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Acute Kidney Injury and Chronic Kidney

Disease

1. Kidney Failure also called renal failure = partial or complete impairment of


kidney function
- results in an inability to excrete metabolic waste prod- ucts
and water and contributes to disturbances of ALL body
systems
can be acute or chronic
- AKI- acute kidney injury has rapid onset, potentially
reversible but mortality rates 60%
- chronic kidney disease usually develops slowly over
months to years, and is linked with development of car-
diovascular disease
- focus of CKD is managing disease requires long term
care- dialysis or transplant
note acute kidney injury and acute kidney failure - same thing

2. Acute Kidney In- - term used to encompass entire range of syndrome


jury/ Acute Kid- - from slight deterioration of kidney function to severe
ney Failure- impairment
what is it - characterized by a rapid loss of kidney function
- this loss is accompanied by a rise in serum creatinine and
or reduction in urine output
- can develop to progressive azotemia- accumulation of
nitrogenous wastes in the blood
- although potentially reversible, high mortality rate
- most commonly, affects people with other life threaten- ing
conditions
3. AKI severe prolonged, hypotension or hypovolemia or expo- sure
Commonly to a nephrotoxic agent
follows

4. AKI develops - over hours or days with progressive elevation of BUN,


creatinine, and potassium with or without a reduction in urine
output
- hospitalized patients develop Aki at a high rate and have a
high mortality rate

5. Common Prerenal- perfusion related - sudden and severe drop in BP or


causes of AKI interruption in blood flow to kidneys from severe
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injury or illness
1. Hypovolemia- dehydration, hemorrhage, GI loses, di-
uresis, burns
2. Decreased CO- dysrhythmias, HF, MI
3. Decreased PVR- anaphylaxis, neurologic injjiry, septic
shock
4. Decreased renal blood flow - embolism, remarry artery
thrombosis

Intrarenal- in the tissue of the kidney- direct damage to the


kidneys by inflammation, toxins, drugs, infection, or
reduced blood supply
1. Nephrotoxic injury- drugs, contrast media, blood trans-
fusion reaction, severe crush injury, chemical exposure
2. Interstital nephritis- allergies, antibodies, ace inhibits,
infections- bacterial
3. Other causes- prolonged prerenal ischemia, acute
glomerulonephritis, thrombotic disorders, malignant hy-
pertension, systemic lupus erythematous

Postrenal- sudden obstruction of urine flow due to en-


larged prostate, kidney stones, bladder tumor or injury
1. benign prostatic hyperplasia, bladder cancer, cal-
culi formation, neuromuscular disorders, prostate cancer,
strictures, trauma to back, pelvis

6. Bladder cancer postrenal acute kidney failure cause


is an example
of
- external to the kidneys
7. Acute Kidney - reduce systemic circulation causing reduction in renal blood
In- jury Patho- flow= decease glomerular perfusion and filtration of kidneys
Prer- enal
- in prerenal oliguria there is NO damage to the kidney
tissues- parenchyma- the oliguria is caused by decrease in
8. Distinguish pre- circulating blood volume- severe dehydration, HF, de-
renal oliguria creased CO and is readily reversible with treatment- pre-
from oliguria of renal azotemia results in a reduction in the excretion of
intrarenal AKI

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sodium increased sodium and water retention, decreased urine
output
- prenreal conditions can lead to intrarenal disease if renal
ischemia is prolonged

9. Intrarenal caus- - conditions that cause direct damage to kidneys resulting in


es of AKI impaired nephron function
- usually from prolonged ischemia, nephrotoxins (amino
glycoside antibiotics, contrast media) hemoglobin re- leased
from hemolyzed RBC or myoglobin released from necrotic
muscle cells
- nephrotoxins can cause obstruction of intrarenal struc- tures
by crystallizing or by causing damage to epithelial cells
- hemoglobin and myoglobin can block the tubules and cause
vasoconstriction- disease of the kidney can cause cause like
glomerulonephritis or systemic lupus erythe- matousis

= most common intrarenal cause of Aki and is primarily


result of ischemia, nephrotoxins or sepsis
10. Acute - severe kidney ischmeia causes a disruption in the base- ment
Tubular membrane and patchy destruction of the tubular epithelium
Necrosis - nephrotoxic agents cause necrosis of tubular epithelial cells,
which slough off and plug the tubules
- ATN is potentially reversible if the basement membrane is
not destroyed and tubular epithelium regretters
- ATN is most common cause of AKI for hospitalized
patients

