbubble-mediated kidney-specifically transferring SARS-CoV-2 N-expressing plasmids in CRP wide-type (WT) and Transgenic (Tg) mice. We also developed a novel therapy for SARS-CoV-2 N-induced by targeting CRP signaling with a neutralizing anti-CD32 antibody both in vivo and in vitro. Results In COVID-19 patients with AKI, serum levels of CRP were significantly elevated when compared with non-AKI group. In mice, kidney-specifically overexpressing SARS-CoV-2 N protein caused AKI including tubular necrosis and elevated levels of serum creatinine and BUN in CRP WT mice, which became more severe in CRP Tg mice. Importantly, targeting CRP-CD32 signaling with a neutralizing antibody to CD32 significantly inhibited SARS-CoV-2 N protein-induced AKI in CRP Tg mice. Mechanistically, we uncovered that CRP promoted SARS-CoV-2-N protein-induced AKI via the Smad3-p21-dependent G1 cell cycle arrest and NF-κB/p-p65-driven renal inflammation, which was blocked by anti-CD32 antibody in vivo and in vitro. Conclusion CRP is not only a biomarker or risk factor, but also a mediator in SARS-CoV-2 N protein-induced AKI. CRP signals through CD32 mediate SARS-CoV-2 N-induced AKI via mechanisms associated with the Smad3-p21-dependent G1 cell-cycle arrest and NF-κB/p-p65-driven renal inflammation. Targeting CRP-CD32 signaling may represent as a novel therapy for COVID-19-associated AKI.

Crosstalk between COVID-19 Infection and Kidney Diseases: A Review on the Metabolomic Approaches.

The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19, a respiratory disorder. Various organ injuries have been reported in response to this virus, including kidney injury and, in particular, kidney tubular injury. It has been discovered that infection with the virus does not only cause new kidney disease but also increases treatment difficulty and mortality rates in people with kidney diseases. In individuals hospitalized with COVID-19, urinary metabolites from several metabolic pathways are used to distinguish between patients with acute kidney injury (AKI) and those without. This review summarizes the pathogenesis, pathophysiology, treatment strategies, and role of metabolomics in relation to AKI in COVID-19 patients. Metabolomics is likely to play a greater role in predicting outcomes for patients with kidney disease and COVID-19 with varying levels of severity in the near future as data on metabolic profiles expand rapidly. Here, we also discuss the correlation between COVID-19 and kidney diseases and the available metabolomics approaches.

The association between vitamin D3 deficiency and acute kidney injury in COVID-19 patients

Introduction: Vitamin D deficiency is a common clinical finding in the general population and hospitalized patients, including patients in the intensive care unit (ICU). Acute kidney injury (AKI) occurs in more than 50% in ICU admitted patients. Objectives: There are few studies regarding AKI in COVID-19 patients, therefore we investigated the relationship between vitamin D3 deficiency and the occurrence of AKI in COVID-19 patients. Patients and Methods: This cross-sectional study was conducted on 69 COVID-19 patients who were hospitalized in the ward for 12 months. Their serum vitamin D3 levels were measured in the first 24 hours of hospitalization in the ward. Patients were divided into three groups based on the serum levels of vitamin D3: &gt;50 ng/mL as normal, 20-50 ng/mL as insufficient and &lt;20 ng/mL as deficiency status. The patients were studied until the occurrence of acute renal injury or the occurrence of death. Results: Out of 69 hospitalized patients in the ward with COVID-19, there were 39 patients in group vitamin D3&lt;20 ng/mL, 21 patients in group vitamin D3 of 20-50ng/mL and 9 patients in group of vitamin D3&gt;50 ng/mL. The frequencies of AKI in groups of vitamin D3&lt;20 ng/mL, 20-50 ng/mL, and &gt;50 ng/mL were 46%, 28%, and 23%, respectively. A significant relationship was observed between AKI and our study groups (P=0.011). Furthermore, there was a significant association between our study groups and mortality (P=0.014), ICU admission (P=0.041) and hospital length of stay (P=0.017). In another division in patients with different levels of vitamin D3 in the presence or absence of AKI, there were significant associations between patients with vitamin D3&lt;20 ng/mL and the presence of AKI and also with mortality (P=0.042), ICU admission (P=0.024) and additionally with hospital length of stay (P=0.027). Conclusion: Our study showed significant association between vitamin D deficiency and AKI in ICU-admitted COVID-19 patients. Moreover, there were relationships between vitamin D deficiency and mortality, ICU admission and hospital length of stay. These results suggest the correction of vitamin D deficiency may be beneficial to reduce AKI in patient with COVID-19.

