FROM ONSET TO OUTCOME: ACUTE KIDNEY INJURY INSIGHTS FOR HEALTHCARE PROFESSIONALS
Liz Fredrickson, PharmD, BCPS
Liz Fredrickson is an Associate Professor of Pharmacy Practice and Pharmaceutical Sciences at the Northeast Ohio Medical University College of Pharmacy. She serves as Director of Instructional Labs and is course director for the Basic Pharmaceutics Lab and Parenteral Products and Parenteral Products Lab courses.
Acute kidney injury (AKI) represents a complex clinical challenge, often demanding swift diagnosis, interdisciplinary collaboration, and judicious therapeutic intervention. The implications of AKI range from transient renal dysfunction to severe complications. The landscape of AKI management continues to evolve, and this continuing education program aims to provide healthcare providers with a holistic perspective on the latest developments in AKI. This monograph will discuss the pathophysiology of AKI, methods by which to detect and risk stratify AKI, and modalities for prevention and treatment.
RxCe.com LLC is accredited by the Accreditation Council for Pharmacy Education (ACPE) as a provider of continuing pharmacy education.
Universal Activity Number (UAN): The ACPE Universal Activity Number assigned to this activity is
Pharmacy Technician 0669-0000-23-215-H01-T
Credits: 1 contact hour of continuing education credit
Type of Activity: Knowledge
Media: Internet/Home study Fee Information: $4.99
Estimated time to complete activity: 1 contact hour, including Course Test and course evaluation
Release Date: December 13, 2023 Expiration Date: December 13, 2026
Target Audience: This educational activity is for pharmacists and pharmacy technicians
How to Earn Credit: From December 13, 2023, through December 13, 2026, participants must:
Read the “learning objectives” and “author and planning team disclosures;”
Study the section entitled “educational activity;” and
Complete the Course Test and Evaluation form. The Course Test will be graded automatically. Following successful completion of the Course Test with a score of 70% or higher, a statement of participation will be made available immediately. (No partial credit will be given.)
Credit for this course will be uploaded to CPE Monitor®.
Learning Objectives: Upon completion of this educational activity, participants should be able to:
Recall the pathophysiological mechanisms, causes, and diagnostic biomarkers of acute kidney injury (AKI).
Recall evidence-based therapeutic interventions for AKI
Describe the role of interdisciplinary collaboration in AKI management.
Describe tools and techniques to effectively educate and guide patients regarding AKI.
The following individuals were involved in the development of this activity: Liz Fredrickson, PharmD, BCPS, and Pamela Sardo, PharmD, BS. Pamela Sardo was an employee of Rhythm Pharmaceuticals until March 2022 and has no conflicts of interest or relationships regarding the subject matter discussed. There are no financial relationships relevant to this activity to report or disclose by any of the individuals involved in the development of this activity.
© RxCe.com LLC 2023: All rights reserved. No reproduction of all or part of any content herein is allowed without the prior, written permission of RxCe.com LLC.
Acute kidney injury represents a complex clinical challenge, demanding swift diagnosis, interdisciplinary collaboration, and thoughtful therapeutic intervention. A thorough understanding of the diagnosis and management of acute kidney injury is critical to ensure optimal patient outcomes. It is vital for healthcare providers, including pharmacists and staff, to thoroughly understand the pathophysiology, etiology, and management of acute kidney injury. Additionally, healthcare providers should be familiar with ways to engage in the collaborative care of a patient presenting with acute kidney injury. This monograph will discuss the pathophysiology of acute kidney injury, methods by which to detect acute kidney injury, and modalities for prevention and treatment. Information regarding patient education and collaborative care strategies will be discussed.
