INTRODUCTION — At the end of 2019, a novel coronavirus (ie, SARS-CoV-2) was identified as the cause of a cluster of pneumonia cases in Wuhan, a city in the Hubei Province of China. By 2020, it led to a pandemic that has spread throughout most countries of the world. SARS-CoV-2 disease (COVID-19) primarily manifests as a lung infection with symptoms ranging from those of a mild upper respiratory infection to severe pneumonia, acute respiratory distress syndrome, and death. COVID-19 disproportionately affects patients with preexisting comorbidities, such as patients with various types of kidney disease. All medical professionals, including nephrology clinicians, are tasked with rapidly adjusting their practice to curtail the spread of the virus while providing life-sustaining care to their patients.
This topic will discuss issues related to COVID-19 and delivery of nephrology care in patients with acute kidney injury, glomerular disease, chronic kidney disease, and hypertension. Issues related to the care of patients who have end-stage kidney disease or who are candidates for or have a kidney transplant are discussed separately. (See "COVID-19: Issues related to end-stage kidney disease" and "COVID-19: Issues related to solid organ transplantation".)
Other important aspects of COVID-19 that may affect this population are discussed at length elsewhere:
●(See "COVID-19: Epidemiology, virology, and prevention".)
●(See "COVID-19: Clinical features" and "COVID-19: Diagnosis".)
●(See "COVID-19: Infection prevention for persons with SARS-CoV-2 infection".)
●(See "COVID-19: Management in hospitalized adults".)
●(See "COVID-19: Myocardial infarction and other coronary artery disease issues".)
●(See "COVID-19: Questions and answers".)
ACUTE KIDNEY INJURY — Patients with suspected or confirmed COVID-19 may present with acute kidney injury (AKI) as part of their overall illness [1-6]. In a meta-analysis of approximately 13,000 mostly hospitalized patients, the incidence of AKI was 17 percent, although the range of AKI incidence in the included studies was broad (range 0.5 to 80 percent). Approximately 5 percent of patients required kidney replacement therapy (KRT) [6]. The incidence seems to vary by geographic location and proportion of critically ill patients included in each study.
While there are only limited data on temporal trends in the incidence of COVID-19-associated AKI, early data suggest that rates of AKI have declined over the duration of the pandemic, although the reason for these trends is unclear [7,8].
Clinical characteristics and histopathology — Kidney disease among patients with COVID-19 can manifest as AKI, hematuria, or proteinuria, and portends a higher risk of mortality [3,6,7,9-14]. It remains unclear if AKI is largely due to hemodynamic changes and cytokine release or if the virus also leads to direct cytotoxicity.
The reported incidence of AKI among patients with COVID-19, especially those who are hospitalized, varies depending upon the severity of disease in the patients who are studied. In two large observational studies of over 5000 patients hospitalized with COVID-19, AKI was noted among 32 to 37 percent of patients [4,7]. Among patients with AKI, approximately one-half had mild disease (1.5- to 2-fold increase in serum creatinine), and the remaining had moderate or severe disease (more than doubling of creatinine). AKI requiring KRT was noted in 12 to 15 percent of patients. AKI was associated with requirement for mechanical ventilation and with a longer duration of hospitalization. Approximately one-half of the patients with AKI did not achieve complete recovery of their kidney function by hospital discharge [7]. Independent predictors of AKI included being older, Black American, or male; having obesity, diabetes, hypertension, cardiovascular disease, low baseline estimated glomerular filtration rate (eGFR), or higher interleukin-6 level; or requiring mechanical ventilation or vasopressor medications [4,7,15]. Similar findings were reported in another study [13].
In another study of over 3000 critically ill adults with COVID-19, 21 percent developed severe AKI requiring KRT within two weeks of admission to the intensive care unit (ICU) [16]. The 28-day mortality among such patients was approximately 50 percent; risk factors for death included older age, oliguria, and admission to a hospital with relatively limited ICU resources. Of those patients who survived to discharge, 34 percent were KRT-dependent at the time of discharge and more than one-half of those patients were still KRT-dependent by two months. It is unclear if the KRT dependence is related to the severity of critical illness or to the specific pathophysiology related to COVID-19. Long-term outcomes among patients requiring KRT in the setting of COVID-19 have not been studied.
