Module 7: Acute Kidney Injury and Chronic Kidney Disease Flashcards

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1
Q

Kidney (Renal) Failure

A

Partial or complete impairment of kidney function
that results in inability to excrete metabolic waste
products and water

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2
Q

Acute Kidney Injury

A

Ranges from slight deterioration to severe
impairment
 Rapid loss of kidney function with:
 Rise in serum creatinine and/or reduction in urine
output
 Elevated BUN and K+
 Azotemia—accumulation of nitrogenous waste
products
 High mortality rate; other life-threatening conditions

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3
Q

Etiology and Pathophysiology of AKI - Prerenal

A

Prerenal
 Causes: factors that reduce systemic circulation
causing reduction in renal blood flow which leads to
oliguria
* Severe dehydration, heart failure, decreased CO
 Autoregulatory mechanisms attempt to preserve
blood flow
 Prerenal azotemia results in Na+ excretion, increased
Na+ and H2O retention and decreased urine output

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4
Q

Etiology and Pathophysiology of AKI - Intrarenal

A

Intrarenal
 Causes: problems that cause direct damage to kidney
tissue
* Prolonged ischemia
* Nephrotoxins
* Hemoglobin released from hemolyzed RBCs
* Myoglobin released from necrotic muscle cells
* Kidney diseases—acute glomerulonephritis and SLE

Intrarenal
 Acute tubular necrosis (ATN)
* Results from ischemia, nephrotoxins, or sepsis
* Severe ischemia causes disruption in basement
membrane and patchy destruction of tubular epithelium
* Nephrotoxic agents cause necrosis of tubular epithelial cells—clog tubules
* Potentially reversible

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5
Q

Etiology and Pathophysiology of AKI - Postrenal

A

Postrenal
 Causes: mechanical obstruction of outflow which
results reflux into renal pelvis, impairing kidney
function
* Benign prostatic hyperplasia, prostate cancer, calculi,
trauma, and extrarenal tumors
 Bilateral ureteral obstruction—hydronephrosis; relieve obstruction in 48 hours increased chance of recovery

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6
Q

Acute Kidney Injury
Clinical Manifestations: Oliguric phase

A

Three phases: oliguric, diuretic, and recovery
 RIFLE classification (Table 51.3 in the textbook)
 Risk (R)
 Injury (I)
 Failure (F)
 Loss (L)
 End-stage renal disease (E)

Oliguric phase
 Urinary changes—*oliguria
* Urinary output less than 400 mL/day
* Occurs within 1 to 7 days after injury
* Lasts 10 to 14 days (longer is poor prognosis)
* Urinalysis—casts, RBCs, WBCs, protein
* Specific gravity 1.010
* Osmolality 300 mOsm/kg
 50% patients nonoliguric; greater than 400 mL
urine/day

Oliguric phase
 Fluid volume
* Hypovolemia may exacerbate AKI
* Decreased urine output leads to fluid retention
 Neck veins distended
 Bounding pulse
 Edema
 Hypertension
* Fluid overload can lead to heart failure, pulmonary
edema, and pericardial and pleural effusions

Oliguric phase
 Metabolic acidosis
* Impaired kidney cannot excrete hydrogen ions or acid
products of metabolism
* Serum bicarbonate production is decreased
 Reabsorption and regeneration defective
* Severe acidosis develops
 Kussmaul respirations—increasing exhaled CO2

Oliguric phase
 Sodium balance
* Increased excretion of sodium—damaged tubules
* Hyponatremia can lead to cerebral edema
 Potassium excess
* Impaired ability of kidneys to excrete K+
* Increased risk with massive tissue trauma
* Usually asymptomatic
* ECG changes—peaked T waves, widened QRS, ST
depression

Oliguric phase
 Hematologic disorders
* Leukocytosis—infection may be fatal
 Urinary and respiratory infections
 Waste product accumulation
* Increased BUN and *serum creatinine levels
 Neurologic disorders
* Fatigue and difficulty concentrating
* Seizures, stupor, coma

