Acute Kidney Injury: Challenges and Opportunities

Acute kidney injury: Challenges and opportunities

Abstract: Community-acquired acute kidney injury (CA-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 CA-AKI and its implications for APRNs.

By Nhan L.A. Dinh, MSN, CNP, AGACNP-BC, CCRN

cute kidney injury (AKI) is a heterogeneous risk of CKD, but if clinicians do not recognize the kidney disorder that increases in-hospital diagnosis, they cannot follow up or intervene. An AKI A morbidity and mortality. In 2016 data, the diagnosis also increases the chance of another AKI incidence of AKI was 20% for Medicare patients with episode, with a 30% risk of a recurrent AKI episode both chronic kidney disease (CKD) and diabetes.1 Us- within 1 year.1 ing Veterans Affairs (VA) 2016 data, AKI occurred in Mortality is increased with an AKI episode. Medi- more than 25% of hospitalized veterans over age 22, care data from 2016 shows an in-hospital mortality of but less than 50% of those with lab-documented AKI 8.2% but this increases to over 13% when includ- were coded as such.1 The chief concern here is a missed ing patients who were discharged to hospice.1 The in- opportunity for intervention. AKI increases long-term hospital mortality for patients without AKI was only

Keywords: acute kidney injury (AKI), Acute Kidney Injury Network (AKIN), chronic kidney disease (CKD), community-acquired acute kidney injury (CA-AKI), hospital-acquired acute kidney injury (HA-AKI), Kidney Disease Improving Global Outcomes (KDIGO), SvetaZi / Shutterstock Nephrotoxic Injury Negated by Just-in-time Action (NINJA), sick day rules

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

49.1

8.2 68.8 1.8 Home Death 4.7 Other 7. 6 Institution Hospice 22.7 5.0

30.1

2.0

With AKI diagnosis Without AKI diagnosis

1.8% (3.8% if including patients discharged to hos- and AKIN) into one coherent classifi cation.2 (See Clas- pice).1 Patients with AKI also were more likely to be sifi cations of AKI.) referred to a long-term skilled facility. (See Hospital Using this chart and per international KDIGO con- discharge status of fi rst hospitalization for Medicare pa- sensus criteria, AKI is diagnosed when there is an in- tients ages 66+, 2016.) crease 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 ■ AKI defi ned baseline known or presumed to have occurred within AKI was previously known as acute renal failure.2 the prior 7 days before AKI diagnosis.2 The guidelines However, many patients with kidney injury did not also specify that the diagnosis can be made when there progress to kidney failure, but they still had signifi cant, is a urine volume of less than 0.5 mL/kg/h for 6 hours.2 often permanent, loss of kidney function. Researchers AKI can be divided into two categories: community- worked to better defi ne AKI and noted that it is a po- acquired AKI (CA-AKI) and hospital-acquired AKI tential but often reversible rapid deterioration of kid- (HA-AKI). Patients who present to a hospital meeting ney function, with or without kidney damage. It may criteria for AKI as listed above are defi ned as having or may not be associated with oliguria. Numerous CA-AKI.5 HA-AKI has been the focus of research over groups attempted to defi ne AKI from both a clinical the last 2 decades as rates of AKI have steadily increased and physiologic point of view to allow for epidemio- and continue to do so.6 However, CA-AKI has gained logic studies. A consensus group developed the fi rst more attention recently because of its prevalence; it was criteria with a defi nition relying on changes in the recently stated that nearly 50% of AKI incidents begin serum creatinine (SCr), glomerular filtration rate in the community setting.7,8,10 This statistic is concern- (GFR), and/or urine output, known as Risk of renal ing and practitioners need to be alert to patients in dysfunction, Injury to the kidney, Failure of kidney their practice who are at risk. In 2013, the International function, Loss of kidney function, and End-stage kid- Society of Nephrology launched the “0by25” initiative ney disease (RIFLE).3 The Acute Kidney Injury Net- as a global target to ensure zero death of patients with work believed RIFLE mixed outcomes with severity preventable and treatable AKI by 2025 while raising classes and developed another classifi cation, the AKIN awareness to change incidence and prognosis world- criteria.4 In 2012, Kidney Disease: Improving Global wide.9 One diffi culty with tracking CA-AKI is that it Outcomes (KDIGO), an international organization, is easier to obtain records and statistics on hospital- standardized the competing defi nitions of AKI (RIFLE ized patients, but CA-AKI is often treated outpatient. www.tnpj.com The Nurse Practitioner • April 2020 49

