Transcript Introduction and Overview of Chronic Kidney Disease

Introduction and Overview of
Chronic Kidney Disease
By
Emily Castro, RN, CCRN, MS
Myung Cho, RN, MS
Mary Fay, RN, ANP-BC, DNP
OBJECTIVES
The learner will be able to:
Identify the anatomical location of Kidneys
Identify what the Kidneys do
Identify the most common causes of Kidney
Disease
Identify signs & symptoms of Kidney problems
Identify those at increased risk for Kidney
Disease
Where are Your Kidneys
and How Do They Function
Two kidneys – the size of a fist
Located on either side of the spine at the lowest level of the
rib cage
Each one contains ~ a million functioning units =
nephrons.
A nephron consists of a filtering unit of tiny blood cells =
glomerulus attached to a tubule
When blood enters the glomerulus it’s filtered & remaining
fluid passes along the tubule. Here chemicals & water are
either added to or removed – whatever is the body’s need
Final product being the urine we excrete.
Kidney Function
Your kidneys are powerful chemical factories that
perform the following functions:
Remove waste products from the body
Remove drugs from the body
Balance the body’s fluids
Help control your blood pressure by expelling surplus
sodium for hi BP & releasing renin for low BP
Help keep your bones healthy by producing an active form
of vitamin D
Helps make red blood cells by producing erythropoieten, a
hormone that effects the number of circulating RBCs
Critical regulation of the body’s salt, potassium and acid
content is performed by the kidneys.
Kidney Facts
The kidneys perform life sustaining job of
filtering & returning to the bloodstream about
200 quarts of fluid every 24 hours.
~ 2 quarts are removed from the body in the
form of urine. ~ 198 quarts are recovered.
The urine we excrete has been stored in the
bladder for anywhere from 1 to 8 hours.
Chronic Kidney Disease
CKD is defined as having some type of
kidney abnormality or “marker” such as
protein in the urine, and having decreased
kidney function for three months or
longer.
Causes of CKD
There are many causes of CKD Some
inherited as:
Polycyctic kidney disease (PKD) the most common – 5%
of dialysis & transplants in US and Europe
Alport’s Syndrome – Hereditary Nephritis
Primary hyperoxaluria – accumulation of oxolate which
causes an accumulation of calcium salts (stones) in the
kidneys
Cystinuria – a metabolic disorder causing stones in the
kidneys, bladder, & ureter
Congenital Reflux Disorder – valve-like mechanism
between the bladder & ureter fails and urine backs up to
the kidney causing infection & possible damage
Other Risk Factors
Diabetes – the leading cause of kidney disease – 50%
High Blood Pressure – 28%
Glomerulonephritis
Inflammation of the glomeruli – filtering units, can happen
suddenly after a strep throat
Kidney Stones
Urinary Tract Infections
Upper UTI – Kidney (Pyelonephritis)
Lowere UTI – Cystitis and Urethritis
Drugs & toxins –
OTC pain relievers, nephro toxic medications, pesticides &
“street” drugs can be harmful to the kidneys
Increased Risk for CKD
Higher incidence among:
The elderly
Have a family member with CKD
African American
Hispanic American
Asians
Pacific Islander
American Indian
Warning Signs of Kidney Disease
High Blood Pressure
Blood and/or protein in the urine
BUN & Creatinine outside normal range
GFR less than 60
Frequent urination, particularly at night;
difficult or painful urination
Puffiness around eyes, swelling of hands and
feet
How to Detect Kidney Disease
Early detection & treatment are key to
keeping kidney disease from
progressing
Blood pressure measurement
Protein in urine – filtering units have been
damaged (fever or heavy exercise). Test
should be confirmed over several weeks
Blood creatinine & GFR – GFR tells how
much kidney function you have
Treatment
Many Kidney diseases can be
successfully treated
Kidney failure may be treated with
Hemodialysis – 3X week in a unit or at home
Peritoneal dialysis – Daily at home
Kidney transplantation – requiring a donor - has
a high success rate
Kidney Transplantation
Objectives
Participants will be able to:
– Identify immediate post-op care for the post renal
transplant patient
– Identify the order set for post renal transplant
patients
– Identify PACU routine and 6 Monti routine
– Identify the importance of venodyne stockings
– Identify the importance of accurate I’s & O’s
calculation and documentation
Definitions
Autograft: transplant of persons own
tissue from one body site to another
Isograft: transplant of tissue between
identical twins
Allograft or Homograft: transplant of
tissue between same species
Xenograft: transplant of tissue
between different species
Historical Events
1933: First human to human kidney transplant in
Ukraine. ABO incompatible patient died two days
later.