Nephrological complications in patients after COVID-19 infection

In this review, we looked for correlations and health consequences between COVID-19 infection and kidney health. Although the main symptoms of COVID-19 are respiratory failure and hypoxemia, kidney involvement is also common. In an attempt to decipher how COVID-19 infection affects the kidneys, this review focuses on the pathophysiological and clinical links between COVID-19 infection and the kidneys. The aim of this work was to find long-term health consequences in patients who were discharged from the hospital and to investigate risk factors. COVID-19-related kidney disease is reported not only in infected patients with chronic kidney disease, but also in people with no previous history of kidney disease. The disease caused by the coronavirus (COVID-19) is a threat to public health. Chronic kidney disease (CKD) has been shown to be a risk factor for side effects. Although initial reports from China showed a low incidence (5%-10%) of acute kidney injury (AKI), subsequent articles documented a much higher incidence of AKI in hospitalized COVID-19 patients. Overall, renal biopsies showed a variety of histopathology, including acute glomerulonephritis and acute tubular injury. The pathophysiology of COVID-19-associated AKI is believed to include local and systemic inflammatory and immunological reactions, endothelial damage, and activation of coagulation pathways and the renin-angiotensin system. Histopathology results revealed both similarities and differences between AKI in COVID-19 patients and AKI patients in non-COVID-19 sepsis. Acute tubular injury is common, although it is often mild despite greatly reduced kidney function. Systemic haemodynamic instability most likely contributes to renal tubular damage. Despite the description of COVID-19 as a cytokine storm syndrome, circulating cytokine levels are often lower in patients with COVID-19 than in patients with acute respiratory distress syndrome from causes other than COVID-19. Also, an impaired response to type I interferon has been detected in patients with severe COVID-19. In the light of these observations, the potential pathophysiological mechanisms of COVID-19-associated AKI may provide knowledge to construct therapeutic strategies.

Measurement of the serum level of Elabela for the early detection of acute kidney injury in hospitalized Iraqi COVID-19 patients

Background: Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is caused coronavirus disease2019 (COVID-19) affecting people worldwide. The angiotensin converting enzyme2 (ACE2) represents areceptor of SARS-CoV-2 on the infected host cell. Apelin or its receptor agonists suppress the production ofangiotensin-converting enzyme (ACE) and angiotensin II (Ang-II) and is characterized by a protective effectagainst SARS-CoV-2.Objective: The study aims to assess the serum level of Elabela biomarker as an early detector for AcuteKidney Injury (AKI) in patients with COVID-19.Cases and Methods: This is a case-control study which included 45 hospitalized adult patients in multiplecenters (public hospitals) receiving COVID-19 cases in Baghdad. These cases had a positive real-time orreverse transcription polymerase chain reaction (RT-PCR) of nasal/oropharyngeal swabs. Excluded from thestudy were those with a negative PCR and comorbidities and 43 apparently healthy adult subjects as controls.The age range of the cases and controls was (20 to 60) yearsResult: There are no a statistically significant differences between the two groups in terms of age and genderdistribution. Statistically significant differences were found in terms of eGFR, S. Creatinine, D. dimer,NEU×103/µL, LYM×103/µL and ELA biomarker. Significant negative correlations were found betweenElabela with D. dimer and NEU×103/µL, and between eGFR with S. creatinine, D. Dimer, and NUT×103/µL.Conclusion: The Elabela biomarker can be used for the early detection of acute kidney injury in COVID-19patients.