CA-AKI can be prevented and treated.10 It is crucial nonsteroidal anti-infl ammatory drugs (NSAIDs) for for healthcare professionals to timely identify patients pain management, angiotensin-converting enzyme with CA-AKI as well as those who are at risk for de- (ACE) inhibitors or angiotensin II receptor block- veloping CA-AKI. ers (ARBs) for hypertension and CKD with diabetes, proton pump inhibitors for gastric refl ux, cyclosporine ■ Etiology of AKI and risk factors for CA-AKI and/or tacrolimus for antirejection management.12,13 AKI is caused by endogenous and/or exogenous condi- Intrarenal AKI can be categorized by the components tions, including but not limited to severe ischemia or of the kidney that are primarily affected: tubular, glo- sepsis, dehydration, gastrointestinal (GI) bleeds, ane- merular, interstitial, and vascular.12,13 mia, and/or use of nephrotoxic agents.11-13 These causes Postrenal AKI, the least common etiology, is usu- are often multifactorial. For example, the septic patient ally caused by an obstruction in the urinary fl ow out is given renal-toxic doses of antibiotics. Etiology of of either a single kidney or both kidneys. In postrenal AKI, kidneys still produce urine but the urine cannot be excreted via the Most patients presenting to a hospital urethra due to blockage. Therefore, with AKI are not aware that they have the urine is backed up into the kid- this condition. neys (retrograde fl ow), impairing the renal functions. Obstruction of the urinary fl ow can be a result of AKI can be divided into three categories: prerenal, obstructing stones or blood clots in the ureters or renal intrarenal/intrinsic kidney disease, and postrenal. (See pelvises, enlarged prostate, dysfunction or obstruc- AKI etiologies.) tion of the bladder, and/or strictures in the urinary Prerenal causes, such as volume depletion from system.12,13 dehydration, GI losses, excessive diuresis, hemorrhage Volume depletion was more commonly the cause from trauma, and/or changes in vascular resistance of CA-AKI than HA-AKI.14 Incidence of AKI increases occurring from disease processes or certain drug use, during summer months, as there is more risk of de- cause hypoperfusion to the kidneys.11-13 These changes, hydration. Two studies found that pre-renal causes in turn, lead to a lower GFR. relating to AKI are almost two-fold higher than all Intrarenal AKI can result from a prolonged pre- other causes together.5,14 Patients are at the highest risk renal state with or without toxic insults related to for CA-AKI when they have signifi cant comorbidities toxins, drugs, or any underlying systemic process along with polypharmacy.15 Diuretics are associated such as sepsis. Infl ammation and ischemia of the kid- with a higher incidence of CA-AKI than ACE inhibi- neys can be the sequela of those insults.12,13 Often, tors and ARBs.6 A combination of these medications over-the-counter (OTC) and prescribed medications puts patients at a greater risk for developing CA-AKI are a common intrarenal cause of CA-AKI such as than diuretics alone. Even though risk factors for

Classiﬁ cations of AKI2-4

Stage Urine Output RIFLE AKIN KDIGO

1 <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

2 <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 RRT 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.