11. Postrenal AKI - involve mechanical obsruction in the outflow of urine


- as flow of urine is obstructed it reflexes into the renal
pelvis, impairing kidney function
- most common causes are being prostatic hyperplasia,
prostate cancer, calculi, trauma tumors
- if bilateral obstruction is relieved within 48 hours of
onset, complete recovery is likely

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- after 12 weeks recovery is unlikely
- postrenal causes account for less than 10% of AKI cases

12. Stages of Acute RIFLE


Kidney Injury R- risk- serum, creatinine increased x1.5 or GFR de-
creased 25%
Injury- serum creatine increased 2x or GFR decreased 50%
Failure- serum creatine increased 3x or GFR decreased 75%
of serum creatine >4 and acute rise >0.5
Loss- persistent acute renal failure, complete loss of kid- ney
function >4 weeks
End stage kidney disease - complete loss of kidney func- tion
>3 months

- prerenal and postrenal AKI that has not caused in- trarenal
13. AKI Clinical damage usually resolves quickly with treatment of the cause
Man- ifestations - when parenchymal damage occurs due to pre or post, AKI
has prolonged course
Phases:
Oliguric, diuretic, and recovery- when do not recovery -->
chronic kidney damage may develop

- most common initial manifestation of AKI = oliguria- a


reduction in urine output to less than 400mL/day
14. AKI: Oliguric - usually occurs within 1-7 days of the injury to the kidneys
Phase - if the cause is ischemia,it occurs with 24 hours. in contrast
with nephrotoxic drugs are involved onset may be delayed
to 1 week
- lasts on average for 10-14 days but can lasts in months
- the longer the oliguric phase lasts, the poorer the prog- nosis
for complete recover
- 50% of patients will NOT be oliguric, making initial
diagnosis more difficult
List
1. Fluid Volume
2. Metabolic Acidosis
3. Sodium Bicarbonate

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3. Potassium Excess
4. Hematologic Disorders
5. Waste product accumulation
6. Neurologic Disorders

15. Oliguria: urinaly- - may show casts, RBC and WBC


sis - the casts are formed mucoprotein impressions of the
necrotic renal tubular epithelial cells, which detach or
slough into tubules
- also show specific gravity fixed at 1.010 and urine osmo-
lality at about 300mOsm/kg- the same specific gravity as the
plasma thus reflecting tubular damage with a loss of
concentrating ability by the kidney
- proterinura may be present if kidney failure is related to
glomeural membrane dysfunction

16. AKI Clinical - hypovolemia has the potential to exacerbate all forms of
Man- ifestations: AKI
Olig- uric Phase- - the reversal of hypovolemia with fluid replacement is
Fluid Volume often sufficient to treat many forms, especially prerenal
causes
- when urine output decreases, fluid retention occurs --> the
neck veins may become distended with bounding pulse
- edema and hypertension develop
- fluid overload can lead to HF, pulmonary edema, and
pericardial and pleural effusions
- as a nurse must monitor when they are getting fluids,
***monitor LUNG SOUNDS if fails if worked about fluid
constantly evaluate lung sounds
- if cannot get in touch with provider and hear crackles and
especially if they are not getting out any urine or hypoxic,
signs that they are drowning from inside out, you can stop IV
fluids

- the kidneys cannot synthesize ammonia in AKI which is


17. AKI Clinical needed for hydrogen ion excretion, or excrete acid products
Man- ifestations: of metabolism
Olig- uric Phase- - the serum bicarbonate level decreases because bicar-
Meta- bolic
acidosis
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bonate is depleted in buffering hydrogen ions
- in addition, defective reabsorption and regeneration of
bicarbonate occur --> acidosis
- may develop Kussmaul respirations to compensate and
increasing exhalation of Co22
- what buffers the acid? the kidneys, in the form of carb so
bicarb is getting used up so the level is decreasing the kidneys
not able to replenish
--> severe acidosis Kussmaul respirations- rapid and deep
respirations

