Transcript Renal Failure and Treatment

CKD/ESRD
&
Management
Note-when viewing lab values in PPT-note that
values are given as both as “common values” as
also the specific values given in textbook
(remember, sources vary slightly-think
ranges.)2010
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.
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REVIEW
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Recall functions of the kidneys?
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Recall normal creatinine & BUN; other lab
tests?
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Review Diagnostic Tools
CKD- Elderly Risk (Review)
•Older Adult-normal aging (plus co-morbidities) > risk kidney dysfunction/renal failure
•Must:
•Identify/prevent damage
•Monitor/risk multiple RX/OTC meds (altered renal blood flow/dec. renal
clearance etc)
•Monitor/risk associated with dehydration (ie diuretics)
•Monitor/risk with dec ability to respond to changes to fluid/electrolyte
status (manifestation may be atypical
Functions of the Kidneys
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Regulates volume and
composition of
extracellular fluid
Excretion of nitrogenous
waste products
BP control via reninangiotensin-aldosterone
system- Recall RAAS
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Vitamin D activation
Acid-base balance
(HCO3 & H) regulation
through process of
_____, ____ and
______. filtration, secretion,
reabsorpton
Prostaglandin synthesis
Erythropoietin
production
Functions of the Kidneys
(cont)
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Erythropoietin Release
If a patient has chronic renal failure, what
condition will occur?
 WHY???
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EPO- glycoprotein hormone that controls
erythropoiesis, or red blood cell production
4/8/2016
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Diagnostic Tools for
Assessing Renal Failure
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Blood Tests
 BUN elevated (norm 10-20 mg/dl) (text 10-30mg/dl)
 Creatinine elevated (norm 0.6 - 1.2 mg/dl) (text 0.51.5mg/dl)
 K elevated (text norm 3.5-5.0 mEq/L)
 PO4 elevated (text norm 2.8-4.5mg/dl)
 Ca decreased (text norm 9-11mg/dl)
Urinalysis
 Specific gravity (text norm 1.003-1.030
 Protein (text norm 0-trace)
 Creatinine clearance (text norm 85-135ml/min)
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BUN
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Normal 8 - 20 mg/dl (text 10-30mg/dl)
Nitrogenous waste product of protein
metabolism
Unreliable in measurement of renal function
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Relevance assessed in conjunction with serum
creatinine
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Creatinine
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A waste product of muscle metabolism
Normal value 0.6 - 1.2 mg/dl (text 0.51.5mg/dl)
2 times normal = 50% damage
8 times normal = 75% damage
10 times normal = 90% damage
Exception - severe muscular disease can greatly 
serum creatinine levels
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Diagnostic Tools
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Ultrasound
X-Rays
Biopsy *most definitive
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Chronic Renal Failure/
Chronic Kidney Disease (CKD)
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Slow progressive renal disorder related to
nephron loss, occurring over months to years
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Culminates in End Stage Renal Disease (ESRD)
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Characteristics of CKD > ESRD
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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
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Causes of CKD
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*Diabetes
*Hypertension
Glomerulonephritis
Cystic disorders
Developmental Congenital
Infectious Disease
•Neoplasms
•Obstructive disorders
•Autoimmune diseases
(lupus)
•Hepatorenal failure
•Scleroderma
•Amyloidosis
•Drug toxicity-(overuse some
common drugs, as aspirin, NSAID as
ibuprofen, cocaine and
acetaminophen)
NSAIDs-…cause prerenal ARF by blocking prostaglandin production > also alters
local glomerular arteriolar perfusion… (reduces renal blood flow)
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Glomerular Filtration Rate (GFR)-determine stage
CKD (most accurate evaluation)
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24 hour urine for creatinine clearance
Formula- urine creatinine X urine volume
serum creatinine
Can estimate creatinine clearance by:
140 – {age x weight (kg)}
72 x serum creatinine
What is normal GFR?
90 - 120 mL/min
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Stages of CKD (“old”
terminology)
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Reduced Renal Reserve
Renal Insufficiency
End Stage Renal Disease (ESRD)
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Stages of CKD
NKF Classification System
Stage 1:
Stage 2:
GFR > 90 ml/min despite kidney
damage
Mild reduction (GFR 60 – 89
ml/min)
1. GFR of 60 may represent 50%
loss in function.
2. Parathyroid hormones starts to
increase. (why?)
*kidneys unable to reabsorb calcium, blood calcium levels fall, stimulating
continual secretion of parathyroid hormone to maintain normal calcium
levels in blood.
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During Stage 1 - 2
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No symptoms
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Serum creatinine doubles*
(Up to 50% nephron loss
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FYI-older adult- may
impaired renal function even in
presence of normal serum
creatinine
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Stages of CKD
NKF Classification System
Stage 3: Moderate reduction (GFR 30 – 59
ml/min)
1. Calcium absorption decreases
(from the GI tract)
2. Malnutrition onset
3. Anemia
4. Left ventricular hypertrophy
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Stages of CKD
NKF Classification System
Stage 4:
Oopstrouble!
Severe reduction (GFR 15 – 29
ml/min)
1. Serum triglycerides
2. Hyperphosphatemia
3. Metabolic acidosis
4. Hyperkalemia
K Effect & EKG
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During Stage 3 - 4
