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Label
Acute Kidney Injury (AKI) overview

DefinitionEtiologyEpidemiologyPathophysiologyClinical Presentation
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Definition:

 

Acute kidney injury (AKI): Has replaced the term "acute renal failure". It covers the entire spectrum of injury from less severe cases to more advanced injury that may require renal replacement therapy (RRT), characterized by a rapid reduction in kidney function with ensuing failure to maintain fluid, electrolyte and acid-base homoeostasis.

 

Acute Kidney Injury Network (AKIN) criteria for the diagnosis of AKI includes:

 

1) Rapid time course (less than 48 hours)

2) Reduction of kidney function

  • Rise in serum creatinine
    • Absolute increase in serum creatinine of ≥0.3 mg/dL (≥26.5 μmol/l)
    • Percentage increase in serum creatinine of ≥50%
  • Reduction in urine output, defined as <0.5 ml/kg/hr for more than 6 hours

 

Kidney Disease: Improving Global Outcomes (KDIGO) staging classification* of acute kidney injury (AKI)

 

Improving Global Outcomes (KDIGO) staging classification* of acute kidney injury (AKI)

 

Staging

 

The RIFLE criteria (Risk, Injury, Failure, Loss of function, and End-stage renal disease), proposed by the Acute Dialysis Quality Initiative (ADQI) group, aid in the staging of patients with AKI.

 

RIFLE criteria

 

RIFLE criteria

 

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Etiology:

 

The etiology is divided into:

 

Pre-renal:

Decreased renal perfusion leads to a decrease in glomerular filtration rate (GFR). If left untreated may progress to acute tubular necrosis (ATN)

 

  • Decreased renal perfusion
    • Renal artery stenosis
    • Hypovolemia (excessive diuresis, hemorrhage, dehydration, burns, trauma)
  • Change in vascular resistance
    • Sepsis
    • Anaphylaxis
    • Anesthesia
    • After-load reducing drugs
    • Hepato-renal syndrome I/ II, large volume paracentesis
  • Low cardiac output
    • Cardiogenic shock
    • Congestive heart failure
    • Pulmonary embolism
    • Pericardial tamponade
    • Valvular disorder
    • Arrhythmias
    • Positive pressure ventilation in ICU

 

Intra-renal (intrinsic):

Causes that leads to intrinsic renal disease and damage, responsible for 10-40% of acute renal failure.

 

  • Hypoxia
    • From prerenal causes
    • Renal vein thrombosis
    • Thrombotic microangiopathy
      • Thrombotic thrombocytopenic purpura (TTP)
      • Hemolytic uremic syndrome (HUS)
      • Scleroderma renal crisis
  • Acute tubular necrosis
    • Nephrotoxins; contrast-induced nephropathy (CIN)
    • Ischemia caused by cholesterol crystal emboli
    • Infection
  • Tissue injury
    • Haemoglobinuria
    • Myoglobinuria
    • Uric acid (tumour lysis)
  • Inflammatory nephritides
    • Glomerulonephritis/ rapidly progressive glomerulonephritis (RPGN)
    • Interstitial nephritis
    • Polyarteritis
  • Multiple myeloma
    • Direct tubular injury
    • Hypercalcemia due to tumor lyses syndrome

 

Post-renal:

Various types of obstruction in the voiding and collecting parts of the urinary system and is responsible for 5-10% of ARF.

  • Bladder neck obstruction
  • Blocked ureteric system
  • Pelvis surgery
  • Prostatic enlargement
  • Raised intra-abdominal pressure
  • Renal or ureteric
    • Calculi
    • Clots
    • Necrotic papillae
    • Retroperitoneal fibrosis (RPF)

 

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Epidemiology:

 

AKI is common among hospitalized patients. It affects some 3-7% of patients admitted to the hospital and approximately 25-30% of patients in the intensive care unit.

