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Introduction

Acute kidney injury (AKI), previously referred to as acute renal failure, is a complex medical condition that has many facets and affects the renal system in multiple ways. An AKI impacts the patient’s length of stay, increases the cost of care, and utilizes resources.  

AKI manifests itself in many diagnoses, which include a temporary condition that resolves without harm, a short-term condition with minimal harm, an insidious insult to kidney function, and chronic injury that leads to permanent kidney damage. Due to the prevalence of AKI, understanding this condition, its assessment parameters, treatment options, and quality outcome monitoring and reporting is essential. 

Defining AKI 

What is an AKI? 

What is an AKI? 

It is a global term used to describe all types of impaired or reduced kidney function. AKI was previously known as acute renal failure. The Kidney Disease Improving Global Outcomes (KDIGO) Foundation published guidelines for a consistent definition and criteria for AKI plus recommended treatment strategies.  

However, a standard definition has not been adopted into clinical practice and varies by organization. Although the KDIGO guidelines are the most used, the Acute Kidney Injury Network (AKIN) and RIFLE (risk of renal failure, injury to the kidney, failure of kidney function, loss of kidney function, and end-stage renal disease) are also used [3]. 

The following are three examples of how AKI is defined: 

1. AKI is described as an abrupt (less than two days) decrease in kidney function, which encompasses both injuries [7].
2. 2. KDIGO definition includes any of the following:
3. Increase in serum creatinine (SCr) by X0.3 mg/dL or more in 2 days (48 hours)
4. Increase in serum creatinine 1.5 times or greater than the patient’s baseline from the prior week (7 days)
5. Urine output less than 0.5 mL/kg/hour over at least 6 hours [3]. 

 There is a similarity between these two definitions, but additional research is needed to reach global consensus on the definition for AKI. 

Incidence 

Identification of the incidence of AKI is typically identified from data collected on inpatient admissions.  Published data depicted an AKI incidence of 5.0% to 7.5% of hospitalized patients, and 50-60% of these patients are within the intensive care units [2]. In 2020, our world turned upside down with the emergence of the COVID-19 pandemic; healthcare as we knew it changed drastically. The impact of COVID-19 on short- and long-term health is still being determined.  

A small clinical investigation conducted on COVID -19 patients identified that AKI was present in 36% of diagnosed hospitalized patients, and there was a 35% mortality rate [4].. Although the results of this study were small; it demonstrates a five-fold increase from the previous study. Thus, more research about the impacts of the pandemic on patient kidney health is needed.    

Drug-induced AKI is a significant portion of the condition. However, data on the prevalence of drug-induced AKI is limited and inconsistent. Published literature shared that 20%-40% of hospitalized patients with acute kidney injury were drug-induced AKI. Furthermore, medication induced AKI could be represented in up to 60% of elderly patients [2]. Variation in AKI definition coupled with inconsistent data definitions could be a limiting factor in obtaining more specific statistical information and research. 

Identification of AKI  

The identification of AKI begins with a thorough physical assessment and in-depth patient history to determine the risk for or confirmation of AKI and its timeline of progression.  Ideally, the early risk assessment for a community-based population should occur in a primary care physician’s office. However, this is not always the case when acute kidney injury occurs, due to the nature of an acute-onset illness. If detected early, providing early intervention and hospitalization may help decrease severity and lessen the likelihood of disease progression to potential chronic kidney disease (CKD) [3].   

A comprehensive history and physical examination are warranted if acute kidney injury is suspected. The history portion should include evaluating current and past medical diagnoses, and urine output and characteristics. The healthcare provider should also review current and past prescriptions, including over-the-counter medications. Nonsteroidal anti-inflammatory drugs (NSAIDs) are a contributing cause of AKI, especially in the elderly population [3].     

