NOTES Chronic Kidney Disease/RRT/Transplants
A.
Module #13: Nursing Care of the Individual with Genitourinary Disorders: Chronic Kidney
Disease/RRT/Transplant
Chronic Kidney Disease/RRT/Transplant (click here)
Etiology/Pathophysiology (general) CKD *more common than AKI
1.
Normal physiology-(ref to AKI-A & P)
2.
Progressive renal tissue destruction and loss of function

Incidence inc- older adults; African Americans , Native Americans; large Hispanic
population locally area; over million trt for ESRD; read statistics Fig 47-4-think
underlying disease cause; high mortality

*Diabetes-leading cause CKD; then HTN; also glomerulonephritis, cystic disorders,
developmental disorders, infectious disease (HIV), neoplasms, obstructive disorders,
autoimmune disorders such a s *lupus, *scleroderma; hepatorenal failure, drug toxicity
such as recreational heroin, crack cocaine, *NSAIDs

Progresses over years w/o being recognized until kidneys unable to excrete metabolic
wastes/ electrolytes/irreversible loss kidney function- End-stage Renal Disease (ESRD)
1) Presence of Kidney damage-pathological abnormalities
2) Glomerular filtration rate (GFR) -<60 ml/min for 3 mo or longer

Chronic KD- diffuse bilateral disease of kidneys with progressive destruction and
scarring; loss of function precedes lab abnormalities- renal size usually dec.

*Disease staging based on dec GFR ( 47-6)
*Do not need to “memorize” -recognize/identify needed action /when RRTneeded
1)
2)
3)
Stage 1 & 2 -asymptomatic, but with renal damage; at risk , parathyroid
hormone start to inc.
Stage 3- with moderate reduction, calcium absorption form GI tract, have
onset malnutrition (GFR- 30-59ml/min), anemia, left ventricular hypertrophy
Stage 4-5: Renal Failure/ESRD
a)
Less than 5% GFR always considered ESRD: dialysis or
transplant required or death occurs
b)
As 90% or more nephrons destroyed = ESRD, BUN, and
creatinine clearance dec, serum creatine inc, urine specific
gravity fixed at 1.010 (if urine produced at all)
c)
*UREMIA; “urine in the blood”-uremic toxins
(1)
Syndrome- incorporates all signs/symptoms seen in
vAKIous systems throughout body
(2)
Loss of erythropoietin>chronic anemia (lowered H &
H); fatigue
(3)
Fluid and sodium retention, hyperkalemia,
hypermagnesemia, hyperphosphatemia and
hypocalcemia; metabolic acidosis due to impaired
hydrogen ion excretion
(4)
*Renal function declines > end products of protein
metabolism ( typically excreted in urine) accumulate
in blood) > all body systems adversely affected
RNSG 2432  1
3.
*Note- similar to AKI- exaggerated/more pronounced with ALL systems affected, long term
effects (not reversible) Pathophysiology principles, lab apply
Clinical Manifestations (all body systems affected!) See text * review carefully; “know
why/how” each body system affected); early manifestations: nausea, apathy, weakness,
fatigue; progress to frequent vomiting, increasing weakness, lethargy, confusion *Uremiasyndrome in which kidney function declines to point symptoms develop in multiple body
systems.l
1.
Urinary
a. Initial polyuria-inability to concentrate urine-fixed sp gravity, most often at night (nocturia)
b. Oliguria as CKD worsens; proteinuria and hematuria
c. Anuria-output <40 ml per 24 hrs
2. Metabolic disturbance-waste product accumulation
a. As GFR ↓, BUN ↑ and serum creatinine levels ↑
b. BUN ↑ -due to kidney failure also by protein intake, fever, corticosteroids, and catabolism >
N/V, lethargy, fatigue, impaired thought processes, and headaches
3. Carbohydrate/Triglyceride metabolism/Endocrine System
a. Cell insensitivity to normal action of insulin- exact nature of insulin resistance unclear-may
be related to circulating insulin antagonists, alterations in hormone receptors, or abnormalities
of transport mechanisms; moderate hyperglycemia and hyperinsulinemia occur. Patients with
diabetes who become uremic may require less insulin than before the onset of CKD-because
insulin, which is dependent on kidneys for excretion, remains in circulation longer.
b. High triglyceride/elevated HDL> accelerated atherosclerotic process-most with CKD die
from CV
c. *Caution in dosing diabetic who are uremic; insulin is normally excreted by kidneys
d. Elevated uric acid levels; risk for gout
4. Electrolyte/acid-base balance/Musculoskeletal System Effects
a...Hyperkalemia- Most serious electrolyte disorder>muscle weakness, paresthesia, *EKG changes
(fatal arrhythmias at 7-8 mEg/L; need to lower when reaches 6 mMEq/L; due to dec excretion
by kidneys, breakdown of cellular protein, bleeding and metabolic acidosis, food, drugs, IV.
(Know hyperkalemia develops; dangers, how to manage? ( Tab 47-5)
B.
Tent shaped “T”
b.
c.
Sodium/water retention; if large amounts body water retained, have dilutional hyponatremia;
lead to CHF, HTN, edema; may have normal or low sodium levels; *sodium intakeindividually determined, generally restricted to 2 g per 24
*Calcium, phosphate, magnesium effect- Hyperphosphatemia, hypocalcemia,
hypermagnesia (*kidneys unable to eliminate Mg) *Read-understand how kidney function
affects bone and calcium balance? See text p. 1174 What is role of PTH (*See effect on
Musculoskeletal system) See text & Fig. 47-3
2  RNSG 2432
i.
Calcium and phosphorous> reciprocal relationship; one rises, other dec.
1.
↓ kidney filtration > ↑ serum phosphate level with reciprocal ↓
serum calcium level (Ca & PHO4 bind)
ii.
