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70 Cards in this Set
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Acute Kidney Injury
• Abrupt decline in GFR • Characterized by:??????? |
– Decrease urine output (oliguria or anuria)
– Increase waste products (urea, creatinine) – Fluid and electrolyte imbalance – Acid‐base imbalance |
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Renal Failure
• Duration – Acute is ???? |
Renal Failure
• Duration – Acute < 1 month – Rapidly progressive > 1 month < 3 months – Chronic > 3 months • Often difficult to tell without previous lab data |
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Renal Failure
• Duration – Acute < 1 month – Rapidly progressive -??????? |
Renal Failure
• Duration – Acute < 1 month – Rapidly progressive > 1 month < 3 months – Chronic > 3 months • Often difficult to tell without previous lab data |
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Renal Failure
• Duration – Acute < 1 month – Rapidly progressive > 1 month < 3 months – Chronic > ???????? |
Renal Failure
• Duration – Acute < 1 month – Rapidly progressive > 1 month < 3 months – Chronic > 3 months • Often difficult to tell without previous lab data |
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3 etiologies of Acute Kidney Injury
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Acute Kidney Injury
• Etiology –Prerenal azotemia –Intrinsic renal disease –Postrenal azotemia |
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what are these:
–Prerenal azotemia –Intrinsic renal disease –Postrenal azotemia |
3 etiologies of Acute Kidney Injury
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Adaptive response to severe volume
depletion, hypotension or effective circulating volume depletion |
Prerenal Acute Kidney Injury
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Prerenal Acute Kidney Injury is
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Adaptive response to severe volume
depletion, hypotension or effective circulating volume depletion |
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• Single most common cause of renal
failure (all settings) |
Prerenal Acute Kidney Injur
Adaptive response to severe volume depletion, hypotension or effective circulating volume depletion |
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persistant hypoperfusion of the kidney leads to
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ischemia and Intrinsic renal failure
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what happens in the kidney in the begining of Prerenal Azotemia
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Prerenal Acute Kidney Injury
• Compromised renal perfusion • Intact glomerular and tubular function • Renal adaptation – Afferent vasodilatation • Myenteric reflex • Vasodilator prostaglandins – Efferent vasoconstriction • Angiotensin II – Increased tubular reabsorption of solute and water |
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• Most potent Na retaining hormone
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Angiotensin II
• Renin released from JG cells • Increased angiotensin II • Most potent Na retaining hormone • Increases Na and water reabsorption – Increasing blood pressure – Restoring extracellular fluid volume |
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at what BP is the kidney no longer able to autoregulate itself and maintain GFR
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70 and below
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• Decreases peritubular capillary hydrostatic
pressure • Increases filtration fraction increasing COP in peritubular capillary |
– A‐II constricts efferent arteriole
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– Stimulates Na/K ATPase basolateral membrane
– Stimulates Na/H exchanger PCT |
Angiotensin II
• Effects – A‐II stimulates aldosterone secretion – A‐II constricts efferent arteriole • Decreases peritubular capillary hydrostatic pressure • Increases filtration fraction increasing COP in peritubular capillary – Stimulates Na/K ATPase basolateral membrane – Stimulates Na/H exchanger PCT |
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• Increases filtration fraction increasing COP in
peritubular capillary |
Angiotensin II
• Effects – A‐II stimulates aldosterone secretion – A‐II constricts efferent arteriole • Decreases peritubular capillary hydrostatic pressure • Increases filtration fraction increasing COP in peritubular capillary – Stimulates Na/K ATPase basolateral membrane – Stimulates Na/H exchanger PCT |
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Prerenal Acute Kidney Injury
• Causes – Intravascular volume depletion |
• Hemorrhage
• Diarrhea, vomiting, polyuria • Burns |
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Prerenal Acute Kidney Injury
• Causes ???? |
Prerenal Acute Kidney Injury
• Causes – Intravascular volume depletion • Hemorrhage • Diarrhea, vomiting, polyuria • Burns – *Cardiac failure • Congestive heart failure • Arrhythmias and valvular disease |
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Prerenal Acute Kidney Injury
• Causes: Changes in Vascular Resistance |
Prerenal Acute Kidney Injury
• Causes: Changes in Vascular Resistance – Peripheral vasodilation • Anaphylactic shock • Drugs/anesthesia • *Sepsis/severe infections • Liver failure – Primary renal hemodynamic abnormalities • Renal artery stenosis, embolism, thrombosis • *Medications (nonsteroidal anti angiotensin converting enzyme inhibitors) anti‐inflammatory agents, |
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• Causes: Changes in Vascular Resistance
– Peripheral vasodilation • Anaphylactic shock • Drugs/anesthesia • *Sepsis/severe infections • Liver failure – Primary renal hemodynamic abnormalities • Renal artery stenosis, embolism, thrombosis • *Medications (nonsteroidal anti angiotensin converting enzyme inhibitors) anti‐inflammatory agents, |
Prerenal Acute Kidney Injury
• Causes: Changes in Vascular Resistance – Peripheral vasodilation • Anaphylactic shock • Drugs/anesthesia • *Sepsis/severe infections • Liver failure – Primary renal hemodynamic abnormalities • Renal artery stenosis, embolism, thrombosis • *Medications (nonsteroidal anti angiotensin converting enzyme inhibitors) anti‐inflammatory agents, |