One study compared the incidence of AKI among hospitalized patients with and without COVID-19 [17]. The incidence of AKI was higher among the 2600 patients who had COVID-19 compared with over 19,500 patients who were hospitalized for other reasons (31 versus 18 percent). This higher incidence of AKI could not be explained by differences in the traditional risk factors for AKI between the groups. COVID-19 remained associated with a higher rate of AKI despite controlling for demographic variables, comorbidities, frequency of hypotension, selected laboratory results (eg, complete blood count, baseline eGFR), and use of nephrotoxic medications, vasopressors, or mechanical ventilation (adjusted hazard ratio 1.40, 95% CI 1.29-1.53). Markers of inflammation, such as C-reactive protein and ferritin, appeared to be higher among patients who had COVID-19 compared with those who did not have COVID-19. However, the comparison of AKI between groups controlling for these inflammatory markers was not possible because only a few patients without COVID-19 had these checked during their hospitalization. In another study that compared outcomes among patients with similar baseline comorbidities who were hospitalized either for influenza or COVID-19, those with COVID-19 had AKI at a higher frequency (41 versus 29 percent) and greater severity (stage 3 AKI in 26 versus 6 percent) [18]. In addition, the 90-day mortality was higher among patients who had COVID-19 compared with those who had influenza (35 versus 9 percent). These findings raise questions about the various mechanisms of AKI among patients with COVID-19.
Kidney histopathology was examined in an autopsy series of 42 patients who died with COVID-19 [19]. Mean age of the patients included was 72 years (range, 39 to 97 years); 88 percent were over the age of 60 years. Comorbidities, such as hypertension (73 percent), diabetes (42 percent), coronary artery or cerebrovascular disease (32 percent), obesity (31 percent), and chronic kidney disease (29 percent) were common; only two patients had no underlying comorbidities. AKI (mostly stage 3) was noted among 31 of 33 patients. Most patients (62 percent) exhibited varying degrees of acute tubular necrosis (ATN), one had collapsing focal segmental glomerulosclerosis (FSGS), and many had sequelae of their medical comorbidities (eg, hypertensive nephrosclerosis).
ATN was also the predominant kidney pathologic finding in other studies [3,20-25]. Glomerular lesions were reported in a minority of patients with COVID-19. In addition, COVID-19 may also be associated with renal infarction [26-31]. (See 'COVID-19 associated glomerular disease' below and "Renal infarction", section on 'Etiology and pathogenesis'.)
Whether SARS-CoV-2 causes a direct kidney infection remains controversial [32]. The presence of virus-like particles has been reported in the kidneys of patients with COVID-19 [24,33]. However, these may instead be endosomal subcellular structures (eg, clathrin-coated vesicles and multivesicular bodies) [34]. Ultrastructural in-situ hybridization used in some studies has confirmed presence of viral RNA [35] or viral proteins [10] in kidney tissue. Other studies have failed to demonstrate the presence of virus in the kidney [19-21].
Evaluation of AKI in hospitalized patients — In patients with suspected or confirmed COVID-19 who develop AKI, an emphasis should be placed on optimization of volume status to exclude and treat prerenal (functional) AKI while avoiding hypervolemia, which may worsen the patient's respiratory status.
The evaluation for other AKI etiologies should be undertaken in a manner similar to other critically ill patients with AKI. As an example, manual urine sediment examination should be performed, if appropriate, since urine samples are not considered to be highly infectious.
Management of AKI in hospitalized patients
AKI requiring dialysis — The indications for KRT for AKI remain the same regardless of the COVID-19 status of any given patient.