Renal failure, active- Vit D lacking; unable to absorb calcium from GI tract;
low serum Ca stimulates PTH > resorption of calcium and phosphate from
bone; excess phosphate binds with calcium > formation of insoluble
metastatic calcification deposited throughout body > renal osteodystrophy
(syndrome-of skeletal changes, weakened bones, fx risk)
1.
Osteomalacia: lack of mineralization of newly formed bones
2.
Osteitis fibrosa; ca absorbed from bones, replaced by fibrous
tissues
3.
Metastic calcifications
4.
Bones fragile, break easily; bone tenderness, pain
iii.
*Magnesium; primAKIly excreted by kidneys; generally no problem unless
ingests magnesium; *Avoid mg containing products- milk of
magnesium, magnesium citrate, etc.
d. Metabolic acidosis
i.
Impaired kidneys unable to excrete acid load (mostly from NH3) and
defective reabsorption/regeneration of HCO3 > Kussmaul respiration,
(found in ESRD, AKI) reduces severity of acidosis > inc CO2 excretion.
Multisystem Effects
Review carefully,
5.
6.
7.
Hematologic
a. Due to ↓ production erythropoietin (megaloblastic)
b. RBC lifespan (effect of PTH), Iron deficient
c. Bleeding tendencies -impaired platelet function
d. Impaired immune system
ii. WBC ↓ -changes in leukocyte function and altered immune response; ↓
inflammatory response
iii. Cellular and humoral immune responses suppressed-(good -transplant
success!)
Cardiovascular effects
a. HTN, usually present prior to ESRD, inc with sodium retention and inc. extracellular fluid
b. Inc. risk for MI, atherosclerotic vascular disease, elevated triglyceride levels
c. HF > pulmonary edema; peripheral edema; *dysrhythmias from electrolyte imbalances,
HF; left ventricular hypertrophy
d. Pericarditis (due to uremia): metabolic toxins irritate pericardial sac
Respiratory
a. Kussmaul respirations (why?)
b. Dyspnea- due to fluid overload, pulmonary edema,
c. Uremic pleuritis (why?), pleural effusion
d. Predisposition to respiratory infections, depressed cough reflex
e. “Uremic lung”= uremic pneumonitis
RNSG 2432  3
8.
C.
GI effects
a. All parts affected-inflammation of mucosa due to excessive urea
b. Mucosal ulcerations due to inc. NH3 - by bacterial breakdown of urea; uremic fetor
c. Anorexia, nausea, vomiting, hiccups
d. GI bleeding due to GI irritation, platelet defect; diarrhea from hyperkalemia
e. Diabetic gastroparesis worsens
9.
Nervous system-expected as disease progresses
a. Mood swings; impaired judgment/mental acuity, inability to concentrate and perform
simple math functions; psychotic symptoms
b. Tremors, twitching, seizures > coma
c. Peripheral neuropathy; “restless legs”, foot drop, sensations crawling, prickling
d. High levels uremia (from elevated BUN) toxins > axonal damage; demyelization of
nerve fibers; dialysis may not reverse motor neuropathy> slow general CNS symptoms;
anemia also dec cognition; need at least 33% to function normally
e. Dialysis encephalopathy (if on dialysis)
f. *Neurologic changes dt to in nitrogenous waste products, electrolyte imbalances,
metabolic acidosis and axonal atrophy and demyelination of nerve fibers
10.
Skin
a. Pale, grayish-bronze color due to absorption and retention or urinary pigments that
normally give characteristic color to urine; color pale due to anemia
b. Dry scaly; severe itching; pruritus dt to dry skin plus calcium-phosphate deposition in
skin and sensory neuropathy
c. Bruises easily; platelet abnormalities (petechiae, ecchymosis)
d. Hair dry, brittle and may fall out.
e. Uremic frost; urea crystallizes on skin; see only if BUN extremely high
11.
Eyes
a. Visual blurring and occasional blindness (“Uremic red eye” from irritation due to
calcium-phosphate deposits in the eye)
12.
Reproductive
a. Infertility/menstrual irregulAKIties; reduced testosterone levels
b. Dec. libido, low sperm count
c. Hypothyroidism
d. Gonadal dysfunction
Therapeutic Interventions/Collaborative Care/Diagnostic Tests (review AKI notes; lab 45-8 & Tab
47-7)
Diagnostic Test/Assessment (*know normal values) *Refer to AKI for NA, K, Ca, PH04 etc
1.
Identify CKD (chronic renal failure; monitor renal function by following level or metabolic wastes
and electrolytes
a. Urinalysis: fixed sp gravity 1.010 (low); excess protein, blood cells, cellular casts
b. Urine culture; identify infection
c. *CBC: moderately severe anemia with hematocrit 20-30%; low hemoglobin; reduced
RBC’s and platelets
d. Renal scan, Renal ultrasound (determine kidney size *atropy=CKD
e. BUN and serum creatinine; evaluate kidney function
1)
Mild azotemia: BUN 20-50 mg/dl
2)
Severe renal impairment BUN > 100 mg/dl
3)
Uremic symptoms > BUN 200mg/dl
4)
*Creatinine levels >4 mg/dl = serious renal impairment (**better indicator
than BUN of renal function); elevated BUN –*responsible for neurological
symptoms
f. **Creatinine clearance- **reflects GFR- renal function (most accurate; need 24
hour urine collection (see AKI notes) *Read carefully Tab 47-8 compare GFR
rates with elderly-and young
1) Persistent proteinuria-first indicator kidney damage- 1+ protein on standard
dipstick testing over 3 mo period – need further assessment; urine test for
albumin-to creatinine ratio important- greater thatn 300 mg albumin per 1 gram
creatinine reflects CKDg. *Serum electrolytes: monitored throughout course of CKD
h. CBC: moderately severe anemia with hematocrit 20-30%; low hemoglobin;
reduced RBC’s and platelets
i. Kidney biopsy: diagnose underlying disease process; differentiate acute from chronic
*kidney vascular (risks)
4  RNSG 2432
D.