The physical exam should be detailed and include objective data of blood pressure, heart rate, respiratory rate, pulse oximetry, and actual weight. AKI identification should include the orthostatic vital signs as well. A thorough review of systems (ROS) is needed with focus attention to the following systems: 

1. Skin – livedo reticularis, digital ischemia, butterfly rash, and purpuras to suggest vasculitis. Track marks may suggest endocarditis in an IV drug user, which can contribute to acute kidney injury [3].     
2. Eyes and ears – jaundice in liver disease, band keratopathy in multiple myeloma, signs of diabetes mellitus, and signs of hypertension. [3].     
3. Cardiovascular system – pulse rate, blood pressure, and jugular vein distention (JVD) in establishing the patient’s volume status, especially if there is presence of fluid overload. An irregular heart rhythm, murmur, or friction rub may indicate electrolyte imbalance-related arrhythmias or other potential causes [3].     

Risk Factors 

During the history and physical, it’s important to assess for factors that put the patient at risk for AKI.  Risk factors are patient-specific genetics, behavioral, health care insults, and medications. The table below lists the more common predisposing factors that increase patient risk for AKI for your review. The risk factors are identified in various portions of the history, not necessarily during the review of kidney function. Implementing a simple risk assessment tool that is used to routinely collect information applicable for both the community-based and acute care patients would provide consistency in care as the patient travels across the continuum [1].    The use of a risk assessment tool is the easy part; the challenge is the adoption and consistency, especially between healthcare organizations or during a transfer of patient care.  

Common Predisposing Factors for AKI

Diagnostic Studies  

Initial diagnostic studies may include a complete blood count (CBC), comprehensive metabolic panel (CMP), and urinalysis. These tests are to evaluate the patient’s serum creatinine , urea, electrolytes, blood counts, liver function , glucose level, , and urine A renal ultrasound may also be performed to exclude obstruction [2,3].     

The glomerular filtration rate (GFR) is widely accepted as the best overall index of kidney function.  However, GFR is difficult to measure and is commonly estimated from the serum level of endogenous filtration markers, such as creatinine. Because it’s  complexity, serum creatinine is commonly used to diagnose acute kidney injury [3]. 

The volume of urinary output (UO) is another measurement for diagnosing and monitoring AKI with some limitations. Oliguria typically indicates  AKI, while sudden anuria suggests potential presence of a urinary tract obstruction or acute glomerulonephritis. Gradually diminishing urine output can be secondary to urethral stricture or obstruction related to prostate enlargement or an early indicator of AKI [3].     

However, the decrease or absence of urinary output is not specific to AKI. Changes in volume of UO may also be attributed to dehydration, urinary tract infection, tubular injury, hypovolemia, and hypertension [2, 3].    To make an AKI diagnosis, a comprehensive assessment and patient workup are required. 

Kidney Function 

The kidneys are essential organs for the maintenance of a healthy life. Any insult to the kidneys can impact their function and potentially interfere with the quality of an individual’s daily activities and life expectancy. Insult or decrease in kidney function can be separated into three board categories.  

1) Interference with blood flow to the kidney, also known as prerenal.  

2) Causes within the kidney, also known as intrarenal.  

3) Obstruction or growth that prevents kidney output, also known as postrenal [3.  

It is important to identify the cause of the insult so the appropriate treatment plan can be identified and implemented.  ​

Renal System: Basic Review 

The kidneys are part of the renal system, which includes three structures, the kidney, ureters, and urethra. Typically, a person has two kidneys that are each  four to five inches long. However, people can live with only one functioning kidney. The other kidney may be nonfunctioning, a birth defect, or simply removed due to disease, injury, or through organ donation [8,9].  

The kidney’s main role is blood filtration. Blood enters the kidneys via the renal artery. The kidneys are comprised of many nephrons. The nephron, which is the filter system, has two parts. The first is the glomerulus which separates nutrients and waste from the bloodstream. The second is the tubules, which return the nutrients to the body via the renal vein. The wastes travel (aka urine) in the bladder for elimination. The kidneys process approximately 200 liters per day, but only a portion of this amount  are eliminated as urine [9]. 

