Read” Acute kidney injury: Challenges and opportunities ‘article?then the two additional articles ( ?Challenges of targeting vascular stability in acute kidney injury ?&

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Acute kidney injury: Challenges and opportunities

BY NHAN L.A. DINH, MSN, CNP, AGACNP-BC, CCRN

Abstract: Acute kidney injury (AKI) can be a devastating diagnosis for any patient and can increase mortality during hospitalization. There can be long-term consequences for those who survive the initial insult. This article discusses AKI and its implications for nurses.

Keywords: acute kidney injury, Acute Kidney Injury Network, AKI, chronic kidney disease, CKD, community-acquired acute kidney injury, hospital-acquired acute kidney injury, KDIGO, Kidney Disease Improving Global Outcomes, Nephrotoxic Injury Negated by Just-in-time Action, sick day rule

ACUTE KIDNEY INJURY (AKI) is a heterogeneous kidney disorder that increases in-hospital morbidity and mortality. In 2016 data, the inci- dence of AKI was 20% for Medicare patients with both chronic kidney disease (CKD) and diabetes.1 Based on Veterans Affairs (VA) 2016 data, AKI occurred in more than 25% of hospitalized veterans over age 22, but less than 50% of those with lab-documented AKI were coded as such.1 The chief concern here is a missed opportunity for intervention. AKI increases long-term risk of CKD, but if clinicians do not recognize the diagnosis, they cannot follow up or intervene. An AKI diagnosis also increases the chance of another AKI episode, with a 30% risk of a recur- rent AKI episode within 1 year.1

Mortality is increased with an AKI episode. Medicare data from 2016

shows in-hospital mortality of 8.2%, but this increases to over 13% when including patients who were dis- charged to hospice.1 The in- hospital mortality for patients without AKI was only 1.8% (3.8% if including patients discharged to hospice).1 Pa- tients with AKI also were more likely to be referred to a long-term-care facility. (See Hospital discharge status of first hospitalization for Medicare patients ages 66+, 2016.)

AKI defined AKI was previously known as acute renal failure.2 However, many pa- tients with kidney injury did not progress to renal failure, yet still had significant, often permanent, loss of kidney function. Researchers worked to better define AKI and noted that it is a potential but often reversible rapid deterioration of kidney func-

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tion, with or without kidney dam- age. It may or may not be associated with oliguria.

Numerous groups attempted to define AKI from both a clinical and physiologic point of view to allow for epidemiologic studies. A consensus group developed the first criteria with a definition relying on changes in the serum creatinine (SCr), glo- merular filtration rate (GFR), and/or urine output, known as Risk of renal dysfunction, Injury to the kidney, Failure of kidney function, Loss of kidney function, and End-stage kid- ney disease (RIFLE).3 The Acute Kid- ney Injury Network (AKIN) believed RIFLE mixed outcomes with severity classes and developed another classi- fication, the AKIN criteria.4 In 2012, Kidney Disease: Improving Global Outcomes (KDIGO), an international organization, standardized the com- peting definitions of AKI (RIFLE and AKIN) into one coherent classifica- tion.2 (See Classifications of AKI.)

Using this chart and per interna- tional KDIGO consensus criteria, AKI is diagnosed when there is an increase in SCr from baseline by at least 0.3 mg/dL within 48 hours

or an increase in SCr to at least 1.5 times from baseline known or pre- sumed to have occurred within the 7 days before AKI diagnosis.2 The guidelines also specify that the di- agnosis can be made when there is a urine volume of less than 0.5 mL/ kg/h for 6 hours.2

AKI can be divided into two cat- egories: community-acquired AKI (CA-AKI) and hospital-acquired AKI (HA-AKI). Patients who present to a hospital meeting criteria for AKI as listed above are defined as having CA-AKI.5 HA-AKI has been the focus of research over the last 2 decades as rates of AKI have steadily increased and continue to do so.6 However, CA-AKI has gained more attention recently because of its prevalence; it was recently stated that nearly 50% of AKI incidents begin in the com- munity setting.7,8,10 This statistic is concerning and healthcare providers need to be alert to patients in their practice who are at risk. In 2013, the International Society of Nephrology launched the “0by25” initiative as a global target to ensure zero death of patients with preventable and treatable AKI by 2025 while raising

awareness to change incidence and prognosis worldwide.9 One difficulty with tracking CA-AKI is that it is easier to obtain records and statistics on hospitalized patients, but CA-AKI is often treated outpatient. CA-AKI can be prevented and treated.10 It is crucial for healthcare professionals to promptly identify patients with CA- AKI as well as those who are at risk for developing CA-AKI.

