Download Renal Failure and Treatment

Renal Failure
and
Treatment
Vicky Jefferson, RN, CNN
Capital Dialysis of Texas
Bones can break, muscles can atrophy, glands
can loaf, even the brain can go to sleep
without immediate danger to survival. But -should kidneys fail.... neither bone, muscle, nor
brain could carry on.
Homer Smith, Ph.D.
Functions of the Kidneys



Renin secretion and the
regulation of volume and
composition of
extracellular fluid.
Excretion
Blood pressure control

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Vitamin D activation
Acid-base balance
regulation.
Erythropoietin
production
Urine formation
Renin


Renin is important in the regulation of blood pressure.
It is released from the granular cells of the efferent
arteriole in response to decreased arteriole blood
pressure, renal ischemia, extracellular fluid depletion,
increased norepinephrine, and increased urinary Na+
concentration.
Blood Pressure Regulation
4 mechanisms are involved
Volume control
 Aldosterone effect
 Renin-angiotensin-aldosterone
 Renal prostaglandin

Prostaglandin
Prostoglandins (PGs)- synthesized by most
body tissues. In the kidney, PGs are synthesized
in the medulla and have a vasodilating action
and promote Na+ excretion. PGs counteract the
vasoconstrictor effect of angiotensin and
norepinephrine. Renal PGs systemically lower
blood pressure by decreasing systemic vascular
resistance.
Vitamin D


Acquired by the body through diet or through
synthesis by ultraviolet radiation on the
cholesterol in the skin.
The liver and the kidney make the vitamin active
in the body.
Erythropoietin
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Erythropoietin is produced and released by the
kidneys in response to decreased oxygen tension
in the renal blood supply that is created by the
loss of red blood cells.
Erythropoietin stimulates the production of
RBCs in the bone marrow.
Erythropoietin deficiency leads to anemia in
renal failure.
RBC Synthesis & Maturation
Kidney secrete Erythropoietin, it stimulates the
bone marrow to produce RBC’s
 in oxygen delivery simulates release
 in response the RBC count rises in 3 - 5 days
 speeds the maturation of RBC’s

Acid Base Balance
Kidneys regulate acid-base balance by stabilizing
body fluid volume & flow rate to enhance the
reabsorption or excretion of bicarbonate &
hydrogen ions
Electrolyte Regulation

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Sodium
Potassium
Calcium
Phosphate
Magnesium
Chloride
Need to Know:
Normal Values
Functions
Factors affect
Excretion of Metabolic Waste


Over 200 waste products excreted
Only 2 are used for clinical assessment
BUN
 Creatinine

Excretion of Metabolic Waste


Over 200 waste products excreted
Only 2 are used for clinical assessment
BUN
 Creatinine

BUN

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
Normal 8 - 20 mg/dl
Nitrogenous waste product of protein
metabolism
Unreliable in measurement of renal function

Relevance is assessed in conjunction with Creatinine
Factors Affecting BUN

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Urine flow
low renal perfusion
Volume depletion
Metabolic rate
Protein metabolism
Drugs
Creatinine
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A waste product of muscle metabolism
Normal value0.6 - 1.5 mg/dl
2 times normal = 50% damage
8 times normal = 75% damage
10 times normal = 90% damage
Exception - severe muscular disease can greatly
 Creatinine levels
Diagnostic Tools for Assessing
Renal Failure

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Blood Tests
 BUN elevated (norm 10-20)
 Creatinine elevated (norm 0.7-1.3)
 K elevated
 PO4 elevated
 Ca decreased
Urinalysis
 Specific gravity
 Protein
 Creatinine clearance
Diagnostic Tools
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Biopsy
Ultrasound
X-Rays
Acute Renal Failure (ARF)
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Sudden onset - hours to days
Often reversible
Severe - 50% mortality rate overall; generally
related to infection.
Characteristics of ARF

Homeostatic functions affected most
Electrolyte imbalances
 Volume regulation
 Blood pressure control
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Endocrine functions affected lease
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Require time to evolve
Renal size is preserved
Evidence of acute illness or insult exists
Chronic Renal Failure

Slow progressive renal disorder related to
nephron loss, occurring over months to years

Culminates in End Stage Renal Disease
Characteristics of Chronic Renal
Failure
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Cause & onset often unknown
Loss of function precedes lab abnormalities
Lab abnormalities precede symptoms
Symptoms (usually) evolve in orderly sequence
Renal size is usually decreased
Causes of Chronic Renal Failure
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Diabetes
Hypertension
Glomerulonephritis
Cystic disorders
Developmental - Congenital
Infectious Disease
Causes of Chronic Renal Failure
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Neoplasms
Obstructive disorders
Autoimmune diseases
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Lupus
Hepatorenal failure
Scleroderma
Amyloidosis
Drug toxicity
Stages of Chronic Renal Failure
Old System

