Clinical characteristics and factors associated with acute kidney injury among patients hospitalized with coronavirus disease: an observational retrospective study.

BACKGROUND: Coronavirus disease 19 (COVID-19) is a multisystemic disease with high incidence of acute kidney injury (AKI). OBJECTIVE: To describe the clinical characteristics and factors associated with AKI among patients hospitalized with COVID-19. DESIGN AND SETTING: Retrospective cohort conducted at Hospital Civil de Culiacan, Mexico. METHODS: We included 307 patients hospitalized due to COVID-19. AKI was defined and staged based on serum creatinine levels in accordance with the criteria of the Acute Kidney Injury Network (AKIN). Multivariate logistic regression analysis was used to determine factors associated with AKI. RESULTS: The patients' age was 56 ± 15 years (64.5% male). The incidence of AKI was 33.6% (n = 103). Overall, 53.4% of patients had community-acquired AKI, and 46.6% had hospital-acquired AKI. Additionally, 15.5% of them presented AKIN stage 1; 34% had AKIN stage 2; and 50.5% had AKIN stage 3. Hemodialysis was required for 10.7% of the patients. The factors associated with AKI were chronic kidney disease (odds ratio, OR: 10.8; P = 0.04), use of norepinephrine (OR: 7.3; P = 0.002), diabetes mellitus (OR: 2.9; P = 0.03), C-reactive protein level (OR: 1.005; P = 0.01) and COVID-19 severity index based on chest tomography (OR: 1.09; statistical trend, P = 0.07). Hospital stay (11 ± 7 days; P < 0.001) and mortality (83.5 versus 31.4%; P < 0.05) were greater among patients with AKI. CONCLUSION: AKI was a frequent and serious complication in our cohort of patients hospitalized with COVID-19, which was associated with high mortality and long hospital stay.

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

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

Utilization of Palliative Care for Patients with COVID-19 and Acute Kidney Injury during a COVID-19 Surge.

BACKGROUND AND OBJECTIVES: AKI is a common complication of coronavirus disease 2019 (COVID-19) and is associated with high mortality. Palliative care, a specialty that supports patients with serious illness, is valuable for these patients but is historically underutilized in AKI. The objectives of this paper are to describe the use of palliative care in patients with AKI and COVID-19 and their subsequent health care utilization. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: We conducted a retrospective analysis of New York University Langone Health electronic health data of COVID-19 hospitalizations between March 2, 2020 and August 25, 2020. Regression models were used to examine characteristics associated with receiving a palliative care consult. RESULTS: Among patients with COVID-19 (n=4276; 40%), those with AKI (n=1310; 31%) were more likely than those without AKI (n=2966; 69%) to receive palliative care (AKI without KRT: adjusted odds ratio, 1.81; 95% confidence interval, 1.40 to 2.33; P<0.001; AKI with KRT: adjusted odds ratio, 2.45; 95% confidence interval, 1.52 to 3.97; P<0.001), even after controlling for markers of critical illness (admission to intensive care units, mechanical ventilation, or modified sequential organ failure assessment score); however, consults came significantly later (10 days from admission versus 5 days; P<0.001). Similarly, 66% of patients initiated on KRT received palliative care versus 37% (P<0.001) of those with AKI not receiving KRT, and timing was also later (12 days from admission versus 9 days; P=0.002). Despite greater use of palliative care, patients with AKI had a significantly longer length of stay, more intensive care unit admissions, and more use of mechanical ventilation. Those with AKI did have a higher frequency of discharges to inpatient hospice (6% versus 3%) and change in code status (34% versus 7%) than those without AKI. CONCLUSIONS: Palliative care was utilized more frequently for patients with AKI and COVID-19 than historically reported in AKI. Despite high mortality, consultation occurred late in the hospital course and was not associated with reduced initiation of life-sustaining interventions. PODCAST: This article contains a podcast at https://www.asn-online.org/media/podcast/CJASN/2022_02_24_CJN11030821.mp3.

Human Kidney Spheroids and Monolayers Provide Insights into SARS-CoV-2 Renal Interactions.