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AKI etiologies

Prerenal AKI Intrarenal AKI Postrenal AKI ↓ Intravascular volume Acute tubular necrosis Upper urinary tract obstruction • Dehydration/hemorrhage • Ischemic: • Intrinsic • GI, cutaneous, or kidney losses – Sepsis – Stone • Third spacing – Hypotension – Papillary necrosis • Nephrotoxic: – Blood clot ↓ Effective blood volume – Drugs – TCC • Congestive heart failure – Pigments • Extrinsic • Cirrhosis – Retroperitoneal ﬁ brosis • Nephrotic syndrome Acute interstitial nephritis – Malignancy • Sepsis • Drug-induced – Ligation • Anesthesia • Infection-related – Pelvic mass • Systemic diseases Altered renal hemodynamics • Malignancy Lower tract obstruction • Preglomerular constriction • Urethral stricture • Postglomerular vasodilation Acute glomerulonephritis • Benign prostatic hypertrophy • Medications: ACE inhibitors, NSAIDs, CSA • Prostate cancer • Hepatorenal syndrome, surgery Acute vascular syndrome • Bladder cancer • Renal artery dissection • Stones: bladder Renal vascular obstruction • Renal artery thromboembolism • Neurogenic bladder • Renal vein thrombosis • Malpositioned indwelling Abdominal compartment syndrome • Atheroembolic disease urinary catheter

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

CA-AKI and HA-AKI are similar, CA-AKI is common electrolyte concentrations, pH, and excretion of wastes in elderly males with comorbidities including diabetes and toxins in the body, AKI does not manifest any spe- mellitus, hypertension, heart disease, existing CKD, cifi c signs and symptoms until other organs or systems cancer, and/or dementia.1,6,14 Gender also plays a role are affected. Patients with AKI can present with either in CA-AKI development. Men across all age groups oliguria or nonoliguria. Signs and symptoms of AKI are at higher risk for CA-AKI compared with their also depend on the causes that dictate how rapid and female counterpart. This factor is thought to be medi- severe the decline of kidney function is.11-13 Most pa- ated in part by testosterone.16,17 According to a Vander- tients presenting to a hospital with AKI are not aware bilt University study, testosterone has been found to that they have this condition. Patients often present increase renal EGFR expression, which is associated with symptoms that later cause AKI (such as hemor- with the likelihood of progressive kidney injury.17 The rhage, severe nausea and vomiting, or medication exact mechanism remains unclear and is currently overdoses) or the symptoms due to the complications being further investigated. Further, Black, Hispanic, of AKI (including altered mental status, severe edema, and hospitalized patients with previous diagnosis of shortness of breath, malaise/lethargy, hemodynamic AKI are more likely to develop AKI than those from instability, arrhythmias). These signs and symptoms different ethnic groups or those without risk fac- are often related to uremia or its underlying causes.11-13 tors.1,6,14,16,18 As noted previously, patients with diabetes mellitus and CKD tend to have more incidents of AKI ■ AKI management than those without comorbidities.1 Although CKD has AKI management varies, depending on the underlying consistently been shown to increase risk for the devel- etiology and the severity of kidney injury. Since the opment of AKI, one study found that it does not pose mortality rate is high in patients with AKI, the most any signifi cant differences in the severity of AKI.14 important goal of therapy is preventing life-threatening complications.11-13 However, current AKI interventions ■ Signs and symptoms of AKI are limited to supportive care and prevention of Although the kidneys are responsible for regulating ex- causative factors. Any possible causes of AKI and its tracellular and intravascular fl uid volume, osmolality, contributing factors should be prevented, treated, or www.tnpj.com The Nurse Practitioner • April 2020 51