Diagnostic and Staging Criteria
Acute kidney injury (AKI) is a rapid loss of kidney function, occurring within hours to days, and having a duration of 7 days.1 This sudden loss of kidney function is determined on the basis of increased serum creatinine levels and reduced urinary output.1,2 The implications of AKI range from temporary renal dysfunction to severe complications for patients.1,2
KDIGO Diagnostic Criteria for AKI 1-3
|Rise in serum creatinine of at least 0.3 mg/dL over a 48-hour period
|Rise in serum creatinine >/1.5 the baseline value within seven previous days
|Urine volume </0.5 mL/kg per hour for the past six hours
There is no single, definitive definition of AKI. Overall, the staging systems utilized for AKI still require validation in the assessment and management of patients with AKI.1 The most referenced diagnostic criteria are provided by The Kidney Disease: Improving Global Outcomes (KDIGO) 2012 Clinical Practice Guidelines for Acute Kidney Injury.1-3 Per the KDIGO
criteria, AKI occurs when any of the three criteria listed in Table 1 are present. Table 2 lists the KDIGO staging criteria.1-3
KDIGO Staging Criteria for AKI 1-3
|1.5-1.9 times baseline OR ≥0.3 mg/dL increase
|<0.5 mL/kg/hr for 6-12 hours
|2.0-2.9 times baseline
|<0.5 mg/kg/hr for >/12 hours
3.0 times baseline OR increase in serum creatinine to ≥4.0 mg/dL OR initiation of renal replacement therapy OR a decrease in eGFR to
<35 mL/min in patients
<18 years of age
|<0.3 mL/kg/hr for >/24 hours OR anuria for >/12 hours
Outside of KDIGO, other diagnostic criteria have been proposed. The RIFLE criteria (Risk, Injury, Failure, Loss, End-stage kidney disease) provide a structured framework for staging AKI.4 RIFLE categorizes patients into different stages based on changes in serum creatinine levels, glomerular filtration rate (GFR) and urine output as seen in Table 3.4
Injury: In this stage, there is a two-fold increase in serum creatinine or a GFR decrease of ≥50% or urine output <0.5 mL/kg/h for ≥12 hours.
Risk: Patients with a risk of A Jim KI have a 1.5-fold increase in serum creatinine or a GFR decrease of ≥25% or urine output <0.5 mL/kg/h for ≥6 hours.
RIFLE AKI Staging Criteria
Failure: Patients in this stage experience a three-fold increase in
serum creatinine or a GFR decrease of ≥75% or urine output <0.3 mL/kg/h for ≥24 hours.
|Loss: This stage represents a persistent, complete loss of kidney function for more than four weeks.
|End-stage kidney disease (ESKD): ESKD indicates the need for renal replacement therapy for more than three months.
The Acute Kidney Injury Network (AKIN) criteria is a third staging system. The AKIN diagnostic criteria include the following: an increase in serum creatinine of ≥0.3 mg/dL or ≥50% within 48 hours or a urine output of
<0.5 mL/kg/hour for >6 hours. AKIN staging criteria further refine the RIFLE criteria (Table 4).5 This criteria places a greater emphasis on small increases in serum creatinine and overcomes two shortcomings of the RIFLE system: a required baseline creatinine value and a lack of guidance at which stage to begin RRT.5,6 While KDIGO and AKIN provide both diagnostic and staging criteria, the RIFLE criteria offer a definition for AKI that is included within the staging criteria.1 Overall, the KDIGO diagnostic criteria is preferred given it considers both the RIFLE and AKIN criteria.6
AKIN AKI Staging Criteria
|Stage 1: Serum creatinine increase of ≥0.3 mg/dL within 48 hours or a 1.5 to 2-fold increase from baseline.
|Stage 2: Serum creatinine increase of >2 to 3-fold from baseline.
|Stage 3: Serum creatinine increase of >3-fold from baseline or serum creatinine ≥4.0 mg/dL with an acute increase of ≥0.5 mg/dL or the initiation of renal replacement therapy.