18. AKI Clinical - damaged tubules cannot conserve sodium


Man- ifestations: - urinary excretion of sodium may increase, resulting in
Olig- uric Phase- normal or below norm sodium
sodi- um - excessive intake of sodium should be avoided because it can
balance lead to volume expansion, hypertension and HF
- uncontrolled hyponatremia or water excess --> cerebral
edema
note urine is hypernatremic and serum is hyponatremic

- the kidneys normally excrete 80-90% potassium


19. AKI Clinical - in AKI the potassium level is increased because kidneys
Man- ifestations: normal ability s impaired
Olig- uric Phase- -hyperkalemia is more of a risk of AKI is caused by massive
Potassium tissue trauma because damaged cells release additional
potassium into ECF
- bleeding, blood transfusions may cause cellular destruc- tion
--> more potassium
- acidosis worsens hyperkalemia as hydrogen ions enter the
cells and potassium is driven out of the cells into the ECF
- may be asymptotic usually but some may have weak- ness
- hyperkalemia: peaked T waves, widening QRS, ST seg-
ment depression

- hospital acquired AKI often occurs in patients with multi-


grain failure
- leukocytosis is often present with AKI
20. AKI Clinical
Man- ifestations:
Olig- uric Phase-
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Hematologic Dis- - most common cause of death in AKI is infection
orders - most common sites of infections are urinary and respi-
ratory system
- a complete blood count with eosinophilia suggests an
allergic response
21. AKI Clinical - kidneys are primary excretory organs for urea and cre-
Man- ifestations: atinine
Olig- uric Phase- - BUN and serum creatinine levels are ELEVATED in
waste product kidney failure
accumulation - an elevated BUN must be elevate with caution can also be
caused by dehydration, corticosteroids, or catabolism
resulting from infections, fever, injury or GI bleed
22. Best indicator of creatinine because it is not sig altered by other factors
AKI - BUN is for example by corticosteroids
23. AKI Clinical - changes occur as the nitrogenous waste products accu-
Man- ifestations: mulate in the brain and other nervous tissue
Olig- uric Phase- - can be mild as fatigue and difficulty concentrating and
Neu- rologic escape to seizures, stupor and cam
Disor- ders - asterixis: flapping tremor when the wrist is extended is most
common in liver failure but can be seen in severe kidney
dysfunction- flapping resembles a bird flapping its wings
when the hands and wrist extending outward
24. AKI Diuretic - daily orient is around 1-3L but may reach 5L or more
Phase - although urine output is increasing, the nephrons are still
NOT fully functional
- the high urine volume is caused by osmotic diuresis from the
high urea concentration in the glomerular filtrate and the
inability of the tubules to concentrate the urine
- the kidneys have received their ability to excrete wastes, but
NOT ability to concentrate the urine
- hypovolemia and hypotension can occur from massive
fluid losses
- because of the large losses of fluid and electrolytes monitor
for hyponatremia, hypokalemia and dehydration
- diuretic phase may last 1-3 weeks

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29. What is often the first test for AKI

25. AKI-
Recover
Phase

26. Outcome of AKI


influenced by

27. AKI
Diagnostic
Studies

28. Urine sediment


containing
abun- dant cells,
casts, or
proteins sug-
gests

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Acute Kidney Injury and Chronic Kidney
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- near the end of this are no better criteria for AKI diagnosis
phase, acid base, - an increase in serum creatine may not be evident until there
electrolytes and BUN, is a loss of more than 50% of kidney function
creatine values begin - the rate of increase in serum creatinine is also v impor- tant
to normalize -urinalysis is v important

- begins when GFR Intrarenal disorders


increases, allowing - the urine osmolality, sodium content and specific gravity
BUN and serum help distinguish types
creatinine levels to - urine sediment may be normal in prerenal and postrenal AKI
plateau and then - in intrarenal problems- hematuria, pyuria and crystals may
dcrease be seen
- although major Prerenal: low sodium, normal urine sediment
improvements occur in Intrarenal: high sodium, urine casts, high sediment = no pee
the first 1-2 week of
this phase, kidney - kidney ultrasound provides imaging without exposure to
function may take 12 potentially nephrotoxic contrast agents
months to stabilize - usefl for evaluating for possible kidney disease and

- patients overall heath,


severity of kidney
failure, number and the
of complications
- some do not recover and
go to end stage
- most patient who
recover achieve
clinically normal kid-
ney function with no
complications- some
scar tissue remains but
no loss of function is
sig

