key: cord-0697176-qwrinmot
authors: Hirsch, Jamie S.; Ikizler, Talat Alp; Sharma, Shuchita; Mohammed, Azeem
title: Acute Kidney Injury and Advanced Kidney Disease in the COVID-19 Pandemic: Proceedings From a National Kidney Foundation Symposium
date: 2021-04-17
journal: Kidney Med
DOI: 10.1016/j.xkme.2021.03.003
sha: 12022c26f0c85930a37834e868b186d2fd520299
doc_id: 697176
cord_uid: qwrinmot

The coronavirus disease 2019 (COVID-19) pandemic is an unprecedented and historic public health crisis that continues to expand and evolve. The National Kidney Foundation (NKF) held a two-part CME live virtual symposium on July 16th and July 24(th) 2020 to address the multiple challenges of COVID-19 in the context of advanced chronic kidney disease (CKD). Faculty addressed the pathophysiology, impact, risks, and management of COVID-19 as it relates to advanced kidney disease. Testing, risk mitigation, and inpatient and outpatient management were also addressed. This concise review addresses major findings of the symposium along with certain updates regarding vaccinations since then. These findings include: 1) Severe COVID-19 has been associated with acute kidney injury (AKI); 2) It is essential to prevent and actively manage AKI to decrease mortality in these critically ill patients; 3) Management of patients with advanced kidney disease should be geared towards minimizing their risk of exposure while making sure they are receiving adequate treatments. 4) Patients with kidney disease, especially ones in advanced stages, should be prioritized for vaccination.

Similar to severe acute respiratory syndrome (SARS) observed during previous coronavirus epidemics, SARS-CoV2 uses the receptor angiotensin-converting enzyme 2 (ACE2) for cell entry. 1,2,3 ACE2 is highly represented in lung tissues, which is why certain SARS-CoV2 is believed to predominantly infect lower airways first. However, COVID-19 is a multisystem disease and can impact the lungs, as well as the heart, brain, liver, and kidney. SARS-CoV2 can also induce inflammatory cytokine releases and the resultant "cytokine storm" or "cytokine cascade" is believed to play a major role in organ damage.

Severe COVID-19 or mortality can occur in healthy individuals of any age, but it predominantly occurs in adults with advanced age or underlying medical comorbidities, including cardiovascular disease (CVD), diabetes mellitus, hypertension, chronic lung disease, cancer and chronic kidney disease (CKD). 4, 5, 6, 7, 8 Early reports from China suggested a low incidence of AKI (3-7 %) in hospitalized patients with COVID-19. 9, 10, 11, 12 However, these cohorts had relatively low burden of comorbid illness. More recent data indicate that AKI can occur in over one third patients with COVID-19. For example, a retrospective observational cohort study by Hirsch et al analyzed the data of 5,449 adult patients (median age 64 years) hospitalized with COVID-19 from March 1, 2020 to April 5, 2020 in a New York Health System (13 hospitals). The study showed that AKI occurred in 36.6% of hospitalized patients, and was particularly prominent in patients admitted to the intensive care unit or requiring invasive mechanical ventilation. 13 AKI also appears to be associated with higher admission and mortality rates ( Figure 1 ). The median urine specific gravity was J o u r n a l P r e -p r o o f high (1.020) and most patients (65.6%) had urinary sodium less than 35 mEq/L. Fairly high rates of proteinuria (2-3+ positive in 42.1%) and hematuria (2+ to 3+ positive in 46 .1%) were also observed.

Research on the pathophysiology of AKI in COVID-19 patients is ongoing.