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Signs and symptoms worsen if kidneys stressed
ability to maintain homeostasis
75% nephron loss
glomerular filtration rate, solute clearance,
ability to concentrate urine and secrete hormone
Symptoms: BUN & Creatinine, mild
azotemia, anemia
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Stages of CKD-NKF Classification System
Stage 5: Kidney failure (GFR < 15 ml/min) ESRD!!!
 Azotemia
 Residual function < 15% of normal
 Excretory, regulatory, hormonal functions
severely impaired
 Metabolic acidosis (Kussmaul breathing)
 Marked
: BUN, Creatinine, Phosphorous
 Marked : Hemoglobin, Hematocrit, Calcium
 Fluid overload
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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 CKD
Fatal if no treatment
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Manifestations of Chronic Uremia
Syndromecombination
of common
symptoms
*greater
build-up
waste
products =
greater
symptoms
Fig. 47-5
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What happens when kidneys
don’t function correctly?
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Manifestations of CKD 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
Manifestations due to inc nitrogenous waste products, electrolyte imbalances, metabolic
acidosis and axonal atrophy and demyelination of nerve fibers & dec erythropoietin*
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Manifestations of CRF
Skin
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Pale, grayish-bronze color
Dry scaly
Severe itching
Bruise easily, petechiae, ecchymosis
*Uremic frost
*Manifestations due to…calcium-phosphate deposition in skin, sensory
neuropathy, platelet abnormalities; urea crystallizes (uremic frost) >if
BUN extremely high
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Medical Mystery?
What do lab studies, etc indicate ? What causes uremic frost?
*57-year-old with HTN and CKD (Stage 5), refused dialysis found in respiratory distress after week of
upper respiratory symptoms due to viral infection
Before admission to hospital >developed asystolic cardiac arrest, was resuscitated by EMT, admitted to ICU,
required vasopressor support.
PE- diffuse deposits tiny white crystalline material on skin > lab studies- BUN 208 mg/dl; creatinine 15 mg/dl;
bicarbonate level 5 mmol per liter; anion gap-26; arterial pH of 6.74, and arterial partial pressure of carbon
dioxide of 50 mm Hg. Blood cultures- revealed-Staphylococcus aureus pneumonia, likely due to prior
Walsh S and Parada N. N Engl J Med 2005;352:e13
influenza infection. *Aggressive care measures withdrawn after consultation with patient's family >patient
died.
*Uremic frost- uncommon skin manifestation due to profound azotemia;
occurs when urea and other nitrogenous waste products accumulate in sweat
and crystallize after evaporation.
Manifestations of CKD
Eyes
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Visual blurring
Occasional blindness
“Red eye”
Due to calcium-phosphate
deposits in eyes
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Manifestations of CKD
Fluid - Electrolyte - pH
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Volume expansion and fluid overload
Due to impaired kidneys unable to excrete acid load (mostly
Metabolic Acidosis from NH3); defective reabsorption/regeneration of HCO3.
Electrolyte Imbalances
Potassium
 Magnesium
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Sodium
Due to dec excretion by kidneys, breakdown of cellular
protein, bleeding, metabolic acidosis, food, drugs, etc
Kidneys unable to excrete (too much magnesium
causes hyporeflexia and can lead to cardiac arrest)
Kidneys retain > water retention> fluid overload
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Manifestations of CKD
GI Tract/Bleeding Risk
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Uremic fetor
Anorexia, nausea, vomiting
GI bleeding Due to GI irritation, platelet defect; diarrhea from hyperkalemia
Anemia
Platelet dysfunction
Anemia-due to insufficient production of erythropoietin, protein
naturally produced in functioning kidneys…circulates through
bloodstream to bone marrow, stimulating production of RBCs.
Platelet dysfunction-subnormal platelet aggregation -due to fibrinogen fragments,
usually absent in normal human blood but present in uremic plasma may lead to
platelet dysfunction in uremia.
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Manifestations of CKD-Musculoskeletal
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Muscle cramps
Soft tissue calcifications
Weakness
Related to calcium phosphorous imbalances
RENAL OSTEODYSTROPHY
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Fracture risk!
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Manifestations of CKD- Heart & Lungs
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Hypertension
Heart failure > pulmonary edema
Pericarditis due to uremia
Pulmonary edema
Pleural effusions- “Uremic Lung”
Atherosclerotic vascular disease*
Cardiac dysrhythmias (from HF, electrolyte imblaances)
*Major Problem!
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Manifestations of CKD- Endocrine Metabolic
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Erythropoietin
Hypothyroidism
Insulin resistance
Growth hormone
Gonadal dysfunction
Parathyroid hormone
Hyperlipidemia
and Vitamin D3
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Treatment Options
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Conservative Therapy * (Severe restrictions, dietary, fluids
maintain renal function as long as possible- if GFR > 10ml/min)
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Hemodialysis
Peritoneal Dialysis
Transplant
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Nothing > Death
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Conservative Treatment
Goals
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Detect/treat potentially reversible causes of
renal failure
Preserve existing renal function
Treat manifestations
Prevent complications
Provide for comfort
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Conservative Treatment
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Control
Hyperkalemia
 Hypertension
 Hyperphosphatemia
 Hyperparthryoidism
 Anemia
 Hyperglycemia
 Dyslipidemia
 Hypothyroidism
 Nutrition : Describe a renal diet?