While the filtration of the blood is the main function of the kidneys, they have other responsibilities, too; including the production of hormones to help blood pressure control, stimulate red blood cell  production, and keeping bones strong and healthy [8,9].  

Nephrotoxicity and Kidney Function Affected   

Medications are a huge part of the healthcare treatment plan. Patients with comorbiditiessuch as acute or chronic liver disease, heart disease, pulmonary hypertension, malignancies and surgery are at greater risk for drug-induced AKI.   

Different classes of medication attack different parts of the kidney function and structure. Patients who take nonsteroidal anti-inflammatory drugs (NSAIDs), renin-angiotensin-aldosterone system blockers, high dose system vasoconstrictors, and calcineurin inhibitors are at risk for developing prerenal AKI because of decrease glomerular pressure [2,3]. 

A type of intrarenal injury, acute tubular necrosis (ATN) results from aminoglycosides, vancomycin, radiocontrast media, cisplatin, amphotericin B, foscarnet, and osmotically active agents [2,3]. 

Acute interstitial nephritis (AIN) defects occur from antimicrobials such as b-lactams, sulfa-based drugs, quinolones, anti-ulcer agents, anticonvulsants, and diuretics [2,3]. 

Postrenal injury due to crystal-induced luminal obstruction can occur from patients exposed to acyclovir, ciprofloxacin, and methotrexate. There is also an abundance of other common medications that can cause glomerular disease, impacting kidney function [2,3]. 

Monitoring prescribed medications for potential risk to a patient’s kidney function is the responsibility of all healthcare providers. New medications incorporated into the treatment plan should be reviewed with all current medications to determine if an additional risk to AKI is present. ’It first starts with the prescribing provider and then the pharmacist should also review the patient’s medications before dispensing the medication. Furthermore, if the patient is hospitalized, the final review is with the nurse administering the medication.  

Treatment of AKI and the Role of the Nurse 

The treatment plan for AKI is dependent on the identified underlying cause and may require multiple interventions for treatment. The patient’s treatment plan is individualized and is based on the diagnosis (pre, intra, or postrenal), symptoms, and comorbidities.   The healthcare provider and team are responsible for the treatment plan. Furthermore, the nurse is integral to implementation, monitoring, and education of the patient in treatment goals. 

The types of treatments include [2,3]. 

• Necessity of fluid therapy is based on the patient’s hemodynamic status (hypovolemic or hypervolemic) .   
  • The nurse plays an  integral role through  assessment, monitoring vital signs (VS), hemodynamic status, and urinary output, and contacting the healthcare provider when deviations from the patient’s baseline occur.  
• Use of vasopressors, if necessary.  
  • If the patient becomes hemodynamically unstable, vasopressors or other medications may be required. The nurse should alert the healthcare provider immediately if symptoms appear.’  
• Use of diuretics and urinary output monitoring.   
  •  Measures the patient’s urine output, which is traditionally done using an indwelling urinary catheter (IUC). However, nurses are patient advocates and should  promote utilizing alternative urine output measurements whenever feasibly possible. 
• Identifying and managing drug-induced nephrotoxicity.   
  • Patient assessment and continuous monitoring of diagnostic results is vital for early recognition of drug-induced nephrotoxicity. When multiple medications are used to manage patient care, it becomes more important to pay attention to critical lab values and patients’ symptoms.  
• Renal Replacement Therapy  
  •  Renal replacement therapy is sometimes necessary in an acute care setting to remove a buildup of toxins in the body and help to eventually restore kidney function. Examples of renal replacement therapies include hemodialysis (HD), continuous renal replacement therapy (CRRT)slow, low-efficiency dialysis (SLED), and peritoneal dialysis (PD). These procedures are well established, and the nurse typically has standards of care, algorithms, or specialized training to implement these complicated procedures when ordered by the healthcare provider.  