Possible risk factors for AKI in COVID-19 patients can include hyper-/hypovolemia, nephrotoxins, secondary infections (i.e., sepsis), hypercoagulability, direct SARS-COV2 virulence, and impact of cytokine storm. Primary causes of AKI in COVID-19 include acute tubular injury (acute tubular necrosis), collapsing glomerulopathy, rhabdomyolysis, thrombotic microangiopathy, pauci-immune glomerulonephritis and kidney infarction. 14, 15, 16, 17 The most common pathology appears to be acute tubular injury, while the most common glomerular pathology found is collapsing glomerulopathy. Initial studies suggested direct SARS-CoV2 viral infection in the kidney. 18, 19 However, other evidence points to a lack of direct renal invasion, due to a possible lack of specificity for some immunohistochemical staining and the possibility that cellular components, such as clathrin-coated vesicles or multivesicular bodies, may have appeared as viral particles during these initial studies. 20, 21 Presence of underlying CKD has been associated with worse COVID-19 disease although granular data for different stages of kidney disease are limited. Two studies have found that 13% and 21% of patients hospitalized for severe COVID-19 illness also had underlying CKD at the time of admission, respectively. 22, 23 A meta-analysis by Henry et al found that presence of CKD diagnosis at the time of admission appears to be associated with increased risk of severe COVID-19 infection. 24 A study from a New J o u r n a l P r e -p r o o f York City hospital system found that patients with CKD and COVID-19 had a higher risk of mortality. 25 In the study 6.2% of the 3,391 patients with COVID-19 had CKD.

Patients with ESKD, especially those undergoing maintenance dialysis, are at higher risk of SARS-CoV2 infection. 26 Once infected, ESKD patients experience exponentially increased risk for severe COVID-19 disease. 26, 27, 28, 29 Most recent data suggest mortality rates approximating 20% in patients with ESKD depending upon their underlying co-morbidities or geographical region. Current management recommendations for these patients are similar to those for patients with severe COVID-19 disease and also include anti-metabolite reduction for transplant patients, which centers generally perform albeit based on limited data.

The use of certain medications in the context of COVID-19 has come under scrutiny; however, recommendations regarding use of RAAS inhibitors and avoidance of NSAIDs remain unchanged in the absence of any compelling data supporting the change in current practices.

Debate continues as to whether or not patients with COVID-19 receiving angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) are at increased risk for adverse outcomes. 30, 31, 32 Coronaviruses, such as COVID-19, bind to their target cells through ACE2, which is expressed by epithelial cells of the lung, intestine, kidney, and blood vessel. 33 However, there is no direct evidence to support an association with these agents specifically; and stopping these agents in some patients may exacerbate comorbid cardiovascular or kidney disease. 30, 34 On the basis of J o u r n a l P r e -p r o o f current evidence, RAAS inhibitors should be continued in patients in otherwise stable condition who are at risk for, being evaluated for, or have COVID- 19. There has been speculation regarding whether NSAIDs use increases the likelihood of contracting COVID-19 and/or exacerbate symptoms in people with COVID-19. Concern about possible negative effects of non-steroidal anti-inflammatory drugs NSAIDs was raised by reports about individuals with COVID-19 receiving NSAIDs early in the course of infection and experienced severe disease. 30, 33 There has also been speculation in the possible role as an anti-inflammatory, given the "cytokine storm" is believed to cause most of the negative outcomes of COVID-19. Current data shows no strong evidence in favor of or disputing use of NSAIDs with COVID-19

infection. CKD patients should be advised to avoid NSAIDs, as they can negatively impact kidney function. 35

It is essential to prevent and actively manage AKI in critically ill patients with COVID-19 to help decrease mortality. Supportive and critical care strategies should include adjustment of fluid balance according to volume responsiveness, hemodynamic monitoring in patients with kidney involvement, avoidance of nephrotoxins, and treatment of secondary infections and sepsis. 36 Volutrauma and barotrauma could be mitigated through the application of lung-protective ventilation, which may also lower the risk of AKI by limiting ventilation-induced hemodynamic effects. Volutrauma refers to lung injury due to overdistention during mechanical ventilation, while barotrauma refers to physical damage to body tissues caused by a difference in pressure between a gas space inside and the surrounding fluid. 37 Early and aggressive anticoagulation and J o u r n a l P r e -p r o o f efforts to inhibit cytokine release syndrome (CRS) should also be considered where appropriate. 38 Aggressive extracorporeal ultrafiltration may precipitate or worsen hypotension among COVID-19 patients with marked hemodynamic instability and/or refractory fluid overload. 39, 40 In these situations, initial support with CRRT can offer more consistency in ultrafiltration, greater hemodynamic tolerance, and less metabolic and osmotic fluctuations. 39 Patients with COVID-19 infection require frequent mobilization and pronation; therefore, alternative therapies, such as prolonged intermittent kidney replacement therapy (PIRRT), slow low-efficiency dialysis (SLED), and slow continuous ultrafiltration (SCUF) represent a reasonable compromise between continuous and intermittent modalities. 39 PIRRT can be considered as an alternative to continuous kidney replacement therapy (CKRT) if there is not sufficient equipment to meet demand. 41 Peritoneal dialysis has also been utilized in patients with COVID-19 and AKI during periods of increased demand. 38, 57 Indication for CKRT can include oliguria with refractory hypovolemia, hyperkalemia, severe acidosis and azotemia. Medium cutoff or high cutoff dialyzers, or hemadsorption devices for special cases can be considered. 39, 42, 43, 44 It is also important to ensure the availability of CRRT machines and additional supplies, ICU staff, special membranes, or sorbent cartridges, especially in an area of high COVID-19 incidence.