6/17/50: Cadeveric transplant on Ruth Tucker,
lasted 10 months – no immunosuppressive
therapy. She lived an additional 5 years
12/23/54: First successful Living donors –identical
twins in Boston – survived 8 years
1962: Tissue typing protocol – first cadaveric renal
transplant
Historical Events
1970’s: Harvard Brain Death Criteria
1972: Kidney Transplants included in
Health Insurance
1978: Cyclosporin introduced – major
immunosuppressant
1984: Established National Organ
Transplant Act
1989: Tacrolimus introduced
Overview
The need is great – over 70,000
waiting nationally with a 7 – 8 year
wait in New York, 4 years in New
Jersey
Living donor recipients have higher
success rate short and long term.
ESRD cause: 50%- DM, 28%- HTN
Kidney transplant is an allograft
Surgery for the Recipient
New kidney is placed in the pelvis:
the anterior iliac fossa extraperitoneally
Renal artery anastomosed to hypogastric or
external iliac artery
Renal vein anastomosed to external iliac vein
Ureter tunneled into the bladder or anastomosed
end to side to native ureter
Time of surgery 2 – 4 hours
Living donor kidney usually works immediately
– deceased donor kidney may be delayed in 3040% of patients
Post Operative Care
Post-op routines focus on close
monitoring of the function of the
transplanted kidney and close
observation for complications or signs
of rejection of the kidney.
A newly planted kidney may begin to
function immediately, or may not
function for some time.
Immediate Post-Op Care
Once patient is in PACU
1. Duplex Ultrasound of Transplanted Kidney on arrival to
PACU
2. LABS on arrival to PACU STAT and 6 hours post: CBC
with platelet count, Phosphorous, Serium Magnesium, Basic
Metabolic Panel, Calcium level, (PT/PTT, INR in 6 hr)
3. VS per PACU routine – call MD is SBP >160 or <100 &DBP
>100
4. No BP or IV in fistula arm
5. No IM injections
6. Strict I & O’s every hour – call MD if u/o < 200 ml/hr or >
800 ml/hr
7. FS glucose every 4 hr – call MD for glucose < 80 or > 250
8. Venodynes to lower extremities at all times – even when
sitting in the chair. Discontinue when ambulatory
9. Daily weights with same standing scale.
Orders 3 through 9 follow the patient when they are transferred to 6
Monti
IV Fluids & Oxygen
Sodium Chloride 0.9% at 70 ml per hr.
Replace u/o ml for ml every hr. with Sodium
Chloride 0.9%
account for baseline fluid rate; if u/o 200ml give 130 ml of
0.9% Sodium Chloride in addition to the 70 ml over next
hour
Oxygen: 4LPM – humidified NC continuously
– keep O2 Sat >92% - call MD if <92%.
These orders follow the patient when they
are transferred to 6 Monti
6 Monti
VS every 15 minutes X 3 hours, then every 1 hour X 3 hours, then
every 2 hours X 18 hours – unless otherwise specified by MD and
MD to approve further changes to every 4 hrs.
NPO except for MEDS, until fully awake
Ambulate 3 – 5 times a day with assistance, starting on post-op day
one
Don’t forget those venodynes!!! D/C when ambulating
Incentive spirometer 10 X every hour while awake– encourage
coughing and deep breathing
Labs every AM: CBC with Diff & Platelet ct., phosphorous, calcium
level, Magnesium – serium, Comp. Metabolic panel, LDH, FK506
(Tacrolimus/Prograf level (trough) and u/a.