BACKGROUND: Although coronavirus disease 2019 (COVID-19) causes significan t morbidity, mainly from pulmonary involvement, extrapulmonary symptoms are also major componen ts of the disease. Kidney disease, usually presenting as AKI, is particularly severe among patients with COVID-19. It is unknown, however, whether such injury results from direct kidney infection with COVID-19's causative virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), or from indirect mechanisms. METHODS: Using ex vivo cell models, we sought to analyze SARS-CoV-2 interactions with kidney tubular cells and assess direct tubular injury. These models comprised primary human kidney epithelial cells (derived from nephrectomies) and grown as either proliferating monolayers or quiescent three-dimensional kidney spheroids. RESULTS: We demonstrated that viral entry molecules and high baseline levels of type 1 IFN-related molecules were present in monolayers and kidney spheroids. Although both models support viral infection and replication, they did not exhibit a cytopathic effect and cell death, outcomes that were strongly present in SARS-CoV-2-infected controls (African green monkey kidney clone E6 [Vero E6] cultures). A comparison of monolayer and spheroid cultures demonstrated higher infectivity and replication of SARS-CoV-2 in actively proliferating monolayers, although the spheroid cultures exhibited high er levels of ACE2. Monolayers exhibited elevation of some tubular injury molecules-including molecules related to fibrosis (COL1A1 and STAT6) and dedifferentiation (SNAI2)-and a loss of cell identity, evident by reduction in megalin (LRP2). The three-dimensional spheroids were less prone to such injury. CONCLUSIONS: SARS-CoV-2 can infect kidney cells without a cytopathic effect. AKI-induced cellular proliferation may potentially intensify infectivity and tubular damage by SARS-CoV-2, suggesting that early intervention in AKI is warranted to help minimize kidney infection.

The mechanism underlying extrapulmonary complications of the coronavirus disease 2019 and its therapeutic implication.

The coronavirus disease 2019 (COVID-19) is a highly transmissible disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that poses a major threat to global public health. Although COVID-19 primarily affects the respiratory system, causing severe pneumonia and acute respiratory distress syndrome in severe cases, it can also result in multiple extrapulmonary complications. The pathogenesis of extrapulmonary damage in patients with COVID-19 is probably multifactorial, involving both the direct effects of SARS-CoV-2 and the indirect mechanisms associated with the host inflammatory response. Recognition of features and pathogenesis of extrapulmonary complications has clinical implications for identifying disease progression and designing therapeutic strategies. This review provides an overview of the extrapulmonary complications of COVID-19 from immunological and pathophysiologic perspectives and focuses on the pathogenesis and potential therapeutic targets for the management of COVID-19.

Development of a europium nanoparticles lateral flow immunoassay for NGAL detection in urine and diagnosis of acute kidney injury.

BACKGROUND: AKI is related to severe adverse outcomes and mortality with Coronavirus Disease 2019 (COVID-19) patients, that early diagnosed and intervened is imperative. Neutrophil gelatinase-associated lipocalin (NGAL) is one of the most promising biomarkers for detection of acute kidney injury (AKI), but current detection methods are inadequacy, so more rapid, convenient and accuracy methods are needed to detect NGAL for early diagnosis of AKI. Herein, we established a rapid, reliable and accuracy lateral flow immunoassay (LFIA) based on europium nanoparticles (EU-NPS) for the detection of NGAL in human urine specimens. METHODS: A double-antibody sandwich immunofluorescent assay using europium doped nanoparticles was employed and the NGAL monoclonal antibodies (MAbs) conjugate as labels were generated by optimizing electric fusion parameters. Eighty-three urine samples were used to evaluate the clinical application efficiency of this method. RESULTS: The quantitative detection range of NGAL in AKI was 1-3000 ng/mL, and the detection sensitization was 0.36 ng/mL. The coefficient of variation (CV) of intra-assay and inter-assay were 2.57-4.98 % and 4.11-7.83 %, respectively. Meanwhile, the correlation coefficient between europium nanoparticles-based lateral fluorescence immunoassays (EU-NPS-LFIA) and ARCHITECT analyzer was significant (R2 = 0.9829, n = 83, p < 0.01). CONCLUSIONS: Thus, a faster and easier operation quantitative assay of NGAL for AKI has been established, which is very important and meaningful to diagnose the early AKI, suggesting that the assay can provide an early warning of final outcome of disease.

A 67-Year-Old Male Patient With COVID-19 With Worsening Respiratory Function and Acute Kidney Failure.

CASE PRESENTATION: A 67-year-old obese man (BMI 38.0) with type 2 diabetes mellitus (DM), chronic atrial fibrillation, and chronic lymphocytic leukemia stage II, stable for 8 years after chemotherapy, and a history of smoking presented to the ED with progressive dyspnea and fever due to SARS-CoV-2 infection. He was admitted to a general ward and treated with dexamethasone (6 mg IV once daily) and oxygen. On day 3 of hospital admission, he became progressively hypoxemic and was admitted to the ICU for invasive mechanical ventilation. Dexamethasone treatment was continued, and a single dose of tocilizumab (800 mg) was administered. On day 9 of ICU admission, voriconazole treatment was initiated after tracheal white plaques at bronchoscopy, suggestive of invasive Aspergillus tracheobronchitis, were noticed. However, his medical situation dramatically deteriorated.