Comprehensive monitoring of CRRT in critically ill COVID-19 includes catheter position (after pronation), circuit patency (pressures), fluid balance, hemodynamics and delivered dialysate/filtrate/effluent rate. Approaches to management may evolve as additional studies and evidence become available.

Severely ill patients with COVID-19 are at elevated risk of multi-organ dysfunction due to CRS. Increased levels of IL-2, IL-6, IL-7, IL-8, IL-10, granulocytecolony stimulating factor (G-CSF), interferon INF-gamma, and TNF (tumor necrosis factor) have all been identified. 38 A dysregulated host response to infection can lead to multi-system organ failure. This process can depend on systemic inflammation from innate immunity and possibly severe immunosuppression from adaptive immunity.

Therapies, such as INF-gamma inhibitors, corticosteroids, intravenous immunoglobulin G (IVIG), TNF blockers, and tocilizumab have been postulated to be beneficial in the treatment of the cytokine storm. 38 Modalities that may aid cytokine removal or modulation include cascade hemofiltration, HVHF (high volume hemofiltration), highadsorption hemofiltration, plasmapheresis, hemoperfusion, and high cut off/medium cutoff membranes. 42 The aim of these interventions is to modify the cytokine-to-chemokine ratio from the tissues to the blood and/or decrease the peaks of cytokine concentrations.

The removal of cytokines via extracorporeal therapies has been an active area of study. 42, 44, 45 Extracorporeal treatments should theoretically not interfere with experimental antibody-based therapies used in COVID-19 (e.g., tocilizumab, convalescent plasma, intravenous immunoglobulins), as hemodialysis filters and hemadsorption cartridges do not remove antibodies. The size of these antibodies exceed the size of molecules that can be removed with extracorporeal treatments. Studies indicate that certain filters can remove inflammatory markers in critically ill COVID-19 patients. 42, 44, 45 However, further research is necessary to explain the outcomes related to these therapies.

Other therapies, such as hydroxychloroquine, vitamins, selenium, zinc and pyrithione have been proposed as treatments, but all lack substantial evidence for use in patients to treat COVID-19, including those with advanced kidney disease. 46 Remdesivir has been approved for severe symptoms in hospitalized patients with COVID-19. The use of remdesivir in the context of AKI in COVID-19 has been an area of research. Patients with advanced kidney disease were not included in remdesivir trials, due to concerns about the drug's potential toxicity among these patients. These concerns relate to remdesivir's actions and to the potential accumulation of its sulfobutylether-bcyclodextrin (SBECD) carrier. However, remdesivir has a limited duration of treatment (5-10 days) and a relatively low concentration of SBECD carrier. Therefore, the benefits may outweigh risk in select COVID-19 patients with eGFR <30 ml/min per 1.73m 2 . 47

Patients with advanced kidney disease, such as those with ESKD, are at increased risk of SARS-CoV-2 infection and complications of COVID-19 due to multiple risk factors, including older age, comorbid conditions (e.g., CVD, hypertension, diabetes, chronic lung disease), and an underlying immune-compromised state. Patients receiving maintenance dialysis are at high risk of SARS-CoV2 exposure because of their obligation to congregate frequently for prolonged periods with other patients, dialysis staff, and transportation providers. 48 Patients with advanced kidney disease are also more likely than the general population to reside in skilled nursing facilities, and have higher rates of hospitalization and doctor visits, further increasing risk of exposure.