A retrospective cohort study sought to characterize the epidemiology of AKI according to KDIGO and compare it with three other definitions.7 Within the study, the incidence of AKI was highest according to the KDIGO definition (18.3%), followed by the AKIN (16.6%) and RIFLE (16.1%) definitions. Additionally, the incidence of AKI was significantly higher in patients with low baseline serum creatinine according to the KDIGO, AKIN, and RIFLE
definitions.7 Acute kidney injury was also associated with a significantly higher risk of death and higher resource utilization, according to all definitions.7 It has been shown that changes in serum creatinine and urine output are neither sensitive nor specific to AKI.8 Changes in urine output might be more sensitive but are less specific.8
Acute kidney injury is estimated to occur during 7% of hospital admissions and 30% of intensive care unit (ICU) admissions.9 There is a yearly incidence of 500 cases per 100,000 individuals, which has increased in recent years.9 Patients who experience AKI in the ICU have an estimated morbidity rate of 50%.9 The two most common causes of AKI in this cohort are sepsis and the use of nephrotoxic drugs.6 These patients are at risk of long-term complications that include chronic kidney disease (CKD) and end-stage kidney disease (ESKD).9
Etiology and Risk Factors
Several factors put patients at risk of AKI. These can be grouped into two categories: modifiable and non-modifiable.10,11 Non-modifiable risk factors include chronic kidney disease, chronic liver disease, congestive heart failure, diabetes, renal arterial stenosis, and age greater than 65.11 Modifiable risk factors include anemia, hypertension, hypercholesteremia, nephrotoxic drug use, sepsis, and rhabdomyolysis.10,11
Causes of AKI can be categorized into three primary groups: prerenal, intrarenal, and postrenal, as outlined in Table 5.8 While this classification serves as a valuable tool for establishing a differential diagnosis, it is crucial to acknowledge that AKI typically arises from multiple factors, and there is significant overlap in underlying pathophysiology across these categories.8 Furthermore, AKI often involves numerous contributing factors that not only trigger its onset but also contribute to its progression.8
Causes of AKI Category Abnormality Possible Causes
Hemorrhage Poor oral intake
Gastrointestinal losses (vomiting,
True volume depletion
Impaired cardiopulmonary functions
Decreased vascular resistance
Intrarenal hemodynamic changes
Third space losses (pancreatitis, peritonitis, burns)
Renal losses (over diuresis) Skin or respiratory losses Congestive heart failure Pericardial tamponade Pulmonary thromboembolism Systemic vasodilation
Sepsis Neurogenic shock Anaphylaxis
Medications (NSAID, RAS blockers, CNIs)
Hypercalcemia Renal ischemia Nephrotoxins Endogenous
Myoglobin, hemoglobin Tumor lysis syndrome
Medications (e.g., contrast agents) Acute glomerulonephritis
Vasculitis Malign hypertension
Interstitial damage Infections (Bacterial or viral)
Category Abnormality Possible Causes
Medications (Antibiotics, NSAIDs) Renal artery/vein thrombosis
Vasculitis (Polyarteritis nodosa) Atheroembolism
Intrarenal obstruction Nephrolithiasis Benign prostate hypertrophy
Prostate, bladder, rectal or cervical cancer
Acute neurogenic bladder Urethral stenosis or clotting Retroperitoneal fibrosis Renal papillary necrosis
Prerenal AKI, characterized by reduced renal perfusion, accounts for a significant portion of AKI cases (estimated at 25-60%).8,9 Prerenal AKI is associated with a decreased GFR due to issues such as hypovolemia and impaired cardiac function that cause intravascular volume depletion.2,8 A rise in serum creatinine or blood urea nitrogen concentrations due to poor renal plasma flow and intraglomerular hydrostatic pressure is designated as prerenal azotemia, or functional AKI.9 Clinicians should be familiar with medications that can lead to prerenal azotemia, including nonsteroidal anti- inflammatory drugs (NSAIDs), angiotensin-converting enzyme inhibitors (ACE-Is) and angiotensin receptor blockers (ARBs).9
Understanding the common causes and risk factors for prerenal AKI is crucial for early recognition and intervention. They include hypovolemia, hypotension, hepatorenal syndrome, reduced cardiac output, and renal artery stenosis, and prerenal AKI may be caused by a patient’s medications.