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7
Q

AKI Diagnostic Studies

A

Diagnostic studies
 Thorough history
 Serum creatinine, BUN, electrolytes
 Urinalysis
 Renal ultrasound
 Renal scan
 CT scan
 Renal biopsy

Diagnostic studies
 Contraindications for contrast medium
* MRI or MRA with gadolinium contrast medium—may be fatal
* Contrast-induced nephropathy (CIN)
* Diabetics taking metformin: hold 48 hours before and
after use of contrast medium; risk of lactic acidosis
* If contrast is needed for high-risk patients—use low-
dose and optimal hydration

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8
Q

AKI Care

A

Ensure adequate intravascular volume and cardiac
output
 Loop diuretics (e.g., furosemide [Lasix])
 Osmotic diuretics (e.g., mannitol)
 Closely monitor fluid intake during oliguric phase
 Fluid restriction calculation: All fluid losses for
previous 24 hours + 600 mL

Hyperkalemia therapies
 Temporary—move K+ into cells
* Insulin and sodium bicarbonate
  dysrhythmias—stabilizes myocardium
* Calcium gluconate
 Remove K+ from body
* Sodium polystyrene sulfonate (Kayexalate) or
Patiromer (Veltassa)
* Dialysis
 Dietary restriction

Indications for renal replacement therapy (RRT)
 Volume overload
 Elevated serum potassium level
 Metabolic acidosis
 BUN level > 120 mg/dL (43 mmol/L)
 Significant change in mental status
 Pericarditis, pericardial effusion, or cardiac
tamponade
 Clinical status of patient

Renal replacement therapy (RRT)
 Peritoneal dialysis (PD)
* Not frequently used
 Intermittent hemodialysis (HD)
* Emergent therapy
 Continuous renal replacement therapy (CRRT)
* Cannulation of artery and vein
* Continuously 24 hours

Nutrition therapy
 Maintain adequate caloric intake
* Primarily carbohydrates and  fat
* Adequate protein to prevent breakdown
 Restrict sodium, K+, phosphate
 Calcium supplements or phosphate-binding agents
 Enteral/parenteral nutrition

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9
Q

Gerontologic Considerations
Acute Kidney Injury

A

Decreased GFR with aging
 More susceptible to AKI
 Dehydration
* Polypharmacy- diuretics, laxatives
* Illness and immobility
 Hypotension, diuretic therapy, aminoglycoside
therapy, obstructive disorders, surgery, infection, and
contrast medium
 decreased reduced ability to recover
 RRT still an option

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10
Q

Chronic Kidney Disease

A

Progressive, irreversible loss of kidney function
 Greater than 26 million American adults have
CKD; more common than AKI
 Increased prevalence related to aging population,
increased obesity, increased diabetes and HTN
 Over half a million Americans are receiving
treatment for ESRD; high mortality rate

Kidney disease improving global outcomes (KDIGO)
defines CKD as
 Kidney damage
* Pathologic abnormalities
* Markers of damage
 Blood, urine, imaging tests
 Low glomerular filtration rate (GFR)
* <60 mL/min/1.73m2 for longer than 3 months

Leading causes
 Diabetes—50%
 Hypertension—25%
 Other: glomerulonephritis, cystic diseases, urologic
diseases
 Persons with CKD are often asymptomatic; ~ 70%
aware
 Underdiagnosed and untreated

Course and prognosis are variable
 Medicare covers ~80% of the costs
 Considered a disability
 See Promoting Health Equity Box
 Increased incidence with Blacks, Native Americans,
and Hispanics

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11
Q

CKD Clinical Manifestations

A

Result of retained substances
 Urea
 Creatinine
 Phenols
 Hormones
 Electrolytes
 Water
 Uremia