Depends on lab values-usually low
NA, K, restricted protein,
phosphorous, & fluids (See text)
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Hemodialysis
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Removal of soluble substances and water from the blood by
diffusion through a semi-permeable membrane.
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Early animal experiments began 1913
1st human dialysis 1940’s by Dutch physician Willem Kolff (2 of
17 patients survived)
Considered experimental through 1950’s, No intermittent blood
access; for acute renal failure only.
1960 Dr. Scribner developed Scribner Shunt-1960’s machines
expensive, scarce, no funding.
“Death Panels” panels within community decided who got to
dialyze.
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Hemodialysis Process
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Blood removed from patient into extracorporeal
circuit.
Diffusion and ultrafiltration take place in
dialyzer.
Cleaned blood returned to patient.
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Extracorporeal Circuit
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How Hemodialysis Works
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.
How Dialysis Works-Interactive!
An Introduction to Dialysis-How
Stuff Works! (Step by Step)
YouTube- Hemodialysis! Great!
Vascular Access (click)
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Arterio-venous shunt (External Shunt) *used
now for Continuous Renal Replacement
Therapy (CRRT)-temporary access
Arterio-venous (AV) Fistula (AKA-native or primary
fistula)
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PTFE Graft
Temporary catheters
“Permanent” catheters
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External Shunt (Schribner 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
*Used now only for
CRRT-temporary
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Arterio-venous (AV) Fistula
Primary (native) Fistula
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Patients own artery and vein surgically anastomosed.
Advantages
 patient’s own vein/artery
 longevity
 low infection and thrombosis rates
Disadvantages
 long time to mature, 1- 6 months
 “steal” syndrome
 requires needle sticks
davita.com
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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 1-4 weeks
 prominent vessels
Disadvantages
 clots easily
 “steal” syndrome more frequent
 requires needle sticks
 infection may necessitate removal of graft
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Temporary Catheters
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Dual lumen catheter placed into a central veinsubclavian, jugular or femoral.
Advantages
 immediate use
 no needle sticks
Disadvantages
 high incidence of infection
 subclavian vein stenosis
 poor flow-inadequate dialysis
 clotting
 Restricts movement
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Cuffed Tunneled Catheters (Dacron cuff)
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Dual lumen catheter with Dacron cuff
surgically tunneled into subclavian,
jugular or femoral vein.
Advantages
 immediate use; *permanent/long
term 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
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Above Native fistula (in place for over 20 years)
*Remember- assess circulation-listen for bruit,
feel for thrill!
Buttonhole technique-individual cannulates
own fistula for home dialysis YouTube video
“Temporary” vascular access catheters- if tunnelled,
with Dacron cuff, can be used long-term as Permacath,
below.
Care of Vascular Access
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NO BP’s, needle sticks to arm with vascular access.
This includes finger sticks.
Place ID bands on other arm whenever possible.
Palpate thrill and listen for bruit.
Teach patient nothing constrictive, feel for
thrill.
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Potential
Complications of Hemodialysis
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During dialysis
 Fluid and electrolyte related
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Cardiovascular
 arrhythmias
Associated with the extracorporeal circuit
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Disequilibrium Syndrome & seizures
Musculoskeletal
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exsanguination
Neurologic
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hypotension
cramping
Other
 fever & sepsis
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blood born diseases
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Potential Complications of Hemodialysis
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Between treatments
Long term (due to disease process &
management)
•Metabolic
Hypertension/Hypotension
•Hyperparathyroidism
 Edema
•Diabetic complications
 Pulmonary edema
•Cardiovascular
 Hyperkalemia
CHF
 Bleeding
AV access failure
 Clotting of access
Cardiovascular disease
•Respiratory
Pulmonary edema
•Neuromuscular
Neuropathy
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Complications Hemodialysis- con’t-long term, ESRD
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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
Long term cont’d
•Genitourinary
•infection
•Sexual dysfunction
•Psychiatric
•depression
•Infection
•blood borne
pathogens
Rheumatologic
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amyloid deposits
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Dietary Restrictions-Hemodialysis
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Fluid restrictions Urine output + 500-600
Phosphorous restrictions Approx 800-1200 mg/day
Potassium restrictions Approx 1-2 g/day; 40 mg/kg/IBW
Approx 1-2 g/day
Sodium restrictions
Protein to maintain nitrogen balance (complete)
too high - waste products
 too low - decreased albumin, increased mortality
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Calories to maintain or reach ideal weight
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Peritoneal Dialysis
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1.
2.
3.
Removal of soluble substances and water from blood by diffusion through a
semi-permeable membrane (peritoneum) that is intracorporeal (inside