removed as soon as possible.11,12 Prevention and early dehydration and the need to adjust certain medica- detection are the keys to improving outcomes for pa- tions. In addition, many patients present to urgent tients with AKI. For example, ACE inhibitors and ARBs care and are treated for the problem and labs are not should be held temporarily in those with decreased checked for existing kidney disease. Often, patients oral intake or those who present with prerenal AKI will self-medicate with OTC combination or multi- that can be started from the community setting, as they symptom medications containing NSAIDs, such as may exacerbate a prerenal state. While waiting for the naproxen or ibuprofen. This compounds the chance kidneys to recover on their own, restricting or avoiding of developing AKI. The National Kidney Foundation substances and medications that are known to impair has a patient website that highlights medication dosing kidney function is vital. In the event of significant for the at-risk patient.21 electrolyte derangement and/or fluid overload, an emergent dialysis can be performed to prevent further ■ Prevention complications related to cardiac dysrhythmia, heart Multiple studies have shown an improvement of out- failure, or respiratory failure during hospitalization. comes in patients with AKI with early detection as well Collaboration with or without a formal in-service as preventive measures when AKI is diagnosed.8,10,14,16,22 among the healthcare interdisciplinary team, including Stress to patients in the community setting the impor- primary care physicians, hospitalists, nephrologists as tance of optimization of hemodynamic and volume well as advanced practice providers, is crucial in opti- status as well as avoiding exposures to any nephrotoxic mizing AKI management. agents.10 When primary prevention fails to prevent AKI from occurring, the Recognition-Action-Result frame- ■ CA-AKI outcomes work can act as a secondary prevention by properly CA-AKI has been identifi ed as the most common type diagnosing and evaluating AKI when it occurs with a of AKI.14 CA-AKI accounted for almost 80% of the goal of limiting duration and severity to prevent com- patients with a discharge diagnosis of AKI at a single plications.10 A multidisciplinary approach has been VA hospital, and its severity was found as signifi cant recommended for tertiary prevention of AKI. This as HA-AKI.14 If present at admission, CA-AKI has a includes close monitoring, medication review, and signifi cant impact on hospital length of stay and is reassessment of patients, especially those with a history associated with a substantially higher risk of death and of AKI.2,10,12 Outpatient preventive measures after the CKD progression.14,19 The rate of rehospitalization in fi rst episode of AKI are vital in improving quality of life, alleviating long-term complications and limiting recurrences. Early treatment is the key to preventing One of the most promising pre- further complications of electrolyte ventive methods is implementing imbalances as well as progression of AKI. “sick day rules” developed by the National Health Service of the Unit- ed Kingdom.23 Sick is defined as patients with CA-AKI versus HA-AKI did not differ, vomiting or diarrhea (unless minor), fevers, sweats, and early temporary dialysis may improve the outcome and shaking. When these symptoms occur, patients are of CA-AKI.10,18 However, those who initially present directed to temporarily hold the following: with CA-AKI exhibit the highest incidence of CKD at • NSAIDs. These can impair renal autoregulation by their 5-year follow-up.19 Two studies found that 40.2% inhibiting prostaglandin-mediated vasodilatation of patients developed CKD stage 3 (GFR 30 to 60 ml/ of the afferent arteriole and may increase the risk of min) or higher, and nearly 27% progressed to either AKI. CKD stage 5 (GFR less than 15 ml/min) or end-stage • ACE inhibitors and ARBs. These reduce systemic BP renal disease (ESRD) requiring dialysis.19 and also cause vasodilatation of the efferent arteriole, CA-AKI is often underappreciated as a clinic or further reducing glomerular perfusion pressure. offi ce-based issue.14,20 In patients presenting with up- • Diuretics (including spironolactone and eplere- per respiratory or GI complaints, clinicians may focus none). These can cause hypovolemia and AKI. on the presenting condition and may not consider • Other BP-lowering medications.