Early stages
 No change in urine output
 Polyuria may be present related to diabetes.
 CKD progression—increasing fluid retention; need
diuretic
 After a period on dialysis, patients may become
anuric

Waste product accumulation
 As GFR decreases, BUN and serum creatinine levels
increase
 BUN level increase
* From kidney failure and protein intake, fever,
corticosteroids, and catabolism
* N/V, lethargy, fatigue, impaired thought processes, and headaches occur
 *Serum creatinine clearance—most accurate indicator

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12
Q

Uremia

A

Uremia
 Syndrome in which kidney function declines to the
point that symptoms occur in multiple body systems
 Often occurs when GFR is less than or equal to
15 mL/min
 Manifestations vary depending on cause, co-
morbidities, age, and adherence to medical regimen

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13
Q

Defective Carb Metabolism

A

Altered carbohydrate metabolism
 Caused by impaired glucose metabolism
* From cellular insensitivity to normal action of insulin
* Mild-moderate hyperglycemia and hyperinsulinemia

Defective carbohydrate metabolism
 Patients with diabetes who develop uremia may
require less insulin than before the onset of CKD
 Excretion of insulin dependent on kidneys
 Insulin dosing must be individualized
 May improve after starting dialysis

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14
Q

Elevated Triglycerides

A

Elevated triglycerides
 Hyperinsulinemia stimulates hepatic production of
triglycerides
 Altered lipid metabolism
* Decreased levels of enzyme lipoprotein lipase
– Important in breakdown of lipoproteins
 Increased VLDLs and LDLs, decreased HDLs
 Most patients with CKD die from CV disease

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15
Q

Electrolyte Imbalances

A

Potassium (K+)
 Hyperkalemia
* Most serious electrolyte disorder in kidney disease
* Fatal dysrhythmias
 When serum potassium level reaches 7 to 8 mEq/L (7 to 8 mmol/L)
* Decreased excretion, breakdown of cellular protein,
bleeding, and metabolic acidosis leads to increased K+
 Other sources: food, dietary supplements, drugs, and IV infusions

Sodium (Na+)
 May be high, normal, or low
 Impaired excretion causes sodium and water
retention
 Dilutional hyponatremia may occur
* Edema
* Hypertension
* HF

Calcium and phosphate
 See section on Musculoskeletal System (CKD mineral
and bone disorder)

 Magnesium
 Hypermagnesemia
* Related to ingestion of magnesium (e.g., milk of
magnesia, magnesium citrate, antacids)
* Can result in absence of reflexes, decreased mental
status, cardiac dysrhythmias, hypotension, respiratory
failure

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16
Q

Metabolic Acidosis

A

Metabolic acidosis
 Results from
* Impaired ability of kidneys to excrete excess acid
* Defective reabsorption and regeneration of bicarbonate
 Plasma bicarbonate level usually falls to
approximately 16 to 20 mEq/L (16 to 20 mmol/L)

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17
Q

Anemia

A

Anemia
 Due to decreased production of erythropoietin
* Hormone stimulates bone marrow to make RBCs
 Other factors: nutritional deficiencies, decreased RBC
life span, increased hemolysis, blood sampling, GI
bleeding, HD, increased PTH
 Also decreased iron stores
 Folic acid lost in dialysis

Bleeding tendencies
 Defect in platelet function
 Infection
Changes in WBC function
 Altered immune response and function
 Hyperglycemia and external trauma

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18
Q

Cardiovascular Disease closely linked

A

CV disease and CKD closely linked
 Death often related to MI, ischemic heart disease,
PAD, HF, cardiomyopathy, and stroke
 Traditional CV risk factors
* Hypertension and elevated lipids
 Nontraditional CV risk factors
* Vascular calcification and arterial stiffness

Calcium deposits associated with stiffness of blood
vessels
 Vascular smooth muscle cells change
* Chondrocytes or osteoblast-like cells
 High calcium and phosphate totals
 Impaired renal excretion
 Drug therapies to treat bone disease