Etiology of AKI and risk factors for CA-AKI AKI is caused by endogenous and/ or exogenous conditions, including but not limited to severe ischemia or sepsis, dehydration, gastrointestinal (GI) bleeding, anemia, and/or use of nephrotoxic agents.11-13 These causes are often multifactorial. For example, patients with sepsis are given renal- toxic doses of antibiotics.

Etiology of AKI can be divided into three categories: prerenal, intrarenal/ intrinsic kidney disease, and postrenal. (See AKI etiologies.) Prerenal causes, such as volume depletion from de- hydration, GI losses (vomiting, diar- rhea, bleeding), excessive diuresis, hemorrhage from trauma, and/or

Hospital discharge status of first hospitalization for Medicare patients ages 66+, 20161

49.1

8.2

7.6

30.1

5.0

68.8 1.8

4.7

22.7

2.0

Home

Death

Other

Institution

Hospice

With AKI diagnosis Without AKI diagnosis

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changes in vascular resistance occur- ring from disease processes or certain drug use, cause hypoperfusion to the kidneys.11-13 These changes, in turn, lead to a lower GFR.

Intrarenal AKI can result from a prolonged prerenal state with or without toxic insults related to toxins, drugs, or any underlying systemic process such as sepsis. Inflammation and ischemia of the kidneys can be sequelae of those insults.12,13 Over-the-counter (OTC) and prescribed medications are a common intrarenal cause of CA- AKI. Examples include nonsteroidal anti-inflammatory drugs (NSAIDs) for pain management, angiotensin- converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) for hypertension and CKD with diabetes, proton pump inhibi- tors for gastric reflux, and cyclospo- rine and/or tacrolimus for antirejec- tion management.12,13 Intrarenal AKI can be categorized by the compo- nents of the kidney that are primarily affected: tubular, glomerular, intersti- tial, and vascular.12,13

Postrenal AKI, the least common etiology, is usually caused by an obstruction in urinary flow out of either a single kidney or both kid- neys. In postrenal AKI, kidneys still produce urine, but the urine cannot be excreted via the urethra due to blockage. Therefore, the urine backs

Classifications of AKI2-4

Stage Urine Output RIFLE*

Intrarenal AKI can result from a prolonged prerenal state with or without toxic insults related to drugs or

an underlying systemic process.

up into the kidneys (retrograde flow), impairing renal functions. Obstruction of urinary flow can result from obstructing stones or blood clots in the ureters or renal pelvises, an enlarged prostate, dys-

AKIN

function or obstruction of the blad- der, and/or strictures in the urinary system.12,13

Volume depletion is more com- monly the cause of CA-AKI than HA-AKI.14 Incidence of AKI increas- es during summer months, when the risk of dehydration is greater. Two studies found that pre-renal causes relating to AKI are almost two-fold higher than all other causes together.5,14

Patients are at the highest risk for CA-AKI when they have significant comorbidities along with polyphar- macy.15 Diuretics are associated with a higher incidence of CA-AKI than ACE inhibitors and ARBs.6 A combi- nation of these medications puts pa- tients at a greater risk for developing CA-AKI than diuretics alone.

