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 48 The Nurse Practitioner • Vol. 45, No. 4 www.tnpj.com Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved. Acute kidney injury: Challenges and opportunities 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 Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved. Acute kidney injury: Challenges and opportunities 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. 50 The Nurse Practitioner • Vol.