Hypovolemia: One of the most common causes of prerenal AKI is hypovolemia, which can result from excessive fluid loss or inadequate fluid intake, including vomiting, diarrhea, use of diuretics, and burns.9
Hypotension: Hypotensive episodes, whether due to sepsis, shock, or other causes, can lead to decreased renal blood flow, triggering prerenal AKI.12
Hepatorenal Syndrome: In patients with hepatic cirrhosis, hepatorenal syndrome can lead to AKI via afferent arterial vasoconstriction.8
Reduced Cardiac Output: Conditions that reduce cardiac output, such as heart failure or arrhythmias, can compromise renal perfusion and contribute to prerenal AKI.8 Cardiorenal syndrome reduces circulatory volume while increasing central venous pressure.8
Renal Artery Stenosis: Functionally, this can be viewed as any of the above conditions. But any blockage of blood supply, whether from tumor, stenosis, or malformation, can cause decreased perfusion as above.9
Medications, including angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, can lead to prerenal AKI.9
Intrarenal AKI is characterized by conditions that affect the renal parenchyma, including the renal tubules, glomeruli, and interstitium.2,8 Prolonged or severe ischemia leads to acute tubular necrosis.12
Acute Tubular Necrosis (ATN): ATN is the most common type of intrinsic kidney injury and is often seen in the context of ischemic injury or exposure to nephrotoxic agents, such as certain medications.8 Major
causes include the use of nephrotoxic medications, sepsis, and renal ischemia.8 Medications associated with AKI are presented in Table 6.8
Acute Interstitial Nephritis results from hypersensitivity reactions to medications, including beta-lactam antibiotics and NSAIDs.2 It may also result from infections.2
Sepsis-Associated AKI: This is the most common trigger for AKI among critically ill patients and is due to the presence of severe and sustained prerenal factors.8
Rhabdomyolysis: Rhabdomyolysis is the breakdown of skeletal muscle resulting in muscle compartment leakage into extracellular fluid (ECF) and circulation.8 In these cases, myoglobin and other substances lead to intratubular obstruction and damage.8
Pharmacy team members play a pivotal role in medication management and should collaborate with healthcare teams to monitor and adjust medications for patients at risk of intrinsic AKI.
Medications Associated with AKI13
Aminoglycosides (Tobramycin, gentamycin)
β-Lactam antibiotics Fluoroquinolones Rifampin
Tenofovir Cidofovir Foscarnet Acyclovir Indinavir
Antifungals Amphotericin B
Analgesics NSAIDs (Naproxen, ibuprofen)
Tyrosine kinase inhibitors PD-1/PD-L1 inhibitors CTLA-4 inhibitors
Proton pump inhibitors Furosemide
Intravenous immunoglobulin Iodinated contrast media
Postrenal AKI is caused by urinary tract obstruction that prevents urine from being excreted from the kidneys.8 This can occur at any level of the urinary system.7 Healthcare providers should be familiar with the causes and clinical presentations of postrenal AKI.8 Causes include neurogenic bladder and retroperitoneal fibrosis.2
Urinary tract Obstruction can occur at various points in the urinary tract, including the ureters, bladder, or urethra.14 Common causes include urinary stones, tumors, or prostatic hypertrophy.8 An estimated 5-10% of all AKI cases are due to a urinary tract obstruction, with an increased incidence in elderly patients.8
Understanding postrenal AKI is essential for timely intervention and relief of urinary tract obstruction, which can be life-threatening if left untreated.8 Often, the diagnosis will require imaging studies to evaluate the source of the obstruction.8 Images often start with ultrasonography; this is done to rule out potential obstructions. Renal ultrasonography can assess the structure of the kidney and evaluate for hydronephrosis (excessive fluid
backup in the kidney) or other lesions. Bladder ultrasonography can reveal if the source of the obstruction lies distal to the bladder (for example, the urethra), if the bladder is overdistended, or if it implies neurologic or muscular issues that prevent full emptying.9 A post-void residual (PVR) can quickly identify the quantity of remaining urine in the bladder.9 If more than 50- 100mL remains, there is incomplete emptying, which can be treated by catheterization for evacuation of the urine.9
Clinical Presentation and Diagnosis
Recognizing the clinical presentation of AKI is vital for early diagnosis and intervention. Many patients are asymptomatic and diagnosed based on laboratory findings. Healthcare professionals should be vigilant in assessing patients for AKI signs and symptoms if AKI is suspected.