Suppressed renoprotective purines in COVID-19 patients with acute kidney injury

Acute kidney injury (AKI) is common in patients hospitalized for COVID-19, complicating their clinical course and contributing to worse outcomes. Animal studies show that adenosine, inosine and guanosine protect the kidney against some types of AKI. However, until now there was no evidence in patients supporting the possibility that abnormally low kidney levels of adenosine, inosine and guanosine contribute to AKI. Here, we addressed the question as to whether these renoprotective purines are altered in the urine of COVID-19 patients with AKI. Purines were measured by employing ultra-high-performance liquid chromatography-tandem mass spectrometry with stable-isotope-labeled internal standards for each purine of interest. Compared with COVID-19 patients without AKI (n = 23), COVID-19 patients with AKI (n = 20) had significantly lower urine levels of adenosine (P < 0.0001), inosine (P = 0.0008), and guanosine (P = 0.0008) (medians reduced by 85%, 48% and 61%, respectively) and lower levels (P = 0.0003; median reduced by 67%) of the 2nd messenger for A2A and A2B adenosine receptors, i.e., 3’,5’-cAMP. Moreover, in COVID-19 patients with AKI, urine levels of 8-aminoguanine (endogenous inhibitor of inosine and guanosine metabolism) were nearly abolished (P < 0.0001). In contrast, the “upstream” precursors of renoprotective purines, namely 5’-AMP and 5’-GMP, were not significantly altered in COVID-19 patients with AKI, suggesting defective conversion of these precursors by CD73 (converts 5’-AMP to adenosine and 5’-GMP to guanosine). These findings imply that an imbalance in renoprotective purines may contribute to AKI in COVID-19 patients and that pharmacotherapy targeted to restore levels of renoprotective purines may attenuate the risk of AKI in susceptible patients with COVID-19.

ACUTE KIDNEY INJURY AS A PREDICTOR OF MORTALITY IN PATIENTS WITH COVID-19

ACUTE KIDNEY INJURY AS A PREDICTOR OF MORTALITY IN PATIENTS WITH COVID-19

Acute kidney injury and its association with mortality in Asian COVID-19 patients: A meta-analysis.

Previous evidence suggests that acute kidney injury (AKI) is common in patients with COVID-19 and associated with adverse outcomes. Moreover, the incidence and mortality of AKI in Asia are ambiguous. Evaluating the risk factors and risk of death from AKI in -COVID-19 patients in Asia. We conducted a meta-analysis of clinical observational studies of -COVID-19 patients in Asia. Outcome measures included: AKI in COVID-19 patients, overall mortality in COVID-19 patients, and mortality assessment in patients with AKI. The random-effects model was adopted, with heterogeneity and sensitivity analysis. 27 clinical studies (18,216 Asian patients with COVID-19) have been included in the study. The pooled incidence of AKI was 0.19 (95% CI 16-23%; I2=98.9%, p<0.001); the pooled incidence of total mortality was 0.19 (95% CI 17-22%; I2=98.9%, p<0.001). No publication bias was found (Egger's test, p=0.396, 0.213). The pooled mortality in AKI patients with COVID-19 was 50% (95% CI 33-67%; I2 by random-effects model =98.4%, p<0.001). AKI was found to be a risk factor for death in stepwise regression analysis; age, diabetes, and hypertension were influencing factors for AKI risk in -COVID-19 patients. AKI is a common complication in Asian COVID-19 patients, and it is associated with an increase in mortality of Asian COVID-19 patients. Any treatment that protects the kidney may be a practical intervention to reduce the mortality of COVID-19 patients in Asia.

Cystatin C is a marker for acute kidney injury, but not for mortality among COVID-19 patients in Mexico

BackgroundPatients 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. AimThis work aimed to assess the level of cystatin C as an indicator of AKI and mortality among COVID-19 patients from Mexico. MethodsA 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. ResultsA 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). ConclusionThe 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.

13 THE ROLE OF HYPERTENSION AS A RISK FACTOR FOR ACUTE KIDNEY INJURY IN COVID-19 AT RSUP HAJI ADAM MALIK MEDAN: A CROSS-SECTIONAL STUDY IN 2020

Background and aim: Acute kidney injury (AKI) is a common complication in hospitalized patients. The incidence of AKI in COVID-19 ranges from 0.5% to 56.9% in various case series. AKI in COVID-19 is also associated with a higher risk of death. Some risk factors reported to confer a poor prognosis in COVID-19 such as increased age, male gender, patients with comorbidities such as hypertension or diabetes and higher BMI. The aim of this study was to identify the prevalence and risk factor of AKI among COVID-19 patients. Material and methods: We conducted a cross sectional analysis from moderate, severe, and critical COVID-19 patients that developed to AKI at RSUP Haji Adam Malik Medan during 2020. The data was collected during July to September 2021. Results: Form 465 hospitalized COVID-19 patients, there were 64 people with inclusion and exclusion criteria suffered from AKI during the COVID-19 treatment period (13.8%). 71.9% of the patients were men, 70.3% had more than 1 comorbidities, and 60.9% had hypertension as comorbid. Among patients with comorbid hypertension, 12 patients had stage 1 AKI (30.8%), 2 patients had stage 2 AKI (5.1%), and 25 had stage 3 AKI (64.1%). Although bivariate analysis showed no significant relationship between hypertension and AKI stadium (p 0.155), multivariate analyses showed that hypertension has an OR of 4.24 (p 0.049; CI 95% 1.01 — 17.9) which means that in patients with hypertension, the incidence rate for stage 3 AKI is 4.24 times greater and statistically significant. Conclusion: Hypertension is proven as a risk factor of AKI in COVID-19 patients.