Even though risk factors for CA- AKI and HA-AKI are similar, CA-AKI is common in older adult males with comorbidities including diabetes mellitus, hypertension, heart disease, CKD, cancer, and/or dementia.1,6,14

Gender also plays a role in CA-AKI development. Men across all age groups are at higher risk for CA-AKI compared with their female coun- terparts. This factor is thought to be mediated in part by testosterone.16,17

According to a Vanderbilt University study, testosterone has been found to increase renal GFR expression, which is associated with the likelihood of

KDIGO

<0.5 mL/kg/h Risk: Increase in SCr of 1.5x Increase in SCr 1.5–2x Increase in SCr of 1.5–1.9x for 6 h or decrease in GFR >25% baseline or ≥0.3 mg/dL baseline or ≥0.3 mg/dL

<0.5 mL/kg/h Injury: Increase in SCr 2x Increase in SCr 2–3x baseline Increase in SCr of 2–2.9x for 12 h or decrease in GFR >50% baseline

3 <0.3 mL/kg/h Failure: Increase in SCr 3x Increase in SCr 3x baseline or Increase in SCr of >3x base- for 24 h or or decrease in GFR >75% SCr of ≥4 mg/dL (with acute line or increase in SCr ≥ 4.0 anuria for 12 h rise of ≥0.5 mg/dL) mg/dL or initiation of renal

replacement therapy

* Loss and ESRD of the RIFLE criteria are not included in this staging chart, as they are considered outcome variables.

Used with permission from Erica Davis, PA-C: AAPA presentation. 2017. New Orleans, La.

www.Nursing2020.com September l Nursing2020 l 47

1

2

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progressive kidney injury.17 The exact mechanism remains unclear and is currently being investigated. Further, Black, Hispanic, and hospitalized patients with a previous diagnosis of AKI are more likely to develop AKI than those from different ethnic groups or those without risk fac- tors.1,6,14,16,18

As noted previously, patients with diabetes mellitus and CKD tend to have more incidents of AKI than those without comorbidities.1 Al- though CKD has consistently been shown to increase risk for the devel- opment of AKI, one study found that it does not pose any significant dif- ferences in the severity of AKI.14

Signs and symptoms of AKI Although the kidneys are responsible for regulating extracellular and in- travascular fluid volume, osmolality, electrolyte concentrations, pH, and excretion of wastes and toxins in the body, AKI does not manifest any specific signs and symptoms until

AKI etiologies Prerenal AKI

other organs or systems are affected. Patients with AKI can present with either oliguria or nonoliguria. Signs and symptoms of AKI also depend on the causes that dictate how rapid and severe the decline of kidney function is.11-13 Most patients pre- senting to a hospital with AKI are not aware that they have this condition. Patients often present with signs and symptoms that later cause AKI (such as hemorrhage or severe nausea and vomiting) or signs and symptoms related to complications of AKI (in- cluding altered mental status, severe edema, shortness of breath, malaise/ lethargy, hemodynamic instability, and dysrhythmias). These signs and symptoms are often related to uremia or its underlying causes.11-13

AKI management AKI management depends on the underlying etiology and the severity of kidney injury. Because mortal- ity is high in patients with AKI, the most important goal of therapy is

Intrarenal AKI

preventing life-threatening compli- cations.11-13 However, current AKI interventions are limited to support- ive care and prevention of causative factors. Any possible causes of AKI and its contributing factors should be prevented, treated, or removed as soon as possible.11,12

Prevention and early detection are the keys to improving outcomes for patients with AKI. For example, ACE inhibitors and ARBs should be held temporarily in patients with decreased oral intake and in those who present with prerenal AKI that may have started in the community setting, because these drugs may exacerbate a prerenal state. While waiting for the kidneys to recover on their own, restricting or avoid- ing substances and medications that are known to impair kidney func- tion is vital. In the event of signifi- cant electrolyte derangement and/ or fluid overload, emergent dialysis can be performed to prevent further complications related to cardiac dys-

Postrenal AKI

↓ Intravascular volume Acute tubular necrosis Upper urinary tract obstruction • Dehydration/hemorrhage • Ischemic: • Intrinsic • GI, cutaneous, or renal losses – Sepsis – Stone • Third spacing – Hypotension – Papillary necrosis

• Nephrotoxic: – Blood clot ↓ Effective blood volume – Drugs – Tumor • Heart failure – Heme pigments • Extrinsic • Cirrhosis – Retroperitoneal fibrosis • Nephrotic syndrome Acute interstitial nephritis – Malignancy • Sepsis • Drug-induced – Ligation • Anesthesia • Infection-related – Pelvic mass