As part of the patient's history, clinicians should inquire about potential risk factors for AKI, such as recent surgery, nephrotoxic medication use, or preexisting conditions like diabetes and hypertension.12 For example, a patient with a history of diabetes and recent use of nephrotoxic antibiotics may be at increased risk for AKI.12
Acute kidney injury may present with a spectrum of symptoms, from mild to severe. Common clinical manifestations include the following.2
Decreased Urine Output: Oliguria (urine output <0.5 mL/kg/h) or anuria (complete absence of urine output) is a hallmark of AKI and should raise suspicion.
Fluid Retention: Patients with AKI may exhibit signs of fluid overload, such as edema, weight gain, and elevated jugular venous pressure.
Electrolyte Imbalances: AKI can lead to electrolyte disturbances, resulting in symptoms like muscle weakness, palpitations, and altered mental status
Other signs and symptoms may include skin rashes, such as a maculopapular rash, jaundice, uveitis, cardiac murmurs, hearing loss, and pelvic or rectal masses.2 The specific signs and symptoms can alert clinicians to the underlying cause.2
Important urine and lab findings can help establish the diagnosis.
Imaging may also be needed.
Serum creatinine and blood urea nitrogen (BUN) levels are diagnostic criteria.2 However, serum creatinine is a slow-changing surrogate for decreased GFR.2 A ratio of BUN to creatinine above 20:1 can suggest prerenal disease.
Serial creatinine clearance levels provide a direct measure of GFR and an efficient assessment of renal function.2
Urinalysis and urine microscopy provide information related to the location and cause of AKI.2
Urine electrolytes: fractional excretion of urea and sodium can be used to identify prerenal azotemia (Table 7).2 A fractional excretion of sodium less than 1% is suggestive of a prerenal cause, and a fractional excretion of urea <35% suggests a prerenal cause.2
Other tests that may be needed include renal ultrasound and renal biopsy. 2
Calculating Fractional Excretion of Sodium and Urea
|Fractional excretion of sodium
|Fractional excretion of urea
Healthcare professionals can contribute significantly to AKI prevention by identifying at-risk patients and implementing preventive measures. Strategies for prevention are detailed below. Implementing these strategies for AKI prevention can have a significant impact on patient outcomes and reduce the burden on healthcare systems.
Medication Review: A thorough medication review should focus on nephrotoxic medications. Medications that pose a high risk of causing or exacerbating AKI should be discontinued.12
Fluid Management: Appropriate fluid management should be implemented, especially in patients with AKI risk factors. Aggressive fluid resuscitation should be avoided in patients at risk of volume overload.12
Blood Pressure Management: Patients with hypertension should have blood pressure control measures in place to reduce the risk of hypertensive emergency-related AKI.12 Care should be taken to avoid hypotension as well.
Diabetes Management: Patients with diabetes should have optimized glucose control to prevent diabetic nephropathy-related AKI.12
Surgical and Procedural Care: Providers should actively assess and manage perioperative factors contributing to AKI, such as hypotension and contrast use in perioperative settings.12
High-Risk Populations: High-risk patient populations should have targeted AKI prevention efforts in place. For example, elderly patients are at increased risk of AKI due to age-related changes in renal function. Additionally, patients with conditions like diabetes, hypertension, and
chronic kidney disease are at higher risk for AKI. Tailor prevention strategies to address their specific needs.
The management of AKI primarily focuses on supporting patients while aiming to prevent further renal damage and promote the recovery of renal function.2 Timely diagnosis and addressing the underlying cause of AKI are paramount in achieving successful outcomes.2 This multifaceted approach encompasses several key components, including fluid resuscitation, avoidance of nephrotoxicity, and correcting electrolyte or other biochemical abnormalities present.2
Assessing Volume Status and Hemodynamic Stability
Assessing volume status and hemodynamic stability is pivotal when managing patients with AKI, as fluid overload has been linked to increased mortality.2 If fluid resuscitation is warranted, isotonic crystalloids such as 0.9% normal saline, lactated Ringer solution, or Plasma-Lyte A are recommended as the initial therapy.2 These options are preferred over colloids like albumin or dextran due to concerns about excess chloride levels, which can worsen renal function and disrupt acid-base balance. Studies have demonstrated that a chloride-restrictive resuscitation strategy is associated with a lower incidence of AKI and reduced need for renal replacement therapy.2 Maintaining a mean arterial pressure goal of 65 mm Hg or higher is acceptable, and vasopressors may be necessary if fluid resuscitation cannot achieve this target.2 Protocol-based strategies are recommended to prevent and improve AKI, especially in high-risk patients such as those postoperative or in septic shock.