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19
Q

HTN

A

Hypertension
 Both a cause and a consequence of CKD
* Aggravated by sodium and water retention
* Increased renin production may contribute
 HTN, ECF volume overload, and anemia may
develop into left ventricular hypertrophy, which may
lead to cardiomyopathy and HF
* HTN can cause retinopathy, encephalopathy,
nephropathy

*BP control—one of most important goals
 Dysrhythmias
 Hyperkalemia and decreased coronary artery
perfusion
 Uremic pericarditis can progress to effusion and
tamponade
 Friction rub, chest pain, and fever

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20
Q

Respiratory

A

Kussmaul respirations related to acidosis
 Dyspnea may occur with
 Fluid overload
 Pulmonary edema
 Uremic pleuritis
 Pleural effusions
 Respiratory infections

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21
Q

GI

A

Every part of GI system is affected
 Cause: excessive urea
* Stomatitis with exudates and ulcerations
* Uremic fetor (urinous odor of breath)
* Anorexia, nausea, and vomiting
* Diabetic gastroparesis
* GI bleeding
* Constipation

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22
Q

CNS Depression

A

CNS depression
 Lethargy, apathy
 Decreased ability to concentrate
 Fatigue, irritability
 Altered mental ability (late)
 Seizures
 Coma
 Hypertensive encephalopathy

Peripheral neuropathy
 Restless legs syndrome
 Paresthesias
 Motor involvement
 Footdrop
 Muscle weakness and atrophy
 Loss of deep tendon reflexes
 Muscle twitching, jerking, asterixis, and nocturnal leg
cramps

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23
Q

Bones/Minerals

A

CKD mineral and bone disorder (CKD-MBD)
 Systemic disorder of mineral and bone metabolism
 Results in
* Skeletal complications (osteomalacia, osteitis fibrosa)
* Soft tissue complications (vascular calcifications)

24
Q

Other

A

Pruritus
 Calcium-phosphate deposits and sensory neuropathy
 Itching may be intense
 Leads to bleeding or infection

Uremic frost
 Urea crystalizes on skin
 BUN > 200 mg/dL

 Infertility and decreased libido
 Experienced by both sexes: low sperm counts;
amenorrhea
 Sexual dysfunction
 Physical, psychological, and medication side effects
 Pregnancy during dialysis poses significant risk to
mother and infant
 Personality and behavioral changes
 Emotional lability
 Withdrawal
 Anxiety, depression, and grief
 Fatigue, lethargy
 Changes to: body image, lifestyle, occupation,
finances, and family roles and responsibilities

25
Q

CKD Diagnostic Studies

A

History and physical assessment
 Dipstick evaluation of protein
 Albuminuria
 Urinalysis
 Renal ultrasound, scan, CT scan, biopsy
 Albumin-to-creatinine ratio (1st am void)
 Serum BUN, creatinine, creatinine clearance,
electrolytes, lipids, hemoglobin, hematocrit
 GFR

26
Q

CKD Care

A

Management
 Stages 1 to 4
 Control HTN, hyperparathyroid disease, CKD-MBD,
anemia, and dyslipidemia
 Correct of ECF volume overload or deficit
 RRT
 Treat CV disease
 Nutritional therapy
 Drug therapy

Hyperkalemia
 Restriction of high-potassium foods and drugs
 Acute
* IV glucose and insulin
* IV 10% calcium gluconate
 Sodium polystyrene sulfonate (Kayexalate)
* Cation-exchange resin; bowel exchanges Na+ for K+ ions
* Osmotic laxative action (diarrhea)
 Patiromer (Veltessa)—binds K+ in GI tract
* May bind other oral meds; take 6 hours before or 6 hours after ; delayed onset
 Dialysis—most effective

Hypertension
 Weight loss (if indicated)
 Therapeutic lifestyle changes
 Diet recommendations (DASH Diet)
 Antihypertensive drugs; often need 2 or more
* If diabetic—give ACE inhibitors and ARBs