Several issues specific to KRT in patients with COVID-19 are discussed below:
●Circuit thrombosis during KRT occurs more frequently in patients with COVID-19 than in other patients [36,37]. In the absence of contraindications, patients with COVID-19 should receive anticoagulation during KRT. This can be in the form of regional anticoagulation using unfractionated heparin or citrate, or systemic anticoagulation with unfractionated or low-molecular-weight heparin. Based on low quality data, regional citrate anticoagulation appears to be less effective among COVID-19 patients [36,37]; the reason for this is unclear. Additional details regarding anticoagulation for the hemodialysis procedure are presented separately, as is the issue of hypercoagulability in the setting of COVID-19. (See "Anticoagulation for the hemodialysis procedure" and "Anticoagulation for continuous kidney replacement therapy" and "COVID-19: Hypercoagulability".)
●For patients on continuous kidney replacement therapy (CKRT), no special provisions or methods for disposal of the CKRT effluent are necessary. This is because neither presence of SARS-CoV-2 nor other similar viruses have been demonstrated in the effluent.
●Extracorporeal hemoperfusion devices for cytokine removal, such as Cytosorb, have had no clear role in management of sepsis prior to the COVID-19 pandemic. Due to lack of proven benefit, we do not use Cytosorb or other similar devices among critically ill COVID-19 patients with or without dialysis-requiring AKI. (See "Investigational and ineffective therapies for sepsis", section on 'Cytokine and endotoxin inactivation or removal'.)
AKI not requiring dialysis — Patients who have AKI that is not dialysis-requiring should be managed with limited contact as much as possible. Physical examination and ultrasound evaluations should be coordinated with the primary/consulting teams to minimize contact, when possible.
Differences in management of AKI among patients with COVID-19 may include limited use of intravenous fluids. Most patients with COVID-19 characterized by pneumonia have variable degree of oxygen requirements and/or airway control. Fluid resuscitation goals are understandably conservative as per various acute respiratory distress syndrome criteria. Thus, fluid resuscitation should be individualized and based on trackable objective measures (eg, inferior vena cava collapse on ultrasound).
Kidney function impairment after AKI — The risk of developing chronic kidney disease (CKD) is high in patients with COVID-19-associated AKI. In an observational study from the United Kingdom, 16 percent of patients with AKI progressed to CKD by 90 days [38]. Similarly, in a study of United States veterans who survived at least 30 days after COVID-19 infection, the annual decrease in eGFR relative to controls not infected with COVID-19 was 3.3, 5.2, and 7.7 mL/min/1.73 m2 in nonhospitalized patients, hospitalized patients, and patients requiring intensive care, respectively [39]. Corresponding decreases in eGFR were even more pronounced in patients who had COVID-19 associated AKI.
GLOMERULAR DISEASE
COVID-19 associated glomerular disease — Glomerular lesions were reported in a minority of patients with COVID-19, with collapsing focal segmental glomerulosclerosis (FSGS), also called COVID-associated nephropathy (COVAN), being the most common [20]. Such patients present with nephrotic-range proteinuria and acute kidney injury (AKI) [9,11,25,40-44]. Similar to HIV-associated nephropathy, COVAN occurred exclusively in Black individuals, and a high proportion tested possessed high-risk APOL1 genotypes [25,44]. (See "Collapsing focal segmental glomerulosclerosis not associated with HIV infection", section on 'Genetic factors'.).
Thrombotic microangiopathy is another uncommon finding among patients who develop AKI and nephrotic-range proteinuria [25]. There are case reports of other glomerular diseases associated with COVID-19, including antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis [45], anti-glomerular basement membrane antibody disease [46], and IgA nephropathy [47].
COVID-19 vaccine-associated glomerular disease — Both de novo glomerular disease and relapse of preexisting glomerular disease have been reported shortly after administration of COVID-19 messenger RNA (mRNA) vaccines (Moderna mRNA-1273 and Pfizer-BioNTech BNT162b2) [48-60]. (See "COVID-19: Vaccines".)
However, these are overall rare and a causal link with the COVID-19 vaccine is not firmly established. Our approach to COVID-19 vaccination among patients with glomerular disease is discussed below. (See 'COVID-19 vaccination in patients with glomerular disease' below.)