 

  • 5% of hospital admissions are due to renal failure
  • 30% of ICU admissions are due to acute renal injury
  • 25% of hospitalized patients develop renal failure
  • 1% of post-op cases develop renal injury
  • Approximately 10% require dialysis or transplant
  • Death is usually the result of complications rather than the renal failure itself

 

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Pathophysiology:

 

The mechanisms of AKI

 

The mechanisms of AKI

 

Phases of urinary output in acute tubular injury

 

Phases of urinary output in acute tubular injury

 

 

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Clinical Presentation:

 

- Distinguish between AKI (rapid over 48 hr) from chronic

renal failure (progressive loss of renal function over a

period of months and years)

 

- Distinguish one type of AKI from another based on

underlying cause:

 

Prerenal azotemia:

  • Volume depletion
    • Hemorrhage, GI loses, burns, trauma, dehydration etc
  • Low cardiac output
    • Cardiac failure (shock, tamponade, CHF), arrhythmia, pulmonary embolism etc.
  • Change in vascular resistance
    • Afterload reducing drugs
    • Anaphylaxis
    • Septic shock
      • High morbidity and mortality associated with AKI plus sepsis
    • Hepatorenal syndrome (HRS)
      • In patients with cirrhosis and ascites
      • Secondary to renal vasoconstriction
      • Type 1 HRS: Rapidly progressive, grave prognosis
      • Type 2 HRS: Less severe

Post renal azotemia:

  • Obstruction of urine flow
    • Structural
      • BPH, malignancies, strictures
    • Non-structural
      • Medication e.g. anticholinergics

Intrinsic renal failure:

  • Inflammatory conditions including autoimmune etiology, thrombosis, infections
  • Contrast-induced nephropathy (CIN) is a leading cause of AKI in the hospitalized patients that occurs within 72 hrs post contrast administration
  • Nephrogenic systemic fibrosis (NSF)
    • May occur in patient with reduced renal function following exposure to gadolinium
    • Scleromyxedematous condition with high mortality
  • HIV associated nephropathy
    • Rapidly progressing
    • Associated with poorly controlled HIV infection
  • Highly active antiretroviral therapy (HAART) related renal disease
    • Tenofovir → ATN
    • Indinavir → crystalline-induced kidney injury

 

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Differential Diagnosis:

 

- Distinguish between AKI (rapid over 48 hr) from chronic

renal failure (progressive loss of renal function over a

period of months and years)

 

- Distinguish one type of AKI from another based on

underlying cause:

 

Prerenal azotemia:

  • Volume depletion
    • Hemorrhage, GI loses, burns, trauma, dehydration etc
  • Low cardiac output
    • Cardiac failure (shock, tamponade, CHF), arrhythmia, pulmonary embolism etc.
  • Change in vascular resistance
    • Afterload reducing drugs
    • Anaphylaxis
    • Septic shock
      • High morbidity and mortality associated with AKI plus sepsis
    • Hepatorenal syndrome (HRS)
      • In patients with cirrhosis and ascites
      • Secondary to renal vasoconstriction
      • Type 1 HRS: Rapidly progressive, grave prognosis
      • Type 2 HRS: Less severe

Post renal azotemia:

  • Obstruction of urine flow
    • Structural
      • BPH, malignancies, strictures
    • Non-structural
      • Medication e.g. anticholinergics

Intrinsic renal failure:

  • Inflammatory conditions including autoimmune etiology, thrombosis, infections
  • Contrast-induced nephropathy (CIN) is a leading cause of AKI in the hospitalized patients that occurs within 72 hrs post contrast administration
  • Nephrogenic systemic fibrosis (NSF)
    • May occur in patient with reduced renal function following exposure to gadolinium
    • Scleromyxedematous condition with high mortality
  • HIV associated nephropathy
    • Rapidly progressing
    • Associated with poorly controlled HIV infection
  • Highly active antiretroviral therapy (HAART) related renal disease
    • Tenofovir → ATN
    • Indinavir → crystalline-induced kidney injury

 

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Investigation and Workup:

 

History:

 

  • Determine whether renal failure is acute or chronic
  • Renal size may be normal or increased in several chronic renal diseases (e.g. diabetic nephropathy, amyloidosis, polycystic kidney disease)
  • Accurate drug history plays important role

 

Labs:

 

  • Urinalysis
  • Complete blood count (CBC) and ESR
  • Serum electrolytes
  • BUN, creatinine
  • Uric acid
  • Cryoglobulins
  • Lactate dehydrogenase (LDH)
  • Multiple myeloma screen
  • Sclearoderma panel

 

Other investigations may need, such as:

 