CKD-mineral and bone disease (MBD)
 Phosphate not restricted until patient requires renal
replacement therapy
* Phosphate intake then restricted to
< 1 g/day

CKD-MBD
 Phosphate binders
* Calcium acetate (PhosLo)
* Calcium carbonate (Caltrate)
 Bind phosphate in bowel and then excreted
* Sevelamer hydrochloride (Renagel)
 Lowers cholesterol and LDL levels
Phosphate binders
* Should be administered with each meal
* Side effect: constipation

CKD-MBD
 Avoid aluminum and magnesium preparations
 Supplementing vitamin D
* Cholecalciferol
* Serum phosphate level must be lowered before calcium or vitamin D is administered

27
Q

CKD Care Continued

A

Control secondary hyperparathyroidism
* Calcimimetic agents
 Cinacalcet (Sensipar)
– Increase the sensitivity of calcium receptors in
parathyroid glands
* Subtotal or total parathyroidectomy

Anemia
 Erythropoietin (EPO)
* Epoetin alfa (Epogen, Procrit)
* Darbepoeitin alfa (Aranesp)
* Given IV or subcutaneously
* Increased hemoglobin and hematocrit in 2 to 3 weeks
* Side effects: thromboembolism, hypertension
* Use lowest possible dose; contraindicated in
uncontrolled HTN

Anemia
 Iron supplements
* If plasma ferritin level is <100 ng/mL
* Side effects: gastric irritation,
constipation
* May make stool dark in color

Anemia
 Folic acid supplements
* Needed for RBC formation
* Removed by dialysis
 Avoid blood transfusions
* Increase the development of antibodies
* May lead to iron overload

Dyslipidemia
 Statins (HMG-CoA reductase inhibitors)
* Most effective for lowering LDL level
* Atorvastatin (Lipitor)
 Fibrates (fibric acid derivatives)
* Used to lower triglyceride levels and increase HDLs
* Gemfibrozil (Lopid)

28
Q

CKD Nutriton Therapy

A

Nutrition therapy
 Designed to maintain good nutrition
 Dietician referral
 Calorie-protein malnutrition
* Monitor laboratory parameters
Protein intake
 Normal for Stages 1 to 4 and HD patient
 Increased for PD patient
Fluid restriction with HD
 Intake depends on daily urine output
Sodium restriction
 Diets vary from 2 to 4 g/day
 Avoid high-sodium foods
 Salt substitutes should be avoided because they
contain potassium chloride
Potassium restriction
 Limit: 2 to 3 grams
 High-potassium foods should be avoided with HD
Nutrition therapy
Phosphate restriction in ESRD
 Limit: 1 gram per day
 Foods high in phosphate
* Meat and dairy products
 Most foods high in phosphate are high in protein
* Phosphate binders essential with dialysis

29
Q

Dialysis

A

Movement of fluid/molecules across a
semipermeable membrane from one
compartment to another
 Used to correct fluid and electrolyte imbalances
and removes waste products in kidney failure
 Can be used to treat drug overdoses

2 methods of dialysis available
 Peritoneal dialysis (PD)
 Hemodialysis (HD)

Started when patient’s uremia can no longer be
adequately treated conservatively; GFR < 15
mL/min/1.73 m2
 Nephrologist determines when to start
 Uremic complications require dialysis

ESRD treated with dialysis because
 There is a lack of donated organs
 Some patients are physically or mentally unsuitable
for transplantation
 Some patients do not want transplants
 Age is not a factor in determining candidacy

30
Q

General Principles of Dialysis

A

Diffusion
 Movement of solutes from an area of greater
concentration to an area of lesser concentration

Osmosis
 Movement of fluid from an area of lesser
concentration of solutes to area of greater
concentration
* Glucose in dialysate creates osmotic gradient to pull
fluid from the blood