The following de novo glomerular diseases have been described following COVID-19 vaccination:
●IgA nephropathy [48,49]
●Anti-neutrophilic cytoplasmic antibody (ANCA)-associated vasculitis [48]
●Minimal change disease [50-53,61]
●Anti-glomerular basement membrane (anti-GBM) nephritis [49]
In addition, a relapse of the following glomerular diseases has been reported following COVID-19 vaccination:
●IgA nephropathy [54-56]
●Minimal change disease [57-59]
●Primary membranous nephropathy [60]
●Complement-mediated thrombotic microangiopathy (C-TMA) [62]
Data delineating the risks of new onset or relapse of glomerular disease in the setting of COVID-19 vaccination are sparse. In an observational Swiss study, COVID-19 vaccination was not associated with a higher risk of incident glomerular disease [63]. In a cohort study of patients with preexisting glomerular disease, exposure to a second or third (but not first) COVID-19 vaccine dose was associated with a doubling of risk of relapse [64]. However, the increase in absolute risk of relapse associated with COVID-19 vaccination in this study was small: 1 to 2 percent for ANCA-associated vasculitis, minimal change disease, membranous nephropathy, and FSGS, and 3 to 5 percent for IgA nephropathy and lupus nephritis.
Modifications to the management of preexisting glomerular disease — Patients with glomerular disease who are treated with immunosuppressive therapies may be at a heightened risk of infections (COVID-19 or other infections). However, there are no rigorous studies to guide pandemic-related modifications to the treatment of glomerular disease. We modify the immunosuppressive therapy in some patients with glomerular disease depending upon their risk of progression to end-stage kidney disease and the local transmission of COVID-19 [65].
Among patients who are at low risk of acquiring COVID-19 because of limited community transmission and their ability to self-isolate (eg, ability to work from home and have limited or no interaction with outsiders), we continue with their previously planned treatment for their glomerular disease. Additionally, we reinforce the risks and benefits of undergoing immunosuppressive therapy in the context of the pandemic to ensure adherence to strict isolation while on treatment.
Among patients who are at risk of acquiring COVID-19 due to regional transmission rates and other factors (eg, inability to quarantine because of their occupation), we take the following approach:
●If the patient's glomerular disease is being treated with calcineurin inhibitors or hydroxychloroquine, no treatment modification is necessary (these drugs do not increase the risk of COVID-19).
●However, among other patients at risk of acquiring COVID-19, we modify our approach as follows:
•For patients who are not yet on immunosuppressive therapy for their glomerular disease, we postpone treatment among the following groups:
-Patients with membranous nephropathy who have uncomplicated nephrotic syndrome and preserved estimated glomerular filtration rate (eGFR)
-Patients with IgA nephropathy who do not have features associated with a high risk of progression (eg, heavy proteinuria, impaired eGFR, or crescents on histopathology)
-Patients who have glomerular diseases for which it is unclear that immunosuppressive therapy is beneficial (eg, infection-related glomerular disease)
•For patients who were initiated on immunosuppressive therapy before the pandemic and who are not yet in remission, an individual risk-benefit assessment is needed regarding continuation of such therapy. According to institutional policies, arrangements should be made for administration of necessary intravenous (IV) infusions at home rather than in an institutional infusion center. In addition, when possible, IV infusions should be changed to equivalent oral alternatives. As examples:
-IV cyclophosphamide could be changed to either oral cyclophosphamide or oral mycophenolate mofetil
-IV pulse methylprednisolone could be changed to either oral high-dose prednisone or oral methylprednisolone
In patients who have glomerular diseases for which there is no widely accepted immunosuppressive strategy (eg, glucocorticoid-resistant FSGS), we avoid cytotoxic drugs (eg, cyclophosphamide), rituximab, and antimetabolites (eg, mycophenolate mofetil).
•For patients who were initiated on immunosuppressive therapy before the pandemic and who are already in remission, we lower the doses of their immunosuppressive medication to a minimum level that will maintain remission. Among patients who have been in remission for >12 months, we favor immediate cessation of antimetabolites, such as mycophenolate mofetil or azathioprine, and avoidance of maintenance rituximab infusions.
