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<b>Speakers Bureau: </b>
<b>Needed a Better Way to Assess AKI</b>
<b>Needed a Better Way to Monitor Kidney Stress In Real </b>
<b>Time</b>
<b>Use of ScR and Urine Output is Too Slow and Lagging</b>
<b>Increasing Biomarker Presence In Clinical Care</b>
<b>AKI Is Expensive and Has Negative Effect on Metrics</b>
<b>and Patients!!</b>
*Genetic and Inflammatory Markers of Sepsis (GenIMS) study.
<i>[1] Murugan R, Karajala-Subramanyam V, Lee M, et al. Acute Kidney Injury in Non-Severe Pneumonia is Associated with an Increased Immune Response and Lower Survival. Kidney Int. </i>
2010;77:527-535.
<b>AKI was found to be prevalent (34%) in a study of 1836 hospitalized patients with </b>
<b>community acquired pneumonia*,1</b>
Severe AKI (n = 189, 10%)
Moderate AKI (n = 135, 7%)
Mild AKI (n = 307, 17%)
No AKI (n = 1205, 66%)
<b>Mortality in </b>
<b>Sepsis was identified as the presumed etiology in 19% of AKI cases in the ICU in one </b>
<b>study2</b> <b><sub>and septic shock was found to be a contributing factor to AKI in 48% of cases </sub></b>
<b>in another study.3</b>
<b>Hospital </b>
<b>Mortality3</b>
[<i>2] Mehta RL, Pascual MT, Soroko S, et al. Spectrum of Acute Renal Failure in the Intensive Care Unit: the PICARD Experience. Kidney Int. 2004;66:1613-1621.</i>
<i>[3] Uchino S, Kellum JA, Bellomo R, et al. Acute Renal Failure in Critically Ill Patients: a Multinational, Multicenter Study. JAMA. 2005;294:813-818</i>
<b>28%</b>
<b>57%</b>
<b>0%</b>
<b>10%</b>
<b>20%</b>
<b>30%</b>
[15] Bihorac A et al. National Surgical Quality Improvement Program Underestimates the Risk Associated with Mild and Moderate Postoperative Acute
<i>Kidney Injury. Crit Care Med. 2013;41(11):2570-2583.</i>
0,6% 3%
7%
26%
0%
10%
20%
30%
No AKI Mild (Risk) Moderate
(Injury) (Failure)Severe
3%
6%
11%
29%
0%
10%
20%
No AKI Mild (Risk) Moderate
(Injury) (Failure)Severe
<b>Hospital Mortality</b> <b>90-Day Mortality</b>
In a single-center cohort of 27,841 adult surgical patients undergoing major surgery, it was
identified that hospital and 90-day mortality were significantly higher among patients with AKI
<i>[16] Hobson CE et al. Acute Kidney Injury is Associated with Increased Long-Term Mortality After Cardiothroacic Surgery. Circulation.</i>
2009;119:2444-2453.
<i>N = 2973 CT Surgery Patients16</i>
0%
10%
20%
30%
40%
50%
60%
70%
80%
All Types Isolated CABG Valve Surgery Aortic Surgery Thoracic
Surgery TransplantHeart
<b>% of </b>
<b>CT</b>
<b> S</b>
<b>ur</b>
<b>ger</b>
<b>y </b>
<b>w</b>
<b>ith </b>
<b>A</b>
<b>K</b>
<b>I</b>
Moderate
AKI Severe AKI
Mild AKI
No AKI
<i>[9] Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Inter, Suppl. 2012; 2:1-138</i>
<i>[10]Tolwani A. Continuous Renal-Replacement Therapy for Acute Kidney Injury. N Engl J Med. 2012;367:2505-2514.</i>
Acute Kidney Injury (AKI) is a rapid (typically within about 48 hours) loss of kidney function9
• 96% of AKI does NOT require RRT10
RIFLE/AKIN/KDIGO criteria were validated over the past decade and provide a standardized
definition of AKI
The criteria are based on increases and serum creatinine and decreases in urine output and stratify
AKI into three severity levels:9
1. Mild AKI (RIFLE-R or Stage 1)
2. Moderate AKI (RIFLE-I or Stage 2)
3. Severe AKI (RIFLE-F or Stage 3)
The criteria are good for epidemiological studies but difficult to apply at the bedside; AKI thus
remains largely a clinical diagnosis9
8
[4] Massicottee-Azarniouch, Magder S, Goldberg P, Alam A. Acute Kidney Injury in the Intensive Care Unit: Risk Factors and Outcomes of Physician Recognition Compared with KDIGO Classification. Poster presented at: Society of Critical
Care Medicine; February 2016; Orlando, FL.