  • Antiglomerular basement membrane antibodies
    • Rule out good pasture syndrome
  • Anti-neutrophil cytoplasmic antibodies
    • Rule out vasculitis
  • Anti-nuclear antibodies
    • Rule out systemic lupus erythematosus (SLE)
  • Anti Streptolysin-O
    • Rule out post streptococcal glomerulonephritis
  • Creatine phosphokinase (CPK)
    • Rule out rhabdomyolysis
  • Complement titers
    • Rule out post infectious glomerulonephritis, SLE, subacute bacterial endocarditis, cholesterol embolization

 

Laboratory findings in Acute Kidney Injury (AKI)

 

Fractional excretion of sodium:

 

Most useful in distinguishing between prerenal and renal ARF

Fractional excretion of sodium

 

Imaging

 

  • Bladder scan
    • Useful to rule out urinary retention
  • Renal ultrasound
    • Rule out post renal causes, confirm there are 2 kidneys
    • Rule out hydronephrosis
  • CT scan
    • Rule out ureteral obstruction; CT can detect non-radiopaque calculi
    • Assess bladder distension
    • Rule out hydronephrosis
  • Renal arteriography/venography
    • Indicated if vascular causes are suggested clinically, rule out renal artery disease and renal vein thrombosis
  • Magnetic resonance arteriography
    • Used for diagnosing renal artery stenosis as well as thrombosis of both arteries and veins
  • Retrograde or anterograde pyelography
    • Provides precise localization of site of obstruction
  • Plain films of the abdomen
    • Initial screening tool in suspected nephrolithiasis

 

Post void residual:

 

  • Catheter is inserted immediately after urinating to measure fluid retention the bladder; 50-100 ml suggests neurogenic bladder

 

ECG:

 

  • Peaked T waves
  • PR prolongation
  • QRS widening
  • Long QT if hypocalcaemia is present
  • Criteria for left ventricular hypertrophy (LVH) - may suggest long standing hypertension

 

Renal biopsy

  • Reserved for patients with uncertain diagnosis

 

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Treatment:

 

  • Determination of preexisting renal disease is important
  • Adequate hydration before, during and after any procedure requiring NPO
  • Avoid drugs (or use with caution) which are excreted through the kidneys
  • Monitor analgesic use
  • Avoid infection; provide meticulous care to patients with indwelling catheters and I.V. lines
  • Correct reversible cause of acute renal failure (e.g., improves renal perfusion; maximize cardiac output, surgical relief of obstruction)
  • Adjustment of drug regimen
  • Elimination of triggering agents (whenever possible)
  • Disease-specific therapies
  • Draining wounds, burns etc, can lead to dehydration and sepsis and progressive renal damage
  • For patient at risk of contrast induced(CI) AKI:
    • Prevention of CI-AKI with N-acetylcysteine and NaHCO3 combination therapy is controversial as ACT study did not show any benefits
    • Consider forced diuresis to reduce transit time and potential nephrotoxicity in patients with severe baseline chronic kidney as per the REMEDIAL II trial

 

Emergency Treatment:

 

  • Prevent and treat shock with blood and fluid replacement, as prescribed
  • Monitor intake/output and CVP hourly in critically ill patients to detect onset of renal failure at the earliest moment
  • Monitor blood pressure and maintain nutrition
  • Determination of fluid overload and deficit is critical
  • Initiate hemodialysis, peritoneal dialysis, or continuous renal replacement therapy for patients with progressive disease or complications

 

Treat the life threatening conditions appropriately in ICU setting.

 

- Pulmonary edema:

  • Oxygen
    • 100% by non rebreather mask
  • Diuretics
    • Furosemide IV 0.5 to 1.0 mg/kg
  • IV vasodilators (eg, nitroglycerin)
    • Nitroglycerin 0.4 mg sublingually every 5 min
    • Followed by an IV drip at 10 to 20 μg/min
    • Titrated upward at 10 μg/min every 5 min as needed to a maximum 300 μg/min if systolic BP is >100 mmHg
  • Morphine
    • 1 to 5 mg IV once or twice daily
  • Ventilatory assistance as needed
    • If hypoxia is significant
      • Bi-level positive airway pressure (BiPAP)
    • If CO2 retention is present or the patient is obtunded
      • Tracheal intubation and assisted ventilation are required
  • Treat the underlying cause

 

- Hyperkalemia:

 

If no ECG changes are present and renal function is intact:

 