•For patients with glomerular disease who are receiving immunosuppressive therapy that includes antimetabolites and who have suspected or confirmed COVID-19, we discontinue antimetabolites for 7 to 10 days after symptom onset. In addition, among patients who are on long-term glucocorticoids and who require hospitalization for moderate to severe COVID-19, we also administer stress-dose glucocorticoids. Patients with nephrotic-range proteinuria who receive hydroxychloroquine or azithromycin for treatment of COVID-19 should have an electrocardiogram performed to check the corrected QT interval. This is because patients with nephrotic syndrome can have a low ionized calcium.
•For patients with glomerular disease who are enrolled in research studies that entail having kidney biopsies purely for research purposes (rather than for clinical decision-making), such biopsies should be postponed or cancelled.
COVID-19 vaccination in patients with glomerular disease — Our approach to COVID-19 vaccination depends upon the timing of the onset or relapse of the glomerular disease (see 'COVID-19 vaccine-associated glomerular disease' above):
●Glomerular disease not associated with vaccination – Among patients who develop glomerular disease (de novo or relapse) that is not temporally associated with a COVID-19 vaccination (ie, disease that occurs >30 days after an administered vaccine), we encourage vaccinations as recommended for the general population. For patients whose immunosuppressive therapy consists of rituximab and for whom delaying therapy would be safe, we administer rituximab four to six weeks after COVID-19 vaccination. Other relevant pandemic-related treatment modifications are discussed above. (See 'Modifications to the management of preexisting glomerular disease' above.)
●Glomerular disease associated with vaccination – Among patients who develop glomerular disease (de novo or relapse) that is temporally associated with a COVID-19 vaccination (ie, disease that occurs ≤30 days after an administered vaccine), it is possible that an additional dose of the vaccine will adversely impact their kidney function. The decision to proceed with additional vaccine doses for such patients should be based upon shared decision-making with the patient. The discussion of risks and benefits of vaccination should be individualized in context of the patient's type and severity of glomerular disease and whether or not they are in remission by the time of the next scheduled dose [66]. As examples, patients with minimal change disease who achieve remission or those with self-limited IgA nephropathy could receive an additional scheduled dose of vaccine. Conversely, patients with ANCA-associated vasculitis, C-TMA, or anti-GBM disease should likely not receive an additional dose.
CHRONIC KIDNEY DISEASE AND HYPERTENSION — Among patients with COVID-19, both chronic kidney disease (CKD) and hypertension are risk factors for more severe disease [67-73]:
●In a meta-analysis of four studies and 1389 infected patients (including 273 patients with severe disease), the prevalence of underlying CKD was more frequent among those with severe disease (3.3 versus 0.4 percent; odds ratio 3.03, 95% CI 1.09-8.47) [70].
●In the same cohort of 1389 patients from these four studies, history of hypertension was more common among those who had severe, as compared with nonsevere, COVID-19 (15 versus 32 percent) [70]. Similarly, in a separate cohort of 1590 hospitalized patients in China, underlying hypertension was independently associated with severe COVID-19 (hazard ratio 1.58, 95% CI 1.07-2.32) [67]. While some studies conducted in the United States and Italy reveal broadly consistent findings [68,69], others suggest that hypertension is not an independent risk factor for severe COVID-19 [71].
Renin angiotensin system inhibitors — Patients receiving angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) should continue treatment with these agents (unless there is an indication for discontinuation such as hyperkalemia or hypotension). There is no evidence that stopping ACE inhibitors or ARBs reduces the severity of COVID-19 [74-79]. In addition, studies conducted prior to the COVID-19 pandemic suggest that discontinuing ACE inhibitors and ARBs in some patients may exacerbate underlying cardiovascular or kidney disease and lead to increased mortality [80-82]. This approach is supported by multiple guideline panels [83-87].