**Management CKD and ESRD (Death if no treatment with ESRD; attempt to delay onset ESRD- See
text , NCP Online Interventions apply to AKI
Medications *(refer also to AKI Notes-& text- read carefully!! & ab. 47-5) Important
1.
General effects of CKD re medication effects (*Important) * complications-additional
consideration patient on dialysis
a. *Inc half-life- inc. plasma levels of meds excreted by kidneys; monitor carefully
b. *Dosages- may change in renal failure due to how drug excreted! Example- do not
give demerol to patients on dialysis (toxicity); digitalis excreted largely by kidney*
Remember patients with CRD-avoid NSAIDsr
c. Dec. drug absorption if phosphate-binding agents administered concurrently
d. *Low plasma protein levels > lead to toxicity when protein-bound drugs are given
e. *Avoid nephrotoxic drugs (Aminoglycosides, penicillin in high doses, carefully
monitor vancomycin due to toxic accumulation); Amphoteracin B very nephrotoxic ;
also contrast-media induced nephrotoxicity
f. **If on dialysis; many drugs removed by dialysis; vAKIes with hemodialysis and
peritoneal dialysis: *CHECK before giving
g. *Typically do NOT give antihypertensive drugs before hemodialysis (BP may drop);
give after dialysis. (work closely with co-nurse & dialysis nurse on this!)
2.
Meds- hyperkalemia present (see AKI (Tab. 47.5)- recall Kayexlate, IV glucose, etc
3.
Meds- Hypertension- review ch 33
a. Antihypertensive drugs- diuretics, B-adrenergic blockers, calcium blockers, ACE inhibitors,
ARBS
b. *Drug selection-depend –patient diabetic/nondiabetic (ACE and ARBs for
diabetics/nondiabetics with proteinuria due to effect on proteinuria and slowing of CKD
c. Diuretic (furosemide, other loop diuretics -reduce edema; dec. blood
pressure, lower potassium) & *
d. Antihypertensive medications: ACE inhibitors preferred
4.
Meds-Renal osteodystrophy *Read carefully
a. Phosphate intake restricted < 1g/day
1) Phosphate binders-calcium carbonate (Caltrate), calcium acetate (Phoslo)bind phosphate in bowel to excrete * note risk if given when phosphate very
elevated; adm of calcium may inc calcium load >inc risk for vascular
calcifications >use non-calcium-based phosphate binders if serum calcium
normal or elevated ( lanthanum carbonate (Fosrenal) and sevelamer
(Renagel); also lowers chlosteral and LDL
2) Aluminum products effective binders-*Note risks toxicity, bone effects
b. *Give with meal-act as binding agent; give between meals to act as calcium
supplement
c. Side effect-constipation
d. Supplement Vit D (recall why needed); likely to be hypocalcemic; trt > hypercalcemia
1) Calcitriol (Rocaltrol)
2) Paricalcitrol (Zemplar)
3) & Serum phosphate level-must lower before administering calcium or vit D >
tissue calcification
e. Control secondary hyperparathyroidism *recall why this develops) (p. 1177),
1) Calciminetic agents- Cinacalcet (Sensipar)- ↑ Sensitivity of ca receptors in
parathyroid glands
2)
Subtotal parathyroidectomy- transplant portion of gland in forearm, thigh-still
produce PTH, but less amt (think caution)
5.
Meds- Anemia
a. Erythropoietin by injection (Epogen or Procrit….inc production RBCs)- IV, or sc
b. Iron supplements if plasma ferritin <100 ng/ml-side effects gastric irritation, constipation
(dark stools) * Don’t give with phosphate binder/calcium
c. Folic acid; require multiple vitamin supplements; removed by dialysis (has to be given post
dialysis (water soluble)
d. *Avoid blood transfusions-suppresses erythropoietin (no hypoxic stimulus)- possible iron
overload
e. Antacids to treat gastric irritation; *No magnesium based- magnesium toxicity
6. Nutrition/fluid management (Why important?)
RNSG 2432  5
a.
*Early in CKD: diet modification-slow kidney failure & avoid uremic symptoms (usual
guidelines) *modify hen on dialysis/type RRT *p. 1178 Tab. 47-10
b. Protein - 0.6-1.0 g/kg body weight/day (about 40-50 g/day)-*remember urea nitrogen and
creatinine are breakdown products of protein-need high biologic value protein-8New
thought keep “norml in stages 1-4 (read EBP p. 1179
i. Guidelines change with hemodialysis begins inc to 1.2-1.3 g/kg body weight
(slightly more liberal)
ii. **If peritoneal dialysis- MUST be enough to compensate for losses through
peritoneal membrane- at least 1.2-1.3 g/kg body weight (60 g/day)
e. Water/fluid (important)- restrictions depend upon output… *Not restricted in pre-ESRD’
*remember 600 plus previous 24 hours output-*generally about 1000ml daily*most…NOT always…patients on dialysis will have less than 400 ml or NO urine output.
Monitor restrictions> fluid overload…restrict weight gain between dialysis- more liberal
fluids on peritoneal dialysis-patients in more “control”- Important-not to gain more than
1-1.5 kg between dialysis *Recall -1 kg=1000 ml weights- *p. 1177-1178
f. Sodium restrictions-diets vary-2-4 gm depend upon degree edema, HTN, lab values; do
not confuse Na and salt; avoid high sodium foods -*No salt substitutes-contain
potassium!
g. Restrict potassium to (2-3 g day);*dialysis depend on lab results- avoid bananas,
prunes, raisins, orange juice, tomatoes, deep green, yellow vegetables;*not restricted
on peritoneal dialysis; p 1178 Tab47-11
h. Inc. carbohydrate intake (30-35kcal/kg/day) *protein sparing
i. Restrict phosphorus food (especially milk, ice cream, cheese; also meat, eggs, dairy
products) to 1g/day
Nursing Management
1. Nursing Diagnosis *identify significance p. 1180-1181 NCP 47-1
a. Excess fluid volume
b. Risk for injury
c. Imbalanced nutrition-less than body requirements
d. Grieving
e. Risk for Infection
2. Heath Promotiona. Identify individuals at risk for CKD
b. See teaching Guidelines p. 1179 47-12 Important!
