Exam #1 Study Guide: Acute Kidney Injury And Renal Transplant Flashcards

1
Q

Acute Kidney Injury vs. Chronic Kidney Disease: Onset

A

AKI: Sudden
CKD: Gradual, often over many years

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2
Q

Acute Kidney Injury versus Chronic Kidney Disease: Most common cause

A

AKI: Acute Tubular Necrosis
CKD: Diabetic Nephropathy

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3
Q

Acute Kidney Injury versus Chronic Kidney Disease: Diagnostic Criteria

A

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

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4
Q

Acute Kidney Injury versus Chronic Kidney Disease: Reversibility

A

AKI: Potentially
CKD: Progressive and Irreversible

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5
Q

Acute Kidney Injury versus Chronic Kidney Disease: Primary cause of death

A

AKI: Infection
CKD: Cardiovascular disease

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6
Q

Acute Kidney Injury: Prerenal etiology and Pathophysiology

A
  • 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.
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7
Q

Prerenal conditions can contribute to intrarenal disease if

A
  • 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)
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8
Q

Prerenal Azotemia results in

A

A reduction in the excretion of sodium (less than 20 mEq/L), increased salt and water retention and decreased UO.

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9
Q

Acute Kidney Injury: Intrarenal Etiology and Pathophysiology

A
  • 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)
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10
Q

How can nephrotoxins cause intrarenal acute kidney injury?

A

Can cause obstruction of intrarenal structures by crystallization or by causing damage to the epithelial cells of the tubules.

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11
Q

How does hemoglobin and myoglobin cause intrarenal AKI?

A

Can block the tubules and cause renal vasoconstriction.

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12
Q

Intrarenal AKI: Acute Tubular Necrosis Pathophysiology and Etiology

A
  • 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.
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13
Q

AKI Postrenal: Etiology and Pathophysiology

A
-Causes include mechanical obstruction of outflow:
Benign prostatic hyperplasia
Prostate cancer
Calculi
Trauma
Extrarenal tumors
Bilateral ureteral obstruction
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14
Q

AKI: Progresses through phases

A
  1. Oliguric
  2. Diuretic
  3. Recovery

*When a patient does not recover from AKI, then CKD may develop.

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15
Q

RIFLE Classification

A
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
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16
Q

AKI Oliguric Phase: Clinical Manifestation

A
  • 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)
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17
Q

Urine Output Requirement

A

0.5 mL/kg/hrs

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18
Q

How long does the oliguric phase last?

A

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)

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19
Q

Prerenal: Specific Gravity

A

High because urine is concentrated.

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20
Q

Fluid retention during the oliguric phase of AKI can lead to

A

HF, pulmonary edema and pericardial and pleural effusions (d/t fluid overload)

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21
Q

Why is metabolic acidosis a clinical manifestation of the oliguric phase of AKI?

A
  • Impaired kidney cannot excrete hydrogen ions
  • Serum bicarbonate production is decreased
  • Severe acidosis develops -> Kussmaul respirations

*Read notes for more information

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22
Q

Clinical Manifestations of the Oliguric Phase of AKI: Sodium Balance

A
  • There is an increased excretion of sodium

- Hyponatremia can lead to cerebral edema (puts them at risk for seizure activity)

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23
Q

Clinical Manifestations of the Oliguric Phase of AKI: Potassium Excess

A
  • Impaired ability of kidneys to excrete potassium
  • Increased risk with massive tissue trauma
  • Usually asymptomatic
  • ECG changes

*Read notes for more info

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24
Q

How do you treat high potassium in oliguric phase of AKI?

A
  • Regular insulin

* May be more

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25
Q

Diuretic Phase of AKI

A
  • 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.
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26
Q

Recovery Phase of AKI

A

-May take up to 12 months for kidney functions to stabilize.