- through history essential


- although changes in
urine output and serum
creatinine occur
relatively late in the
course of AKI, there

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obstruction
- a renal scan can assess abnormalities in kidney flow
- CT can identify lesions, masses, obstructions, vascular
abnormalities
30. What is the - renal biopsy
best method for
confirming in-
trarenal causes
of AKI

31. Last option AKI - MRI or magnetic resonance angiography with contrast
diagnosis media gadolinium is not advised with patients in kidney
failure unless there is a sig reason to do the tests or unless
the ultrasound or CT will not provide the info needed
- administration of gadolinium has been associated with
the development of a devastating and potentially lethal
disorder- nephrogenic systemic fibrosis in patients with
kidney failure- characterized by skin hyper pigmentation
and induration and joint contractures
- in patients with normal kidney function, administration of
contrast media poses minimal risk
- in patients with kidney failure, contrast-in-
duced-nephropathy (CIN) can occur with contrast media
- best way to avoid CIN is avoid exposure to contrast
media
- if contrast media MUST me administered to high risk
patient, the patient needs to have optimal hydration and
a low dose of the contrast agent

32. AKI Care -eliminate cause managemt symptoms


- first step is to determine if there is adequate intravascu-
lar volume and cardiac output to ensure adequate perfu-
sion to the kidneys
- diuretic therapy is often administered but NOT recom-
mended in high doses
- usually loop diuretic- Lasix (act on ascending loop of
Henle) or an osmotic diuretic- mannitol
- if AKI is already established, forcing fluids and diuretics

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Acute Kidney Injury and Chronic Kidney
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will not be effective, may be harmful
- monitor fluid intake during oliguric phase- general rule for
calculating fluid restriction is to add all loses for previ- ous 24
hours (urine, diarrhea, emesis, blood) plus 600mL for
insensible losses
- Hyperkalemia is one of most serious complications- both
insulin and sodium bicarbonate severe as temporary measure
for treatment of hyperkalemia by promoting a shift of
potassium into the cells, but potassium will even- tually be
released
- calcium gluconate raises the threshold at which dys-
rhythmias occur, temporarily stabilize myocardium
- only sodium polystyrene sulfonate- Kayexalate and dial-
ysis actually remove potassium from the body- never give this
drug to a patient with paralytic ileus because bowel necrosis
can occur
Note she said dopaine but it didn't not work like they thought
Vasopressin 3 priorities- levafed, vasopressin, epi?

- treatment of precipitating cause


33. AKI Collabo- - fluid restriction 600mL + previous 24 hour fluid loss
rative - nutritional therapy: adequate protein intake
Therapy (0.6-2g/kg/day) depending on degree of catabolism
Chart in TB potassium restriction, phosphate restriction, sodium re-
striction
- measures to lower potassium
- calcium supplements or phosphate biding agents
- enteral nutrition
- parenteral nutrition
- consider dialysis
- continuous renal replacement if needed

Regular Insulin IV
- potassium moves into cells
34. AKI- - IV glucose is given concurrently to prevent hypo-
Therapies for glycemia
Elevated - when effects of insulin diminish, potassium shifts back out
Potassium of cells

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Acute Kidney Injury and Chronic Kidney
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Sodium Bicarbonate- correct acidosis and cause shift of
potassium into cells
Calcium Gluconate IV
- generally used in advanced cardiac toxicity- ECG
changes, calcium raises threshold for excitation
Hemodialysis
- most effective therapy to remove potassium, works with a
short time
Sodium Polystyrene Sulfonate- Kayexalate
- cation-exchange resin in administered both or retention
enema
- when resin is in bowel, potassium is exchanged for
sodium
- therapy removes 1mEq of potassium per gram of drug
- it is mixed in water with sorbitol to produce osmotic
diarrhea evacuation of potassium rich stool
Dietary restriction
- potassium intake limited to 40 mEq/day
dialysis and kayexale actually remove it, others just push it
into cells then eventually back