Scrutiny of medications, including the consideration of discontinuation, dose adjustments, or monitoring, is crucial.2 Certain medications can exacerbate kidney injury, and it is essential to identify and manage them
appropriately.2 Pharmacist-led quality-improvement programs have shown promise in reducing nephrotoxic exposures and AKI rates within the hospital setting.2
Diuretics are generally not recommended for treating or preventing AKI except when needed to alleviate volume overload.2 Maintaining a plasma glucose target between 110 and 149 mg per dL (6.1 to 8.3 mmol per L) for ICU patients is advisable, although this specific target lacks randomized controlled trial (RCT) validation.2 Nutritional status should be carefully evaluated, and dietary recommendations should align with AKI's underlying cause and severity.2
Hyperkalemia is a clinical emergency and a common complication of AKI. Pseudohyperkalemia should be ruled out initially.15 Emergent pharmacologic treatment of hyperkalemia is presented in Table 8. In some cases, emergent dialysis may be needed.16
Emergent Treatment of Hyperkalemia
|Expected decrease in potassium
|Onset of action
|Duration of effect
gluconate 1 ampule
(1 g) by slow (1–2 min) bolus (may be repeated after 5 min)
|< 3 min
|Caution/avoid if digitalis toxicity strongly suspected
Regular insulin 0.1 IU/Kg BW (up to max 10 IU) by intravenous
(IV) bolus, preceded by (if serum
glucose <250 mg/dL)
50% dextrose 50–
100 mL (25–50 g)
mEq/L after 1 h
|Hypoglycemia (up to 30% in patients with advanced CKD)
|Regular insulin 20 IU by IV infusion over 1 hour together with IV infusion of dextrose 60 g
mEq/L after 1 h
|Hourly monitoring of serum glucose concentration for at least 3 hours necessary
10–20 mg nebulized salbutamol (20 gtt of a 0.5% salbutamol solution repeated up to 8 times in 120 min)
|Within 30 min
|Maximum effect at 90 min
Tremor, tachycardia, palpitations, anxiety More effective if used in conjunction with insulin/dextrose
Use with caution in patients with heart disease
12–40% of patients unresponsive, especially if on treatment with beta- blockers
Avoid in patients with ischemic heart disease
0.5–2.5 mg IV
|Maximum effect at 30 min
1.4% (1/6M) or 8.4%
(1 M) sodium bicarbonate by IV infusion, 10–20 mEq/h
Variable (up to 2 mEq/L
after 10 mEq/L of increase in serum bicarbonate concentration in acidemic
patients with CKD
Use only in acidemic patients
Risk of hypernatremia, volume overload, tetany, and pCO2 increase in patients with respiratory failure
|Furosemide 1 mg/Kg as IV bolus (up to 80 mg), followed by 10 mg/h continuous infusion
|Duration of infusion
|Use only in hypervolemic patients May be combined with thiazides or thiazide-like diuretics
|Sodium polystyrene sulphonate 30 g with 100 ml 20% sorbitol orally or by rectal enema
|Doubtful efficacy in the acute setting
|At least 2 h
Risk of colonic necrosis (low) Bowel obstruction must be ruled out
before administration Not recommended as a first-line treatment of emergency hyperkalemia
Renal Replacement Therapy (RRT)
In severe cases of AKI, renal replacement therapy (RRT) may be necessary to support kidney function and manage fluid and electrolyte imbalances.2 RRT modalities include hemodialysis, peritoneal dialysis, and continuous renal replacement therapy (CRRT).2 RRT should be initiated in patients with severe AKI who exhibit refractory fluid overload, severe acid- base disturbances, or persistent hyperkalemia despite medical therapy. 1 The selection of RRT modality depends on the patient's clinical condition, hemodynamic stability, and the availability of resources.2
The effective management of AKI depends upon the collaborative efforts of a diverse healthcare team, with each member bringing a unique skill set to the table. Nephrologists are central in guiding the diagnosis and treatment of AKI, and they work closely with intensivists who provide critical care expertise. Pharmacists offer their medication management knowledge, ensuring the avoidance of nephrotoxic agents. Dietitians tailor nutrition plans to varying AKI severities, optimizing patient outcomes. This multidisciplinary approach fosters enhanced communication, fosters early intervention, and helps address complex AKI cases.