Reduced Renal Reserve
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Renal Insufficiency
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End Stage Renal Disease (ESRD)
Stages of Chronic Renal Failure
NKF Classification System
Stage 1:
GFR > 90 ml/min despite kidney
damage
Stages of Chronic Renal Failure
NKF Classification System
Stage 2:
Mild reduction (GFR 60 – 89
ml/min)
1. GFR of 60 may represent 50%
loss in function.
2. Parathyroid hormones starts to
increase.
During Stage 1 - 2

No symptoms

Serum creatinine doubles
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Up to 50% nephron loss
Stages of Chronic Renal Failure
NKF Classification System
Stage 3:
Moderate reduction (GFR 30 – 59
ml/min)
1. Calcium absorption decreases
2. Malnutrition onset
3. Anemia secondary to Erythropoietin
deficiency
4. Left ventricular hypertrophy
Stages of Chronic Renal Failure
NKF Classification System
Stage 4:
Sever reduction (GFR 15 – 29
ml/min)
1. Serum triglycerides increase
2. Hyperphosphatemia
3. Metabolic acidosis
4. Hyperkalemia
During Stage 3 - 4
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Signs and symptoms worsen if kidneys are
stressed
Decreased ability to maintain homeostasis
During stages 3 - 4
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75% nephron loss
Decreased: glomerular filtration rate, solute
clearance, ability to concentrate urine and
hormone secretion
Symptoms: elevated BUN & Creatinine, mild
azotemia, anemia
Stages of Chronic Renal Failure
NKF Classification System
Stage 5:
Kidney failure (GFR < 15 ml/min)
1. Azotemia
During Stage 5
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Residual function < 15% of normal
Excretory, regulatory and hormonal functions
severely impaired.
metabolic acidosis
Marked increase in: BUN, Creatinine,
Phosphorous
Marked decrease in: Hemoglobin, Hematocrit,
Calcium
Fluid overload
During Stage 5
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Uremic syndrome develops affecting all body
systems
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can be diminished with early diagnosis & treatment
Last stage of progressive CRF
Fatal if no treatment
What happens when the kidneys
don’t function correctly?
Manifestations of CRF Nervous System
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Mood swings
Impaired judgment
Inability to concentrate and perform simple
math functions
Tremors, twitching, convulsions
Peripheral Neuropathy
restless legs
 foot drop
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Manifestations of CRF
Skin
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Pale, grayish-bronze color
Dry scaly
Severe itching
Bruise easily
Uremic frost
Manifestations of CRF
Eyes
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Visual blurring
Occasional blindness
Manifestations of CRF
Fluid - Electrolyte - pH
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Volume expansion and fluid overload
Metabolic Acidosis
Electrolyte Imbalances
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Hyperkalemia
Manifestations of CRF
GI Tract
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Uremic fetor
Anorexia, nausea, vomiting
GI bleeding
Manifestations of CRF
Hematologic
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Anemia
Platelet dysfunction
Manifestations of CRF
Musculoskeletal
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Muscle cramps
Soft tissue calcifications
Weakness
Related to calcium phosphorous imbalances
Calcium-Phosphorous Balance
Manifestations of CRF
Heart - Lungs
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Hypertension
Congestive heart failure
Pericarditis
Pulmonary edema
Pleural effusions
Manifestations of CRF
Endocrine - Metabolic
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Erythropoietin production decreased
Hypothyroidism
Insulin resistance
Growth hormone decreased
Gonadal dysfunction
Parathyroid hormone and Vitamin D3
Hyperlipidemia
Treatment Options
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Hemodialysis
Peritoneal Dialysis
Transplant
Nothing
Hemodialysis

