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Acute Kidney Injury
Lori A. Cox MSN, ACNP‐BC, ACNPC, CCRN, FCCM
Nurse Practitioner Neuroscience Critical Care
Penn State Hershey Medical Center
Pa Coalition of Nurse Practitioner Annual Conference
November 2015
Intended Audience
APP’s managing adult patients in acute and critical care.
Disclosures
None
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Background of Problem
• Estimated 7% of all hospitalized Pts develop AKI1
• 5‐20% of all Critical Care Pts develop at least one incident of AKI2
• 4‐9% of AKI Pts will need RRT2
• Up to 80% Mortality
• Independent Risk Factor for Mortality
1. Nash K, Hafeez A, Hou S. Hospital‐acquired renal insufficiency. Am J Kidney Dis 2002; 39:930–936.2. Metnitz PGH, Krenn CG, Steltzer H, et al. Effect of acute renal failure requiring renal replacement therapy on outcome in critically ill
patients. Crit Care Med 2002; 30: 2051–2058.
Definition
Abrupt loss of kidney function resulting in the retention of urea and other nitrogenous waste products and in the dysregulation of extracellular volume and electrolytes.
Operational Definition
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Acute Dialysis Quality Initiative (ADQI)
• Expert Nephrologists and Intensivists
• Uniform definition needed
• RIFLE criteria(changes within 7 days)
Bellomo et al. Crit Care 2004; 8:R204.
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:R204
Acute Kidney Injury Network Criteria
• Acute Kidney Injury Network
• After volume resuscitated
• Ruled out obstruction
Mehta et al. Crit Care 2007; 11:R31.
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AKIN Definition
• Abrupt (within 48 h) reduction in kidney function currently defined as an absolute increase in serum creatinine of 0.3 mg/dL or more (≥26.4 μmol/L) or
• A percentage increase in serum creatinine of 50% or more (1.5-fold from baseline) or
• A reduction in urine output (documented oliguria of < 0.5 mL/kg/h for >6 h)
Mehta et al. Crit Care 2007; 11:R31.
Kidney Disease Improving Global Outcomes
• Clinical Practice Guidelines for AKI
• Modified definition‐blend of both RIFLE & AKIN definitions
Kellum, J. et al. KDIGO AKI Work Group Crit Care 2013;17:204
KDIGO Definition of AKI
Any of the following
• Increase in Cr by > 0.3mg/dl within 48 hrs
• Increase in Cr by >1.5 times baseline, which is known or presumed to have occurred within the prior 7 days
• Urine volume <0.5 mk/kg/hr for 6 hrs
Kellum, J. et al. KDIGO AKI Work Group Crit Care 2013;17:204
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KDIGO Staging
Causes of AKI
Exposures Susceptibility
Sepsis
Critical Illness Dehydration/Vol Loss
Circulatory Shock Advanced Age
Nephrotoxic Drugs Female Gender
Radiocontrast Agents Diabetes
Cardiac Surgery(CPB) Black Race
Trauma CKD
Burns Cancer
Intra-abdominal HTN
Kellum et al. Critical Care 2013, 17:204
A1: AKI is defined as any of the following (not graded): • increase in SCr by ≥0.3 mg/dl (≥26.5 μmol/l) within 48 hours; or • increase in SCr to ≥1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or • urine volume <0.5 ml/kg/hour for 6 hours.
A2: AKI is staged for severity according to the criteria presented
A3: The cause of AKI should be determined whenever possible
Kellum, J. et al. KDIGO AKI Work Group Crit Care 2013;17:204
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B1: We recommend that patients be stratified for risk of AKI according to their susceptibilities and exposures (Grade 1B).
B2: Manage patients according to their susceptibilities and exposures to reduce the risk of AKI
B3: Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI (not graded). Individualize frequency and duration of monitoring based on patient risk and clinical course (not graded).