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• *Sepsis/severe infections
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Prerenal Acute Kidney Injury
• Causes: Changes in Vascular Resistance – Peripheral vasodilation |
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• Anaphylactic shock
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Prerenal Acute Kidney Injury
• Causes: Changes in Vascular Resistance – Peripheral vasodilation • Anaphylactic shock • Drugs/anesthesia • *Sepsis/severe infections • Liver failure |
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– Primary renal hemodynamic abnormalities of Prerenal Acute Kidney Injury
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– Primary renal hemodynamic abnormalities
• Renal artery stenosis, embolism, thrombosis • *Medications (nonsteroidal anti angiotensin converting enzyme inhibitors) anti‐inflammatory agents, |
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cyclosporine and tacrolimus vasoconstrict
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the afferant arteriole and can lead to prerenal acute kidney injury
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NSAIDs constrict what arteriole
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afferent and therefore they can cause prerenal kidney injury
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Intrinsic Acute Kidney Injury has what four causes
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Intrinsic Acute Kidney Injury
• Acute tubular necrosis (ATN) – Renal toxins – Prolonged hypotension • Acute i interstitial nephritis (AIN) – Medications • Acute glomerulonephritis (GN) – Post‐infectious GN • Vasculitis |
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Intrinsic Acute Kidney Injury
• Acute tubular necrosis (ATN) – Renal toxins – Prolonged hypotension • Acute i interstitial nephritis (AIN) – Medications • Acute glomerulonephritis (GN) – Post‐infectious GN • Vasculitis |
Intrinsic Acute Kidney Injury has what four causes
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• Acute tubular necrosis (ATN) caused by what
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– Renal toxins
– Prolonged hypotension |
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– Renal toxins
– Prolonged hypotension cause what? |
• Acute tubular necrosis (ATN) caused by what
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Most common cause of intrinsic AKI
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• ATN
– Most common cause of intrinsic AKI – Most common causes are ischemia and toxins – Persistent hypoperfusion renal failure (ATN) – Toxins include: • Common ‐ aminoglycosides and contrast • Less common ‐ heme pigments, chemotherapeutic agents, cyclosporine, multiple myeloma → ischemia and intrinsic |
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– ATN Toxins include:
• Common |
Common ‐ aminoglycosides and contrast
• Less common ‐ heme pigments, chemotherapeutic agents, cyclosporine, multiple myeloma |
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Cr increases 48 hours a after
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– Cr increases 48 hours a after contrast exposure in ATN caused by this
– Prevention • Hydration • N‐acetylcysteine (antioxidant) • Low volume and low osmolality |
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– Common cause of ATN in hospitalized patients
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• Contrast agents
– Common cause of ATN in hospitalized patients – Renal ischemia and direct tubular toxicity – Cr increases 48 hours a after contrast exposure – Prevention • Hydration • N‐acetylcysteine (antioxidant) • Low volume and low osmolality |
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Acute Tubular Necrosis
• Pathogenesis – vulnerable cells????? |
S 3 segment of PCT
– Medullary thick ascending limb LOH – Exposed to chronic hypoxia – High metabolic demand • Primarily Na reabsorption |
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• Loss of cell polarity
• Cell detachment |
Acute Tubular Necrosis
• Pathogenesis – Tubular factors • Loss of cell polarity • Cell detachment |
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Acute Tubular Necrosis
• Pathogenesis – potential factors |
Acute Tubular Necrosis
• Pathogenesis – potential factors – Altered autoregulation – Altered TGF – Tubular factors • Loss of cell polarity • Cell detachment – Inflammatory factors • Neutrophils (? ICAM‐1) • Macrophages |
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– Cell swelling (decreased ATP)
– Calcium influx – Phospholipase A 2 (breakdown membrane PL) – Reactive oxygen species – Complement activation |
Acute Tubular Necrosis
• Pathogenesis – mediators of cell injury, either ischemia or cytotoxic – Cell swelling (decreased ATP) – Calcium influx – Phospholipase A 2 (breakdown membrane PL) – Reactive oxygen species – Complement activation |
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flattening of the epithelium
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early ATN
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• ATN – time course
– Cr plateaus |
Acute Kidney Injury
• ATN – time course – Cr plateaus 7‐10 days (injury phase) |
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• ATN – time course
– Cr plateaus 7‐10 days (injury phase) – Maintenance phase????? |
• ATN – time course
– Cr plateaus 7‐10 days (injury phase) – Maintenance phase 10 nonoliguric) |
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• ATN – time course
– Cr plateaus 7‐10 days (injury phase) – Maintenance phase 10 nonoliguric) – Recovery????? |
• ATN – time course
– Cr plateaus 7‐10 days (injury phase) – Maintenance phase 10 nonoliguric) – Recovery 14‐21 days (recovery phase) |
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• ATN – time course
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• ATN – time course
– Cr plateaus 7‐10 days (injury phase) – Maintenance phase 10 nonoliguric) – Recovery 14‐21 days (recovery phase) • Mortality rate remains high – ICU patients 40‐80% 10‐14 days (oliguric or |
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Intrinsic Acute Kidney Injury
• Small vessel and or glomerular injury causes?????? |
Intrinsic Acute Kidney Injury