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27
Q

AKI: Diagnostic Studies

A
  • Thorough history
  • Serum creatinine
  • Urinalysis
  • Kidney ultrasonography
  • Renal scan
  • CT scan
  • Renal biopsy

*Add notes in to this from slide 15

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28
Q

AKI Diagnostic Studies: Contraindications

A
  • MRI with gadolinium contrast medium
  • Magnetic resonance angiography (MRA) with gadolinium contrast medium: Nephrogenic systemic fibrosis and Contrast-induced nephropathy (CIN)

*Add notes

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29
Q

AKI: Primary Goals

A
  • Eliminate cause
  • Manage signs and symptoms
  • Prevent complications (i.e infection)
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30
Q

AKI Interprofessional Care Includes

A
  1. Ensure adequate intravascular volume and CO: Force fluids, loop diuretics and osmotic diuretics
  2. Closely monitor fluid intake during oliguric phase
  3. Treat hyperkalemia
  4. Renal replacement therapy
  5. Nutritional Therapy
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31
Q

What is the general rule for calculating the fluid restriction?

A

Add all loses for previous 24 hours plus 600 mL for insensible losses.

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32
Q

How to treat hyperkalemia associated with AKI?

A
  • Insulin and sodium bicarbonate
  • Calcium carbonate
  • Sodium polystyrene sulfonate (Kayexalate)

*Add notes

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33
Q

AKI: What are indications for renal replacement therapy?

A
  • Volume overload
  • Elevated serum potassium level
  • Metabolic acidosis
  • BUN level > 120 mg/dL (43mmol/L)
  • Significant change in mental status
  • Pericarditis, pericardial effusion, or cardiac tamponade

*Add notes

34
Q

AKI: Types of Renal Replacement Therapy

A
  1. Intermittent hemodialysis (method of choice when rapid changes are required in a short period of time)
  2. Continuous renal replacement therapy: involves cannulation of artery and vein
35
Q

AKI Interprofessional Care: Nutritional Therapy

A
  • Maintain adequate caloric intake: Primarily carbohydrates and fat; limited protein (to prevent further breakdown of body protein for energy purposes)
  • Restrict sodium
  • Increase dietary fat
  • Enteral nutrition

*Add more info from notes

36
Q

AKI: Nursing Assessment includes

A
  • Measure vital signs
  • Measure fluid intake and output
  • Examine urine for color, SG, glucose, protein, blood and sediment.
  • Assess general appearance (i.e color, edema, neck vein distention)
  • Observe dialysis access site for inflammation and exudate
  • Mental status/level of consciousness
  • Oral mucosa for dryness and inflammation
  • Lung sounds
  • Heart rhythm
  • Laboratory values and diagnostic test results.
37
Q

AKI: Nursing Diagnoses and Collaborative Problem

A
  • Excess fluid volume RT kidney failure and fluid retention
  • Risk for infection RT invasive lines, uremic toxins and altered immune response secondary to kidney failure
  • Fatigue RT anemia, metabolic acidosis and uremic toxins
  • Anxiety RT disease processes, therapeutic interventions and uncertainty of prognosis
  • Potential complication: dysrhythmia RT electrolyte imbalances
38
Q

AKI Planning: The patient with AKI will

A
  • Completely recover without any loss of kidney function
  • Maintain normal fluid and electrolyte balance
  • Have decreased anxiety
  • Adhere to and understand need for careful follow-up care
39
Q

AKI Nursing Implementation: Health Promotion

A
  • Identify and monitor populations at high risk
  • Control exposure to nephrotoxic drugs and industrial chemicals
  • Prevent prolonged episodes of hypotension and hypovolemia
40
Q

Slide 28

A

??

41
Q

AKI: Acute Care

A
  • Accurate intake and output
  • Daily weights
  • Assess for signs of hypervolemia or hypovolemia
  • Assess for potassium and sodium disturbances
  • Meticulous aseptic technique
  • Careful use of nephrotoxic drugs
  • Skin care measures/mouth care

*Read notes

42
Q

AKI: Ambulatory Care

A
  • Regulate protein and potassium intake
  • Follow-up care
  • Teaching
  • Appropriate referrals

*Add notes

43
Q

AKI Evaluation: The expected outcomes are that the patient with AKI wil

A
  • Regain and maintain normal fluid and electrolyte balance
  • Adhere to the treatment regimen
  • Experience no complications
  • Have complete recovery
44
Q

AKI: Vascular Access

A

Uses vascular access catheter

45
Q

During Hemodialysis, what is added to prevent clotting?