Complications
Objectives
Participants will be able to:
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Identify complications post renal transplant
Identify different types of rejection
Identify s/s of infection
Identify different viral infections
Identify causes of Acute tubular necrosis
Identify vascular complications
Identify ways to monitor kidney function
Identify the significance of Resistive Index (RI)
Identify immediate, early & late complications
Complications Post-Transplant
•Acute Tubular Necrosis
•Infection – viral, fungal
&/or bacterial
•Polyoma BK Virus
•Lymphocele
•Rejection
•High Blood Pressure
•Post-Transplant Diabetes
Immediate Complications
Immediate = < 1 week
ATN or delayed graft function – from reversible ischemic
damage to the renal tubular cells prior to engraftment =
most frequent complication in first 48 hours
Risk factors:
– Cadeveric grafts (20-60% associated with ATN)
– Hypotension in donor prior to
Accelerated Acute Rejection
Renal vein Thrombosis (RVT) or obstruction
Renal artery Thrombosis (RAT)
Ureteral edema
Hematoma, Abscess
Hemorrhage
Renal AV Fistula
Pseudoaneurysm
EARLY COMPLICATIONS
One Week to1 Month
Acute rejection – body recognizes transplant as
foreign and tries to destroy it. Most can be
treated
Urinary Fistula – 3 weeks post op
Urinoma – collection of urine, usually in pelvis
Ureteral obstruction – from fibrosis caused by
rejection or ischemia to ureter. Also clots and
edema post op
Late Complications
The period between 1 and 6 months after transplantation is the
most crucial time
74% of rejections
58% of all graft losses
22% of deaths
Hypertension is a common finding
Cyclosporine toxicity
Renal artery stenosis
Disease recurrence
Ureteral strictures
Lymphoceles
Acute Tubular Necrosis
Acute tubular necrosis is a relatively
innocent complication of renal
transplantation and, if one avoids
assaulting patients with invasive
diagnostic procedures, does not give
rise to an increased mortality nor, in
the long run, to an increased loss of
kidneys. Therefore, kidneys should
not be discarded because of fear they
might develop this complication
Acute Tubular Necrosis
Also known as delayed graft function or
“sleepy kidney” after transplant – expected
when kidneys are from cadaveric donors or
when there is a long cold ischemic time.
Generally not associated with kidneys from live
donors – 9% of cases.
S & S: nausea, vomiting, decreased urine
output, increased creatinine, proteinuria, edema
Causes of ATN
Intraoperative manipulation of the
kidney
Laparoscopic removal of kidneys
Recipient factors
Drug-related complications
Kidneys from older donors
Any technical element of narrowing
ATN or Delayed Graft Function
ATN results from
reversible ischemic damage
to the renal tubular cells
prior to engraftment
Most frequent
complication in first 48
hours
Risk factors:
Cadaveric grafts(20-60%
associated with ATN)
Hypotension in donor prior to
implantation (diuretics,
vasoconstrictors to maintain
urinary output or BP)
Long warm (>30 minutes) or
cold (>24 hrs) ischemic times
Usually fully reversible
Resistive Index
Resistive Index (RI) = Peak systolic velocity
- lowest diastolic velocity
Peak systolic Velocity
• RI = S-D / S
• Elevation of the RI >0.9 or progressive
elevation above a normal baseline is good
evidence of renal dysfunction
Causes of Elevated Resistive Index
Acute Rejection
ATN
Pyelonephritis
Renal Vein Thrombosis
Hypertension
Ureteral Obstruction
Graft Compression
Monitoring Kidney Function PostTransplant
Ultrasound: safe imaging of graft and
perfusion
Doppler: allows rapid assessment of
global renal arterial perfusion and
venous patency
Prompt graft function correlates with
shorter hospital stay, improved short
(1 year) and long-term (5 year)
survival
Infection
Viral, Fungal &/or bacterial: Immunosuppressive therapy interferes with
immunity and more susceptible to infection
Herpes-simplex virus type I and II
Most often infect the skin but can occur in other areas including eyes and
lungs
Most infections are mild
Symptoms
Type I: cold sores and blisters around mouth
Type II: genital sores transmitted sexually
Weakness
Painful fluid-filled sores in mouth or genital area
In women, unusual vaginal discharge
Treatment
No cure but can be treated (topical, oral or IV route)
Herpes zoster (shingles)
Appear as rash or small water blisters usually on chest, back or hip
Rash may/may not be painful
Notify transplant team
Viral Infections
Cytomegalovirus (CMV)
Occurs most frequently
Highest in the first months post transplant
Post-transplant CMV infections are a source of
significant morbidity.