Complications of AKI 

Nurses have around-the-clock interaction with the patient in the acute care setting. Because of their comprehensive assessment skills and connectivity to the patient, the nurse can identify slight changes in a patient’s condition. In some cases, complications can become life-threatening and require immediate intervention, while others  are non-life-threatening but require treatment. The table below identifies common complications associated with AKI. The nurse should document all identified complications in the electronic medical record. The complication should be recorded on the patient problem list and incorporated into nursing care plans according to their hospital policies. 

Common Complications Associated with AKI

Implementation and Evaluation of Quality Indicators  

Providing high-quality care for patients with AKI or those at risk of AKI occurs across a continuum. It’s a communication hand-off that begins in the community and continues in the emergency department, hospital setting, and after discharge from inpatient care [5].Preventive measures, as well as rapid identification of AKI treatment and handling complications, have been shown to improve outcomes in several small studies. The faster complications are identified, and treatment rendered leads to a positive outcome for the patient. 

AKI patients can recover completely with supportive management, depending on the etiology of the condition and the presence or absence of existing kidney disease. However, these patients will still require ongoing monitoring to maintain their health. Reoccurring AKI can lead to kidney function deterioration over time, where  approximately 12%-15% of patients with AKI will require permanent dialysis [3]. 

Improvements in clinical practice are made through asking questions, posing hypotheses, and collecting data on pre-established indicators. These indicators are defined as structure (policies and procedures), process (adhering to standards of care), and outcome (the impact on patients). One concept that encompasses all three indicators is a care path. A care path is developed using consensus-driven guidelines and practice from all healthcare practice areas. The adoption, modification, and implementation of a path within an organization is accomplished by a work team. The team is co-led by a physician and Clinical Nurse Specialist (CNS) and includes other healthcare providers throughout the ambulatory, acute care, and post-discharge clinical areas. 

Using an AKI care path is an excellent framework for providing consistent care, data collection, evaluation of processes and patient outcomes, along with identifying opportunities for improvement. The information obtained through the use of care paths would improve the health of the AKI patients, decrease hospital stays, cost and resource utilization.  

Unfortunately, there is not a consistent definition for AKI,  standard risk assessment tool, or care paths protocols that are widely used.. To achieve high-quality outcome measures, the healthcare community and organizations should consider implementing use of a care path. The care path bundle includes a validated risk assessment, adoption, and implementation of standard definitions of AKI, implementing standard treatment plans, and monitoring and evaluating outcomes. This is a way to provide safe, quality care and improve the health of the patients served in acute care and community settings.   

Conclusion

AKI identification and treatment should begin in the community and across the continuum to aid in reducing the incidence of the condition. The lack of adoption of the universal definition of AKI, not using standard risk assessment tools and inconsistency in treatment interventions, missing a consensus-driven care paths, and minimal outcome monitoring is problematic [6].In June 2019, KDIGO convened a consensus conference with the goal to standardize terminology and definitions. The conference identified and published guidelines. However, as these are only guidelines, their use is dependent on adoption and implementation by organizations and clinicians. Publication of outcomes through clinical journals and adoption of standard guidelines should be considered to improve patient outcomes.  

Case Studies 

#1 

Sally Bluebird is a 62-year-old, obese female who presented to her primary care physician (PCP) with symptomsof feeling tired, walking slower, and a slight increase in shortness of breath.  

Past medical history includes right knee bone on bone for 30 years, HTN, sleep apnea, and melanoma. Vital signs B/P 148/94, HR 70, and RR  24 with SPO2 of 98%. Weight 133kg.  

Medications include metoprolol succinate XL  50mg daily, meloxicam 15mg daily.    

Her self-monitoring blood pressure trends are 140-180/84-98 over the last two weeks.   

PCP completed the physical exam and reviewed the medical record. A follow-up to wide incision biopsy for melanoma showed trended elevated LDH. A CT was ordered. Results showed no sign of malignancy but evidence of pulmonary arterial hypertension (PAH).    