  • Eliminate K+ supplements and K+ sparing diuretics
  • Insulin 5 to 10 units regular and Dextrose, 50 mL of 50% dextrose
    • Infusion of 10% D/W should follow at 50 mL/h to prevent hypoglycemia
  • Ventolin 4 puffs
  • Kexylate or calcium resonium (ion exchange resin), binds with potassium and forms a complex which cannot be absorbed thus lowering the serum potassium levels significantly

 

If there are ECG changes:

 

  • Ca Gluconate 10 to 20 mL 10% (or 5 to 10 mL 22% Ca gluceptate) IV over 5 to 10 minutes
    • Calcium: Caution to patients taking digoxin, because it may precipitate hypokalemia-related arrhythmias
    • The effect of calcium occur within minutes but last only 20 to 30 minutes
  • Insulin 5 to 10 units regular and dextrose IV, 50 mL of 50% dextrose
    • Infusion of 10% D/W should follow at 50 mL/h to prevent hypoglycemia
  • β2-agonist, high dose (as adjunct) - if not contraindicated
    • High dose albuterol 10 to 20 mg inhaled over 10 min (5 mg/mL concentration)
    • Lower serum K+ by 0.5 to 1.5 mEq/L
  • Sodium bicarbonate: If bicarbonate is less than 25 mmol/L
    • Then administer 45 mEq (1 ampule of 7.5% NaHCO3) infused over 5 min and repeated in 30 min
    • May result in alkalinization or the hypertonicity due to the concentrated Na+ in the preparation
    • May be harmful for dialysis patients who also may have volume overload
  • Sodium polystyrene sulfonate
    • 30 g oral or rectal; to reduce total body potassium
  • Dialysis (with low K+ dialysate)

 

- Metabolic acidosis:

 

Usually not treated unless the serum bicarbonate concentration is <20mmol/L or arterial pH is <7.2

 

  • NaHCO3 IV slow infusion
    • ≤ 150 mEq NaHCO3 in 1 L of 5% D/W at a rate of 50 to 100 mL/h or 75 mEq NaHCO3 in 1L of ½ normal saline

 

HEMODIALYSIS

 

- Indications:

 

  • Uncontrollable severe hyperkalemia
  • Severe sodium and water overload (unresponsive to diuretics)
  • Severe uremia
  • Metabolic acidosis (unresponsive to drug treatment)
  • Uremic encephalopathy or neuropathy
  • Pulmonary edema (unresponsive to diuretics)
  • Severe hypertension (poorly responsive to anti HTN medications)
  • Persistent nausea and vomiting
  • Serum creatinine concentration >10 mg/dL
  • Blood urea nitrogen >100 mg/dL
  • GFR <6 ml- 15/min/1.73m2
  • Poisons and drug intoxication

 

- Contraindications:

 

  • There is no absolute contraindication

 

- Prognosis of acute renal failure:

 

  • Age, cause and clinical presentation of the patient
  • Blood pressure, nutritional status, and electrolytes
  • Comorbid conditions
  • Diabetes mellitus (DM)

 

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MEDICATIONS:

Antidote/ Mucolytic agent

  • ➢ N-acetylcysteine

Mechanism

  • May act as an oxygen-derived free-radicals scavenger to prevent radiographic contrast-induced nephropathy
  • It also causes endothelium-dependent vasodilation by combining with oxide of nitric oxide to form a potent vasodilator, S-nitrosothiol

 

Dose:

N-acetylcysteine

Orall

  • Oral: 600 mg PO (BID) on day prior to and day of contrast

 

  • IV-Cardiac catheterization: 1200 mg IV over 5-10 min prior to procedure, then 1200 mg PO BID x 48 hr

 

Diuretic, Loop

  • ➢ Furosemide

Mechanism

  • Inhibits the reabsorption of sodium and chloride from the ascending loop of Henle, proximal and distal renal tubules
  • Increases renal excretion of water, sodium, chloride, magnesium, potassium, and calcium
  • It also has some renal vasodilator effect

 

Dose:

Furosemide

  • Intravenous (IV): 20-40 mg/dose; may repeat the same dose or increase by 20 mg/dose every 1-2 hrs if required; Max. 200 mg/dose

 

  • IV infusion: Bolus 0.1 mg/kg followed by 0.1 mg/kg/hr, then double every 2 hrs to a maximum of 0.4 mg/kg/hr

 

  • Oral: Initial 20-80 mg x 1; may repeat the same dose or increase by 20-40 mg every 6-8 hrs

 

Acute pulmonary edema

 