CMV infection is due either to reactivation of latent
infection or is transmitted along with the renal allograft
and manifested as a primary infection
Cytomegalovirus (CMV)
Signs & Symptoms:
Fatigue
High temperature
Aching joints
Headaches
Visual disturbances
Pneumonia
Treatment
May require hospitalization
Polyoma BK Virus
Dormant in 80% of population – no
symptoms
First isolated in 1971 from urine of a
renal transplant patient, initials B.K.
The necessary use of
immunosuppressant medications has
the side-effect of allowing the virus to
replicate within the graft, a disease
called BK nephropathy.
Signs & Symptoms of BKV
A primary BKV infection may have no symptoms. If
your immune system is weak, you may have any of
the following:
Abdominal (stomach) problems.
Blurry vision or trouble seeing things.
Brown or reddish-colored urine.
Burning pain or trouble when passing urine, or passing
more urine than usual.
Cough, colds or trouble breathing.
Fever, muscle pain, or weakness.
Seizures (convulsions).
Treatment of BK Virus
The cornerstone of therapy is reduction in
immunosuppression.
A recent surge in BKV correlates with use of
potent immunosuppressant drugs, such as
tacrolimus and mycophenolate mofetil
(MMF- CellCept).
Studies have not shown any correlation
between BKV and a single
immunosuppressive agent but rather the
overall immunosuppressive load.
Fungal Infections
Candida (yeast)
Usually appears in mouth/throat (thrush)
May also appear in surgical wound, eyes, respiratory or urinary tracts,
esophagus or vagina
Most often infect the skin but can occur in other areas including eyes
and lungs
Candida is most severe in bloodstream
Most infections are mild
Symptoms
Thrush
– White, patchy lesions
– Pain or tenderness
– White film on tongue
– Difficulty swallowing
Vaginal infection
– Yellow or white discharge
Treatment
Notify transplant team
Bacterial Infections
Wound Infections
Occur at surgical site
Symptoms
Fever
Redness/swelling
Tenderness
Drainage
Treatment
Antibiotics
Other Infections
Pneumocystis carinii
Germ similar to fungus normally found in lung
May cause pneumonia (PCP) in immunosupressed patients
Patient presents with cold or flu-like symptoms
Signs & Symptoms
Signs & symptoms of Infection:
Fever > 100°
Urinary frequency & burning
Pain or tenderness over transplant site
Cough
Drainage from wound
Prevention of Infection
Handwashing
Meticulous care of IV lines & foley
Wound care
Adequate nutrition for wound healing
Good oral & skin hygiene
Frequent assessment for S & S of
infection
Lymphocele
Lymphoceles:
The most common fluid collections in transplant
population (5-15% of patients)
Most frequently associated with ureteral obstruction
Most develop within one year of transplantation
Risk factors
Incomplete ligation of pelvic lymphatics
Prior episode of severe rejection
Clinical Findings:
Palpable mass, leg pain and edema
Impaired graft function due to compression of the
ureter
REJECTION
Rejection occurs when the body
recognizes the transplanted kidney as
not belonging, and tries to destroy it
Most rejections can be treated and
reversed
There are different types of rejection,
diagnosed by renal biopsy
REJECTION
Several types:
Hyperacute – immediate - no compatibility
– Seldom occurs with improved matching techniques
Accelerated acute – first few days post op – kidney may
never function
– Antibody screening very important while waiting for a
transplant
Acute Rejection – first week to several months to years
after
– Can be treated with medication
Chronic Rejection – can occur anytime – results in loss of
kidney function
– Does not respond to medication
Signs & Symptoms of Rejection
Acute, acute accelerated and chronic
S&S: fever>100, chills, headache, body
aches, fatigue, dizziness, pain or
tenderness over graft, sudden weight
gain, swelling of hands, feet, legs or
eyelids, sob, decreased urine output, pain
or burning during urination
Diagnosed through renal biopsy
REJECTION
Rejection can occur at any time
Critical time for rejection 2-4 weeks post
transplant, with greatest risk within first 3
months
Higher doses of immunosupressive medications
given during this time
Immunosupression that allows the graft to
survive past this period improves long term
survival dramatically
While less common, rejection can occur
years after transplant
Rejection Prevention
Administer immunosuppressive
medications at the right time and the right
amount
Prednisone
Mycophenolate mofectiI (CellCept)
Basiliximab (Simulect) or Thymoglobin
Adherence to medication regimen is
essential for survival of the transplanted
organ.