Potential impact of serpin peptidase inhibitor clade (A) member 4 SERPINA4 (rs2093266) and SERPINA5 (rs1955656) genetic variants on COVID-19 induced acute kidney injury

BackgroundSARS-CoV-2 has a number of targets, including the kidneys. Acute Kidney Injury (AKI) might develop in up to a quarter of SARS-CoV-2 patients. In the clinical environment, AKI is linked to a high rate of death and leads to the progression of AKI to chronic renal disease. AimWe aimed to investigate rs2093266 and rs1955656 polymorphisms in SERPINA4 and SERPINA5 genes, respectively, as risk factors for COVID-19 induced AKI. Subjects and methodsA case-control study included 227 participants who were divided into three groups: 81 healthy volunteers who served as controls, 76 COVID-19 patients without AKI and 70 COVID -19 patients with AKI. The TaqMan assay was used for genotyping the SERPINA4 (rs2093266) and SERPINA5 (rs1955656) polymorphisms by real-time PCR technique. ResultsLymphocytes and eGFR showed a significantly decreasing trend across the three studied groups, while CRP, d-Dimer, ferritin, creatinine, KIM-1and NGAL showed a significantly increasing trend across the three studied groups (P < 0.001). Rs2093266 (AG and AA) genotypes were significant risk factors among non-AKI and AKI groups in comparison to controls. Rs1955656 (AG and AA) were significant risk factors among the AKI group, while AA was the only significant risk factor among the non-AKI group. Recessive, dominant, co-dominant, and over-dominant models for genotype combinations were demonstrated. The GG v AA, GG + AG v AA, and GG v AG + AA models of the rs2093266 were all significant predictors of AKI, whilst only the GG v AA model of the rs1955656 SNP was a significant predictor. The logistic regression model was statistically significant, χ2 = 56.48, p < 0.001. AKI was associated with progressed age (OR = 0.95, 95% CI: 0.91–0.98, p = 0.006), suffering from chronic diseases (OR = 3.25, 95% CI: 1.31–8.01, p = 0.010), increased BMI (OR = 0.89, 95% CI: 0.81–0.98, p = 0.018), immunosuppressive (OR = 4.61, 95% CI: 1.24–17.16, p = 0.022) and rs2093266 (AG + AA) (OR = 3.0, 95% CI: 1.11–8.10, p = 0.030). ConclusionSingle nucleotide polymorphisms (rs2093266) at SERPINA4 gene and (rs1955656) at SERPINA5 gene were strongly linked to the development of AKI in COVID-19 patients.

Acute Kidney Injury in Critically-Ill COVID-19 Patients.

Purpose: Acute kidney injury (AKI) is common in patients with COVID-19, however, its mechanism is still controversial, particularly in ICU settings. Urinary proteinuria profile could be a non-invasive tool of interest to scrutinize the pathophysiological process underlying AKI in COVID-19 patients. Material and Methods: We conducted a retrospective study between March 2020 and April 2020. All patients with laboratory-confirmed COVID-19 and without end-stage kidney disease requiring renal replacement therapy before ICU admission were included. Our objectives were to assess the incidence and risk factors for AKI and to describe its clinical and biological characteristics, particularly its urinary protein profile. Results: Seventy patients were included; 87% needed mechanical ventilation and 61% needed vasopressor during their ICU stay; 64.3% of patients developed AKI and half of them needed dialysis. Total and tubular proteinuria on day 1 were higher in patients with AKI, whereas glomerular proteinuria was similar in both groups. The main risk factor for AKI was shock at admission (OR = 5.47 (1.74–17.2), p < 0.01). Mortality on day 28 was higher in AKI (23/45, 51.1%) than in no-AKI patients (1/25, 4%), p < 0.001. Risk factors for 28-days mortality were AKI with need for renal replacement therapy, non-renal SOFA score and history of congestive heart failure. Conclusions: AKI is common in COVID-19 patients hospitalized in ICU; it seems to be related to tubular lesions rather than glomerular injury and is related to shock at ICU admission.