body).
 Solution warmed to body temperature prior to instillation into
peritoneal cavity via peritoneal catheter
 Metabolic waste products and excessive electrolytes diffuse into
dialysate while it remains in abdomen
 Fluid removal controlled by glucose (dextrose) concentration in
dialysate (acts as “osmotic” agent)
 Excess fluid/solutes removed- gradual/constant Fluid drained by gravity into sterile bag at set intervals“Clear” solution ‘fills” abdomen
“Yellow” urine-like fluid drains out (like urine, clear)
Types of Peritoneal Dialysis
1.
*CAPD: Continuous ambulatory peritoneal dialysis
2.
CCPD: Continuous cycling peritoneal dialysis/Aka. *APD – Automated
Peritoneal Dialysis
3.
IPD: Intermittent peritoneal dialysis (also)
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Phases of Peritoneal
Dialysis Exchange
1. Fill (inflow): fluid infused into
peritoneal cavity (usually 10-15
min).
2. Dwell time (equilibrium):
time solution (dialysate) fluid
remains in peritoneal cavity
(duration depends on method- as
CAPD 4-5 exchanges/day).
3. Drain (equilibrium): time
fluid drains from peritoneal cavity
by gravity flow (usually 20-30
min); facilitate by gently
massaging abdomen, changing
position.
CAPD
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CAPD
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APD
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Catheter into peritoneal cavity
Exchanges 4 - 5 times per day
Treatment 24 hrs; 7 days a week
Solution remains in peritoneal cavity
except during drain time
Independent treatment
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Click to play animation
Videos-Dialysis, all types!
Click to locate desired video
Automated Peritoneal Dialysisfluid exchanges automatically
by machine-(also known as
continuous cycling peritoneal
dialysis (CCPD), requires
“cycler machine”programmable- to automate
filling and draining process.
Treatment at home, typically at
night (while sleeping-thus no
fluid in “the belly” at daytime
Complications of Peritoneal Dialysis
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Infection
 peritonitis
 tunnel infections
 catheter exit site
Hypervolemia
 hypertension
 pulmonary edema
Hypovolemia
 hypotension
Hyperglycemia
Malnutrition
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Obesity
Hypokalemia
Hernia
Cuff erosion
Low back pain
Hyperlipidemia
Peritoneal Catheter Exit Site
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Advantages of PD
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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
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59
Multi-prong system
occasionally used
with PD patients in
hospital settings
Which dialysis
“bags” have already
been infused?
The “yellow”
ones!- dialysis
nurse sets up
bags, staff nurse
infuses, drains
according to
schedule.
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Medications - Dialysis Patients & CKD (Stages 4-5)
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Vitamins - water soluble
Phosphate binder - (Phoslo, Renagel, Calcium,
*Aluminum hydroxide-risks) Give with meals
Iron - don’t give with phosphate binder or calcium
Antihypertensives – typically hold prior to dialysis
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
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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
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Patient
Education
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Alleviate fear
Dialysis process
Fistula/catheter care
Diet and fluid restrictions
Medication
Diabetic teaching
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Case Study
A 48 year old female with a history of uncontrolled
diabetes presents to the ER. Her chief complaints are
nausea, vomiting and fatigue.
Lab: BUN 100; Creatinine 10; H&H 7.0/21.4;
K+ 6.0, PO4 5.5; Ca++ 7.5
What do you suspect? How would she possibly be
treated?
*Access Evolve Apply Case Study- Chronic Renal Failure
*Access Renal Case Study
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Transplantation
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Treatment not cure
View also Organ Donation video
66
Kidney Awaiting Transplant
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“Old” kidneys typically left in place
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Advantages
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Restoration of “normal”
renal function
Freedom from dialysis
Return to “normal” life
Reverses pathophysiological
changes related to RF
Less expensive than dialysis
after 1st year
Disadvantages
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Life long medications
Multiple side effects
from medication
Increased risk of tumor
Increased risk infection
Major surgery
Care of 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
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Post-op Care
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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-careful monitor
Ultrasound
Renal scans
Renal biopsy
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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
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Prevention of Infection
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Major complication of transplantation due to
immunosuppression
HANDWASHING
Avoid Crowds, Kids
Patient Education
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Rejection
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Hyperacute - preformed antibodies to donor antigen
function ceases within 24 hours
 Rx = removal
Accelerated - same as hyperacute but slower, 1st week to month
 Rx = removal
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
Chronic - gradual process of graft dysfunction
 Repeat rejection episodes- not completely resolved with
treatment
 4 months to years after transplant
 Rx = return to dialysis or re-transplantation
74
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Immunosuppressant Drugs
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CorticosteroidsPrednisone
 Prevents infiltration of
T lymphocytes
Side effects
 cushingnoid changes
 Avascular Necrosis
 GI disturbances
 Diabetes
 infection
 risk of tumor