*When renal function at approx <15% = ESRD…following options must be considered
Renal Replacement Therapies/Treatment Options; used when medications and dietary modifications no
longer effective
1.
Hemodialysis: establish vascular access (create AV fistula) months
2.
Peritoneal Dialysis: can be initiated when indicated; training of patient and/or family required
3.
Transplantation
4.
Death
A. Dialysis: manages ESRD; does not cure it*
Principles of dialysis (p. 1182, Fig 47-4) *understand this
1. *Dialysis- Movement of fluid/molecules across semipermeable membrane
from one compartment to another; used to correct fluid/electrolyte imbalances and remove waste
products in renal failure; treat drug overdoses
2. Two methods of dialysis available- Peritoneal dialysis (PD) & Hemodialysis (HD)
3. Dialysis- begun when uremia can’t be adequately managed conservatively- GFR (or creatinine
clearance) <15 ml/min
4. *Diffusion- Movement of solutes from area of greater concentration to area of lesser
concentration (in renal failure-urea, creatinine, uric cid, electrolytes –potassium, phosphate, move
from blood to diaysate- WBC, RBC, plasma proteins do NOT cross)
5. *Osmosis-movement of fluid from area of lesser to area of greater concentration of solutes
*Glucose pulls excess fluid-peritoneal dialysis-osmotic gradient
6. *Ultrafiltration- Water/ fluid removal, results when there is osmotic gradient across membrane- in
PD- *Glucose pulls excess fluid-acts as ultrafiltration; in HD- hemodialysis machine uses positive
pressure or negative pressure to cause ultrafiltration.
7. Osmosis and Diffusion occur across semipermeable Membrane
Hemodialysis
1.
Hemodialysis See text p. 1284-+-*Uses principles- diffusion and ultrafiltration to remove
electrolytes, waste product/ excess water (soluble substances and water) from body through a
semi-permeable membrane-know definitions! Requires vascular access!!
6  RNSG 2432
a.
2.
Hemodialysis
1) Do 3-4 times a week; takes 3-4 hours at a time
2) Early animal experiments in 1913; first dialysis in 1940; 2 0f 17 patients
survived; experimental until 1950’s due to lack of intermittent blood access
(only AKI)
3) 1960-Dr. Scribner developed Schribner shunt; initially “Death Panels” determine
who could dialyze! 1972title XVIII-SS ACT –Medicare coverage for ESRD to all
for dialysis; 425, 000 +now on hemodialysis!
b. *Continuous renal replacement therapy (CRRT): used for clients with AKIwho cannot
tolerate hemodialysis and rapid fluid removal (see text p. 1188)- Blood continuous
circulated through highly porous hemofilter from artery to vein or vein to vein; for less
stable clients
Vascular access- A challenge; 3 types used mostly today: internal arteriovenous fistulas (AVFs),
and grafts (AVGs), temporary and semipermanent catheters subcutaneous ports and shunts.
*Shunts- external device- U-shaped silastic tube, rarely used now except with CRRT due to risk of
complications, infection, thrombosis (p. 1184- fig. 47-8; 47-9)
a. External shunt- today CRRT- external U-shaped silastic tube, temporary dialysis access
(Schribner shunt) See below- one end into artery; other end into vein *not in text
1) Advantages-put in place at bedside; can use immediately
2) Disadvantages- *accidental separation (bleeding!), skin erosion, infection, limit
use of extremity
b.
Temporary /Long-term access-insert double lumen catheter into subclavian, jugular
or femoral vein (temporary) (p. 1186 Fig 47-10) Which vein cannulation is associated
with lowest incidence of thombosis?
1) Advantages-immediate use, no needle sticks
2) Disadvantage- high incidence infections (leave subclavian 1-3; femoral1 week in place),
subclavian vein stenosis, poor flow-inadequate dialysis, clotting, restrict movement-
*Fig 47-10-Temporary double lumen catheters-Blood drawn from proximal portion of catheter
and returned to circulation through distal end of catheter
3). Cuffed Tunneled Catheters (Dacron cuff)-duel lumen catheter with Dacron cuff
surgically tunneled into subclavian, jugular or femoral vein (Permacath, common type
locally)
1) Advantages/Disadvantages same as above EXCEPT- can allow for LONG term use for
patients with no other access (not candidates for fistula/graft
2 ) New types- inc blood flow- dec rates infection and pvt clotting Important- *Do not
access- accessed by trained dialysis staff- must not administer meds, draw blood
from vascular access catheters (patient’s life- has large quantities heparin, high bleed
risk! p. 1186 Fig 47-11“Permanent” vascular access catheter- Permacaths “new”
ones as Lifesite Ports (not often used locally)- provide access into IJ, femoral,
subclavian; tunneled- ex- Lifesite Port; good blood flow, implanted under skin and
tunneled into internal jugular (IJ)
c. Vascular Access- Internal Arteriovenous Fistula/Graft- patient’s own
artery and vein surgically anastmosed –either own artery/vein or with graft
RNSG 2432  7
*Arteriovenous (AV) fistula (click to direct link) (p. 1184 Fig 47-8)- Surgical
anastomosis of patient’s own artery/ vein in non-dominant arm, usually radial artery
and cephalic vein preferred (also called primary or native AV fistula)
1) Advantages: patient’s own vein; lasts longer; less prone to clotting and infection; low
thrombosis rate
2) Disadvantages: Requires needle stick; long time to “mature” (before can use),requires
“good” vessels for placement; 1-6 mo.; risk of “steal” syndrome p. 1185 (define)
d. Arteriovenous graft (PTFE (Polytetraflourethylene) graft-synthetic “vessel” anastomosed
into artery and vein
1) Advantages: patients with inadequate vessels; use within 2-4 weeks (maybe earlier);
vessels easy to visualize.