Vascular Complications
Renal Artery Stenosis
(RAS)
Seen in ~12% of
transplants
Almost always occurs
within 1cm of the
anastomosis
Renal Vein Thrombosis
or occlusion (RVT)
Low occurrence rate
(<1-2%)
Other Complications
Hypertension and heart disease
Increased occurrence as patients age
Treatment
Diuretics and antihypertensive medications
Diabetes
May be induced by immunosupressive medications
Symptoms
Elevated serum glucose
Increased frequency of urination
Blurred vision
Confusion
Increased thirst
Treatment
Weight loss
Diet management
Exercise
Insulin preparations (oral or sq)
Procedure Related Complications
Hemorrhage:
Complication rate associated with percutaneous biopsy of
renal graft approx. 5-8%
Perinephric hematomas account for 25-30% of all
complications
Most hematomas are small and do not require treatment
Hematomas may compress ureter and produce hydronephrosis
Containment of an acute or enlarging hematoma within the
renal capsule or adjacent tissues may compress renal
parenchyma sufficiently to impair function (rarely results in
hypertension)
Procedure Related Complications
Pseudoaneurysm:
Rare
Cause
consequence of renal biopsy
infection within graft
Dehiscence of the arterial anastomosis
Treatment:
Most regress spontaneously
Symptomatic lesions treated with embolizaton or
surgical repair depending on location
Procedure Related Complications
Arteriovenous Fistula (AVF):
Occurs as a consequence of simultaneous laceration
of a renal artery branch and an adjacent vein during
biopsy
Occur in up to 18% of biopsied kidneys
Usually small and asymptomatic
Treatment:
Most spontaneously thrombose requiring no further
treatment
Embolizaton required for 1-2% of fistulae associated
with hemodynamically significant AV shunting or
recurrent hematuria
Signs & Symptoms
S&S: fever>100, chills, headache, body
aches, fatigue, dizziness, pain or
tenderness over graft, sudden weight
gain, swelling of hands, feet, legs or
eyelids, sob, decreased urine output, pain
or burning during urination
Diagnosed through needle biopsy
Immunosuppressive Therapy
Objectives
The learner will be able to:
– Identify the different immunosuppressive agents
– Identify the importance of daily administration of
immunosuppressive agents
– Identify the signs & symptoms of
immunosuppressive toxicity
– Identify the administration protocol for IVIg
Immunosuppressive Drugs
Inhibit or prevent activity of the immune
system.
Central issue in organ transplantation
remains suppression of allograft rejection.
Immunosuppressive drugs is the key to
successful allograft function.
Immunosuppressive drugs are used for
induction, maintenance, and reversal of
established rejection.
Immunosuppressive Therapy
Immunosuppressive drugs can be
classified into five groups:
Glucocorticoids
Cytostatics
Antibodies
Drugs acting on immunophilins
Other drugs
The common side-effect of many
immunosuppressives is immunodeficiency
Glucocorticoids
Also called corticosteroids or steroids, are
powerful drugs that can quickly reduce
inflammation and pain.
A general classification of adrenal cortical
hormones that are primarily active in protecting
against stress and in affecting protein and
carbohydrate metabolism.