• Systemic diseases Altered renal hemodynamics • Malignancy Lower urinary tract tract obstruction • Preglomerular constriction • Urethral stricture • Postglomerular vasodilation Acute glomerulonephritis • Benign prostatic hyperplasia • Medications: ACE inhibitors, NSAIDs • Prostate cancer • Hepatorenal syndrome, surgery Acute vascular syndrome • Bladder cancer

• Renal artery dissection • Bladder stones Renal vascular obstruction • Renal artery thromboembolism • Neurogenic bladder

• Renal vein thrombosis • Malpositioned indwelling urinary Abdominal compartment syndrome • Atheroembolic disease catheter

Used with permission from Catherine Wells, DNP: NKF presentation. 2013. Orlando, Fla.

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rhythmias, heart failure, or respira- tory failure during hospitalization. Collaboration among the interdisci- plinary team, including primary care physicians, hospitalists, nephrolo- gists, nurses, and advanced practice providers, is crucial in optimizing AKI management.

CA-AKI outcomes CA-AKI has been identified as the most common type of AKI.14 CA- AKI accounted for almost 80% of the patients with a discharge diagnosis of AKI at a single VA hospital, and its severity was found to be as significant as HA-AKI.14 If present at admission, CA-AKI has a significant impact on hospital length of stay and is associ- ated with a substantially higher risk of death and CKD progression.14,19

The rate of rehospitalization in pa- tients with CA-AKI versus HA-AKI did not differ, and early temporary dialysis may improve the outcome of CA-AKI.10,18 However, those who initially present with CA-AKI exhibit the highest incidence of CKD at their 5-year follow-up.19 Two studies found that 40.2% of patients developed CKD stage 3 (GFR 30 to 60 mL/min) or higher, and nearly 27% progressed to either CKD stage 5 (GFR less than 15 mL/min) or end-stage renal dis- ease (ESRD) requiring dialysis.19

CA-AKI is often underappreciated as a clinic or office-based issue.14,20

In patients presenting with upper re- spiratory or GI complaints, clinicians may focus on the presenting condition and may not consider dehydration and the need to adjust certain medica- tions. In addition, many patients pres- ent to urgent care and are treated for the problem and labs are not checked for existing kidney disease.

Some patients self-medicate with OTC combination or multisymptom medications containing NSAIDs, such as naproxen or ibuprofen. This compounds the chance of develop- ing AKI. The National Kidney Foun- dation has a patient website that

An AKI diagnosis increases the chance

of another AKI episode, with a 30% risk of

recurrence within 1 year.

highlights medication dosing for the at-risk patient.21

Prevention Multiple studies have shown an im- provement of outcomes in patients with AKI with early detection as well as preventive measures when AKI is diagnosed.8,10,14,16,22 Stress to patients in the community setting the im- portance of optimization of volume status as well as avoiding exposures to any nephrotoxic agents.10 When primary prevention fails to prevent AKI from occurring, the Recognition- Action-Result framework can act as a secondary prevention by properly diagnosing and evaluating AKI with a goal of limiting duration and severity to prevent complications.10

A multidisciplinary approach has been recommended for tertiary pre- vention of AKI. This includes close

monitoring, medication review, and reassessment of patients, especially those with a history of AKI.2,10,12

Outpatient preventive measures after the first episode of AKI are vital in improving quality of life, alleviating long-term complications, and limit- ing recurrences.

One of the most promising preventive methods is implement- ing “sick day rules” developed by the National Health Service of the United Kingdom.23 Sick is defined as vomiting or diarrhea (unless minor), fevers, sweats, and shaking. When these symptoms occur, patients are directed to temporarily stop taking: • NSAIDs, which can impair re- nal autoregulation by inhibiting prostaglandin-mediated vasodilation of the afferent arterioles and may increase the risk of AKI. • ACE inhibitors and ARBs, which reduce systemic BP and also cause vasodilation of the efferent arterioles, further reducing glomerular perfu- sion pressure. • Diuretics (including spironolactone and eplerenone), which can cause hypovolemia and AKI. • Other BP-lowering medications. • Medications that may accumulate due to decreased kidney function caused by hypotension, increasing the risk of adverse reactions. Ex- amples include metformin (risk of lactic acidosis), sulfonylureas (risk of hypoglycemia), and trimethoprim (risk of hyperkalemia).