2) Disadvantages: clots easily; “steal syndrome more frequent; requires needle stick;
infection may require removal of graft
Site for cannulation/needle
access to dialyze with AV graft
(PTFE)
c.
Care of vascular access-fistula/graft for complications (regardless if primary AV
fistula or graft)
1) No BP’s, needle sticks to arm with vascular access (includes finger sticks)
2) Place ID bands on other arm whenever possible
3) Palpate thrill and listen for bruit (determine patency)
4) Assess for thrombosis, infection
5) Teach Patient –nothing constrictive bands, feel for thrill
6) Post-op care with placement fistulas/grafts- elevate, assess patency, no constrictive
bands, monitor for circulation (“steal” syndrome) For information on grafts/fistulas-
click here
Graft material used in this photo; listen
for bruit, feel for thrill; no BP’s on this
arms, no restrictive bands!
8  RNSG 2432
3.
Hemodialysis process (p. 1186, Fig 47-12) (*understand principles of operation) *Read carefully
p. 1186-1187 *Read Procedure
Diffusion takes places here-in
dialyzer
a.
b.
4.
Blood removed from patient into extracorporeal circuit (flow at about 200-500 ml/min)
Diffusion occurs in dialyzer (long plastic cartridge containing thousands of parallel
hollow tubes or fibers-semi-permeable membrane made of cellulose-based/other
synthetic materials). Blood pumped into top of cartridge- dispersed into all of fibers).
Pump pressure >pressure gradient >ultrafiltration >fluid removal
c. Two needles placed in fistula or graft (or temporary or semi-permanent vascular device
as Permacath is accessed“); “needle” closer to fistula or red catheter (identifies arterial
blood) pulls blood from patient then to dialyzer; blood returned from dialyzer to patient
through second needle or blue catheter (identifies venous blood)
d. Dialyzer/blood lines primed with saline solution-eliminate air; hepAKIn added to blood;
terminated by flushing dialyzer with saline to remove all blood; post procedure- needles
removed, frim pressure required (with graft/fistula)
e. During procedure-*glucose, electrolytes, water pass through dialyzer -larger molecules
(protein, red blood cells)-blocked from passing through semi-permeable membrane
(dialyzer) *Important
f. Substances can be added to dialysate to diffuse into blood of patient (i.e. additional K if
level is low)
Complications/comparison/consideration-hemodialysis (*important to understand these!)
See also p. 1187 Tab. 47-13
a. *Prior to treatment- assessment of fluid status (weight before and after dialysis- *Bestlimit wt gain-1-1.5 kg between dialysis ); condition of access, temperature, skin
condition; during treatment- monitor changes in condition, perform vital signs every 3060 minutes
b. Note-MOST medications- HOLD prior to dialysis/give after (except phosphate
binders-give with meals!)- “dialyze out” ie many antibiotics, water soluble antibiotics;
*meds as BP cause significant drop in BP...(unless informed otherwise)- check with
staff/dialysis nurse; *caution with insulin- make sure patient will/can eat-dialysis may
cause nausea- hypoglycemic response-careful monitoring! *Check Dialyziability of
Drugs (PDF reference)
During dialysis
c.
d.
e.
f.
Hypotension, most common- related to changes in osmolality, rapid removal from
vascular department, vasodilation -FYI-Osmolality- measure of solute concentration,
(number of osmoles of solute per liter of solution (osmol/L); Osmolality-measure of
osmoles of solute per kilogram of solvent (osmol/kg). * Avoid- hold BP meds prior to
dialysis, additional fluids given during dialysis
Muscle cramps-due to altered fluid and electrolytes
Cardiovascular; arrhythmias associated with fluid and electrolyte alterations; bleeding
due to altered platelet function (uremia); *Cardiovascular disease –most common cause
death-ESRD/dialysis
Complications associated with extracorporeal circuit- (dialysis)
RNSG 2432  9
Bleeding- heparinn to prime circuit; “central line” access catheters contain
Heparin typically- risk line separation, bleeding during access; accidental
line separation-high pressure in line-arterial-venous connection=high flow!
> *rapid bleeding
g. Neurologic: seizures (*know why this happens!) *Not in text (happen with initial
dialysis
1)
Disequilibrium syndrome especially with initial dialysis
a) Urea, sodium and other solutes removed more rapidly from blood
than from cerebrospinal fluid and brain
b) Creates high osmotic gradient in brain > shift of fluid into brain and
cerebral edema > nausea, vomiting, confusion, headaches, twitching
and seizures
h. *Infection: local or systemic
1)
Staphylococcus aureus septicemia-infected vascular access; high rates
of hepatitis B and C, CMV, HIV
Potential Complications Hemodialysis
Between Treatments- risks of hypertension/hypotension (HTN greatest risk); edema; pulmonary
edema; hyperkalemia; bleeding; clotting of access > uremia *
Long term complications with hemodilaysis (relate to ESRD manifestations) p. 1204-1209)
including hyperparathyroidism, diabetic complications, CHF, cardiovascular disease, respiratory
disease as “uremic lung” etc.
*Hemodialysis -prevent long term complications by dietary control, fluid management,
medication adherence; and adherence to dialysis schedule.