Kellum, J. et al. KDIGO AKI Work Group Crit Care 2013;17:204
Pathogenesis of AKI
PreRenal AKI
• Extracellular Fluid Loss– Hemorrhage
– GI losses
– Renal losses(diuretics/DI)
– Cutaneous losses(Burns)
• Fluid Sequestration– Capillary leak(sepsis)
– GI(pancreatitis/peritonitis)
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PreRenal AKI
• Decreased CO– HF/Cardiogenic Shock
• Systemic Vasodilation– Septic Shock
– Cirrhosis
• Alt Intrarenal Hemodynamics– Hepatorenal
– Meds(ACEI, NSAIDS, Contrast)
Intrinsic AKI
• Acute Tubular Necrosis(85-90%)– Ischemia/Hypoperfusion
• Shock
• CPB
• Post Cardiac Arrest
– Nephrotoxic• Myoglobin
• Drugs– Vanc
– Aminoglycosides
– Contrast
Intrinsic AKI
• Acute Interstitial Nephritis(5-10%)– Drug Induced
• PCN
• NSAIDS
• Rifampin
• PPI
• Allopurinol
• Quinolones
• Acute Glomerulonephritis– Post Infectious
– Systemic Lupus Erythematous
– Systemic vasculitis
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Intrinsic AKI
• Acute Vascular Disease– Large vessel disease
• Renal artery thrombosis
• Renal artery dissection
• Renal vein thrombosis
– Renal Microvasculature• Malignant HTN
• Hemolytic Uremic Syndrome
• Thrombotic Thrombocytopenic Purpura
• Intratubular Obstruction– Crystalline nephropathy
• Ethylene glycol poisoning
• Methotrexate
• Acyclovir
– Myeloma cast nephropathy
Post-Renal AKI
• Upper Urinary Tract– Nephrolithiasis
– Stricture
– Malignancy
• Extrinsic– RP Hematoma
– Surgical ligation
• Lower Urinary– BPH
– Prostate Ca
– Bladder Ca
– Urethral stricture
Types of Acute Kidney Injury
• Pre-renal (40 - 80%)
– renal artery disease
– systemic hypotension
– Dehydration
• Intra-renal (10 - 50%)
– acute tubular necrosis
– interstitial nephritis
• Post-renal (< 10%)
– obstruction
Significant overlap
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Diagnosis and Evaluation
• History– Drugs including OTC and herbal remedies
– Exposures
– Previous renal impairment
• Physical Exam
Diagnostic Studies
• Labs– BMP/Neph Panel
– Osmolality
– CBC
– UA
– Urine Lytes/Osmo
– FeNe or Fe Urea
• Renal US
Urine Analysis
• Presence of RBC’s always pathological
– Eumorphic RBC’s-bleeding
– Dysmorphic/casts- glomerular inflammation
• WBC’s
– Infection
– AIN
• Myoglobin
• Urine eosinophil's(Wright or Hansel stain)
– Interstitial nephritis
• Uric Acid Crystals
– ATN from uric acid nephropathy
• Calcium oxalate crystals
– Ethylene Glycol toxicity
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Urine Sodium
Low
• Diuretics
• Heart Failure
• Adrenal Insufficiency
• Hepatic Failure
High
• Prerenal Azotemia
• HepatoRenal Syndrome
• Hyperladosteronism
• Hyponatremia
FeNa
FENa = (UNa/PNa) / (UCr/PCr) X 100
• Only useful if oliguric
• <1% PreRenal Azotemia
• >1% ATN– Except radiocontrast nephropathy,
severe burns, acute glomerulonephritis, and rhabdomyolysis
Fe Urea
FEUrea = (Uurea/Purea) / (UCr/PCr) X 100
• Use for Pts receiving diuretics
Urine IndicesEtiology Urine Na FeNa FeUrea Urine Sediment
Pre-Renal <20mmol/L <1% <35% WNL or hyaline or rare granular casts
ATN >40mmol/L >2% >60% Epithelial casts, muddy brown casts
AIN Variable:maybe >40mmol/L
May be <1% RBC’s, QBC’s, WBC casts, Eosinophils
Adapted from Critical Care Medicine (2014) Chapter 55; Table 55.4
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NephroCheck
• First test to assess risk of developing moderate to severe AKI
• Identifies 2 proteins in urine
• NephroCheck accurately detected 92 percent of AKI patients in one study and 76 percent in the other. In both studies, NephroCheck incorrectly gave a positive result in about half of patients without AKI.
FDA News Release September 5, 2014
Management of AKI
• Identify Underlying Cause• Reverse
• Prevent further injury
• Determine Volume Status
Volume Depletion
• Clinical History– Vomiting/Diarrhea
– Diuretic use
• Physical Exam Findings/VS– Tachycardia
– Hypotension
– Dry mucous membranes
• Treatment– Volume Replacement
• Limit further injury
– Crystalloids
– Target endpoints• MAP/HR
• SVV
• Passive leg raise
• UOP
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Volume Overload
• May be intrinsic or secondary to fluid resuscitation or daily care
• Evaluate I/O’s
• Edema/Anasarca
• CXR w signs of volume overload
• Loop Diuretics– May need high
doses/infusions
• If refractory, try thiazide such as Chlorothiazide(Diuril)
C1: Evaluate patients with AKI promptly to determine the cause, with special attention to reversible causes (not graded).
C2: Monitor patients with AKI with measurements of SCr and urine output to stage the severity, according to Recommendation A2 (not graded).
C3: Manage patients with AKI according to the stage and cause (not graded).
C4: Evaluate patients 3 months after AKI for resolution, new onset, or worsening of pre-existing chronic kidney disease (CKD) (not graded).