Ultrafiltration
 Water and fluid removal
 Results when there is an osmotic gradient or pressure
gradient across membrane
* PD—glucose in dialysate
* HD—pressure gradient
 Excess fluid moves into dialysate

31
Q

Peritoneal Dialysis

A

Peritoneal access is obtained by inserting a catheter
through anterior abdominal wall
 Technique for catheter placement varies; usually
done via surgery
 PD may start right away or bed delayed until site
healed
 Aseptic technique important to avoid peritonitis

Three phases of PD cycle (manual):
 Inflow (fill)—2 to 3 L over 10 minutes
 Dwell (equilibration) 20 to 30 minutes—8 hours
 Drain 15 to 30 minutes

Cycle is repeated
 Called an exchange
 Volume depends on size of peritoneal cavity
 Dextrose—osmotic agent

Automated peritoneal dialysis (APD)
 Cycler delivers the dialysate during sleep Times and
controls fill, dwell, and drain phases; alarms and
monitors for safety
 Continuous Ambulatory peritoneal dialysis (CAPD)
 Manual exchange four times during the day

32
Q

Peritoneal Dialysis Complications

A

Exit site infection
 Redness, tenderness, drainage
 Treat with antibiotics

Peritonitis—Exit site or tunnel infection
 Abdominal pain, rebound tenderness, or cloudy
effluent with increased WBCs or bacteria, may
have fever

GI: diarrhea, vomiting, distention, increased bowel sounds
 Treat with antibiotics
 Repeated infections may cause adhesions

Hernias
 Increased intrabdominal pressure from dialysate
 Treatment: hernia repair

Lower back problems
 Intraperitoneal infusion increases pressure
 Treatment: binders and exercise

Bleeding
 Common with initial catheter placement
 New—active intraperitoneal bleeding; check BP and
hematocrit
 Pulmonary complications
 Decreased lung expansion  atelectasis, pneumonia, or bronchitis
 Elevate HOB, repositioning and deep breathing
 Protein loss—monitor nutrition

33
Q

Hemodialysis
Settings and Schedules

A

Most treated in a community-based center
 Dialyzed for 3 to 4 hours, 3 days/wk
 Other schedule options
 Short daily HD
 Long nocturnal HD
 Home HD

34
Q

Hemodialysis
Complications

A

Hypotension
 Hypovolemia, decreased CO and SVR
 Light-headed, nausea, seizures, vision changes, and chest pain
 Treatment: decreasing volume of fluid removal and IV NSS
 Muscle cramps
 Decreased BP, hypovolemia, increased ultrafiltration, and low-sodium dialysate
 Treatment: decrease ultrafiltration and IV fluids

Loss of blood
 Blood not rinsed from dialyzer, accidental separation of tubing, dialysis membrane rupture or bleeding after
needles removed; heparin
 Treatment: rinse all blood back, avoid excess heparin, and hold pressure to access sites
 Hepatitis—8% to 10% hepatitis C
 Infection control precautions
 Hepatitis B—low incidence; administer vaccine

35
Q

Continual Renal Replacement
Therapy

A

Method for treating AKI (acute kidney infection)
 Means by which uremic toxins and fluids are
removed
 Acid-base status and electrolyte are adjusted slowly
and continuously in hemodynamically unstable
patients
 Over 24 hours
 Can used with HD

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

Various types of CRRT
 Continuous venovenous hemofiltration (CVVH)
 Slow continuous ultrafiltration (SCUF)
 Continuous venovenous hemodialysis (CVVHD)
 Continuous venovenous hemodiafiltration (CVVHDF)

Infusion of replacement fluid determined by
degree of fluid and electrolyte imbalance
 Anticoagulants are needed to prevent blood
clotting
 Customized to patient’s needs

CVVHD and CVVHDF
 Uses dialysate
 Dialysis fluid is attached to distal end of hemofilter