*See previous discussion dietary/fluid management in CKD
Refer to difference mgt-hemodialysis/peritoneal dialysis;& fluid restrictions; (Tab 47-10)
phosphorous, potassium, sodium; protein (maintain nitrogen balance-too high > excessive waste
products, too low, dec albumin, inc mortality; caloric requirements to maintain/reach ideal weight.)
1)
5.
6.
7.
8.
Peritoneal Dialysis p. 1182-1184, See Fig 47-5–*read carefully-Removal of soluble substances and water
from blood by diffusion through a semi-permeable membrane intracorporeal (inside body); *treatmentongoing, usually 24 hrs a day/7 days/wk/ongoing
1.
Peritoneal dialysis: access by inserting catheter through anterior wall of abdomen-requires
consent, surgically placed-immediate irrigation; usually delay 7-14 days prior to start peritoneal
dialysis; 2-4 wks after implantation, exit site > clean, dry, free of redness/tenderness Fig 47-6
catheter, exit site
2.
Solutions (dialysate)- available in 1-2 L plastic bags with glucose concentration of 1.5 %, 2.5%,
4.25%- composition similar to plasmaa. Solution warmed to body temperature prior to instillation into peritoneal cavity via
peritoneal catheter
b. Metabolic waste products/ excessive electrolytes diffuse into dialysate while it remains
in abdomen
c. Fluid removal controlled by glucose (dextrose) concentration in dialysate (acts as an
“osmotic” agent- *What is osmosis?)
d. Excess fluid/solutes removed- gradual/constant-less risk for unstable client
e. Fluid drained by gravity into sterile bag at set intervals-removing waste products/
excess fluid
1)
“Clear” solution ‘fills” abdomen
2)
“Yellow” urine-like fluid drains out (like urine, clear)
f. Types of Peritoneal Dialysis (*understand principles)
1) CAPD- Continuous ambulatory peritoneal dialysis- manual exchange systemindividual controls exchanges
CAPD- individual controls daily schedule; trt-ongoing 24 hrs a day; 7
days a week; 2 l solution in peritoneal cavity except during drain
time; independent treatment; disconnect catheter during dwell time.
10  RNSG 2432
2)
APD- -automated peritoneal dialysis- fluid exchanges done automatically by
machine-treatment done at home at night while sleeping-thus no fluid in “the belly”
at daytime (uses a cycler)
The cycler — automatically fills and drains
abdomen, usually at night during sleep — can
be programmed to deliver specified volumes
dialysis solution on specified schedule
2.
g. Terminology:
1) Dwell time (equilibrium): time solution (dialysate) fluid remains in peritoneal cavity
(duration depends method-CAPD, or CCPD)-usually 4-5 exchanges daily
2) Fill (inflow): fluid infused into peritoneal cavity (usually takes 10-15 minutes);
facilitate by gently massaging abdomen, chg position
3) Drain (equilibrium): time fluid drains from peritoneal cavity by gravity flow (usually
takes 20-30 minutes)
Complications (see also p 1184, Tab. 47-13)
a. *Infection: peritonitis (dialysate return looks cloudy; abdominal tenderness), tunnel
infections, catheter exit site infections; priority problem!
b. Abdominal pain; outflow problems; hernias, lower back problems; cuff erosion
c. Bleeding
d. Hypervolemia (hypertension), risk pulmonary edema; excessive fluid intake, poor
management; hypervolemia, excessive fluid removed
e.* Hyperglycemia (dialysate -contains large amounts glucose)- Risk of malnutrition, obesity,
hyperlipidemia, recall solution used); *Hyperglycemia: glucose concentrations high for
osmosis for fluid loss; can add insulin to solution; (early satiety due to glucose)
(carbohydrate/lipid abnormalities)
f.* Hypokalemia: loss of potassium and protein through peritoneal membrane-diet
liberalized; can have more protein
g. Loss of untrafiltration
3. Advantages of CAPD/APD
a. Independence- for patient; not needle sticks; short training program; ease of traveling;
greater mobility than hemodialysis; better blood pressure control; * fewer dietary restrictions
(inc protein)
b.
Disadvantages- see above (complications-ie risk peritonitis, poor clearing etc.
4. *Compare advantages/disadvantages Peritonal Dialysis and Hemodialysis (p. 1182, 1178 Tab 4713, Tab 47-10)
5. Review dietary & other considerations related to hemodialysis/peritoneal dialysis-(*important!)
a. Fluid restrictions
b. Phosphorous, potassium sodium restrictions
c. Protein amts
d. Calories
e. *Medications- generally hold medications (especially BP) prior to
hemodialysis…check before giving medications prior to dialysis.
*Medications common to dialysis patients & pre-end stage patientsInclude water soluble vitamins, iron supplements, antihypertensives,
erythropoietin, calcium supplements (between meals), activated
RNSG 2432  11
6.
vitamin D3; antibiotics after dialysis
c. Invasive procedures (wound care, injections, etc, should not be done during or
immediately after dialysis, have to bleeding risk due to use of heparin during dialysis.
d. Assess for patency of fistula (palpable thrill and audible bruit)
e. Never use access sites or fistula for “regular IV administration of meds etc.!
Patient Education_ Include Alleviate fear; explain dialysis process; fistula/catheter care; diet and
fluid restrictions, medication compliance; diabetic teaching (many diabetics) *See online case study for
additional information.
CRRT/CVVHD- p, 1188-1189, Fig 47-14 *Know definitions
1. CRRT- Continuous Renal Replacement Therapy- large volumes fluid removed hourly, then replaced;
fluid replacement dependent on stability-individualized to needs of patient; uses dialysate bags
attached to distal end of hemofilter; fluid pumped countercurrent to blood flow; *ideal method for
patient who needs/fluid/solute control but cannot tolerate rapid fluid shifts
a. compared to HD- continuous not intermittent; solute removed by convection, not dialysate,
in addition to osmosis and diffusion; less hemodynamic instability; does not require
constant monitoring
b. done in critical care settings
Kidney Transplant (click to learn more!)