Removal of soluble substances and
water from the blood by diffusion
through a semi-permeable membrane.
History
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Early animal experiments began 1913
1st human dialysis 1940 by Dutch physician
Willem Kolff (2 of 17 patients survived)
Considered experimental through 1950’s, No
intermittent blood access; for acute renal failure
only.
History cont’d
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1960 Dr. Scribner developed Scribner Shunt
1960’s Machines expensive, scarce, no funding.
“Death Panels” panels within community
decided who got to dialyze.
Hemodialysis Process
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Blood removed from patient into the
extracorporeal circuit.
Diffusion and ultrafiltration take place in the
dialyzer.
Cleaned blood returned to patient.
Extracorporeal Circuit
How Hemodialysis Works
Vascular Access
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Arterio-venous shunt (Scribner External Shunt)
Arterio-venous (AV) Fistula
PTFE Graft
Temporary catheters
“Permanent” catheters
Scribner Shunt
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External- one end into
artery, one into vein.
Advantages
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place at bedside
use immediately
Disadvantages
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infection
skin erosion
accidental separation
limits use of extremity
Arterio-venous (AV) Fistula
Primary Fistula
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Patients own artery and vein surgically anastomosed.
Advantages
 patients own vein
 longevity
 low infection and thrombosis rates
Disadvantages
 long time to mature, 1- 6 months
 “steal” syndrome
 requires needle sticks
PTFE (Polytetraflourethylene)
Graft
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Synthetic “vessel” anastomosed into an artery and vein.
Advantages
 for people with inadequate vessels
 can be used in 7-14 days
 prominent vessels
Disadvantages
 clots easily
 “steal” syndrome more frequent
 requires needle sticks
 infection may necessitate removal of graft
Temporary Catheters
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Dual lumen catheter placed into a central vein-subclavian,
jugular or femoral.
Advantages
 immediate use
 no needle sticks
Disadvantages
 high incidence of infection
 subclavian vein stenosis
 poor flow-inadequate dialysis
 clotting
Cuffed Tunneled Catheters
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Dual lumen catheter with Dacron cuff
surgically tunneled into subclavian,
jugular or femoral vein.
Advantages
 immediate use
 can be used for patients that can have
no other permanent access
 no needle sticks
Disadvantages
 high incidence of infection
 poor flows result in inadequate
dialysis
 clotting
Complications of Hemodialysis
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During dialysis
 Fluid and electrolyte related
 hypotension
 Cardiovascular
 arrythmias
 Associated with the extracorporeal circuit
 exsanguination
 Neurologic
 seizures
 other
 fever
Complications of Hemodialysis
cont’d
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Between treatments
Hypertension/Hypotension
 Edema
 Pulmonary edema
 Hyperkalemia
 Bleeding
 Clotting of access

Complications of Hemodialysis
cont’d

Long term
 Metabolic
 hyperparathyroidism
 diabetic complications
 Cardiovascular
 CHF
 AV access failure
 Respiratory
 pulmonary edema
 Neuromuscular
 neuropathy
Complications of Hemodialysis
cont’d
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Long term cont’d
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Hematologic
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GI
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bleeding
dermatologic
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anemia
calcium phosphorous deposits
Rheumatologic
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amyloid deposits
Complications of Hemodialysis
cont’d
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Long term cont’d
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Genitourinary
infection
 sexual dysfunction
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Psychiatric
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depression
Infection
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bloodborne pathogens
Dietary Restrictions on
Hemodialysis
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Fluid restrictions
Phosphorous restrictions
Potassium restrictions
Sodium restrictions
Protein to maintain nitrogen balance
too high - waste products
 too low - decreased albumin, increased mortality
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Calories to maintain or reach ideal weight
Peritoneal Dialysis

Removal of soluble substances and water from
the blood by diffusion through a semipermeable membrane that is intracorporeal
(inside the body).
Types of Peritoneal Dialysis
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CAPD: Continuous ambulatory peritoneal dialysis
CCPD: Continuous cycling peritoneal dialysis
IPD: Intermittent peritoneal dialysis
CAPD
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Catheter into peritoneal cavity
Exchanges 4 - 5 times per day
Treatment 24 hours; 7 days a week
Solution remains in peritoneal cavity except
during drain time
Independent treatment
Phases of A Peritoneal Dialysis
Exchange
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Fill: fluid infused into peritoneal cavity
Dwell: time fluid remains in peritoneal cavity
Drain: time fluid drains from peritoneal cavity
Complications of Peritoneal
Dialysis
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Infection
 peritonitis
 tunnel infections
 catheter exit site
Hypervolemia
 hypertension
 pulmonary edema
Hypovolemia
 hypotension
Hyperglycemia
Malnutrition
Complications of Peritoneal
Dialysis cont’d
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Obesity
Hypokalemia
Hernia
Cuff erosion
Advantages of CAPD
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Independence for patient
No needle sticks
Better blood pressure control
Some diabetics add insulin to solution
Fewer dietary restrictions
protein loses in dialysate
 generally need increased potassium
 less fluid restrictions

