Understanding AKIs and How to Treat Them

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Introduction

Acute kidney injury (AKI) 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, plus acute or chronic injury that leads to permeant kidney damage. Due to the inconsistencies in an AKI’s definition, assessments, treatment plans, and poor-quality outcome monitoring and reporting, the condition is an unquantified healthcare crisis that is impacting the population across the continuum.   

Defining AKI 

What is an AKI? 

It is a global term used to describe all types of impaired kidney function. AKI was previously known as renal failure. The Kidney Disease Improving Global Outcomes (KDIGO) foundation published guidelines for a consistent definition and criteria for AKI plus treatment strategies. However, a standard definition has not been adopted in clinical practice. Treatment plans vary, outcome monitoring and evaluation are minimally completed or not at all. These factors contribute to variation in medical journals, reviews, and opinions in defining acute kidney injury.   

The following are three examples of how AKI is defined: 

1. AKI is described as an abrupt (within hours) decrease in kidney function, which encompasses both injuries (structural damage and impairment (loss of function) (1).
2. 2. Using objective criteria from laboratory tests and clinical measures is defined as a rise in creatinine of X 50% from its baseline value and/or a fall in the glomerular filtration (2). 
3. KDIGO definition includes any of the following increase in (serum creatinine) SCr by X0.3 rate (GFR) by X25%, and/or a decrease in urine output below 0.5 ml/kg/h for 6 h or more. The mg/dl (X26.5lmol/l) within 48 hours; or increase Scr to X1.5 times baseline; which is known or presumed to have occurred within the prior 7 days; or urine volume 0).5 ml/kg/h for 6 hours (3).

There is a similarity in two of the 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 (4). 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 (5). The results of this study are small; it demonstrates a five-fold increase from the previous study; more research is needed.    

Drug-induced AKI is a significant portion of the condition. Data on the prevalence of drug-induced AKI is limited and inconsistent. Published literature shared that 20%-40% of admitted patients had drug-induced AKI. Which could be represented in up to 60% of elderly patients (4). Variation in AKI definition coupled with inconsistent data definitions is a limiting factor in obtaining more statistical information. 

Identification of AKI  

The identification of AKI begins with a thorough physical assessment and in-depth history of the patient to determine the risk for AKI or confirmation of AKI and its timeline progression.  Ideally, the early risk assessment for a community-based population would occur in a primary care physician’s office. If identified, this is the time to provide early intervention for AKI patients in a non-critical occurrence; however, most AKI diagnoses occur in the acute care setting.    

A history and physical is a noninvasive way to start the investigation to determine if the patient has AKI.  The history portion should include evaluating current and past medical diagnoses and reviewing prescriptions, including over-the-counter medications. Nonsteroidal anti-inflammatory drugs (NSAIDs) are a contributing cause of AKI, especially in the elderly.     

The physical exam should be detailed and include objective data of blood pressure, heart rate, respiratory rate plus pulse oximetry, and dreaded 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 to suggest endocarditis in an IV drug abuser (6). 
2. Eyes and ears – jaundice in liver disease, band keratopathy in multiple myeloma, signs of diabetes mellitus, atheroemboli in retinopathy, and signs of hypertension. Keratitis, iritis, and uveitis in autoimmune vasculitis. Hearing loss in Alport disease (6).  
3. Cardiovascular system – pulse rate, blood pressure, and jugulovenous pulse in establishing volume status. Irregular rhythm may indicate electrolyte imbalance-related arrhythmias. Pericardial friction rubs in uremic pericarditis (6). 

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 put the patient at 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 (7). The development of a risk assessment tool is the easy part; the challenge is the adoption and consistent use of the tool.  

Common Predisposing Factors for AKI

Diagnostic Studies  

Most diagnostic studies are invasive and include SCr, urea, electrolytes, complete blood count, liver function tests, glucose level, bone profile, urine analysis, and microscopic examination, and a renal ultrasound must be performed to exclude obstruction (4).  

The glomerular filtration rate (GRF) is widely accepted as the best overall index of kidney function.  However, GRF is difficult to measure and is commonly estimated from the serum level of endogenous filtration markers, such as creatinine. Because of the complexity of using GRF, serum creatinine is commonly used to measure AKI (3). 

The volume of urinary output (UO) is another measurement for diagnosing and monitoring AKI with limitations. Oliguria favors AKI; sudden anuria suggests that urinary tract obstruction of acute glomerulonephritis and gradually diminishing urine can be secondary to urethral stricture or obstruction related to prostate enlargement.  

The decrease or absence of UO is not specific to AKI. Changes in volume of UO may also be attributed to dehydration, urinary tract infection, tubular injury, hypovolemia, and hypertension (3). To make an AKI diagnosis comprehensive assessment of the patient is 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 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;  

2) Drug-induced nephrotoxicity; 

3) Obstruction or growth.  

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 bladder. Kidneys are four to five inches long and one of the few organs that the body has, two of them.  People can and do live with only one functioning kidney. The other kidney may be non-functioning or simply not there due to surgical removal for disease or injury; or because the individual chose to promote the gift of life and donated one of their kidneys.  