Sex-related differences in mortality, acute kidney injury, and respiratory failure among critically ill patients with COVID-19.

ABSTRACT: Although the number of deaths due to coronavirus disease 2019 (COVID-19) is higher in men than women, prior studies have provided limited sex-stratified clinical data.We evaluated sex-related differences in clinical outcomes among critically ill adults with COVID-19.Multicenter cohort study of adults with laboratory-confirmed COVID-19 admitted to intensive care units at 67 U.S. hospitals from March 4 to May 9, 2020. Multilevel logistic regression was used to evaluate 28-day in-hospital mortality, severe acute kidney injury (AKI requiring kidney replacement therapy), and respiratory failure occurring within 14 days of intensive care unit admission.A total of 4407 patients were included (median age, 62 years; 2793 [63.4%] men; 1159 [26.3%] non-Hispanic White; 1220 [27.7%] non-Hispanic Black; 994 [22.6%] Hispanic). Compared with women, men were younger (median age, 61 vs 64 years, less likely to be non-Hispanic Black (684 [24.5%] vs 536 [33.2%]), and more likely to smoke (877 [31.4%] vs 422 [26.2%]). During median follow-up of 14 days, 1072 men (38.4%) and 553 women (34.3%) died. Severe AKI occurred in 590 men (21.8%), and 239 women (15.5%), while respiratory failure occurred in 2255 men (80.7%) and 1234 women (76.5%). After adjusting for age, race/ethnicity and clinical variables, compared with women, men had a higher risk of death (OR, 1.50, 95% CI, 1.26-1.77), severe AKI (OR, 1.92; 95% CI 1.57-2.36), and respiratory failure (OR, 1.42; 95% CI, 1.11-1.80).In this multicenter cohort of critically ill adults with COVID-19, men were more likely to have adverse outcomes compared with women.

SARS-CoV-2 N Protein Induces Acute Kidney Injury via Smad3-Dependent G1 Cell Cycle Arrest Mechanism.

COVID-19 is infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and can cause severe multiple organ injury and death. Kidney is one of major target organs of COVID-19 and acute kidney injury (AKI) is common in critically ill COVID-19 patients. However, mechanisms through which COVID-19 causes AKI remain largely unknown and treatment remains unspecific and ineffective. Here, the authors report that normal kidney-specifically overexpressing SARS-CoV-2 N develops AKI, which worsens in mice under ischemic condition. Mechanistically, it is uncovered that SARS-CoV-2 N-induced AKI is Smad3-dependent as SARS-CoV-2 N protein can interact with Smad3 and enhance TGF-ß/Smad3 signaling to cause tubular epithelial cell death and AKI via the G1 cell cycle arrest mechanism. This is further confirmed in Smad3 knockout mice and cells in which deletion of Smad3 protects against SARS-CoV-2 N protein-induced cell death and AKI in vivo and in vitro. Most significantly, it is also found that targeting Smad3 with a Smad3 pharmacological inhibitor is able to inhibit SARS-CoV-2 N-induced AKI. In conclusion, the authors identify that SARS-CoV-2 N protein is a key mediator for AKI and induces AKI via the Smad3-dependent G1 cell cycle arrest mechanism. Targeting Smad3 may represent as a novel therapy for COVID-19-asscoaited AKI.

Acute Kidney Injury in Severe COVID-19 Has Similarities to Sepsis-Associated Kidney Injury: A Multi-Omics Study.