Evolving Risk of Acute Kidney Injury in COVID-19 Hospitalized Patients: A Single Center Retrospective Study.

Background and Objectives: Within a year, COVID-19 has advanced from an outbreak to a pandemic, spreading rapidly and globally with devastating impact. The pathophysiological link between COVID-19 and acute kidney injury (AKI) is currently being debated among scientists. While some studies have concluded that the mechanisms of AKI in COVID-19 patients are complex and not fully understood, others have claimed that AKI is a rare complication of COVID-19-related disorders. Considering this information gap and its possible influence on COVID-19-associated AKI management, our study aimed to explore the prevalence of AKI and to identify possible risk factors associated with AKI development among COVID-19 hospitalized patients. Materials and Methods: A retrospective cohort study included 83 laboratory-confirmed COVID-19 patients hospitalized at the isolation department in a tertiary hospital in Zagazig City, Egypt between June and August 2020. Patients younger than 18 years of age, those diagnosed with end-stage kidney disease, or those on nephrotoxic medications were excluded. All study participants had a complete blood count, liver and renal function tests, hemostasis parameters examined, inflammatory markers, serum electrolytes, routine urinalysis, arterial blood gas, and non-enhanced chest and abdominal computer tomography (CT) scans. Results: Of the 83 patients, AKI developed in 24 (28.9%) of them, of which 70.8% were in stage 1, 8.3% in stage 2, and 20.8% in stage 3. Patients with AKI were older than patients without AKI, with hypertension and diabetes being the most common comorbidities. Risk factors for AKI include increased age, hypertension, diabetes mellitus, and a higher sequential organ failure assessment (SOFA) score. Conclusions: AKI occurs in a considerable percentage of patients with COVID-19, especially in elderly males, those with hypertension, diabetes, and a higher sequential organ failure assessment (SOFA) score. Hence, the presence of AKI should be taken into account as an important index within the risk spectrum of disease severity for COVID-19 patients.

Acute Kidney Injury Incidence, Stage, and Recovery in Patients with COVID-19.

PurposeTo determine the incidence, mortality, stage, and recovery of acute kidney injury (AKI) in COVID-19 patients and further analyze the effect of patient demographics and comorbidities on AKI incidence.Study DesignOur study looked at 1545 charts of patients over 18 years old who presented to BronxCare Hospital in NY with a positive SARS-CoV-2 PCR test. Using the KDIGO criteria, any patient presenting with a creatinine of 1.5 times the baseline or that had an increase in creatinine of 0.3mg/dL in 48 hours was diagnosed with AKI. Pregnant patients, patients with end-stage renal disease (ESRD), and patients with a history of renal transplant were excluded.ResultsThe incidence of AKI in COVID-19 patients was 39% (608), and the mortality rate was 58.2% (354). Of the 254 survivors, 74.8% recovered. Moreover, 42.6% (259) of patients with AKI were admitted to the ICU. Twenty-six of our patients received hemodialysis during admission. There was a statistically significant association between AKI and age, race, hypertension (HTN), diabetes mellitus (DM), hepatitis C (HCV), congestive heart failure (CHF), CKD, patient outcome, and days spent in the hospital. Of the 608 patients with AKI, 294 (48.4%), 185 (30.4%) and 129 (21.2%) had AKI stage 1, 2 and 3, respectively.ConclusionEarly resource planning is necessary when admitting COVID-19 patients. Nephrology should be consulted early, and measures should be in place to optimize outpatient follow-up in the nephrology clinic. Lastly, the use of nephrotoxic agents should be carefully considered and, if possible, avoided from the time of admission in patients with COVID-19.

POS-842 EXTRAPOLATION OF BURDEN OF ACUTE KIDNEY INJURY IN HOSPITALISED COVID-19 PATIENTS

COVID-19 infection is as a global pandemic which is associated with a variety of clinical spectrum including acute kidney injury (AKI). The devastating outcome of AKI in COVID-19 patients will lead to a new subgroup of population with kidney diseases. AKI also has been reported to be strongly associated with mortality of COVID-19 hospitalised patients.