  • Intravenous (IV): 40 mg single dose; may increase dosage to 80 mg after 1 hour if no adequate response

 

Nitrates/ Vasodilator

  • ➢ Nitroglycerin

Mechanism

 

Stimulates intracellular cyclic-GMP, results in

  • Vascular smooth muscle relaxation and peripheral vasodilatation → decreases fluid pressure going into heart and lungs
  • Reduces myocardial oxygen demand by decreasing pre and after-load
  • Nitroglycerin also dilates coronary arteries

 

Dose:

Nitroglycerin

  • 0.4 mg SL every 5 min; followed by an IV drip at 10 to 20 mcg/min; may increase 10 mcg/min every 5 min; Max 200 mcg/min

 

Analgesic, centrally acting

  • ➢ Morphine

Mechanism

 

  • Binds to opiate receptors in the CNS, causing
    • Inhibition of ascending pain pathways
    • Altering the perception of and response to pain
    • Generalized CNS depression
  • It also causes respiratory depression, peripheral vasodilation, decreased gastrointestinal motility, sphincter of Oddi spasm, vomiting and increased bladder tone mood change

 

Dose:

Morphine

  • Intravenous (IV): 1 to 5 mg (QD - BID) diluted in 5% DW or 0.9% sodium chloride solution

 

Insulin

  • ➢ Regular insulin

Mechanism

 

  • Insulin acts via specific membrane-bound receptors on target tissues, stimulates peripheral glucose uptake and inhibits hepatic glucose production, lipolysis and proteolysis
  • Insulin activates sodium-potassium ATPase → increases intracellular movement of potassium

 

Dose:

Insulin (regular)

  • Intravenous (IV): 5 to 10 units infusion mixed with 50 mL of 50% dextrose water

 

Calcium salts

  • ➢ Calcium gluconate

Mechanism

 

  • Calcium is an important activator in many enzymatic reactions and necessary to a number of physiologic processes including
    • Nerve impulses transmission
    • Contraction of cardiac, smooth, and skeletal muscles
    • Renal function/ respiration
    • Capillary permeability/ blood coagulation
  • It reduces the excitability of cardiomyocytes thus lowering the likelihood of developing cardiac arrhythmias

 

Dose:

Calcium gluconate

  • Intravenous (IV): 10 mL of 10% solution over 5 minutes; alternate 10 to 20 mL 10% IV over 5 to 10 min if severe hyperkalemia

 

Beta agonists

  • ➢ Albuterol

Mechanism

 

  • Relaxes bronchial smooth muscle by action on beta2-receptors with little or no effect on alpha-adrenergic receptors

 

Dose:

Albuterol

  • High dose 10 to 20 mg inhaled over 10 min (5 mg/mL concentration)

 

Alkalinizing agent/ Antacid

  • ➢ Sodium bicarbonate

Mechanism

 

  • It increases plasma bicarbonate, buffers excess hydrogen ions, raises blood and urinary pH and it also cause a redistribution of potassium ions into cells

 

Dose:

Sodium bicarbonate

 

Metabolic acidosis, acute

 

  • Intravenous (IV infusion): Start 2 to 5 mEq/kg over 4 to 8 hours; may repeat the dose according to plasma bicarbonate concentration

 

Hyperkalemia

 

  • Intravenous (IV infusion): 45 mEq (1 ampule of 7.5% NaHCO3) over 5 min and repeated in 30 min

 

Cationic exchange resins

  • ➢ Sodium polystyrene sulfonate

Mechanism

 

  • Exchanges sodium ions for potassium ions in the intestine → reduces serum potassium levels

 

Dose:

Sodium polystyrene sulfonate

  • Oral: 15 g one to four times daily in water or sorbitol

 

  • Rectal: 30-50 g once or twice daily with at least intervals of six hours

 

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Clinical Trials:
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Pipeline Agents:

"There are none in PHASE III Trials"

 

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Physician Resources:

1. Tips for Patient Care

Risk factor management:

  • Always consider infectious processes; patients may not always have fever
  • Monitor for hypovolemia or hypervolemia
  • Measure and record intake and output
  • Monitor urinary output and urine specific gravity
  • Monitor serum and urine electrolyte concentrations
  • Watch for cardiac arrhythmia and heart failure from hyperkalemia
  • Prepare for dialysis when rapid lowering of potassium is needed
  • Weigh the patient daily to provide an index of fluid balance