A

Heparin is added to prevent clotting.

46
Q

Hemodialysis Complications

A
  • Risk for bleeding/Blood loss (d/t heparin)
  • Risk for anemia (RBC can get stuck in filter?)
  • Hypotension
  • Muscle cramps (d/t electrolyte loss)
  • Hepatitis

*Read notes

47
Q

Hemodialysis Effectiveness

A
  • Cannot fully replace normal functions of kidneys
  • Can ease many of symptoms
  • Can prevent certain complications
48
Q

Continual Renal Replacement Therapy

A
  • Method for treating AKI
  • Means by which uremic toxins and fluids are removed
  • Acid-base status/electrolyte are adjusted slowly and continuously
  • For those not cardiogenic stable (i.e BP, heart rhythm, etc.)
  • Anticoagulants needed to prevent blood clotting (Higher risk for filter to clot)
49
Q

Continual Renal Replacement Therapy Contraindication

A

Patient has life-threatening manifestations of uremia that require rapid treatment

50
Q

CRRT versus HD

A
  • Continuous rather than intermittent
  • Fluid volume can be removed over days versus hours
  • Solute removal by convection (no dialysate required) in addition to osmosis and diffusion
  • Less hemodynamic instability
  • Does not require constant monitoring by HD nurse
  • Does not require complicated HD equipment
51
Q

CRRT Infusion of replacement fluid is determined by

A

Degree of fluid and electrolyte imbalance

52
Q

CRRT can be continued as long as

A

30-40 days

53
Q

How often should the CRRT hemofilter be changed?

A

24-48 hours

54
Q

What should the ultrafiltrate color be for CRRT?

A

Clear yellow (If the ultrafiltrate becomes bloody or blood tinged, suspect a possible rupture in the filter membrane Treatment needs to be terminated to prevent blood loss)

55
Q

CRRT Specific Nursing Interventions

A
  • Obtain weights
  • Monitor and document laboratory values daily
  • Assess hourly: Intake and output, vital signs, hemodynamic status
  • Care for site to prevent infection
56
Q

Kidney Transplant Recipient Selection

A
  • Candidacy determined by a variety of medical and psychosocial factors that vary among transplant centers
  • Preemptive transplant (before dialysis is required) is possible if recipient has a living donor

*Read notes

57
Q

Contraindications to kidney transplant

A
  • Disseminated malignancies
  • Refractory/untreated cardiac disease
  • Chronic respiratory failure
  • Extensive vascular disease (not being able to perfuse the kidney)
  • Chronic infection
  • Unresolved psychosocial disorders (may not be compliant with medications)
58
Q

Surgical Procedures required before kidney transplant

A
  • Coronary artery bypass or coronary angioplasty
  • Cholecystectomy
  • Bilateral nephrectomy
59
Q

Kidney Transplant Incompatibility Studies

A

Purpose of testing is to identify HLA antigens for both donors and potential recipients

60
Q

Kidney Transplant Donor Sources

A
  • Deceased donors with compatible blood type
  • Blood relatives
  • Emotionally related living donors
  • Altruistic living donors
  • Paired organ donation
61
Q

Kidney Transplant Donor Sources: Live donor needs

A
  • Extensive interprofessional evaluation

- Crossmatches

62
Q

Kidney Transplant Donor Sources: Advantages of Live Donors

A
  • Better patient and graft survival rates
  • Immediate organ availability
  • Immediate function/minimal cold time
  • Opportunity to have recipient in best possible medical condition
63
Q

Kidney Transplant Donor Sources: Live Donor Lab Studies

A
  • 24-hour urine: Creatinine clearance and total protein
  • Complete blood count
  • Chemistry and electrolyte profiles
  • Hepatitis B and C, HIV, CMV testing
64
Q