 Can be continued as long as 30 to 40 days
 Hemofilter should be changed every 24 to 48 hours
 Able to obtain specimens
 Ultrafiltrate should be clear yellow
 If bloody, need to terminate

36
Q

CRRT versus HD

A

CRRT versus HD
 Blood pump is slower than HD
 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
(need ICU nurse)
 Does not require complicated HD equipment

37
Q

CRRT Nursing Interventions

A

Specific nursing interventions
 Obtain weights
 Monitor and document laboratory values daily for fluid and electrolyte balance
 Assess hourly intake and output, VS, and
hemodynamic status
 Care for site to prevent infection

38
Q

Wearable Artificial Kidney (WAK)

A

Recently developed and approved for use
 Miniaturized dialysis machine; ~10 pounds
 Carrier resembles a tool belt
 Connects to patient via catheter
 Designed to filter blood in ESRD
 Can run continuously on batteries

39
Q

Kidney Transplant

A

More than 100,000 patients are currently awaiting kidney transplants
 Average wait time for cadaver is 2 to 5 years
 17,000 transplants take place every year

Advances include:
 Organ procurement and preservation

Surgical techniques
 Tissue typing and matching
 Immunosuppressant therapy
 Prevention and treatment of graft rejection

Best treatment for ESRD
 Very successful
 1-year graft survival rate
 Deceased donor transplants: 90%
 Live donor transplants: 95%
 Reverses pathophysiology of ESRD
 Eliminates dialysis and dietary and lifestyle restrictions
 Less expensive than dialysis after 1st year

40
Q

Kidney Transplant
Recipient Selection

A

Candidacy determined by a variety of medical and
psychosocial factors that vary among transplant centers
 Possible exclusions: obesity, smoker

 Preemptive transplant (before dialysis is required) is
possible if recipient has a living donor

Contraindications to transplant
 Advanced cancer
 Refractory/untreated heart disease
 Chronic respiratory failure
 Extensive vascular disease
 Chronic infection
 Unresolved psychosocial disorders

 HIV+ or hepatitis B or C are not contraindications

Surgical procedures may be required before
transplant
 Coronary artery bypass or coronary angioplasty
 Cholecystectomy
 Bilateral nephrectomy

41
Q

Kidney Transplant
Histocompatibility Studies

A

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

42
Q

Kidney Transplant
Donor Sources

A

 Deceased donors with compatible blood type
 Blood relatives
 Emotionally related living donors
 Altruistic living donors
 Paired organ donation

Live donor
 Extensive interprofessional evaluation
 Crossmatches—check antibodies
 Advantages
* Better patient and graft survival rates
* Immediate organ availability
* Immediate function/minimal cold time
* Opportunity to have recipient in best possible medical
condition since elective surgery

Live donor sees nephrologist for H & P
 Laboratory studies
* 24-hour urine—creatinine clearance and total protein
* Complete blood count, chemistry and electrolyte
profiles
* Hepatitis B and C, HIV, CMV testing

43
Q

Donor Sources: Live Donor

A

Diagnostic studies
 ECG, chest x-ray
 Renal ultrasound, arteriogram, 3-D CT scan

Psychologist or social worker evaluation
 Emotional stability
 Risks and benefits
 Cost covered by recipient’s insurance
 No compensation for lost wages

Paired organ donation
 ABO incompatibility between donor and recipient
 Find another donor/recipient pair with whom to
exchange kidneys
 Plasmapheresis—option to remove antibodies from
recipient
* After transplant, patient gets plasmapheresis

44
Q

Donor Sources
Deceased Donors

A

Deceased (cadaver) kidney donors are relatively
healthy persons that have suffered an
irreversible brain injury and are brain dead
 Must have effective CV functions and on
ventilator to preserve organs
 Permission of next of kin requested even with
signed donor card
 Kidneys removed and preserved up to 72 hours
* Preferred cold time less than 24 hours