Effective patient education is important in preventing AKI.17 Healthcare providers must provide clear and accessible communication to educate
patients on the risks and preventive measures related to AKI. This includes emphasizing the importance of adequate hydration, especially during illness or medical procedures, and avoiding nephrotoxic medications. Patients should be educated on the signs and symptoms of AKI to promote early recognition and timely medical intervention. Furthermore, healthcare professionals can empower patients to actively engage in their own care by encouraging them to communicate medication histories and follow recommended therapeutic care plans.
The Role of the Pharmacists and Staff
Pharmacists and staff can play an important role in patient safety and better outcomes by collaborating on drug management. Drugs may lead to or exacerbate AKI.18 It is important for patients to tell their pharmacist and provider about all medications they are taking. Pharmacy technicians may notice a patient is taking a nephrotoxic medication and can notify the pharmacist.
Pharmacists play important roles in recognizing nephrotoxic medications and working with the healthcare team to discontinue these agents. They can also provide comprehensive reviews of a patient’s entire medication list and offer recommendations related to renal dose adjustments, as well as counsel patients on the safe and effective use of their medications. In institutional settings, pharmacists can assist with developing policies and procedures related to the management of AKI and increase compliance related to these initiatives.
Acute kidney injury can be classified using various criteria, including RIFLE, AKIN, and KDIGO criteria, which consider changes in serum creatinine, glomerular filtration rate (GFR), and urine output. This condition is prevalent, particularly in critical care settings, and is associated with higher morbidity
and mortality rates. Recognizing the clinical presentation of AKI, including decreased urine output, fluid retention, and electrolyte imbalances, is essential for early diagnosis. Strategies for AKI prevention include medication review, fluid management, nephrotoxin avoidance, and addressing risk factors in high-risk populations, and general principles of AKI management involve fluid balance, nephrotoxin avoidance, and electrolyte management.
Which of the following is a diagnostic criterion for acute kidney injury (AKI) according to the KDIGO guidelines
Decreased urine volume over 24 hours
A rise in serum creatinine of at least 0.3 mg/dL over 48 hours
A rise in serum creatinine >/1.5 times the baseline value within seven previous days
A rise in serum creatinine >/2.0 mg/dL over 72 hours
Which of the following is a common cause of prerenal AKI?
Urinary tract obstruction
Increased cardiac output
Which of the following systems stages AKI patients based on changes in serum creatinine only?
Which of the following medications is considered nephrotoxic and, therefore, puts patients at an increased risk of AKI?
Aggressive fluid resuscitation should be avoided in which of the following scenarios?
A patient has a mean arterial pressure of 60 mm Hg.
A patient is at risk of fluid volume overload.
A patient is being supplemented with potassium
A patient has normal glucose levels
What should healthcare providers emphasize in patient education to prevent AKI?
The importance of avoiding all medications
The signs and symptoms of AKI
The need for excessive fluid intake
The benefits of nephrotoxic medications
Renal replacement therapy (RRT) is used in the management of severe AKI
to increase fluid levels
to prevent nephrotoxicity
to promote early recognition of AKI
to support kidney function and manage fluid and electrolyte imbalances
Which of the following is a primary cause of postrenal AKI?
Prerenal factors leading to renal ischemia
Intrinsic renal damage due to nephrotoxins
Urinary tract obstruction preventing urine excretion
Glomerular damage from acute glomerulonephritis
What is the primary goal of medication review in AKI prevention?