There was speculation that patients with COVID-19 who are receiving these agents may be at increased risk for adverse outcomes [88,89]. ACE2 is a receptor for SARS-CoV-2 [90] and some, but not all, evidence suggests that renin angiotensin system inhibitors may increase ACE2 levels [91-94]. In addition, patients with cardiovascular disease, hypertension, and diabetes (a disorder with a high prevalence of renin angiotensin system inhibitors-treated use) often have a more severe clinical course in the setting of infection with SARS-CoV-2.
However, there is no evidence to support discontinuation of renin angiotensin system inhibitors in patients diagnosed with COVID-19. The best data come from a trial of 740 hypertensive adults hospitalized for mild or moderate COVID-19 who were taking either an ACE inhibitor or ARB prior to hospitalization; patients were randomly assigned to continue or discontinue their ACE inhibitor or ARB for 30 days [74]. Compared with those assigned to discontinue therapy, those who continued taking an ACE inhibitor or ARB had statistically similar 30-day mortality (2.8 versus 2.7 percent), need for mechanical ventilation (7.7 versus 9.6 percent), shock requiring vasopressors (7.1 versus 8.4 percent), and median length-of-stay (five days in each group).
The conclusions of this trial are supported by multiple, large observational studies, most of which found no relationship between the use of ACE inhibitors or ARBs and severity of COVID-19 [68,69,75-79,95-97], although some suggested that these drugs may attenuate the severity of disease [72,98-103]. In addition, a meta-analysis of 14 trials that randomly assigned 1838 patients with COVID-19 to either renin angiotensin system inhibitor therapy (ie, continuing or initiating ACE inhibitor or ARB) or to no renin angiotensin system inhibitor therapy (ie, placebo or discontinuation of ACE inhibitor or ARB) reported similar rates of all-cause 30-day mortality in both treatment arms (7.2 percent versus 7.5 percent) [104].
Dialysis access planning in advanced CKD — Patients with stage 4 or 5 CKD who are referred for dialysis access placement should undergo these procedures as planned (and not have their planned procedure deferred).
Although nonessential surgeries should be delayed during the COVID-19 pandemic, guidance from the United States has clarified that placement of arteriovenous fistulas or grafts for hemodialysis and peritoneal dialysis catheters for peritoneal dialysis are essential procedures [105,106].
MANAGING DIALYSIS DURING CRITICAL SHORTAGES — During surges in cases of COVID-19 that result in unanticipated, critical shortages of health care providers and/or equipment, alterations in kidney replacement therapy (KRT) management may be necessary. These include some or all of the following:
●Patients with COVID-19 who require KRT should be colocalized on a floor or ICU, when possible. Colocalization within adjacent rooms can enable one dialysis nurse to simultaneously deliver dialysis to more than one patient. If a patient is in a negative-pressure isolation room, then one hemodialysis nurse will need to be dedicated for the care of that patient in a 1:1 nurse-to-patient ratio.
●If possible, patients with suspected or confirmed COVID-19 who are not critically ill but who require KRT should be dialyzed in their isolation room rather than being transported to the inpatient dialysis unit.
●Even among patients who are hemodynamically stable and could tolerate intermittent hemodialysis, continuous kidney replacement therapy (CKRT) or prolonged intermittent kidney replacement therapy (PIKRT; also called sustained low-efficiency dialysis or SLED) should be performed instead, depending upon machine and staffing availability. This is because CKRT or PIKRT can be managed without 1:1 hemodialysis nursing support. This would potentially help minimize wastage of personal protective equipment and limit exposure among hemodialysis nurses.
●CKRT machines can either be placed inside an isolation room as per standard practice or outside the room with the use of extended tubing. Placing the machine outside of the room minimizes the need for repeated entry to troubleshoot and manage the machine, and therefore reduces wastage of personal protective equipment. However, extended tubing is a scarce resource. In addition, use of extended tubing requires additional tubing connections and increases the likelihood that tubing will become disconnected. Extended tubing also decreases the sensitivity of pressure alarms to detect disconnection of the venous lines and potentially increases the risk of clotting due to the longer tubing length.
