Exam #1 Study Guide: Acute Kidney Injury And Renal Transplant Flashcards
Acute Kidney Injury vs. Chronic Kidney Disease: Onset
AKI: Sudden
CKD: Gradual, often over many years
Acute Kidney Injury versus Chronic Kidney Disease: Most common cause
AKI: Acute Tubular Necrosis
CKD: Diabetic Nephropathy
Acute Kidney Injury versus Chronic Kidney Disease: Diagnostic Criteria
AKI: Acute reduction in urine output and/or Elevation in serum creatinine
CKD: GFR <60 mL/min/1.73 m2 for >3 mo and/or Kidney Damage >3 mo
Acute Kidney Injury versus Chronic Kidney Disease: Reversibility
AKI: Potentially
CKD: Progressive and Irreversible
Acute Kidney Injury versus Chronic Kidney Disease: Primary cause of death
AKI: Infection
CKD: Cardiovascular disease
Acute Kidney Injury: Prerenal etiology and Pathophysiology
- Factors that reduce systemic circulation -> reduction in renal blood flow. (Ex. Severe dehydration, HF, decreased CO)
- Decreases GFR -> causes oliguria
- Autoregulatory mechanisms attempt to preserve blood flow to essential organs.
Prerenal conditions can contribute to intrarenal disease if
- Renal ischemia is prolonged.
- If decreased perfusion persists for an extended time, the kidneys lose their ability to compensate and damage to the kidney parenchyma occurs (intrarenal damage)
Prerenal Azotemia results in
A reduction in the excretion of sodium (less than 20 mEq/L), increased salt and water retention and decreased UO.
Acute Kidney Injury: Intrarenal Etiology and Pathophysiology
- Causes include conditions that cause direct damage to kidney tissue (i.e prolonged ischemia, nephrotoxins, Hgb released from hemolyzed RBC’s, myoglobin released from necrotic muscle cells.)
- Acute tubular necrosis (most common cause)
How can nephrotoxins cause intrarenal acute kidney injury?
Can cause obstruction of intrarenal structures by crystallization or by causing damage to the epithelial cells of the tubules.
How does hemoglobin and myoglobin cause intrarenal AKI?
Can block the tubules and cause renal vasoconstriction.
Intrarenal AKI: Acute Tubular Necrosis Pathophysiology and Etiology
- Results from ischemia, nephrotoxins, or sepsis
- Severe ischemia causes disruption in basement membrane
- Nephrotoxic agents cause necrosis of tubular epithelial cells
- Potentially reversible if the basement membrane is not destroyed and the tubular epithelium regenerates.
AKI Postrenal: Etiology and Pathophysiology
-Causes include mechanical obstruction of outflow: Benign prostatic hyperplasia Prostate cancer Calculi Trauma Extrarenal tumors Bilateral ureteral obstruction
AKI: Progresses through phases
- Oliguric
- Diuretic
- Recovery
*When a patient does not recover from AKI, then CKD may develop.
RIFLE Classification
Used to describe stages of AKI (R)is is the first stage of AKI (I) Injury is the second stage (F) Failure (L) Loss (E) End-stage renal disease
AKI Oliguric Phase: Clinical Manifestation
- Oliguria (UO < 400 mL/day)
- Urinalysis may show casts, RBCs and WBCs
- Hypovolemia
- Fluid retention (d/t decreased UO): Distended neck veins, bounding pulse, edema, HTN
- Metabolic acidosis
- Hyponatremia
- Hyperkalemia
- Neurologic disorders: Fatigue, difficulty concentration, seizures, stupor and coma (occur as waste products accumulate in the brain and other nervous tissue)
- Hematologic Disorders: Leukocytosis (increased risk for infection)
- Waste product accumulation (elevated BUN and serum creatinine levels)
Urine Output Requirement
0.5 mL/kg/hrs
How long does the oliguric phase last?
Occurs within 1-7 days after injury and lasts 10-14 days (the longer the oliguric phase lasts, the poorer the prognosis for complete recovery of kidney function)
Prerenal: Specific Gravity
High because urine is concentrated.
Fluid retention during the oliguric phase of AKI can lead to
HF, pulmonary edema and pericardial and pleural effusions (d/t fluid overload)
Why is metabolic acidosis a clinical manifestation of the oliguric phase of AKI?
- Impaired kidney cannot excrete hydrogen ions
- Serum bicarbonate production is decreased
- Severe acidosis develops -> Kussmaul respirations
*Read notes for more information
Clinical Manifestations of the Oliguric Phase of AKI: Sodium Balance
- There is an increased excretion of sodium
- Hyponatremia can lead to cerebral edema (puts them at risk for seizure activity)
Clinical Manifestations of the Oliguric Phase of AKI: Potassium Excess
- Impaired ability of kidneys to excrete potassium
- Increased risk with massive tissue trauma
- Usually asymptomatic
- ECG changes
*Read notes for more info
How do you treat high potassium in oliguric phase of AKI?
- Regular insulin
* May be more
Diuretic Phase of AKI
- Daily UO is 1-3 L (may reach 5 L or more) (caused by the inability of the tubules to concentrate urine)
- Monitor for hyponatremia, hypokalemia and dehydration (hypovolemia)
- Near the end of this phase, acid-base, electrolyte and waste product values may stabilize.
Recovery Phase of AKI
-May take up to 12 months for kidney functions to stabilize.
AKI: Diagnostic Studies
- Thorough history
- Serum creatinine
- Urinalysis
- Kidney ultrasonography
- Renal scan
- CT scan
- Renal biopsy
*Add notes in to this from slide 15
AKI Diagnostic Studies: Contraindications
- MRI with gadolinium contrast medium
- Magnetic resonance angiography (MRA) with gadolinium contrast medium: Nephrogenic systemic fibrosis and Contrast-induced nephropathy (CIN)
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AKI: Primary Goals
- Eliminate cause
- Manage signs and symptoms
- Prevent complications (i.e infection)
AKI Interprofessional Care Includes
- Ensure adequate intravascular volume and CO: Force fluids, loop diuretics and osmotic diuretics
- Closely monitor fluid intake during oliguric phase
- Treat hyperkalemia
- Renal replacement therapy
- Nutritional Therapy
What is the general rule for calculating the fluid restriction?
Add all loses for previous 24 hours plus 600 mL for insensible losses.
How to treat hyperkalemia associated with AKI?
- Insulin and sodium bicarbonate
- Calcium carbonate
- Sodium polystyrene sulfonate (Kayexalate)
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