1.
Kidney Transplant (p. 1189-1194 & p. 228-232 & view Organ Donation video –TOSA- opt)
&HESI Patient Review
2.
Treatment choice for ESRD; limited by availability of kidneys; improves survival and quality of life
for ESRD client; 90-95% 1 year survival rate (reverses many of pathophysiological changes of
ESRD); can last 25 years+
3.
*Less expensive than dialysis after first year; *Allows return to normal life; eliminates
dependence on dialysis
a.
b.
c.
d.
e.
f.
4.
Subject to chronic rejection
Requires life long medications
Multiple side effects from medications
Increased risk of tumors
*Increased risk of infection
Major surgery-requires detailed assessment donor/recipient before and after procedure
Contraindications to transplantation (generally)
a. Disseminated mailgnanacies
b. Cardiac disease /extensive vascular disease
c. Chronic respiratory failure
d. Chronic infection
e. Unresolved psychological disorders ?who should be a candidate
5.
*Histocompatibility studies- p. 228-229 identify HLA antigens for both donors and potential
recipients (get best match) *What is HLA?
6.
Organ donation- majority from cadavers; transplants from living donors increasing
Living donors- good physical health; nephrectomy major surgery; remaining kidney must be
healthy, procedure starts 1-2 hrs before recipient’s surgery; can be done laparoscopically
*Review care of patient post nephrectomy-include close monitoring renal function, hematocrit
etc- and text p. 1192 + (Live donor pre/post –op care)
Cadaver donors; meet criteria for brain death, age free of systemic disease, malignancy or
infection including HIV, hepatitis B, C
Paired Organ donation > expands donation pool; also paired organ donor exchange- can use if
ABO incompatibility also use plasmapheresis dec. # antibodies inc chance donor success!
(Read p. 1190-1191
7.
Kidney transplant recipient - Kidney removed- preserved by hypothermia; rapid revasculization
critical; donor artery anastomosed to recipient internal/external iliac artery; donor vein
anastomosed to recipient external iliac vein
12  RNSG 2432
a.
b.
8.
Transplant within 24-72 hours (“longer time > greater risk AKI
Do not remove “old” kidney unless extremely large (polycystic or infection source)
Care of the recipient - major surgery; general anesthesia
a.
Pre-op:
1)
2)
3)
4)
5)
b.
c.
Careful pre-op assessment (no infection)
Answer questions/concerns/emotional as well as physical preparation
ECG/ Chest X-Ray, Lab studies
Remain on dialysis as ordered/keep access intact; all PD fluid drained
prior to procedure!
Administer immunosuppressive drugs before surgery
Post-op- when kidney in place-anastomoses complete-clamps released > blood flow reestablished1)
Careful assessment of renal function (fluid and electrolyte balance); daily
weights
2)
Urine may begin to flow or diuretic may be required (oliguric or anuric)
3)
*First priority- maintenance fluid and electrolyte balance- large volumes
urine soon after transplant due to new kidneys ability to filter BUN,
abundance of fluide during surgery; initial tubular dysfunction (unable to
concentrate)
4)
Maintain urinary catheter patency; hourly I&O; keep urine at 100ml/hr;
monitor for ATN (acute tubular necrosis) 59% will experience in
immediate post-op period!!
5)
Monitor for BUN, creatinine and creatinine clearance, daily weights, all
labs
6)
Monitor vital signs and hemodynamic pressure
7)
Replace fluids based on urine output of previous 30-60 minutes (like
treating AKI); diuretics as ordered
8)
Monitor for complications:
a) hemorrhage
b) ureteral anastamosis failure (urine leak into periotoneal cavity);
dec. urine output with abdominal tenderness/swelling
c) renal artery thrombosis; abrupt onset HTN and
d) dec. GFR
e) infection due to immunosuppression
Monitor for rejection *p. 228-232 (Tab 14-19)
1)
Hyperacute
a) Pre-formed antibodies to donor antigen (antibody-mediated,
humoral)rejection
b) function ceases within 24 hours (no treatment; remove kidney)
2)
Acute- occurs days to months after transplantation
a) cell-mediated immune response to HLA antigens
b) occurs days to months after transplant
c) have signs of inflammation; impaired organ function
d) Not uncommon to experience- *reversible; differentiate
between rejection and medication (cyclosporine) toxicity
e) treat with steroids, monoclonial (OKT3) or polyclonal
antibodies (Atgam)
3)
Chronic rejection
a) gradual deterioration of organ function
RNSG 2432  13
b)
c)
d)
d.
starts months to years after transplant
no effective treatment; return to dialysis or re-transplant
*Involves humoral and cellular immune response
*Teach
1)
Prevention infection due to immunosuppression (lead to kidney loss);
major complication: handwashing, avoid crowds, kids
2)
Monitor daily weights; vital signs for inc. temperature; gain in weight
(rejection, loss kidney function)
3)
Avoid crowds, ills persons, crowds, especially first 3 months
4)
Signs of rejections (know them):
a) Inc. weight (daily weight)
b) Pain and/tenderness over transplant site
c) Dec. urine output
d) Fever >100 degrees
e) Progressive azotemia; protenuria, HTN (chronic
f) Rejection > renal failure
9.
Responses to transplant & other facts
a. Rejection of a first kidney “may not” jeopardize the second.
b. Depression occurs with rejection.
c. The longer a person goes without rejection, the better the prognosis.
d. Leading causes of death > infection, (due to pneumonia, wound infection, IV line/drain
site in first months); fungal infections include candida, Cryptococcus, aspergillus, CMVmost common viral infection; Transplant recipients –inc risk atherosclerotic vascular
disease, inc. HTN; malignancies due to immunosuppressive therapy CVA, and MI.
e. Living related donor survival for 1 year is 95%;Living related donor kidney survival for 3
years is 65%.; Cadaveric donor survival for 1 year 78%.; Cadaveric donor kidney
survival for 3 years is 45%.