Early reports on the prevalence and outcomes of SARS-CoV-2 infection in maintenance dialysis patients from Wuhan, China indicated low infection and mortality J o u r n a l P r e -p r o o f rates. However, a study from Xiong et al conducted a retrospective study on 65 centers in Wuhan, China and found a 2.1% incidence rate of COVID-19 among maintenance hemodialysis patients and a mortality rate of 31%. 49 Only about 50% of patients manifested fever; while about 20% of infected patients were asymptomatic. Studies from Europe also indicate high mortality among hemodialysis patients with COVID-19. 50, 51 Data from ERACODA (ERA-EDTA COVID-19 database for patients on dialysis or living with a kidney transplant) indicates that mortality in transplant patients is 18% and in dialysis patients is 20%. 52 A study using data from OpenSAFELY also found lower transmission rates, but high fatality among dialysis patients compared to the general population. 53 The diagnosis of an acute infection cannot be definitively made without microbiologic testing (reverse transcriptase polymerase chain reaction, or rtPCR).

However, testing all patients has been hampered by a limited test capacity and shortages in reagents and other testing supplies. High-priority individuals have been suggested to include symptomatic health care workers, symptomatic people who known risk factors for severe COVID-19 illness and hospitalized patients (in particular those who are critically ill with respiratory illness), 54 Despite their high risk for COVID-19, ESKD patients are not designated as mandatory screening cohort.

Antibodies most commonly become detectable 1-3 weeks after symptom onset.

Therefore it is possible for a person to have a positive viral testing result and a negative antibody testing result. Currently, there is no identified advantage of assays whether they test for IgG, IgM and IgG, or total antibody. 54 Antibody testing has not been standardized and availability for large dialysis organizations is limited. 48 Emotional and mental health check-ins for health care workers is also important.

Management of dialysis patients should be geared towards minimizing their risk of COVID-19 while making sure they are receiving adequate and proper treatments.

COVID-19 presents a catabolic state and patients should not miss their dialysis sessions to avoid the need for hospitalization from preventable causes such as hyperkalemia and hypervolemia. 57 Home dialysis offers a way to help minimize the risk of dialysis patient exposure by supporting social distancing, sheltering in place, and reduction of transportation needs.

Home dialysis requires most patients to visit the clinic once a month for evaluation, barring any complications. In most cases, the patient or the family member performs dialysis, which can also reduce stress on the healthcare workforce. One epidemiological study from Italy showed that the proportion of COVID -19 positive was significantly higher in in-center hemodialysis patient (3.55%) than patients on peritoneal dialysis (1.38%). 51 Multiple strategies can also be applied to help these at-risk patients remain home as much as they can, including utilizing telehealth capabilities (e.g., remote monitoring capability, telehealth platform) and drawing monthly labs at home as much as possible. 58 Contracted courier services can deliver monthly medications (e.g., for anemia and mineral bone disease) and collect samples (e.g., urine and dialysate to bring back to the unit if necessary). 51 

It is important to manage patients proactively in order to prevent hospitalization.

Periodic clinical evaluations can provide reassurance to patients while giving providers valuable updates on clinical status. Volume status should be closely monitored to reduce the risk of hospitalization. Measurements of routine clearances and membrane function can be suspended in areas of peak COVID-19 cases, as long as symptoms, blood urea nitrogen (BUN) and potassium are adequately controlled.

Incident home patients, those with peritoneal dialysis catheter complications, home hemodialysis patients with access trouble, and patients deemed unstable cannot avoid in-person visits. All screening measures described above should be carried out for these visits as well. 57 Patients who are newly started on peritoneal dialysis or home hemodialysis should preferably have a comprehensive first monthly visit at the clinic. 59 Screening and measures to mitigate COVID-19 risk for dialysis patients should also be performed as described above. 

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