●If CKRT capacity at an institution is overwhelmed, CKRT machines can be used to deliver prolonged intermittent treatments (eg, 10 hours rather than continuous) with higher flow rates (eg, 40 to 50 mL/kg/hour). Alternatively, the machine can be rotated between patients every 24 hours or whenever the circuit clots so that use of new filter sets is minimized. This will enable the CKRT machine to become available sooner for care of another patient after terminal cleaning.
●Institutions facing scarcity of replacement fluid for CKRT can lower the delivered dose to 15 mL/kg/hour from the standard 20 to 25 mL/kg/hour, especially among patients who are not hypercatabolic. One institution developed a real-time tracking system to account for and plan redistribution of scarce replacement fluid [107].
When supplies of commercially prepared replacement fluid are exhausted, institutional pharmacies may develop their own replacement fluid by mixing all of the following (in a sterile fashion) [108]:
•1 L of 0.9 percent saline with potassium chloride as needed
•1 L of 5 percent dextrose water with 150 mEq sodium bicarbonate
•1 L of 0.9 percent saline with 1 g magnesium chloride
•1 L of 0.9 percent saline with 1 g calcium chloride
This will yield a 4 L solution containing 153 mEq/L sodium, 37.5 mEq/L bicarbonate, 2.6 mmol/L magnesium, 2.25 mmol/L calcium, and a variable amount of potassium.
Other methods for preparation of dialysate solutions have been formulated at the Cleveland Clinic and Johns Hopkins Hospital [109] in the United States and Guy's and St Thomas' National Health Service Foundation Trust in the United Kingdom [110].
●When available hemodialysis or CKRT machines are scarce, clinicians may need to consider treatment of AKI with peritoneal dialysis [111-116]. Important considerations include:
•Patients with AKI who are treated with peritoneal dialysis have similar rates of all-cause mortality, kidney function recovery, and infectious complications compared with patients treated with other modalities. (See "Use of peritoneal dialysis (PD) for the treatment of acute kidney injury (AKI) in adults", section on 'Outcomes with PD for AKI'.)
•Peritoneal dialysis requires relatively less equipment, infrastructure, and resources relative to other forms of KRT. Nurses and clinicians can be trained expeditiously to provide peritoneal dialysis. (See "Use of peritoneal dialysis (PD) for the treatment of acute kidney injury (AKI) in adults", section on 'Outcomes with PD for AKI'.)
•Peritoneal dialysis can increase intra-abdominal pressure, interfere with respiratory mechanics [117], and may theoretically worsen respiratory failure, particularly among mechanically ventilated patients. However, it can be used among mechanically ventilated patients when other options such as intermittent hemodialysis and CKRT are not available. Performing peritoneal dialysis in a mechanically ventilated patient who requires a prone position may be challenging although one case report found it to be feasible and safe [118]. (See "Use of peritoneal dialysis (PD) for the treatment of acute kidney injury (AKI) in adults", section on 'Complications of PD for AKI'.)
•When peritoneal dialysis is used for management of AKI in patients with COVID-19, automated peritoneal dialysis with a cycler should be used, if available. This minimizes the contact between health care personnel and the patient. (See "Use of peritoneal dialysis (PD) for the treatment of acute kidney injury (AKI) in adults", section on 'Selecting PD modalities for AKI'.)
•Similar to disposal of peritoneal dialysis effluent for patients with end-stage kidney disease, there is a range of opinions for safe disposal of the effluent in the setting of AKI. Data suggesting that peritoneal dialysis effluent is infectious are lacking [112]. (See "COVID-19: Issues related to end-stage kidney disease", section on 'Hospitalized patients'.)
INFECTION CONTROL PRACTICES — Infection control practices specific to the care of patients with kidney disease requiring dialysis are presented in the preceding discussions.