To increase the use of nephrotoxic medications
To identify and discontinue nephrotoxic medications
To administer higher doses of medications
To promote the use of over-the-counter medications
Which of the following criteria is NOT used in the RIFLE staging system for AKI?
Decrease in glomerular filtration rate (GFR)
Increase in serum creatinine
Urine volume measured for at least over 24 hours
Increase in blood urea nitrogen (BUN)
Kellum JA, Romagnani P, Ashuntantang G, Ronco C, Zarbock A, Anders HJ. Acute kidney injury. Nat Rev Dis Primers. 2021;7(1):52. Published 2021 Jul 15. doi:10.1038/s41572-021-00284-z
Mercado M, et al. Acute kidney injury diagnosis and management. Am Fam Physician. 2019;100(11):687-694.
Khwaja A. KDIGO clinical practice guidelines for acute kidney injury.
Nephron Clin Pract. 2012;120(4):c179-c184. doi:10.1159/000339789
Venkataraman R, Kellum JA. Defining acute renal failure: the RIFLE criteria. J Intensive Care Med. 2007;22(4):187-193. doi:10.1177/0885066607299510
Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11:R31
Kulkarni AP, Bhosale SJ. Epidemiology and Pathogenesis of Acute Kidney Injury in the Critically Ill Patients. Indian J Crit Care Med. 2020;24(Suppl 3):S84-S89. doi:10.5005/jp-journals-10071-2339
Zeng X, McMahon GM, Brunelli SM, Bates DW, Waikar SS. Incidence, outcomes, and comparisons across definitions of AKI in hospitalized individuals. Clin J Am Soc Nephrol. 2014;9(1):12-20. doi:10.2215/CJN.02730313
Turgut F, Awad AS, Abdel-Rahman EM. Acute Kidney Injury: Medical Causes and Pathogenesis. J Clin Med. 2023;12(1):375. Published 2023 Jan 3. doi:10.3390/jcm12010375
Waikar SS, Bonventre JV. Acute Kidney Injury. In: Loscalzo J, Fauci A, Kasper D, Hauser S, Longo D, Jameson J. eds. Harrison's Principles of Internal Medicine, 21e. McGraw Hill; 2022.
Nie S, Tang L, Zhang W, Feng Z, Chen X. Are There Modifiable Risk Factors to Improve AKI?. Biomed Res Int. 2017;2017:5605634. doi:10.1155/2017/5605634
Thongprayoon C, Hansrivijit P, Kovvuru K, et al. Diagnostics, Risk Factors, Treatment and Outcomes of Acute Kidney Injury in a New Paradigm. J Clin Med. 2020;9(4):1104. Published 2020 Apr 13. doi:10.3390/jcm9041104
Gameiro J, Fonseca JA, Outerelo C, Lopes JA. Acute Kidney Injury: From Diagnosis to Prevention and Treatment Strategies. J Clin Med. 2020;9(6):1704. Published 2020 Jun 2. doi:10.3390/jcm9061704
Goldstein SL, Mottes T, Simpson K, et al. A sustained quality improvement program reduces nephrotoxic medication-associated acute kidney injury. Kidney Int. 2016;90(1):212-221.
Pickkers P, Darmon M, Hoste E, et al. Acute kidney injury in the critically ill: an updated review on pathophysiology and management.
Intensive Care Med. 2021;47(8):835-850. doi:10.1007/s00134-021- 06454-7
Bianchi S, Aucella F, De Nicola L, Genovesi S, Paoletti E, Regolisti G. Management of hyperkalemia in patients with kidney disease: a position paper endorsed by the Italian Society of Nephrology. J Nephrol. 2019;32(4):499-516. doi:10.1007/s40620-019-00617-y
Lindner G, Burdmann EA, Clase CM, et al. Acute hyperkalemia in the emergency department: a summary from a Kidney Disease: Improving Global Outcomes conference. Eur J Emerg Med. 2020;27(5):329-337. doi:10.1097/MEJ.0000000000000691
Prescott AM, Lewington A, O'Donoghue D. Acute kidney injury: top ten tips. Clin Med (Lond). 2012;12(4):328-332. doi:10.7861/clinmedicine.12-4-328
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