Peritoneal Catheter Exit Site
Medications Common to Dialysis
Patients
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Vitamins - water soluble
Phosphate binder - (Phoslo, Calcium, Aluminum
hydroxide) Give with meals
Iron Supplements - don’t give with phosphate
binder or calcium
Antihypertensives - hold prior to dialysis
Medications Common to Dialysis
Patients cont’d
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Erythropoietin
Calcium Supplements - Between meals, not with
iron
Activated Vitamin D3 - aids in calcium
absorption
Antibiotics - hold dose prior to dialysis if it
dialyzes out
Medications
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Many drugs or their metabolites are excreted by
the kidney
Dosages - many change when used in renal
failure patients
Dialyzability - many removed by dialysis varies
between HD and PD
Patient Education
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Alleviate fear
Dialysis process
Fistula/catheter care
Diet and fluid restrictions
Medication
Diabetic teaching
Transplantation
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Treatment not cure
Kidney Awaiting Transplant
Advantages
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Restoration of “normal” renal function
Freedom from dialysis
Return to “normal” life
Disadvantages
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Life long medications
Multiple side effects from medication
Increased risk of tumor
Increased risk of infection
Major surgery
Care of the Recipient
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Major surgery with general anesthesia
Assessment of renal function
Assessment of fluid and electrolyte balance
Prevention of infection
Prevention and management of rejection
Function
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ATN? (acute tubular necrosis)
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50% experience
Urine output >100 <500 cc/hr
BUN, creatinine, creatinine clearance
Fluid Balance
Ultrasound
Renal scans
Renal biopsy
Fluid & Electrolyte Balance
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Accurate I & O
 CRITICAL TO AVOID DEHYDRATION
 Output normal - >100 <500 cc/hr, could be 1-2 L/hr
 Potential for volume overload/deficit
Daily weights
Hyper/Hypokalemia potential
Hyponatremia
Hyperglycemia
Prevention of Infection
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Major complication of transplantation due to
immunosuppression
HANDWASHING
Crowds, Kids
Patient Education
Rejection
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Hyperacute - preformed antibodies to donor
antigen
function ceases within 24 hours
 Rx = removal

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Accelerated - same as hyperacute but slower, 1st
week to month

Rx = removal
Rejection cont’d
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Acute - generally after 1st 10 days to end of 2nd
month
50% experience
 must differentiate between rejection and
cyclosporine toxicity
 Rx = steroids, monoclonal (OKT3), or polyclonal
(HTG) antibodies

Rejection cont’d

Chronic - gradual process of graft dysfunction
Repeated rejection episodes that have not been
completely resolved with treatment
 Rx = return to dialysis or re-transplantation
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Immunosuppressant Drugs
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Prednisone
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Prevents infiltration of T lymphocytes
Side effects
cushnoid changes
 Avascular Necrosis
 GI disturbances
 Diabetes
 infection
 risk of tumor

Immunosuppressant Drugs
cont’d
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Azathioprine (Imuran)
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Prevents rapid growing lymphocytes
Side Effects
bone marrow toxicity
 hepatotoxicity
 hair loss
 infection
 risk of tumor

Immunosuppressant Drugs
cont’d

Cyclosporin

•
Interferes with production of interleukin 2 which is
necessary for growth and activation of T
lymphocytes.
Side Effects
–
–
–
–
–
Nephrotoxicity
HTN
Hepatotoxicity
Gingival hyperplasia
Infection
Immunosuppressant Drugs
cont’d
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Cytoxan - in place of Imuran less toxic
FK506 - 100 x more potent than Cyclosporin
Prograf
Cellcept
other in trials
Immunosuppressant Drugs
cont’d

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OKT3 - monoclonal antibody used to treat rejection or induce
immunosuppression
 decreases CD3 cells within 1 hour
Side effects
 anaphylaxis
 fever/chills
 pulmonary edema
 risk of infection
 tumors
1st dose reaction expected & wanted, pre-treat with Benadryl,
Tylenol, Solumedrol
Immunosuppressant Drugs
cont’d

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Atgam - polyclonal antibody used to treat rejection or
induce immunosuppression
 decreased number of T lymphocytes
Side effects
 anaphylaxis
 fever chills
 leukopenia
 thrombocytopenia
 risk of infection
 tumor
Patient Education
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Signs of infection
Prevention of infection
Signs of rejection
 decreased urine output
 increased weight gain
 tenderness over kidney
 fever > 100 degrees F
Medications
time, dose, side effects