PCP treatment plan: metoprolol succinate XL increased to 100mg daily, order for pulmonary function test, BMP labs, and cardiology consult. Continue to monitor B/P and work on weight loss. PCP commented that changes might be needed in pain management due to NSAIDs use and age. 

The cardiology consult was scheduled via telephone, duel to the COVID-19 pandemic. The cardiologist used the patients electronic medical record and feedback from Sally to make recommendations. To verify the diagnosis of pulmonary artery hypertension (PAH), a right heart catheterization was ordered. Chlorthalidone 25mg was added to the medication regimen and BMP labs ordered and to recommended continue to work on weight loss. 

The right heart catheterization showed moderate PAH on 9-14-20. Lisinopril 5mg daily and furosemide 40mg daily were added to medications with repeat of BMP labs and f/u visit in 2 weeks. During review of discharge instructions, the nurse stressed the following, lisinopril may cause a cough, and given the number of medications whose side effect could impair kidney function to watch fluid intake and urine output. 

Because of the potential for drug induced AKI, the BMP which included SCr and Bun are important labs to monitor for changes in kidney function. The table below shows the best way to evaluate lab results along with trended data over time; while the labs do not return to baseline, they do decrease.   

Case Study

#2  

Mrs. Holly Gallery is a 67-year-old female, admitted for a right breast lump excision. Mrs. Gallery’s pre-op evaluation cleared her for same day surgery. 

PMH includes a history of heart failure and MI, HTN, hypothyroidism and hysterectomy due to fibroids 25 years ago. 

Medications Furosemide 40mg daily, baby ASA, Lisinopril 5mg daily, clopidogrel 75mg daily (held per-op), amlodipine 5mg daily and levothyroxine 25mcg daily. 

Allergies: none 

VS 138/84, 76,16 and 98.2 F SpO2 92% 

Mrs. Gallery’s surgery started at 0900 and completed without issues. She was transferred to PACU at 1015 in stable condition. During the post-op recovery period, Mrs. Gallery experienced a hypotensive event with B/P 86-90/50-60, HR 120s and RR 24.  No evidence of bleeding on post-op dressing. 250cc LR given as bolus, IV rate increased to 150 ml per hour x2 than return to 100 ml per hour. B/P 110/76 HR 84 and RR 16 at discharge from PACU.    

Mrs. Gallery was transferred to the same day surgery unit at 1230 pm. Upon arrival to unit VS 112/80, 72 and 16.  She is drowsy, but answer’s questions appropriately, denies pain. Dressing dry and intact. IV infusing at 100cc per hour, IV site patent. Lungs sounds are clear and heart rate NSR.  

At 1300, Mrs. Gallery is agitated, complaining that she cannot breathe. B/P 168/86 HR 126, RR 36, lung sounds include scattered rales and wheezing. SpO2 86% on room air. She is positive for a liter and half since admission. Furosemide 40mg IVP given. Exacerbation of heart failure suspected, order placed for CT with contrast to r/o PE and pneumonia, EKG, O2 at 2 liters SpO2 titrate to keep SpO2 greater than 90% plus labs for CBC and BMP. Results Hgb 13.4, WBC 9.78  Hct. 43.9% platelets 317C. Na 136, K+ 4. SCr 2.3 and BUN 42.   

Over the next four hours, Mrs. Gallery improved. Vital signs within normal limits and adequate urinary output. She was discharged in the AM. At discharge, SCr was 1.6 and Bun 32. 

Three days post-op Mrs. Gallery presents to emergency department c/o of increased shortness of breath, and no urinary output for 24 hours. VS 145/92, HR 110, RR 36 and SpO2 86% on room air. Lab results SCr 4.7, BUN 45 and K+ 5.7. Orders to admit to ICU with contrast induced AKI.  ​

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