• Small vessel and or glomerular injury – Vasculitis – Cholesterol emboli – Malignant hypertension – Thrombotic microangiopathy – Acute glomerulonephritis |
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Intrinsic Acute Kidney Injury
• Acute interstitial nephritis what Systemic diseases can cause this shit |
(Sjogren’s syndrome
sarcoidosis, lupus) |
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–Penicillins (methicillin)
–Cephalosporins |
Intrinsic Acute Kidney Injury
• Acute interstitial nephritis caused by meds |
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causes of AIN
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Intrinsic Acute Kidney Injury
• Acute interstitial nephritis – Acute pyelonephritis – Medications (70%) –Penicillins (methicillin) –Cephalosporins – Systemic disease (Sjogren’s syndrome sarcoidosis, lupus) – Other infections (HIV, CMV) |
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Intrinsic Acute Kidney Injury
• Acute interstitial nephritis – Classic triad |
Intrinsic Acute Kidney Injury
• Acute interstitial nephritis – Classic triad – fever, rash, eosinophilia – Urine eosinophils present – β lactam antibiotics (methicillin) – Duration of drug 2‐60 days – Non‐steroidal anti‐inflammatory agents associated with nephrotic syndrome (fenoprofen) |
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NSAIDs cause what type of nephrotic disease
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MCD
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retroperitoneal fibrosis can cause
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Extraureteral obstruction:
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Intraureteral obstruction: ????
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stones, papillary necrosis
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Lower urinary tract obstruction:
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Lower urinary tract obstruction:
neurogenic bladder, anticholinergic medications BPH, cancer |
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Acute Kidney Injury: Evaluation
• Urinalysis • Urine indices • Imaging - ??????????? |
main test is ultrasound
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what type of casts will be seen in someone with myoglobin acute kidney injury
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granular casts
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interstitial disease casts
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white cell casts
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lots of epithelial cells in the urine
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ATN
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• Tubular function assesment
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• Tubular function:
– Fractional excretion of Na reflects % of filtered Na excreted quantity of Na excreted over filtered |
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Prerenal AKI what is the urinary sodium
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< 10 while in ATN it is greater than 20
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Prerenal AKI what is the Urine osmolality
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greater than 550 while in ATN it is less than 250
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type of casts seen in prerenal azotemia compared to ATN
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bland hyaline casts as opposed to the muddy brown granular casts
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what is the fractional excretion of sodium in prerenal
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less than 1 while it is greater than 2 in ATN
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Increase in BUN/Cr ratio > 20:1
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– Prerenal AKI
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– Prerenal AKI
– Gastrointestinal hemorrhage – Catabolic states – Drugs (corticosteroids, tetracycline) |
Acute Kidney Injury: Evaluation
• Increase in BUN/Cr ratio > 20:1 – Prerenal AKI – Gastrointestinal hemorrhage – Catabolic states – Drugs (corticosteroids, tetracycline) |
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• BUN/Cr ratio < 10:1
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• BUN/Cr ratio < 10:1
– Large muscle mass – Muscle injury (rhabdomyolysis) – Ketoacidosis – Medications (TMP/SMX, cimetadine, cephalosporins) |
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– Medications (TMP/SMX, cimetadine,
cephalosporins) may cause |
• BUN/Cr ratio < 10:1
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Acute Kidney Injury: Treatment
• Prerenal AKI???? |
Acute Kidney Injury: Treatment
• Prerenal AKI – Intravascular volume repletion – Maintain euvolemia – Maximize cardiac function in CHF – Stop/avoid nephrotoxic medications – Treat underlying sepsis |
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Acute Kidney Injury: Treatment
• Intrinsic AKI ‐ ATN |
Acute Kidney Injury: Treatment
• Intrinsic AKI ‐ ATN – Optimize renal hemodynamics – Remove and avoid all nephrotoxins – Avoid hyperkalemia – Avoid volume overload – Dose all medications appropriately – Renal replacement therapy – General supportive care |
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Acute Kidney Injury: Treatment
• Intrinsic AKI ‐ AIN |
Acute Kidney Injury: Treatment
• Intrinsic AKI ‐ AIN – Remove offending drug – Renal replacement therapy – +/‐ steroids |
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Acute Kidney Injury: Treatment
• Intrinsic AKI ‐ AIN – Remove offending drug – Renal replacement therapy – +/‐ steroids • Postrenal AKI (obstruction) |
• Postrenal AKI (obstruction)
– Foley catheter – Ureteral stents – Nephrostomy tubes |
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Complications of AKI and Uremia
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Complications of AKI and Uremia
• Neurologic manifestations – Obtundation, asterixis, seizures • Cardiac manifestations – Volume overload, pulmonary edema, pericarditis • Electrolyte abnormalities – Hyperkalemia • Metabolic acidosis |
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Complications of AKI and Uremia
• Electrolyte abnormalities???? |
– Hyperkalemia
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