Influence all types of inflammatory events
Suppress the humoral immunity diminishing B
cell clone expansion and antibody synthesis.
Ex: Prednisone, Deltasone, Orasone
Cytostatics
The word cytostatic describes the way some
drugs work. Most drugs that are used to treat
cancer kill the cancer cells. The word cytotoxic
means toxic to cells, or cell killing.
Chemotherapy is properly called cytotoxic
therapy.
In immunotherapy, they are used in smaller
doses than in the treatment of malignant
diseases.
Inhibit cell division, affect the proliferation
of both T cells and B cells.
Antibodies
Glycoproteins produced by B
lymphocytes in response to the presence
of an antigen.
Linked to Kidney Transplant Rejection
Failure of otherwise well-matched
kidneys may be caused by antibodies.
Immunosuppressive Therapy
Immunosuppressive drugs have three
effects:
The therapeutic effect (suppressing rejection)
Undesidred consequences of immunodeficiency
(infection or cancer)
Nonimmune toxicity to other tissues
Immunosuppressive Therapy
Wide variety of immunosuppressive agents act in different ways:
Azathioprine – (Imuran) the first immunosuppressive agent to
achieve widespread use in organ transplantation – 1988 Interferes with DNS synthesis – 3 to 5 mg/kg P.O. or I.V. daily,
usually beginning on day of transplant, maintained at 1 to 3
mg/kg – based on patient’s response and tolerance.
Cyclosporin – (Sandimmune) Modified (Gengraf, Neoral) – 15
mg/kg P.O. – 4 to 12 hrs pre transplant – daily 1 – 2 weeks
post-op, then reduce by 5% a week to maintenance level of 5 to
10 mg/kg daily. If given IV – 5 to 6mg/kg – 4 to 12 hrs. pre-op
give daily until pt. tolerates P.O. Infuse over 2 to 6 hours.
Inhibits proliferation and function of T lymphocytes and
inhibits production and release of lymphokines.
Immunosuppressive Therapy
Corticosteroids: (Prednisone)Orasone, Deltasone – regulation of
inflammation, immunosuppression)
Daclizumab: (Zenapax) – to prevent acute organ rejection with an
immunosuppressive regimen that includes cyclosporine and
corticosteroids – Standard course IV is1 mg/kg x 5 days. First dose
24 hrs. pre transplant – remaining 4 doses are given at 14 day
intervals. Prevents activation of lymphocytes – once in circulation
impairs response of immune system to antigenic challenges.
Mycophenolate Mofetil (MMF) - (CellCept, Myfortic) IV or PO
– regular release – 1 g 2X day with corticosteroids and
cyclosporine OR 720 mg extended release 2X day 1 hour before or
2 hours after food. Inhibits response of T & B lymphocytes –
suppresses antibody formation.
Immunosuppressive Therapy
Tacrolimus: (FK506) - (Prograf) IV – 0.03 to 0.05
mg/kg/day – at least 6 hours after transplant. PO dose 8
to 12 hrs after stopping IV
0.2 mg/kg daily in two divided doses every 12 hours.
Exact mechanism unknown - inhibits T cell activation,
which results in immunosuppression.
Sirolimus: (Rapamune) – Initially 6 mg PO as one time
dose as soon as possible after transplantation, then
maintenance dose of 2 mg PO once daily. Inhibits T cell
activation and antibody formation.
Know the Drug-drug interactions – many may increase risk of
nephrotoxicity
Side effects of chronic
immunosuppresion
Infections – viral, bacterial, fungal
Malignancies – lymphoma and skin
Toxicity – renal and cardiovascular
Metabolic – Diabetes, osteoporosis and
hyperlipidemia
Cosmetic – hirsuitism and acne
Transplantation
The goal of transplantation is to
improve the quality of life for people
with end stage renal disease (ESRD).
Transplantation is not a cure, but an
alternative to dialysis.
The goal is for the recipient to achieve
a level of activity and health
comparable to a person of their age
who does not have kidney disease.