Screening for children at risk Because AKI can be especially dev- astating in children, researchers at Cincinnati Children’s Hospital (CCH) developed an electronic health record screening and trigger program for the hospital.24 Enrolling all non-critically ill hospitalized children between 2011 and 2015, CCH decreased the exposure rate of nephrotoxic medica- tions by 38%. More important, CCH reduced the incidence of AKI by an impressive 64%.24

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CCH reports the most impor- tant aspect of the program was the person-person interaction. If the pharmacist noted three or more nephrotoxic medications for one patient, he or she would notify the healthcare team. The pharmacist would highlight the risk and discuss other medications that would be less nephrotoxic, but leave the final deci- sion to the healthcare team.24 CCH offered this software application and clinical system to all children’s hospitals nationwide, and more than 14 children’s hospitals have imple- mented it.25

Implications for nurses Because CA-AKI and HA-AKI can both be devastating diagnoses for any patient, nurses must be familiar with the pathophysiology of AKI in order to promptly recognize signs and symptoms. Early treatment is the key to preventing further complica- tions and progression of AKI. For example, nurses in a primary care setting should implement the “sick day rules” to help reduce the risks of CA-AKI development. In the case of AKI trajectory, it is important for the nurse to educate the patient about the acute condition and supportive care for kidney recovery. Nephrology referral is beneficial for follow-up in the event of worsening of AKI or CKD development.

Timely intervention is key AKI is associated with significant clinical consequences and increased healthcare costs. It is crucial that all providers identify patients at risk for AKI and conduct primary prevention. Preventive measures are especially im- portant in high-risk patients, includ- ing those with previous AKI exposure, CKD, older age, or other high-risk comorbidities.

When AKI is present, diagnosis must be made in a timely manner to allow for prompt management. The process of minimizing progression

of AKI, especially with CA-AKI, is important both at hospital admission and at the clinic or office visit.

Though awareness of CA-AKI has increased recently, it is still an under- appreciated clinical presentation. Further research should focus more on comprehensive risk assessment, biomarkers, and management for HA-AKI and CA-AKI to ensure high- quality care.26 Preventive measures can be provided at the community level to patients with a previous AKI diagnosis and patients who may be at risk for developing AKI.2,10 ■

REFERENCES

1. United States Renal Data System. 2018 USRDS Annual Data Report: Epidemiology of Kidney Disease in the United States. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2018.

2. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl. 2012;2:1-138.

3. Bellomo R, Ronco C, Kellum JA, et al. Acute renal failure—definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group Crit Care. 2004;8(4):R204-R212.

4. 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(2):R31.

5. Schissler MM, Zaidi S, Kumar H, Deo D, Brier ME, McLeish KR. Characteristics and outcomes in community-acquired versus hospital-acquired acute kidney injury. Nephrology (Carlton). 2013;18(3):183-187.

6. Stucker F, Ponte B, De la Fuente V, et al. Risk factors for community-acquired acute kidney injury in patients with and without chronic kidney injury and impact of its initial management on prognosis: a prospective observational study. BMC Nephrol. 2017;18(1):380.

7. Jha V, Parameswaran S. Community-acquired acute kidney injury in tropical countries. Nat Rev Nephrol. 2013;9(5):278-290.

8. Sawhney S, Fluck N, Fraser SD, et al. KDIGO- based acute kidney injury criteria operate differently in hospitals and the community- findings from a large population cohort. Nephrol Dial Transplant. 2016;31(6):922-929.

9. International Society of Nephrology. AKI-0by25. 2020. www.theisn.org/all-articles/616-0by25.

10. Kashani K, Rosner MH, Haase M, et al. Quality improvement goals for acute kidney injury. Clin J Am Soc Nephrol. 2019;14(6):941-953.

11. American Nephrology Nurses Association. Core Curriculum for Nephrology Nursing: Acute K

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