10.
Immunosuppressive medication See p. 231. Tab. 14-19 *Read carefully- Immunosuppressive
Therapy & required HESI Pt Review
a. Corticosteroid (prevent infiltration of T lymphocytes) cornerstone drug: side effects:
cushnoid changes; avascular necrosis of hips, knees,, Peptic ulcer disease-GI
disturbances, Glucose intolerance and diabetes, infection, risk of tumorb. Cytoxic Agents
1)
Azathioprine (Imuran); prevents rapid growing lymphocytes: side effects:
bone marrow toxicity, hepatotoxicity, hair loss, infection, risk of tumor
2)
Cellcept (Mycophenolate); Cyclophosphamide (Cytoxan); newer drugs
used instead of Imuran due to decreased toxicity.
3)
*Side effects- this class- bone marrow toxicity, hepatotoxicity, hair loss,
infection risk of tumors
c, Calcineuin Inhibitors -cyclosporine (Sandinimmune, Neoral) also Prograft, FK506
1) Cylosporin (Neoral, Sandimmune)/Prograf, FK506; interferes with production of
interleukin 2 which is needed for growth and activation of T lymphocytes
(Helper T cells); side effects: *nephrotoxicity, HTN, heptotoxicity, gingival
hyperplasia, infection
d. Monoclonal antibody (OKT3 or Orthoclone);; used to treat
rejection or induce immunosuppression; decreases CD3 cells within
1 hour; side effects: *risk*anaphylaxis, fever/chills, pulmonary
edema, risk of infection and tumors (treat prior to administration;
reaction increases chance of success)
e. Polyclonal Antibody-(Antilymphocyte Globulins) Atgam: contain
antilymphocyte antibodies produced by immunizing horses, etc with
human lymphocytes to stimulate production of antibodies; administered to client,
binds to peripheral lymphocytes and mononuclear cells, removes them from circulation
(skin test for sensitivity to horse serum prior to use)
1)
Antithymocyte globulin (ATG (ATGAM)
2)
Side effects- anaphylaxis, fiver chills, leucopenia, thrombocytopenia, risk
infection
Nursing Care/Collaborative Care (CKD, ESRD & Transplant)
1.
Determine stage of renal failure; provide appropriate instruction; critical to caution about drugs,
dehydration, etc that may compromise already impaired renal function
14  RNSG 2432
2.
Nursing diagnoses
CKD/ESRD/management with dialysis
a. Fluid volume excess rt inability of kidneys to excrete fluid, inadequate dialysis, and
excessive fluid intake as manifested by edema, HTN, bounding pulse, weight gain,
SOB, pulmonary edema
b. Impaired tissue perfusion: renal* text p. 784
c. Impaired skin integrity rt decrease in oil and sweat gland activity, hyperphosphatemia,
deposition of calcium-phosphate precipitates, capillary fragility, excess fluid and
neuropathy as manifested by itching, bruising, dry skin, edema, excoriation
d. Imbalanced Nutrition: less than body requirements rt restricted intake of nutrients,
especially protein, nausea, vomiting, anorexia and stomatitis as manifested by loss of
appetite and weight and decreased albumin levels
e. Risk for Infection rt suppressed immune system, access sites, and malnutrition
secondary to dialysis and uremia
f. Risk for injury (fracture rt alteration in the absorption of calcium and excretion of
phosphate, altered vitamin d metabolism
g. Disturbed body image
Kidney transplant (in addition to immediate post-op concerns)
a. *Ineffective protection rt effects of medications that compromise immune
system, loss of tissue integrity
b. *Risk for impaired tissue integrity (graft rejection) rt presence of foreign body
c. Risk for infection rt compromised immune system
3.
Nursing Care of Client Undergoing Hemodialysis
a. Note importance of pre-post weights
b. Identify medications to be held with dialysis (medication will dialyze out; no BP
medications prior to dialysis due to BP fall during dialysis; need for supplement with
water soluble vitamins (give after dialysis); antibiotics typically after dialysis
c. *Fluid intake restricted unless patient has urine output.
d. *Assess vascular access; protect access site
e. Assess for complications related to hemodialysis
f. Provide for teaching (diet/fluid restrictions/cautions related to access)
4.
Nursing Care of Client Undergoing Peritoneal Dialysis
a. Differentiate between hemodialysis and peritoneal dialysis (food and fluid restrictions,
compare advantages/disadvantages of each method
b. Instruct in strict aseptic technique in managing peritoneal dialysis
c. Instruct regarding signs and symptoms of infection
d. Instruct how to manage problems during instillation of dialysate solution
5.
Nursing Care of Client Having a Kidney Transplant
a. Review pre-post-operative care
b. Monitor for signs symptoms of rejection
c. Teaching
1)
Avoid crowds; immune suppressed
2)
Medication compliance; medication information!
Transplant-Keys (View also Organ Donation) and/see Word doc (For Organ Donation-cadavaric-)
1.
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
RNSG 2432  15
–
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.
2.
Official Criteria for Deceased Donors
3.
**Usually irreversible brain injury as MVA, gunshot wounds, hemorrhage, anoxic brain injury
from MI
4.
Must have effective cardiac function*
5.
Must be supported by ventilator to preserve organs
6.
Age 2-70
7.
No IV drug use, HTN, DM, Malignancies, Sepsis, disease
8.
Permission from legal next of kin & pronoucement of death made by MD
9.
Official Criteria for Living Donors
10. Psychiatric evaluation
11. Anesthesia evaluation
12. 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
13. Nurses Role in Event of Potential Donation - Notify TOSA (Texas Organ Sharing Alliance) 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
16  RNSG 2432