IVIg: 15 Facts
1. What is IVIg?
IVIg is a collection of Y shaped
antibodies called IgG
It is formed by taking antibodies
from about 20,000 donors and
mixing them together (FDA sets the
minimum donor pool at 1,000
patients
2. How does IVIg work?
For immune deficiency where the body
does not make enough antibodies, IVIg
supplies them
For autoimmune deficiency, were the
body forms abnormal auto-antibodies
(antibodies that attack the body itself) IVIg
inactivates those antibodies.
After being exposed to toxins and
poisonous chemicals, including carbon
monoxide, the body’s immune system may
mount an attack on the body; IVIg helps to
block this response.
3. How long does it take for IVIg
treatment to have an effect?
Following infusion, patients may see a
response in their disease within 24-48
hours, however it can take 3-4 weeks to
get the desired results
If 4 to 5 cycles do not achieve the desired
results, patients are switched to
plasmapheresis, cytotoxic or other immune
suppressants.
The NIH recommends that if no response
is seen with IVIg infusions, steroids should
be added to the treatment plan.
4. Why is IVIg so expensive?
IVIg is obtained from plasma. Donors are
paid, and then the plasma is sent to a
processing center for mixing, antibody
removal, chemical treatment and flirtation
to remove viruses. From there, the product
is freeze-dried until use.
IVIg costs between $48-$68 / gram, thus, a
single adult dose can cost around
$10,000.
5. How is IVIg administered?
IVIg is reconstituted and given IV at a
rate of 100cc/hr
An adult infusion of IVIg is usually
given over 5 to 6 hours
The rate of administration should be
slowed if the patient develops
symptoms of headache, rash,
fatigue, hyper or hypotension.
6. What are the common side
effects of IVIg?
Headache (more common in females with history
of migranes)
Fatigue (due to antibody interaction)
Rash (pre-medication with Benadryl or steroids
recommended)
Changes in BP
Other side effects: pulmonary edema (from fluid
overload), acute renal failure, venous thrombosis,
aseptic meningitis
REMEMBER: there are a lot of antibodies in IVIg
which can cause any number of allergic responses
7. How can the side effects of IVIg
be reduced?
Hydration: Patients should drink 8 glasses of
water before starting IVIg
Premedication: Tylenol or Benadryl can be used
to counteract headaches and flu-like muscle
soreness
Aspirin: baby ASA may be administered to
prevent thrombophlebitis after IVIg
Steriods: Low dose steroids can be used to
reduce headaches, rash and other side effects
For recurring side effects: slow rate of infusion,
reduce dose, or switch brand of IVIg product
8. How frequently are IVIg
treatments?
Usual dose: 2 grams/kg, divided into
5 doses
Typical dose: 400mg/kg infused daily
for 5 days, followed by a monthly
infusion of 400mg/kg.
9. Is dosing age-adjusted?
Up to age 50: recommended dose
should not exceed 400mg/kg/day
>70 years of age: recommended
dose should not exceed 400mg/kg in
one week.
10. What is the difference between
IVIg Products and Brands?
Generally the difference is in the amount of
IgA content and what it is mixed with:
sucrose, glucose, or another type of sugar,
or what type of preservatives are used.
Patients with CHF or renal dysfunction
are given IVIg with low osmolarity and
low volume
Patients with Diabetes should be given an
IVIg product with no sugar additives
Patients receiving IVIg with sucrose may
be at a higher risk for renal failure
11. What diseases are treated with
IVIg?
FDA Approved Indications:
Allogeneic bone marrow transplant
Chronic Lymphocytic leukemia
Idiopathic Thrombocytopenia purpura
Pediatric HIV
Primary immunodeficiencies
Kawasaki disease
Kidney transplant with high antibody
recipient or ABO incompatable donor
12. What are the off-label uses of
IVIg?