OBJECTIVE: To compare coronavirus disease 2019 (COVID-19) acute kidney injury (AKI) to sepsis-AKI (S-AKI). The morphology and transcriptomic and proteomic characteristics of autopsy kidneys were analyzed. PATIENTS AND METHODS: Individuals 18 years of age and older who died from COVID-19 and had an autopsy performed at Mayo Clinic between April 2020 to October 2020 were included. Morphological evaluation of the kidneys of 17 individuals with COVID-19 was performed. In a subset of seven COVID-19 cases with postmortem interval of less than or equal to 20 hours, ultrastructural and molecular characteristics (targeted transcriptome and proteomics analyses of tubulointerstitium) were evaluated. Molecular characteristics were compared with archived cases of S-AKI and nonsepsis causes of AKI. RESULTS: The spectrum of COVID-19 renal pathology included macrophage-dominant microvascular inflammation (glomerulitis and peritubular capillaritis), vascular dysfunction (peritubular capillary congestion and endothelial injury), and tubular injury with ultrastructural evidence of mitochondrial damage. Investigation of the spatial architecture using a novel imaging mass cytometry revealed enrichment of CD3+CD4+ T cells in close proximity to antigen-presenting cells, and macrophage-enriched glomerular and interstitial infiltrates, suggesting an innate and adaptive immune tissue response. Coronavirus disease 2019 AKI and S-AKI, as compared to nonseptic AKI, had an enrichment of transcriptional pathways involved in inflammation (apoptosis, autophagy, major histocompatibility complex class I and II, and type 1 T helper cell differentiation). Proteomic pathway analysis showed that COVID-19 AKI and to a lesser extent S-AKI were enriched in necroptosis and sirtuin-signaling pathways, both involved in regulatory response to inflammation. Upregulation of the ceramide-signaling pathway and downregulation of oxidative phosphorylation in COVID-19 AKI were noted. CONCLUSION: This data highlights the similarities between S-AKI and COVID-19 AKI and suggests that mitochondrial dysfunction may play a pivotal role in COVID-19 AKI. This data may allow the development of novel diagnostic and therapeutic targets.

Critical analysis of acute kidney injury in pediatric COVID-19 patients in the intensive care unit.

BACKGROUND AND OBJECTIVES: COVID-19 is responsible for the 2019 novel coronavirus disease pandemic. Despite the vast research about the adult population, there has been little data collected on acute kidney injury (AKI) epidemiology, associated risk factors, treatments, and mortality in pediatric COVID-19 patients admitted to the ICU. AKI is a severe complication of COVID-19 among children and adolescents. METHODS: A comprehensive literature search was conducted in PubMed/MEDLINE and Cochrane Center Trials to find all published literature related to AKI in COVID-19 patients, including incidence and outcomes. RESULTS: Twenty-four studies reporting the outcomes of interest were included. Across all studies, the overall sample size of COVID positive children was 1,247 and the median age of this population was 9.1 years old. Among COVID positive pediatric patients, there was an AKI incidence of 30.51%, with only 0.56% of these patients receiving KRT. The mortality was 2.55% among all COVID positive pediatric patients. The incidence of multisystem inflammatory syndrome in children (MIS-C) among COVID positive patients was 74.29%. CONCLUSION: AKI has shown to be a negative prognostic factor in adult patients with COVID-19 and now also in the pediatric cohort with high incidence and mortality rates. Additionally, our findings show a strong comparison in epidemiology between adult and pediatric COVID-19 patients; however, they need to be confirmed with additional data and studies.

Mortality and evolution between community and hospital-acquired COVID-AKI.

BACKGROUND: Acute kidney injury (AKI) is associated with poor outcomes in COVID patients. Differences between hospital-acquired (HA-AKI) and community-acquired AKI (CA-AKI) are not well established. METHODS: Prospective, observational cohort study. We included 877 patients hospitalized with COVID diagnosis at two third-level hospitals in Mexico. Primary outcome was all-cause mortality at 28 days compared between COVID patients with CA-AKI and HA-AKI. Secondary outcomes included the need for KRT, and risk factors associated with the development of CA-AKI and HA-AKI. RESULTS: A total of 377 patients (33.7%) developed AKI. CA-AKI occurred in 202 patients (59.9%) and HA-AKI occurred in 135 (40.1%). Patients with CA-AKI had more significant comorbidities, including diabetes (52.4% vs 38.5%), hypertension (58.4% vs 39.2%), CKD (30.1% vs 14.8%), and COPD (5.9% vs 1.4%), than those with HA-AKI. Patients' survival without AKI was 87.1%, with CA-AKI it was 75.4%, and with HA-AKI it was 69.6%, log-rank test p < 0.001. Only age > 60 years (OR 1.12, 95% CI 1.06-1.18, p <0.001), COVID severity (OR 1.09, 95% CI 1.03-1.16, p = 0.002), the need in mechanical lung ventilation (OR 1.67, 95% CI 1.56-1.78, p <0.001), and HA-AKI stage 3 (OR 1.16, 95% CI 1.05-1.29, p = 0.003) had a significant increase in mortality. The presence of CKD (OR 1.48, 95% CI 1.391.56, p < 0.001), serum lymphocytes < 1000 µL (OR 1.03, 95% CI 1.00-1.07, p = 0.03), the need in mechanical lung ventilation (OR 1.06, 95% CI 1.02-1.11, p = 0.003), and CA-AKI stage 3 (OR 1.37, 95% CI 1.29-1.46, p < 0.001) were the only variables associated with a KRT start. CONCLUSIONS: We found that COVID patients who are complicated by CA-AKI have more comorbidities and worse biochemical parameters at the time of hospitalization than HA-AKI patients, but despite these differences, their probability of dying is similar.