 

Medications:

  • Instruct patient about the importance of following prescribed diet, avoiding foods high in potassium
  • Avoid nephrotoxic drugs such as NSAIDs, ACE inhibitors, and aminoglycosides
  • Consider concurrent risk factors and disease states with the prescribed therapy
  • In elderly patients consider lower starting doses to avoid side effects
  • Compliance with medications

 

Social and Stress factors:

  • Include family or social support in lifestyle modification
  • Ensure patient is well informed about disease and its treatment
  • Patient should know follow up visit and urinalysis are very important

 

Physical activity:

  • Advise to increase activity gradually
  • Patient should be aware to keep themselves well hydrated

 

2. Scales and Table

 

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References:

Core Resources:

  • Compendium of Pharmaceuticals and Specialties (CPS). Canadian Pharmacist association. Toronto: Webcom; 2013
  • Day RA, Paul P, Williams B et al. eds. Brunner & Suddarth's Textbook of Canadain Medical-Surgical Nursing. 2nd edition. Philadelphia: Lippincot Williams and Wilkins; 2010
  • Foster C, Mistry NF, Peddi PF, Sharma S, eds. The Washington Manual of Medical Therapeutics. 33rd edition. Philadelphia: Lippincot Williams and Wilkins; 2010
  • Gray J, ed. Therapeutic Choices. Canadian Pharmacists Association. 6th edition. Toronto: Webcom; 2011
  • Katzung BG, Masters SB, Trevor AJ, eds. Basic and Clinical Pharmacology. 11th edition. New york: McGraw-Hill; 2009
  • Lattanzio MR, Kopyt NP Acute Kidney Injury: New Concepts in Definition, Diagnosis, Pathophysiology, and Treatment. J Am Osteopath Assoc. 2009;109:13-19
  • Longo D, Fauci A, Kasper D et al, eds. Harrison's Principles of Internal Medicine. 18th edition. New York: McGraw-Hill; 2011
  • McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis & Treatment. 49th edition. New York: McGraw-Hill; 2010
  • Skidmore-Roth L, ed. Mosby's drug guide for nurses. 9th ed. St. Louis: Elsevier-Mosby; 2011

 

Online resources:

  • Lewington A, Kanagasundaram S. (2011) Clinical Practice Guidelines Acute Kidney Injury, UK Renal Association 5th Edition; 2011
  • www.renal.org/guideline

 

Online Pharmacological Resources:

  • e-Therapeutics
  • Lexicomp
  • RxList
  • Epocrates

 

Journals/Clinical Trials:

  • Anderson SM, Park ZH, Patel RV. Intravenous N-acetylcysteine in the prevention of contrast media-induced nephropathy. Ann Pharmacother; 2011 Jan;1:101-7
  • ACT Investigators. Acetylcysteine for prevention of renal outcomes in patients undergoing coronary and peripheral vascular angiography: main results from the Randomized Acetylcysteine for Contrast-Induced
  • Brigouri C, Visconti G, Focaccio A et al. for the REMEDIAL II Investigators. Renal Insufficiency After Contrast Media Administration Trial II (REMEDIAL II): RenalGuard system in high-risk patients for contrast-induced acute kidney injury. Circulation. 2011; 124:1260-1269
  • McCullough PA, Khambatta S, Jazrawi A. Minimizing the Renal Toxicity of Iodinated Contrast. Circulation. 2011;124:1210-1211
  • The VA/NIH Acute Renal Failure Trial Network; Intensity of Renal Support in Critically Ill Patients with Acute Kidney Injury. N Engl J Med 2008; 359:7-20
  • Parikh CR, Coca SG, Thiessen-Philbrook H et al. for the TRIBE-AKI Consortium. Postoperative Biomarkers Predict Acute Kidney Injury and Poor Outcomes after Adult Cardiac Surgery. J Am Soc Nephrol. 2011 Sep; 9:1748-1757

 

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Reviewers

EXPERT REVIEWER:
Daniel Sapir, MD, FRCPC, Staff Nephrologist, Oakville Trafalgar Memorial Hospital, Oakville, ON Canada
.......................................... PHARMACY REVIEWER:
Dr. William Semchuk, M.Sc., Pharm.D., FCSHP, Manager, Clinical Pharmacy Services, Regina Qu’Appelle Health Region 14, Regina, SK Canada

 
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