45
Q

Kidney Transplant
Surgical Procedure - Live Donor

A

Live donor
 Donor nephrectomy performed by a transplant
surgeon
 Begins 1 or 2 hours before the recipient’s surgery is
started
 Recipient is surgically prepared in a nearby operating
room

Laparoscopic donor nephrectomy
* Most common approach for removing kidney in living
donor
* Minimally invasive
 Fewer risks, shorter recovery time

Open (conventional) nephrectomy
* Lateral incision
* Rib may need to be removed

46
Q

Kidney Transplant Recipient

A

Kidney transplant recipient
 Transplanted kidney usually placed extraperitoneal in
the iliac fossa
 Right iliac fossa is preferred for anastomosis of blood
vessels and ureter
Before incision
 Urinary catheter placed into bladder
* Antibiotic solution instilled
 Distends the bladder
 Decreases risk of infection
 Crescent-shaped incision

Rapid revascularization critical
 Donor artery anastomosed to recipient internal or
external iliac artery
 Donor vein anastomosed to recipient external iliac
vein

Kidney transplant recipient
 When anastomoses are complete,
clamps are released and blood flow reestablished
 Urine may begin to flow from ureter immediately
 Donor ureter tunneled through bladder submucosa
(ureteroneocystotomy)

47
Q

Pre Op Care

A

Preoperative care
 Emotional and physical preparation
* Stress that dialysis may be required
* Review need for immunosuppressive drugs and
prevention of infection
 ECG
 Chest x-ray
 Laboratory studies
 Dialysis, if needed

48
Q

Post Op Care

A

Live donor
* Care is similar to that for open or laparoscopic
nephrectomy
* Closely monitor renal function
* Closely monitor hematocrit
* Donors usually experience more pain than recipient
* Acknowledge their gift!

Kidney transplant recipient
* Maintenance of fluid and electrolyte balance is the
priority
* Large volumes of urine may be produced soon after
transplanted kidney placed due to
 New kidney’s ability to filter BUN
 Abundance of fluids during operation
 Initial renal tubular dysfunction
* Dehydration must be avoided
* Assess for hyponatremia/hypokalemia
* Acute tubular necrosis can occur
* Monitor urine output; maintain catheter patency
* Patient education: signs and symptoms of rejection,
infection, and surgical complications; follow-up care

49
Q

Kidney Transplant
Immunosuppressive Therapy

A

Goals
 Adequately suppress immune response to prevent
rejection
 Maintain sufficient immunity to prevent overwhelming
infection

50
Q

Kidney Transplant
Complications - Rejection

A

Rejection
 Hyperacute (antibody-mediated, humoral) rejection
* Occurs minutes to hours after transplant
 Acute rejection
* Occurs days to months after transplant
 Chronic rejection
* Process occurs over months or years and is irreversible
* May go back on transplant list

51
Q

Transplant Complications - Infection

A

Risk related to: suppression of normal defense
mechanisms, immunosuppressive drugs, and effects
of ESRD; compounded by systemic illnesses
 Most common infections observed in 1st month:
pneumonia , wound infections, IV line and drain
infections, and UTIs

Fungal infections
* Candida
* Cryptococcus
* Aspergillus
* Pneumocystis jiroveci

Viral infections
* CMV
 One of most common
* Epstein-Barr virus
* Herpes simplex virus (HSV)
* Varicella-zoster virus
* Polyomavirus (e.g., BK virus)

52
Q

Transplant Complications - CVD

A

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

53
Q

Transplant Complications - Cancer

A

Cancers
 Primary cause— immunosuppressive therapy
 Most common
* Skin cancers
* Posttransplant lymphoproliferative disorder
 Regular screening is important
 Preventive care
* Protective clothing and sunscreen

54
Q

Transplant Complications - Recurrence of Kidney Disease

A

Recurrence of original kidney disease
 Glomerulonephritis
 IgA nephropathy
 Diabetic nephropathy
 Focal segmental sclerosis

55
Q
A