OFF-Label Uses Include:
Primary immunodeficiency
thrombocytopenia
Kawasaki disease
Stem cell transplantation
Diabetes
Multiple Myleoma
Aplastic or Hemolytic
anemia
Red Cell aplasia
Von Willebrand disease
Neutropenia
Asthma
Rheumatoid arthritis
Cystic Fibrosis
C-defficile colitis
Alzheimers
Streptococcal Toxic Shock
Acute Renal Failure
Factor VIII deficiency
Refractory response to
platelet transfusion
Solid organ transplantation
HIV
Epilepsy
Guillian-Barre’
Neuropathy
Systemic vasculitis
ALS (Amyotrophic Lateral
Sclerosis)
Acute cardiomyopathy
Chronic Fatigue Syndrome
Congenital heart block
Hemolytic transfusion
reaction
13. Can infections be transferred
from IVIg?
No infections associated with IVIg
transfusion have been reported to the
FDA since 2000.
14. What else should I know about
IVIg?
IVIg is an infusion of IgG antibodies
only. Therefore, peripheral tissues
that are defended mainly by IgA
antibodies (such as the eyes, lungs,
gut and urinary tract) are not fully
protected by IVIg administration.
15. Where can I learn more about
IVIg?
References:
http://www.autoimmunedisease
FDA
NIH
Sending Blood Samples to Rogosin
Institute:
Donor Specific Antigen (DSA)
When clinically indicated blood or
tissue samples are to be sent to
Rogosin Institute for the purpose of
immunological (DSA) and genetic
testing.
Procedure
Verify order for specimen collection
Two types of tubes used for Rogosin Institute
blood samples:
Yellow top tube containing ACD solution A – done pre
transplant – donor & recipient
Red Top tube for serum – post transplant
Tubes must be labeled with patient’s full name and
DOB
Place tubes in the appropriate styrofoam
packaging
Dynamax courier service is to be called – 631231-7200
Account # 30101, Reference is “transplant”
Procedure
Instruct courier service that this is a STAT
pick-up and delivery – specimen must fo
directly to Rogosin Institute without any
stops
Provide pick-up and delivery addresses &
phone numbers
Pick-up: North Shore University Hospital,6 Monti 300 Community Drive, Manhasset, New York 11030,
Tele: 516-562-8600
Delivery: Before 4:30 PM: Rogosin Institute, 430 East
71st St., New York, New York 10021, Tele: 212-7726700, FAX: 212-861-9473. After 4:30 PM: Rogosin
Institute, 435 East 70th St., New York, New York
10021, Tele: 212-772-6700, FAX: 212-861-9437
Living Kidney Donor Patients
Objectives
The learner will be able to:
– Identify the team members of the living kidney
donor program
– Identify the characteristics of a living kidney donor
– Identify the battery of tests for a living kidney
donor
– Describe the surgical technique for a living kidney
donor
– Discuss the advantages of a laparoscopic
nephrectomy
Kidney Donation
Becoming a kidney donor
Questions and fears inevitable re:
donation
Dedicated team to understand the
procedure and reach the decision to
donate
Team: nephrologist, surgeon, nurse,
transplant coordinator, social worker,
and psychiatrist
Kidney Donation
Becoming a kidney donor
Donors’ ages range from 18 yrs. up to
70s
Age-specific good health
Immunological compatibilities (blood
type and antigens) with recipients
Undergo series of tests to determine
eligibility
Kidney Donation
Becoming a kidney donor
Tests: full medical history
A series of blood, urine, EKG, tissuetypings and psychological tests
Donor kidneys need to be evaluated for
suitability for a laparoscopic
nephrectomy
Donor Procedure
Living donors: laparascopic surgery
schedule the operation in advance
operated on at the same time with the
recipient, usually in side-by-side rooms.
One team of surgeons will perform the
nephrectomy-that is, the removal of the
kidney from the donor-while another
prepares the recipient for placement of
the donated kidney
Donor Procedure
Living donors
Three half-inch incisions
Inserts surgical instruments and a
camera
Surgeon frees up the donor kidney and
then make a slightly larger incision
Removed kidney placed in a bag and
chilled on ice until implanted in the
recipient
Donor Procedure
Laparoscopic nephrectomy
reduced post-op pain
Speedier recovery times
Less scaring
Average of 2 days in the hospital
Return to normal activities within 3
weeks
Live a normal life: no special
medications, no restricted diet
Questions