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Cytoxic Agents-Azathioprine
(Imuran); Mycophenolate
(*Cellcept), *Cytoxin (less toxic
than Imuran)
 Prevents rapid growing
lymphocytes
Side Effects
 bone marrow toxicity
 hepatotoxicity
 hair loss
 infection
 risk of tumor
Immunosuppressant Drugs
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Calcineuin InhibitorsCyclosporin, Neoral,
*Prograft, *FK506 (more
potent than cyclosporin)

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Interferes with production of
interleukin 2 which is necessary
for growth and activation of T
lymphocytes.
Side Effects
– Nephrotoxicity
– HTN
– Hepatotoxicity
– Gingival hyperplasia
– Infection

Monoclonal antibodyOKT3 - used to treat
rejection/induce
immunosuppression
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
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


Polyclonal antibody-Atgam-treat rejection or induce
immunosuppression
 decreased number of T lymphocytes
Side effects
 anaphylaxis
 fever chills
 leukopenia
 thrombocytopenia
 risk of infection
 tumor
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Patient Education





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
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Transplants
Notes from Organ Donation slides

Exclusion for Transplant not limited too
Active vasculitis; or
 Life threatening extrarenal congenital
abnormalities; or
 Untreated coagulation disorder; or
 Ongoing alcohol or drug abuse; or
 Age over 70 years with severe co-morbidities; or
 Severe neurological or mental impairment, in
persons without adequate social support, such that
the person is unable to adhere to the regimen
necessary to preserve the transplant.

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






Official Criteria for Deceased
Donors
Usually irreversible brain injury
 MVA, gunshot wounds, hemorrhage, anoxic brain injury
from MI
Must have effective cardiac function
Must be supported by ventilator to preserve organs
Age 2-70
No IV drug use, HTN, DM, Malignancies, Sepsis, disease
Permission from legal next of kin & pronoucement of death
made by MD
*Brain Death is the complete cessation of all brain
& brainstem function. It is death.
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Official Criteria for Living Donors



Psychiatric evaluation
Anesthesia evaluation
Medical Evaluation
Free from diseases listed under deceased donor
criteria
 Kidney function evaluated
 Crossmatches done at time of evaluation and 1 week
prior to procedure
 Radiological evaluation

Nurses Role in Event of
Potential Donation

Notify TOSA of possible organ donation
Identify possible donors
 Make referral in timely manner



Do not discuss organ donation with family
Offer support to families after referral is
made & donation coordinator has met with
family
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