Abnormal Blood Coagulation and Kidney Damage in Aged Hamsters Infected with Severe Acute Respiratory Syndrome Coronavirus 2.

Systemic symptoms have often been observed in patients with coronavirus disease 2019 (COVID-19) in addition to pneumonia, however, the details are still unclear due to the lack of an appropriate animal model. In this study, we investigated and compared blood coagulation abnormalities and tissue damage between male Syrian hamsters of 9 (young) and over 36 (aged) weeks old after intranasal infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Despite similar levels of viral replication and inflammatory responses in the lungs of both age groups, aged but not young hamsters showed significant prolongation of prothrombin time and prominent acute kidney damage. Moreover, aged hamsters demonstrated increased intravascular coagulation time-dependently in the lungs, suggesting that consumption of coagulation factors causes prothrombin time prolongation. Furthermore, proximal urinary tract damage and mesangial matrix expansion were observed in the kidneys of the aged hamsters at early and later disease stages, respectively. Given that the severity and mortality of COVID-19 are higher in elderly human patients, the effect of aging on pathogenesis needs to be understood and should be considered for the selection of animal models. We, thus, propose that the aged hamster is a good small animal model for COVID-19 research.

Modification of immunosuppressive agents in a kidney transplant recipient with COVID-19 and acute kidney injury.

INTRODUCTION: An outbreak of coronavirus disease-19 (COVID-19) has occurred in different parts of the world. Although a large piece of information regarding the epidemiology, clinical features, and management of COVID-19 has been reported in the general population, there is very limited data regarding organ transplant recipients, particularly regarding the management of maintenance immunosuppressive agents during infection. METHODOLOGY: We described a case of kidney transplant recipient from Thailand who had COVID-19 pneumonia and severe acute kidney injury. RESULTS: The patient's serum creatinine peaked at 7.0 mg/dL on day 15 of illness and returned to baseline value of 2.0 mg/dL on day 26 of illness. We have shown how we modified tacrolimus, mycophenolate, and steroids in the patient who had received favipiravir and lopinavir/ritonavir for COVID-19 pneumonia. CONCLUSIONS: In this case, successful modification of this immunosuppressive regimen was accomplished to reduce drug interaction complications, aiming to avoid calcineurin inhibitor nephrotoxicity while maintaining appropriate levels of immunosuppression to prevent organ rejection and to promote the patient's recovery from infection.

[Acute kidney injury caused by rhabdomyolysis as a SARS-CoV-2 infection manifestation. Report of one case]. / Insuficiencia renal aguda secundaria a rabdomiolisis como manifestación de infección por SARS-CoV-2.

SARS-CoV-2 infection has a wide spectrum of clinical manifestations secondary to the impairment of different organs, including kidney. Rhabdomyolysis is produced by disintegration of striated muscle and the liberation of its contents to the extracellular fluid and bloodstream. This may produce hydro electrolytic disorders and acute kidney injury. We report a 35-year-old female with a history of SARS-CoV-2 infection who was hospitalized because of respiratory failure and developed renal failure. The etiologic study showed elevated total creatine kinase levels and a magnetic resonance imaging confirmed rhabdomyolysis. The patient required supportive treatment with vasoactive drugs, mechanic ventilation and kidney replacement therapy. She had a favorable evolution with resolution of respiratory failure and improvement of kidney function.

Clinical profile and outcomes of COVID-19 patients with acute kidney injury: a tertiary centre experience from South India.