Kellum, J. et al. KDIGO AKI Work Group Crit Care 2013;17:204
Renal Replacement TherapyIndications
A- Acidosis(metabolic)
E- Electrolyte Abnormality(Hyperkalemia)
I- Intoxication(ethelene glycol)
O-Overload(acute volume)
U-Uremia(pericarditis, uremic encephalopathy)
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Word Salad of RRT
• CVVH – Continuous VenoVenous Hemofiltration
• CVVHD – Continuous VenoVenous HemoDialysis
• CVVHDF – Continuous VenoVenous HemoDiaFiltration
• IHD – Intermittent HemoDialysis
• SLEDD – Sustained Low-Efficiency Daily Dialysis
Treatments Advantages Disadvantages
IHD Rapid removal of toxins Rapid fluid removal and frequent hypotension
Reduced downtime for procedures Dialysis disequilibrium and risk of cerebral edema
Reduced exposure to anticoagulants Technically complex
Lower cost than CRRT
SLEDD Slower volume and solute removal than IHD Still risk of disequilibrium and hypotension
Faster solute clearance than CRRT Technically complex
Reduced downtime than CRRT
Reduced exposure to anticoagulation
CRRT Continuous removal of toxins/solutesEasy control of fluid balance
Slower solutes clearance than IHD
Better tolerated hemodynamically Need prolonged anticoagulation
User friendly machines Hypothermia
Increased costs
Adapted from Renal Replacement Therapy; Crit Care Clinics(2015) 31:839-848.
Prevention of AKI
• Attention to BP and CO– Fluids
• Colloids Vs Crystalloid
• No Hetastarch
– Vasoactive meds• Renal Dose Dopamine- a myth
• Diuretics– Does not prevent AKI
– Use to Rx fluid overload
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D1: In the absence of hemorrhagic shock, we suggest using isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume in patients at risk for AKI or with AKI (Grade 2B).
D2: We recommend the use of vasopressors in conjunction with fluids in patients with vasomotor shock with, or at risk for, AKI (Grade 1C).
D3: We suggest using protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting (Grade 2C) or in patients with septic shock (Grade 2C).
Kellum, J. et al. KDIGO AKI Work Group Crit Care 2013;17:204
D9: We recommend not using diuretics to prevent AKI (Grade 1B). D10: We suggest not using diuretics to treat AKI, except in the management of volume overload (Grade 2C).
Nutrition and Glycemic ControlD4: In critically ill patients, we suggest insulin therapy targeting plasma glucose 110 to 149 mg/dl (6.1 to 8.3 mmol/l) (Grade 2C).D5: We suggest achieving a total energy intake of 20 to 30 kcal/kg/day in patients with any stage of AKI (Grade 2C). D6: We suggest avoiding restriction of protein intake with the aim of preventing or delaying initiation of RRT (Grade 2D). D7: We suggest administering 0.8 to 1.0 g/kg/day protein in noncatabolic AKI patients without need for dialysis (Grade 2D), 1.0 to 1.5 g/kg/day in patients with AKI on RRT (Grade 2D), and up to a maximum of 1.7 g/kg/day in patients on CRRT and in hypercatabolic patients (Grade 2D). D8: We suggest providing nutrition preferentially via the enteral route in patients with AKI (Grade 2C).
Kellum, J. et al. KDIGO AKI Work Group Crit Care 2013;17:204
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Prevention/Minimize Risk
• Recognize agents w nephrotoxic potential
• Recognize high risk patients
• Prompt diagnosis
• Avoid nephrotoxic agents if possible
• Monitor drug levels if available
• Maintain euvolemia
• Monitor kidney function
Kellum, J. et al. KDIGO AKI Work Group Crit Care 2013;17:204
Contrast Induced AKI
• Rise in SCr of 0.5mg/dl or a 25% increase from baseline
• 48 hours after dye
• Widely known as Contrast Induced Nephropathy(CIN)
Kellum, J. et al. KDIGO AKI Work Group Crit Care 2013;17:204
Assess the risk for CI-AKI and, in particular, screen for pre-existing impairment of kidney function in all patients who are considered for a procedure that requires intravascular (i.v. or i.a.) administration of iodinated contrast medium.
Kellum, J. et al. KDIGO AKI Work Group Crit Care 2013;17:204
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Risk Factors for CI-AKI
• CKD #1
• DM
• HTN
• CHF
• Volume depletion
• Concurrent nephrotoxic meds
Kellum, J. et al. KDIGO AKI Work Group Crit Care 2013;17:204
Pharmacologic Strategies
• HCO3 vs NS
• Non urgent, hospitalized– 1mk/kg/h 12 hrs before
and 12 hrs after
• Urgent– 3ml/kg/hr 1 hr
preprocedure and 1.5ml/kg/hr for 4-6 hrs
• NAC
• Fendolapam
• Dopamine
• Theophylline
• ANP
All of these no benefit demostrated
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We suggest using oral NAC, together with i.v. isotonic crystalloids, in patients at increased risk of CI-AKI. (2D)
Kellum, J. et al. KDIGO AKI Work Group Crit Care 2013;17:204
Kellum, J. et al. KDIGO AKI Work Group Crit Care 2013;17:204
Stage Based Management of AKI
Case Studies