The general approach to infection control in the health care setting, in the home, and in non-hospital institutional settings, as well as the approach to discontinuation of COVID-19 precautions and return-to-work for health care personnel, are presented in detail elsewhere. (See "COVID-19: Infection prevention for persons with SARS-CoV-2 infection".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: COVID-19 – Index of guideline topics".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: COVID-19 overview (The Basics)" and "Patient education: COVID-19 vaccines (The Basics)")
SUMMARY AND RECOMMENDATIONS
●COVID-19 and kidney disease – SARS-CoV-2 disease (COVID-19) disproportionately affects patients with various types of kidney disease. Nephrology clinicians are tasked with rapidly adjusting their practice to curtail the spread of the virus while providing life-sustaining care to their patients. (See 'Introduction' above.)
●Kidney replacement therapy during critical shortages – During surges in cases of COVID-19 that result in unanticipated, critical shortages of health care providers and/or equipment, alterations in kidney replacement therapy (KRT) management may be necessary. These include some or all of the following (see 'Managing dialysis during critical shortages' above):
•Patients with COVID-19 should be colocalized on a floor or intensive care unit (ICU), when possible. Colocalization within adjacent rooms can enable one dialysis nurse to simultaneously deliver dialysis for more than one patient. If a patient is in a negative-pressure isolation room, then one hemodialysis nurse will need to be dedicated for the care of that patient in a 1:1 nurse-to-patient ratio.
•When possible, patients with suspected or confirmed COVID-19 who are not critically ill should be dialyzed in their own isolation room rather than being transported to the inpatient dialysis unit.
•Continuous kidney replacement therapy (CKRT) is preferred among critically ill patients in the ICU who have end-stage kidney disease (ESKD) or acute kidney injury (AKI). Even among patients who are hemodynamically stable and who could tolerate intermittent hemodialysis, CKRT or prolonged intermittent kidney replacement therapy (PIKRT), also called sustained low-efficiency dialysis (SLED), should be performed instead, depending upon machine and staffing availability. This is because CKRT or PIKRT can be managed without 1:1 hemodialysis support. This would potentially help minimize wastage of personal protective equipment and limit exposure among hemodialysis nurses.
•If CKRT capacity at an institution is overwhelmed, CKRT machines can be used to deliver prolonged intermittent treatments (eg, 10 hours rather than continuous) with higher flow rates (eg, 40 to 50 mL/kg/hour). This will enable the CKRT machine to become available sooner for care of another patient after terminal cleaning.
•When available hemodialysis or CKRT machines are scarce, clinicians may need to consider treatment of AKI with peritoneal dialysis. (See "Use of peritoneal dialysis (PD) for the treatment of acute kidney injury (AKI) in adults".)
●AKI in hospitalized patients – In patients with suspected or confirmed COVID-19 who develop AKI, an emphasis should be placed on optimization of volume status to exclude and treat prerenal (functional) AKI while avoiding hypervolemia, which may worsen the patient's respiratory status. Patients who have AKI that is not dialysis-requiring should be managed with limited contact as much as possible. Physical examination and ultrasound evaluations should be coordinated with the primary/consulting teams to minimize contact, when possible. (See 'Evaluation of AKI in hospitalized patients' above and 'AKI not requiring dialysis' above.)
●COVID-19 and glomerular disease – Both COVID-19 and vaccination against COVID-19 may be associated with the development of glomerular disease. In addition, due to the heightened risk of infection among immunosuppressed patients, those who have preexisting glomerular disease may require modifications to their management plan during the COVID-19 pandemic. (See 'Modifications to the management of preexisting glomerular disease' above and 'COVID-19 vaccination in patients with glomerular disease' above.)
●COVID-19 and renin angiotensin system inhibitors – Patients receiving angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) should continue treatment with these agents (unless there is an indication for discontinuation such as hyperkalemia or hypotension). There is no evidence that stopping ACE inhibitors or ARBs reduces the severity of COVID-19. (See 'Renin angiotensin system inhibitors' above.)
●Access planning – Patients with stage 4 or 5 CKD who are referred for dialysis access placement should undergo these procedures as planned (and not have their planned procedure deferred). (See 'Dialysis access planning in advanced CKD' above.)