Kidney Transplant Donor Sources: Deceased Donor

A
  • Deceased (cadaver) kidney donors are relatively healthy individuals
  • Have suffered an irreversible brain injury and are declared brain dead

*Read notes

65
Q

Kidney Transplant Donor Sources: Deceased Donor Data includes

A
  • ABO group
  • HLA typing
  • Age
  • Antibody level
  • Length of time waiting

*Read notes

66
Q

Kidney Transplant Management: Postoperative Care for Live Donor

A
  • Care is similar to that for open or laparoscopic nephrectomy
  • Closely monitor renal function
  • Closely monitor hematocrit
  • Donors usually experience more pain than recipient
67
Q

Kidney Transplant Nursing Management: Postoperative Care for the Recipient

A
  • Maintenance of fluid and electrolyte balance is first priority
  • UO may be as high as 1L/hr and gradually decreases as the BUN and serum creatinine levels return toward normal.
  • Urine output is replaced with fluids milliliter for milliliter hourly for the first 12 to 24 hours.
  • Dehydration must be avoided
  • Assess for hyponatremia/ hypokalemia
  • Acute tubular necrosis can occur
  • Dialysis is required
  • Maintain catheter patency

*Check notes

68
Q

Large volumes of urine may be produced soon after transplanted kidney is placed due to

A
  • New kidney’s ability to filter BUN
  • Abundance of fluids during operation
  • Initial renal tubular dysfunction
69
Q

Kidney Transplant Immunosuppressive Therapy Goals

A
  • Adequately suppress immune response

- Maintain sufficient immunity to prevent overwhelming infection

70
Q

Kidney Transplant Complications: Types of rejection

A
  1. Hyperacute
  2. Acute
  3. chronic
71
Q

Hyperacute (antibody-mediated humoral) Rejection

A

Occurs minutes to hours after transplant

72
Q

Acute rejection

A

Occurs days to months after transplant

73
Q

Chronic Rejection

A
  • Process occurs over months or years and is irreversible.

- Looks the same as chronic liver failure.

74
Q

Kidney Transplant Complications include

A
  • Infection
  • Cardiovascular Disease
  • Malignancies
  • Recurrence of original kidney disease
  • Corticosteroid related complications
75
Q

Kidney Transplant Complications: Most common infections observed in the first month include

A
  • Pneumonia
  • Wound infections
  • IV line and drain infections
  • UTI’s
76
Q

Kidney Transplant Complications: Fungal Infections

A

Candida
Cryptococcus
Aspergillus
Pneumocystis jiroveci

These are difficult to treat, necessitate prolonged treatment periods and involve the administration of nephrotoxic drugs.

77
Q

Kidney Transplant Complications: Viral Infections include

A
  • CMV: One of most common
  • Epstein-Barr virus
  • Herpes simplex virus (HSV)
  • Varicella-zoster virus
  • Polyomavirus (e.g., BK virus)

*Check notes

78
Q

Kidney Transplant Complications: Cardiovascular Disease

A
  • Transplant recipients have increased incidence of atherosclerotic vascular disease
  • Immunosuppressants can worsen hypertension and hyperlipidemia
  • Patients need to adhere to antihypertensive regimen

*Check notes

79
Q

Kidney Transplant Complications: Malignancies

A
  • Primary cause is immunosuppressive therapy

- Regular screening is important

80
Q

Kidney Transplant Complciations: Malignancies Preventive Care

A
  • Protective clothing
  • Sunscreen
  • check notes
81
Q

Kidney Transplant Complciations: Recurrence of original kidney disease

A
  • Glomerulonephritis
  • IgA nephropathy
  • Diabetic nephropathy
  • Focal segmental sclerosis
82
Q

Kidney Transplant Complciations: Corticosteroid-related complications include

A
  • Aseptic necrosis of hips, knees, and other joints
  • Peptic ulcer disease
  • Glucose intolerance and diabetes
  • Dyslipidemia
  • Cataracts
  • Infection
  • Malignancies

*Check notes from last two slides