As of January 1, 2016, 100,791 people are waiting for a kidney transplant. In 2014, there were 17,107 USA kidney transplantations, 32% were from living donors (8). 

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 from the waste. The second is tubules which return the nutrients to the body via the renal vein. The wastes are held in the bladder for elimination. The kidneys process approximately 15 liters per day, but only one to two quarts 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, RBC production, and keeping bones strong and healthy (9). 

Nephrotoxicity and Kidney Function Affected   

Medications are a huge part of the health care treatment plan. Patients with comorbidities of sepsis, 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 (4). 

Acute tubular necrosis (ATN) results from aminoglycosides, vancomycin, radiocontrast media, cisplatin, amphotericin B, foscarnet, and osmotically active agents (4). 

Acute interstitial nephritis (AIN) defects occur from antimicrobials such as b-lactams, sulfa-based drugs, quinolones, anti-ulcer agents, anticonvulsants, and diuretics (4).   

Post renal AKI injury due to crystal-induced luminal obstruction can occur from patients exposed to acyclovir, sulfa-based ciprofloxacin, and methotrexate. There is also an abundance of other common medications that can cause glomerular disease, impacting kidney function (4).  

Monitoring prescribed medications for potential risk to a patient’s kidney function is the responsibility of all health care providers. New medications incorporated into the treatment plan should be reviewed with all current medications to determine if an additional risk to AKI is there. This is everyone’s responsibility. It first starts with the prescribing provider when the medication is ordered. The pharmacist has accountability when preparing and dispensing the medication. The final review is with the nurse who administered the medication and monitors for side effects/complications. 

Treatment of AKI and the Role of the Nurse 

The treatment plan for AKI is dependent on the underline cause and may require multiple interventions to improve patient outcomes. The treatment plan is based on diagnosis, symptoms, and comorbidities.   There is not a standardized AKI care path available for use. The healthcare provider is responsible for the treatment plan, and the nurse is integral in the implementation, monitoring, and education of the patient in reaching the plan’s goal. 

The types of treatments include: 

Fluid Therapy Based on the Patient’s Hemodynamic Status (Hypovolemic or Hypervolemic)

The nurse is integral in patient outcomes through assessment, monitoring VS, hemodynamic status, and UO, and contacting physicians to report deviations from baseline.

Use of Vasopressors

The nurse’s use of head-to-toe assessment skills plus VS and UO monitoring is integral for achieving the best outcome of this intervention.

Use of Diuretics and Urinary Output Monitoring

UO is a measurement that nurses monitor in the acute care setting. Accurate measurement of urine has been traditionally done using an indwelling urinary catheter (IUC). Catheter-associated urinary tract infections (CAUTI) which is a nurse-sensitive patient safety event. Healthcare facilities are financially incentivized by federal programs to reduce the incidence of CAUTIs. The financial reimbursement to reduce the incidence of CAUTI has raised the bar to identify alternative methods for UO measurement.  These include nurse drive foley removal protocols, bladder scanning, condom catheters (male and female), weighing of absorbent pads, and use of intermittent straight catheters. Nurses have a responsibility as patient advocates to promote these utilizing alternative UO measurements whenever feasibly possible.  

Identifying and Managing Drug-induced Nephrotoxicity  

Patient assessment and continuous monitoring of diagnostic results by nurses 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.  Remember those drug cards that were created/used in nursing school. This is where their synergetic value can be seen. 

Renal Replacement Therapy

These are procedure-driven and include hemodialysis (HD), continuous renal replacement therapy (CRRT), which is the most common intervention used in an acute care setting. Slow, low-efficiency dialysis (SLED) and finally 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. Nurses need to use their critical thinking assessment skills to administer these treatments and keep the patient safe. 

Complications of AKI 

Nurses have around-the-clock interaction with the patient in the acute care setting. Because of their connectivity to the patient, typically, the nurse identifies changes in a patient’s condition. In some cases, the complication is life-threatening and requires immediate intervention. Other complications are non-life-threatening but still 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 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 (10). Preventive measures, as well as rapid identification of AKI treatment and handling complications, have been shown to improve outcomes in small studies. The quicker 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 the long term, 12%-15% of patients with AKI will require permanent dialysis (6). 

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 health care 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 health care 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, as there is not a consistent definition for AKI or a standard risk assessment tool, care paths are not widely used or used at all. To achieve outcome measures, the health care community needs to use a bundled care path. The 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.    

Summary 

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 (11). 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 journals and presentations is also needed. Until there is consistent adoption of the guidelines; controversy on the AKI definition and care, AKI will continue to be a diagnosis that impacts 7% of the population, more than a quarter of admitted hospital patients.  

Case Study #1

Sally Bluebird is a 62-year-old, obese female who presented to her primary care physician (PCP) with c/o of 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 PAH, a right heart catherization was ordered. Chlorthalidone 25mg was added to medication regimen and BMP labs ordered and to recommended continue to work on weight loss. 

Right heart cath 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 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 Hx 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 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 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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