<b>AKI Reported by ICU Staff</b> <b>No AKI Reported by ICU Staff</b>
<b>2,393 patients admitted to academic hospital ICU in Montreal, Canada from January 2006 through December 2011. KDIGO AKI </b>
<b>calculated from SCr values. Physician definition of AKI was determined by asking ICU staff if a patient had “acute renal failure”.4</b>
<b>“ICU physicians only identified a small proportion of the patients with AKI. Many of the severe forms </b>
<b>of AKI, which were most associated with adverse outcomes, were missed by the physician reporting.”</b>
<b>79% of the cases </b>
<b>of Moderate and </b>
<b>Severe AKI Were </b>
<b>Reporting </b>
<b>Physician</b>
<b>0</b>
<b>100</b>
<b>200</b>
<b>300</b>
<b>400</b>
<b>500</b>
<b>Moderate AKI</b> <b>Severe AKI</b>
<b>Numb</b>
<b>er </b>
<b>of P</b>
<b>atien</b>
<b>ts</b>
AKI IS DEADLY, COSTLY, AND PREVALENT… AND LOCAL
<b>2016 ANNUAL</b> <b>AKI DIAGNOSES6,7,8*</b>
<b>AVG</b> <b>COST</b>
<b>INCREASE</b> <b>/ </b>
<b>PATIENT7</b>
<b>AVG</b> <b>LENGTH</b> <b>OF</b>
<b>STAY</b> <b>INCREASE</b> <b>/ </b>
<b>PATIENT7</b>
<b>READMISSION</b> <b>RATE</b>
<b>INCREASE9</b>
<b>2200 ICU ADMISSIONS</b>
<b>476 ESTIMATED</b> <b>MODERATE/SEVERE</b> <b>ICU DIAGNOSES</b>
<b>$29,800</b> <b>10.4 DAYS</b> <b>15.9%</b>
<b>Although Often Under-reported5<sub>, AKI Hits Home:</sub></b>
<b>COST</b> <b>INCREASE</b>
<b>LENGTH OF</b> <b>STAY</b>
<b>INCREASE</b>
<b>READMISSION</b> <b>INCREASE</b>
<b>ANNUAL</b> <b>ICU IMPACT: </b>
<b>MODERATE/SEVERE</b> <b>AKI</b>
[5] Massicottee-Azarniouch, Magder S, Goldberg P, Alam A. Acute Kidney Injury in the Intensive Care Unit: Risk Factors and Outcomes of Physician Recognition Compared with KDIGO Classification. Poster presented at: Society of Critical Care Medicine;
February 2016; Orlando, FL.
[6] American Hospital Directory Database, accessed Dec 2017 on 7,104 hospitals, data on file
[7] Hobson CE, Ozrazgat-Baslanti T, Kuxhausen A, et. al. Cost and Mortality Associated With Postoperative Acute Kidney Injury. Annals of Surgery. 2014;00:1–8
[8] SCCM: />
Figure adapted from: [1] Lewington AJP, Certa J, Mehta RL Raising Awareness of Acute Kidney Injury: A Global Perspective of a
<i>Silent Killer. Kidney Int. 2013;84(3):457-467.</i>
<i>[19] Kellum JA, Chawla LS. Cell-Cycle Arrest and acute kidney injury: the light and dark sides. Nephrol Dial Transplant. 2016;1:16-22</i>
Kidney
Stress Decreased Function
Asymptomat
ic Symptomatic (Diagnosis)
Figure adapted from: [1] Lewington AJP, Certa J, Mehta RL Raising Awareness of Acute Kidney Injury: A Global Perspective of a Silent Killer.
<i>Kidney Int. 2013;84(3):457-467.</i>
<i>[20] Martensson J et al. Novel Biomarkers of Acute Kidney Injury and Failure: Clinical Applicability. Brit J Anesth. 2012;109(6):843-50.</i>
<i>[21] Wlodzimirow KA, et al. A comparison of RIFLE with and without urine output criteria for acute kidney injury in critically ill patients. Critical </i>
<i>Care. 2012;16:R200.</i>
[22] Gould CV, et al. Guideline for Prevention of Catheter-Associated Urinary Tract Infections. HICPAC. 2009.