AIM: The rates of development of acute kidney injury (AKI) in COVID-19 have been variably reported from across the world. Prevalence and outcomes of AKI in hospitalised COVID-19 patients in India has not been studied well. METHODS: This was a retrospective observational study amongst adult hospitalised COVID-19 patients admitted at a tertiary care centre between May 1 and October 31, 2020. We estimated the prevalence of AKI and outcomes including mortality and acute kidney disease (AKD) at the time of discharge. Regression analysis was done to study the factors associated with mortality and AKD. RESULTS: Out of 2650 hospitalised patients with COVID-19, 190 (7.2%) patients developed AKI. Mean age of patients with AKI was 62.6 years, 81.6% were male. Comorbidities included diabetes mellitus in 72.1%, hypertension in 66.8%, heart disease in 30% and chronic kidney disease (CKD) in 22.6%. Most patients had stage 1 AKI (71.1%). Overall mortality in patients with AKI was 22.1%, 75% in those requiring dialysis and 74.5% in those requiring ICU. Amongst survivors without pre-existing CKD, 40.9% patients had acute kidney disease at the time of discharge. Higher age, stage 3 AKI and need for mechanical ventilation were associated with higher mortality. On multivariable regression, factors associated with AKD at discharge included pre-existing heart disease and severe albuminuria during hospitalisation. CONCLUSION: In our study population, we found a low prevalence of AKI. Mortality was high in AKI patients requiring ICU care and dialysis. Amongst survivors, a significant percentage had AKD at the time of discharge.

Renal replacement therapy for critically ill patients with COVID-19-associated acute kidney injury: A review of current knowledge.

The outbreak of coronavirus disease 2019 (COVID-19) has rapidly evolved into a global pandemic. A significant proportion of COVID-19 patients develops severe symptoms, which may include acute respiratory distress syndrome and acute kidney injury as manifestations of multi-organ failure. Acute kidney injury (AKI) necessitating renal replacement therapy (RRT) is increasingly prevalent among critically ill patients with COVID-19. However, few studies have focused on AKI treated with RRT. Many questions are awaiting answers as regards AKI in the setting of COVID-19; whether patients with COVID-19 commonly develop AKI, what are the underlying pathophysiologic mechanisms? What is the best evidence regarding treatment approaches? Identification of the potential indications and the preferred modalities of RRT in this context, is based mainly on clinical experience. Here, we review the current approaches of RRT, required for management of critically ill patients with COVID-19 complicated by severe AKI as well as the precautions that should be adopted by health care providers in dealing with these cases. Electronic search was conducted in MEDLINE, PubMed, ISI Web of Science, and Scopus scientific databases. We searched the terms relevant to this review to identify the relevant studies. We also searched the conference proceedings and ClinicalTrials.gov database.

Association of Inflammatory Biomarkers with Immunosuppression Management and Outcomes in Kidney Transplant Recipients with COVID-19.

BACKGROUND: Kidney transplant recipients with coronavirus disease 2019 (COVID-19) are at increased risk for adverse outcomes, such as acute kidney injury (AKI), intensive care unit (ICU) admission, and death. The association of inflammatory biomarkers with outcomes and the impact of changes in immunosuppression on biomarker levels are unknown. METHODS: We investigated factors associated with a composite of AKI, ICU admission, or death, and whether immunosuppression changes correlated with changes in inflammatory biomarkers and outcomes in kidney transplant recipients with a positive severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) polymerase chain reaction. RESULTS: Of 59 patients, 50% had estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2. Patients who discontinued calcineurin inhibitors (CNIs) had higher peak high-sensitivity C-reactive protein (hs-CRP) than those who maintained the same dose (median, 344; interquartile range [IQR], 145-374 vs median, 41; IQR, 22-116 mg/L, P = .03). Of the patients, 73% were hospitalized, 22% had admissions to the ICU, and 20% died. Of the 56% with AKI, 35% required dialysis. All patients with AKI but without pulmonary manifestations recovered to 10% of baseline creatinine levels. Factors associated with the composite outcome were eGFR <60 mL/min/1.73 m2 (odds ratio [OR], 5.833; 95% confidence interval [CI], 1.880-18.099; P = .002), hs-CRP (OR, 1.011/unit increase; 95% CI, 1.002-1.021; P = .019), white blood cell count (OR, 1.173/unit increase; 95% CI, 1.006-1.368; P = .041), and decreased or discontinued CNI (OR, 4.286; 95% CI, 1.353-13.572; P = .013). eGFR<60 mL/min/1.73 m2 (OR, 11.176; 95% CI, 1.581-79.001; P = .016), and peak hs-CRP (OR, 1.010/unit increase; 95% CI, 1.000-1.020; P = .049) remained associated with the composite in the multivariable model. CONCLUSIONS: Kidney transplant recipients with COVID-19 have high rates of ICU admissions, AKI, and death. Those with eGFR<60 mL/min/1.73 m2 are at highest risk. CNI reduction is associated with higher inflammatory biomarkers, correlating with worse outcomes. More studies are needed to determine if this association should drive clinical management.