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• Medications that may accumulate due to decreased Nephrology referral is benefi cial for follow-up in the kidney function due to hypotension leading to risk event of worsening of AKI or CKD development. of adverse effects, such as metformin (risk of lactic acidosis), sulfonylureas (risk of hypoglycemia), and ■ Conclusion trimethoprim (risk of hyperkalemia). AKI is associated with signifi cant clinical consequences and increased healthcare costs. It is crucial that all ■ N ephrotoxic Injury Negated by Just-in-time providers identify patients at risk for AKI and conduct Action (NINJA) primary prevention. Preventive measures are especially Because all AKI can be more devastating in children, the important in high-risk patients, including those with researchers at Cincinnati Children’s Hospital (CCH) previous AKI exposure, CKD, older age, or those pre- developed an electronic health record screening and senting with other high-risk comorbidities. trigger program for the hospital.24 Enrolling all non- When AKI is present, diagnosis must be made in a critically ill hospitalized children between 2011 and timely manner to allow for prompt management. The 2015, CCH decreased the exposure rate of nephrotoxic process of minimizing progression of AKI, especially medications by 38%. More important, CCH reduced with CA-AKI, is important both at hospital admission the incidence of AKI by an impressive 64%.24 CCH re- and at the clinic or offi ce visit. All preventable causes ports the most important aspect of the NINJA program of AKI, especially medications, need to be removed as was the person-person interaction. If the pharmacist soon as possible. Once AKI develops, supportive care noted three or more nephrotoxic medications for one for the kidneys is vital, as is follow-up to identify those patient, he or she would notify the healthcare team. who develop long-term sequela. Nephrology should The pharmacist would highlight the risk and discuss be consulted as soon as possible, especially when there other medications that would be less nephrotoxic, but is a possibility of the need for renal replacement ther- leave the fi nal decision to the healthcare team.24 CCH apy (hemodialysis, peritoneal dialysis, continuous renal offered this software application and clinical system to replacement therapy [RRT]). all children’s hospitals nationwide, and at present more Though awareness of CA-AKI has increased re- than 14 children’s hospitals have implemented it.25 cently, it is still one of many underappreciated clinical presentations. As more NPs are entering the primary ■ Implications for A PRNs care fi eld, they need to be at the forefront of prevent- APRNs diagnose, treat, and educate patients across the ing, recognizing, and treating AKI. Further research lifespan and in all settings. APRNs order and interpret should focus more on comprehensive risk assessment, diagnostic tests and make appropriate diagnoses and biomarkers, and management for AKI and CA-AKI individualized care plans while effectively commu- to ensure high-quality care.26 Preventive measures can nicating with other team members. Since CA-AKI be provided at the community level to patients with and HA-AKI can both be devastating diagnoses for previous AKI diagnosis and patients who may be at any patient and can increase mortality during hos- risk for developing AKI.2,10 pitalization, it is important that the APRN is familiar REFERENCES with the pathophysiology of AKI for ordering and 1. United States Renal Data System. 2018 USRDS annual data report: epidemi- interpreting diagnostic tests and effectively identifying ology of kidney disease in the United States. National Institutes of Health, signs and symptoms of clinical AKI. This also assists National Institute of Diabetes and Digestive and Kidney Diseases. 2018. 2. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury APRNs in establishing individualized care plans while Work Group. KDIGO clinical practice guideline for acute kidney injury. effectively communicating with other team members Kidney Int Suppl. 2012;2:1-138. 3. Bellomo R, Ronco C, Kellum JA, et al. Acute renal failure - defi nition, out- to promptly provide treatment. Early treatment is the come measures, animal models, fl uid therapy and information technology key to preventing further complications of electrolyte needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. 2004;8(4):R204-R212. imbalances, as well as progression of AKI. For example, 4. Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report APRNs in a primary care setting should implement the of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007; 11(2):R31. “sick day rules” to help reduce the risks of CA-AKI de- 5. Schissler MM, Zaidi S, Kumar H, Deo D, Brier ME, McLeish KR. Character- velopment. In the case of AKI trajectory, it is important istics and outcomes in community-acquired versus hospital-acquired acute for the APRN to educate the patient about the 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- condition and supportive care for kidney recovery. acquired acute kidney injury in patients with and without chronic kidney www.tnpj.com The Nurse Practitioner • April 2020 53

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