Kidney
Stress Decreased Function
Asymptom
atic Symptomatic (Diagnosis)
<b>Serum Creatinine</b>
<b>• Lagging indicator20</b>
<b>• Only elevates after 50% of </b>
<b>kidney function lost20</b>
<b>• Non-diagnostic for up to </b>
<b>52% of moderate and </b>
<b>severe AKI21</b>
<b>Urine Output</b>
<b>• Lagging indicator21</b>
<b>• Tedious to measure21</b>
<b>• Affected by HAI </b>
<b>initiatives22</b>
Wouldn’t it be nice to identify
dysfunction occurs?
<i>[10] Kashani K, et al. Discovery and validation of cell cycle arrest biomarkers in human acute kidney injury. Crit Care. 2013;17:R25.</i>
<i>[11] Bihorac A, et al. Validation of Cell-Cycle Arrest Biomarkers for Acute Kidney Injury Using Clinical Adjudication. Am J Respir Crit Care </i>
<i>Med. 2014;189(8):932-939.</i>
<b>340 Biomarkers Evaluated </b>
<i>including NGAL & KIM-1</i>
<b>Discovered in 1,200+ Patients</b>
<i>including sepsis, shock, major </i>
<i>surgery and trauma patients</i>
<b>Urinary [TIMP-2]*[IGFBP-7] stood out as the </b>
<b>best-performing biomarkers to predict development </b>
of moderate or severe AKI within 12 hours10
Candidates identified through hypothesis based
on AKI pathophysiology and evaluated individually
and in combinations of 2-4 biomarkers10
<b>Validated in 500+ Critically Ill </b>
<i><b>Patients from Intended Use </b></i>
<i>Population</i>
<i>Patients had diverse ICU admissions (surgery, </i>
<i>sepsis, trauma) and common comorbidities </i>
<i>(including CKD, diabetes, heart disease) </i>11
<b>Tissue Inhibitor of Metalloproteinase-2 (TIMP-2)</b>
<b>Insulin-like Growth Factor Binding Protein-7 (IGFBP-7)</b>
TIMP-2 and IGFBP-7 are:14
• <b>Biomarkers of cellular stress in the early phase of tubular cell injury caused by a </b>
<i>wide variety of insults (inflammation, ischemia, oxidative stress, drugs, and </i>
<i>toxins)</i>
• <b>Involved in G1 cell-cycle arrest that prevent cells from dividing until damage </b>
can be repaired
• <b>Both biomarkers appear as “alarm” proteins from other nearby cells</b>
This may help explain why urinary TIMP-2 and IGFBP-7 correspond to risk of AKI.
<i>[12] TIMP-2 figure adapted from: Tuuttila A et al. Three-dimensional structure of human tissue inhibitor of metalloproteinases-2 at 2.1 A resolution. J Mol Biol. 1998;284:1133-1140.</i>
[13] IGFBP-7 figure adapted from: ModBase: Database of Comparative Protein Structure Models [accessed 2014 December 10]. Available from:
<i>[14] Gocze I, et al. Urinary Biomarkers TIMP-2 and IGFBP7 Early Predict Acute Kidney Injury After Major Surgery. PLoS ONE. 2015;10(3).</i>
More complete information = personalized medicine
opportunity to consider
before it’s too late
<b>Gauges the Risk of </b>
<b>Injury before </b>
<b>Damage Occurs </b>
<b>• Specific to AKI11</b>
<b>• Fast & Simple: 20 min urine test11</b>
<b>• Commercially Available in USA11</b>
<b>• Peer-reviewed evidence11</b>
<b>• Complementary to HAI and QI </b>
<b>initiatives</b>
<b>• Easy, cost effective to Implement</b>
<b>• When Do I Order the NephroCheck Test?</b>
<b>• Sepsis</b>
<b>• CVI</b>
<b>• Shock</b>
<b>• Logistics</b>
• <b>How Long Does it Take To Get the Results?</b>
<b>• Who to Test</b>
<b>• When to Test</b>
<b>• What Will You Do Different</b>
<b>• Different Treatments Sepsis, Shock, Cardiovascular?</b>
<b>• Reassessment After Intervention</b>
<b>• Trend or Treatment Success</b>
<b>• Value of the Negative Test</b>
[9] Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney inter., Suppl. 2012; 2:
1-138.