POS-857 RISK FACTORS AND SHORT-TERM OUTCOMES OF ACUTE KIDNEY INJURY IN HOSPITALIZED PATIENTS WITH COVID-19: A DOUBLE CENTER RETROSPECTIVE STUDY

Acute kidney injury (AKI) in COVID-19 is considered both a marker of disease severity and a negative prognostic factor for survival. Reported data on AKI in COVID-19 patients in the Philippines is very limited. This study aimed to determine the incidence, risk factors and short-term outcomes of AKI in patients hospitalized with COVID-19 in a tertiary hospital in Cebu. This retrospective, double-center, observational cohort study was done in two separate private tertiary hospitals under the same institution in Cebu. A total of 535 patients were included in this study and all data were gathered through chart review. AKI was defined according to Kidney Disease: Improving Global Outcomes (KDIGO) criteria. Binary logistic regression analyses were performed to determine the risk factors and the association between the stages of AKI and in-hospital mortality. A p-value < 0.05 (two-tailed) was considered statistically significant. Among 535 patients included in this study, AKI developed in 150 (28%). Median age was 65 years and 60.67% were males. Hypertension (74%), diabetes mellitus (50%), and chronic kidney disease (19.33%) were the most common co-morbid conditions and were frequently observed in stage 3 AKI. The peak stages of AKI were stage 1 in 32%, stage 2 in 18.67% and stage 3 in 49.3%. Of these, 35.3% required renal replacement therapy (RRT). The risk factors identified included age, hypertension, CKD, proteinuria, hematuria, pyuria, procalcitonin, mechanical ventilator use, vasopressor use, ICU admission, and illness severity. AKI was observed in greater frequency among patients with respiratory failure, with 67.9% of patients on mechanical ventilation developing AKI compared to only 15% in non-ventilated patients. Among 53 patients who required RRT, 46 (86.79%) were intubated. The median time of intubation to AKI diagnosis was 24 hours. Furthermore, 63% of patients with AKI had major adverse kidney events with in-hospital mortality accounting for 56.6%. The odds of mortality increased by 1.4 times for every increase in AKI stage. Additionally, a total of 113 patients died and of these, 85 (75.2%) had AKI. Acute kidney injury occurred in more than one-fourth of hospitalized patients with COVID-19. Its development occurs in temporal association with respiratory failure and the time of intubation. The rate of in-hospital mortality was significantly higher among patients with AKI. Furthermore, there is a stepwise increase in the mortality rate for every increase in the severity of AKI.

Clinical Features and Outcomes of COVID-19 Patients with Acute Kidney Injury and Acute Kidney Injury on Chronic Kidney Disease.

COVID-19 emerged in Wuhan in December 2019 and soon became a worldwide pandemic. We collected and analyzed the data from 1077 patients with COVID-19 who were admitted to the west campus of Wuhan Union Hospital from January 16 to April 16, 2020. Sixty (5.6%) of the 1077 COVID-19 patients were diagnosed with acute kidney injury (AKI) during hospitalization, and 18 of them (30%) had AKI on chronic kidney disease (AKI/CKD). COVID-19 patients with AKI had a worse prognosis, with higher intensive care unit (ICU) admission (28.3%) and fatality (65%) rates than patients without AKI (3.4% and 10.7%, respectively). Among the COVID-19 patients, AKI was more likely to occur in male patients, the elderly, patients with more severe disease states and those with comorbidities (such as hypertension, diabetes, coronary heart disease (CHD), chronic obstructive pulmonary disease (COPD) and CKD). COVID-19 patients with AKI were more likely to develop respiratory failure, gastrointestinal bleeding, acute liver injury, acute myocardial injury, heart failure, acute respiratory distress syndrome (ARDS), cerebrovascular accident, and disseminated intravascular coagulation (DIC) than those without AKI. Compared with patients without AKI, COVID-19 patients with AKI had lower platelet counts, lymphocyte counts, albumin levels and serum calcium levels but had elevated leukocyte counts, neutrophil counts and serum potassium levels. Inflammatory indicators, such as C-reactive protein (CRP), interleukin-6 (IL-6), and procalcitonin (PCT), were significantly higher in patients with AKI than in those without AKI. COVID-19 patients with AKI also exhibited a longer prothrombin time (PT), a longer activated partial thromboplastin time (APTT), and a higher D-dimer level than those without AKI. Survival analysis revealed that COVID-19 patients with AKI had a reduced survival rate compared with those without AKI. Furthermore, COVID-19 patients with AKI/CKD had a lower survival rate than those with AKI or CKD only. Multiple logistic regression indicated that the predictors of AKI in COVID-19 patients included complications, such as respiratory failure and acute myocardial injury, and higher creatinine and PCT levels during hospitalization.