[11] Murugan R et al. Acute Kidney Injury in Non-Severe Pneumonia is Associated with an Increased Immune Response and Lower Survival. Kidney Int. 2010;77:527-535.
[13] Uchino S et al. Acute Renal Failure in Critically Ill Patients: a Multinational, Multicenter Study. JAMA. 2005;294:813-818.
[23] Ronco C, Ricci Z. The concept of risk and the value of novel markers of acute kidney injury. Crit Care. 2013;17:117-118.
<b>Patient Risk Factors9</b>
• Dehydration or volume depletion
• Advanced Age
• Female gender
• Black race
• CKD
• Chronic Disease (heart, lung, liver)
• Diabetes Mellitus
• Cancer
• Anemia
<b>Acute Risk Factors9,11,13</b>
• Sepsis
• Pneumonia
• Cardiogenic Shock
• Major Surgery
• Cardiac Surgery
• Nephrotoxic Drugs
• Radiocontrast Agents
[9] Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney inter., Suppl. 2012; 2: 1-138.
[23] Ronco C, Ricci Z. The Concept of Risk and the Value of Novel Markers of Acute Kidney Injury. Crit Care. 2013;17:117-118.
<i><b>What if we could get ahead of </b></i>
<b>AKI? </b>
<i><b>Instead of saying, “wait and </b></i>
<i><b>see</b></i><b>…”</b>
<b>• Early Warning</b>
<b>• Stratify Patient Risk</b>
<b>• Attention on “At Risk” </b>
<b>patients </b>
<b>Target patients – High risk for AKI such as: </b>
<b>CV surgery</b>
- Shock – septic, cardiogenic, hemorrhagic
- Acute decompensated CHF with cardiogenic shock
- ARDS for P/F ratio <200
- Oliguria – persistent after resuscitation
<b>Exclusion: </b>
- Age < 18 years
- Previous renal transplant
*For moderate-severe AKI in the next 12 hours.
<b>The NEPHROCHECK®</b> <b>Test cutoff (AKIRISK®</b> <b>Score > 0.3) was prospectively </b>
<b>selected prior to validation studies to achieve*:</b>
<b>High sensitivity and negative predictive value are important in risk </b>
<b>assessment to ensure that:</b>
• <b>The majority of patients who will develop AKI test positive </b>
• <b>Few patients with a negative test result will be at risk of developing AKI</b>
<b>Study A (408 patients)</b> <b>Study B (126 patients)</b>
High sensitivity 92% 76%
Acceptable specificity 46% 51%
High negative predictive
value 96% 88%
<b>High sensitivity and negative predictive value for confidence in identifying the majority of patients at risk for AKI.</b>
Confidence the AKIRISK® <b>Score is not elevated due to common comorbidities such as </b>
CKD, diabetes, surgery, sepsis and trauma.
<i>Results from Study A and B are not statistically different (p>0.05)</i> 25
<b>AK</b>
<b>IR</b>
<b>ISK</b>
<b>®</b> <b>Sc</b>
<i>[9] Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Inter, Suppl. 2012; 2:1-138</i>
<i>[19] Kellum JA, Chawla LS. Cell-Cycle Arrest and acute kidney injury: the light and dark sides. Nephrol Dial Transplant. 2016;1:16-22</i>
<b>LOW AKI RISK: ≤ 0.3</b> <b>HIGH AKI RISK: > 0.3</b>
- Standard of Care – document
UOP AND Foley remove ASAP
- Monitor & document hourly UOP & consider Foley insertion/maintain
- Daily Serum BUN, Cr. - Serum BUN, Cr. Q 12
- Urine Na, Cr, Eos x 1
- Consider repeat NephroCheck in 12hrs
- CI/SVV/SVI not monitored <sub>- Mandatory hemodynamic monitoring for CI/SVV/SVI Q8 </sub><b><sub>POP algorithm</sub></b>
- Check IVC compressibility with US
- Goals -- MAP>70, SVV < 13, CI >2.0
- Vasopressors (phenylephrine, nor-epinephrine, vasopressin)
- Inotrope support (dobutamine or milrinone)
- Low threshold for inotropes if CI < 2, ScvO2 < 70, and/or Lactic Acid increasing
despite adequate MAP and volume expansion
- Diuretics or fluids as needed
based on <b>physiology</b>
- Diuretics and fluids to be utilized ONLY after determining fluid status <b>POP</b>
- For oliguria or hypotension, IVV expansion <b>SV optimization POP</b>
- Crystalloid, blood products rarely albumin, clinical decision
<b>LOW AKI RISK: ≤ 0.3</b> <b>HIGH AKI RISK: > 0.3</b>
- Repeat NephroCheck if new
insult (Same incl/excl criteria)
- Consider repeat NephroCheck testing at 12 hr intervals if there is a need to
reevaluate renal stress/intervention
- Avoid & resolve hypervolemia (> 10% fluid gain)
<b>address hemodynamics using physiology POP</b>
- Can use ACEI/ARB
- Cautious use of NSAIDs
- No NSAIDS or ACEi/ARB
- Avoid all unnecessary IV IODINATED contrast dye studies
- Minimize exposure to nephrotoxins (i.e. vancomycin, piperacillin/tazobactam,
aminoglycosides)
- ADJUST MEDICATION DOSING ANTICIPATING DECREASED GFR ESPECIALLY IF UOP
REMAINS LOW
<b>Consider RRT/CRRT Initiation: Inadequate UOP > 12-24 hrs, symptomatic volume </b>
Patient History:
• 61 yo Male with DM, CAD-stent, Afib, COPD
– Creatinine 1.0
– MICU With Active GI Bleed
– Intubated, Central IV Access, A-line Placed
– Bedside UGI Endoscopy For Active Bleed—Vessel Cauterized
– Rebleed > IR for Embolization
• Day 1
– Fluid Resuscitation
– 7 Units RBC’s and 8 Liters Crystalloid
Clinical Status:
• The physician managing the patient realized an early bump in NC
required extremely aggressive fluid resuscitation, especially with such
high blood loss. Concern was “over-resuscitation” of fluid.
Clinical Issue:
ã NephroCheckđ Test Interpretation: Elevated AKIRisk® Score (> 0.3) Indicates
Higher Risk for Mod/Sev AKI
– AKIRisk Score 0.31 (high kidney stress)
Assessment & Intervention:
• After Successful Resuscitation and Embolization
• CI 2.4 / SVV 10
• Day 2
• CI 2.2 / SVV 11
• Max Creatinine Over Extended Stay
• Creatinine 1.1 Max With NO AKI
Patient Outcome:
• Patient Completely Recovered with no Kidney Damage
Patient History:
• 84 yo Female with Hx of Sjogrens Disease and Arterio-Venous
Malformations Throughout Bowel
• 95Kg pt Admitted to ED With Hgb 7.6 With GI Bleed/Pain
Clinical Status:
• Day 1--Admitted to MICU
• Hgb Fell to 6, BP 60/40, Unresponsive, Shock
• Intubated and Resuscitated Aggressively with 2 pRBC’s, Fluid and
Pressors
• Taken to Interventional Radiology for Embolization
Clinical Issue:
ã NephroCheckđ Test Interpretation: Elevated AKIRisk® Score (>
0.3) indicates higher risk for mod/sev AKI
Assessment & Intervention:
• Day 2: Successful Resuscitation
• Extubated
• Creatinine 1.2, Hgb 9.5
• Pt Transferred to Floor on Day 3
• Surprised to Learn of Low Renal Stress but This Gave Confidence
to Quickly Move pt on to Lower Level of Care:
Key Take Away – Value of Negative Score
<b>• When we test with NephroCheck: As soon sepsis is suspected</b>
• Nurse Alerts
• Hospitalist Training
<b>• Why we test: AKI shows up with Sepsis more than any other reported DRG</b>
• Real Time Picture of the Kidneys
• Did Interventions Make a Difference
• Positive Predictive of the Negative Test
• Helps with Family Discussion of Care Plan
<b>• What we do with the results: Including kidney care in sepsis treatment</b>
• Maintain MAP
• Volume Status
• Review Medications
<b>Build A Team </b>
<b>Lab, Nephrology, CT Surgeon, Nursing, Administration</b>
<b>Education </b>
<b>Before Implementation</b>
<b>After Adoption</b>
<b>Feedback To the Team Of Success!!! </b>