35. AKI- - may be necessary until kidney function improves


Conserva- tive - RRT- renal replacement therapy indications
Therapy + 1. Volume overload resulting in compromised cardiac or
criteria pulmonary status
2. elevated serum potassium
3. metabolic acidosis- serum bicarb <15
4. BUN level >120
5. Sig changes in mental status - cerebral edema
6. Pericarditis, pericardial effusion or cardiac tamponade
- best guide to treatment is clinical assessment
-if RRT is required, many options are available
- Peritoneal dialysis is technically considered option for
RRT not used often- stable but cannot leave their home
- Intermittent hemodialysis- HD intervals 4 hours daily or
every other day or 4-3x a week- stable can leave there home
- continuous renal replacement therapy- has been effec- tive-
provided continuously over 24 hours through cannu-

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Acute Kidney Injury and Chronic Kidney
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lation of an artery and vein
**as little as potassium possible for these patients remem- ber
80-90% excreted in kidneys
36. When rapid - Hemodialysis
changes are re- - technically more complicated because staff and equip-
quired in a short ment and requires anticoagulation therapy
time is pre- - rapid fluid shifts during HD may cause hypotension
ferred

37. AKI- Nutritional - adequate calories to prevent catabolism despite re-


Therapy strictions to prevent electrolyte and fluid disorders and
azotemia
- adequate caloric intake: 30-35kcal/kg and 0.801.9 of
protein per kg of body weight to prevent the further break-
down of body protein for energy purposes
- adequate energy should be primarily from CHO and fate
sources to prevent ketosis from endogenous fat break-
down
- supplementation of essential AA can be given- because
limit protein
- sodium and potassium regulatd- sodium is restricted to
prevent edema, hyerptwension, HF
- dietary fary intake is increased to that receive 30-40%
of calories from fat- Fat emulsion IV infusion given as
nutritional supplement as a good source of nonprotein
calories
- if cannot maintain adequate oral inake, enteral nutrition
is preferred
- when GI is not functioning, parental nutrition is neces-
sary

38. If patient is re- - site for inflammation and exudate


ceiving dialysis - evaluate mental status and LOC
assess - examine oral mucosa for dryness and inflammation
- auscultate lung sounds
- monitor heart for S3 gallop, murmurs or pericardial
friction rub

39.
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Acute Kidney Injury and Chronic Kidney
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AKI- Health - prevention and early recognition
Pro- motion - careful monitor I/O and fluid and electrolyte balances
- assess and record external losses
- the individual who are taking nephrotic drugs should have
kidney function monitored and used sparingly, given in
smallest effect dose for shortest time, caution the pa- tient
about abuse of NSAIDs because ma worsen kidney function
- antibiotics, cocaine, heroin, nitrosources, NSAIDs, ri-
fampin, gold, heavy metals
- ACE inhibitors can also decrease perfusion pressure and
cause hyperkalemia therefore may need to reduce or
eliminate- yet ACE inhibitors are frequently used to prevent
proteinuria and progression of kidney disease, especially in
diabetic patient

- manage fluid and electrolyte balance during oliguric and


40. AKI Acute Inter- diuretic phases
vention - observe and record I/O
- daily weights at the same time to detect gains or loss 1kg
= 1000mL of fluid
- assess for s/s of hypervolemia in oliguric phase or
hypovolemia in diuretic phase
- infection is the leading cause of death in AKI, aseptic
technique is CRITICAL- protect patient- be alert for local
manifestations of infectin- swelling, redness pain, and
systemic- fever, malice, but realize temp may NOT always be
elevated
- patients with kidney failure have a blunted febrile re-
sponse to an infection
- if antibiotics are used to treat the infection, dose and fre-
quency must be considered because kidneys are primary route
of excretion for many antibiotics
- perform skin care and mouth care to prevent stomatitis
- painful swelling and sores in the mouth

41. AKI- Home care - recovery is variable


- diet high in calories, regular protein and potassium and
kidney function

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Acute Kidney Injury and Chronic Kidney
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- teach patient s/s
- the long term convalesce of 3-12 months may case psy-
chosocial and financial hardship- referrals to counseling
- if kidneys do not fully recover, need to transition to life
on dialysis or possible future transplantation
- note 3 month mark is transition to chronic
42. AKI- Geronto- - older adults are a ta risk for same causes of AKI but
logic Considera- MORE susceptible to AKI
tions - dehydration = predisposing factor - associated with
polypharmacy, immobility from bed ridden
- also caused by hypotension, diuretic therapy, amino-
glysodie therapy, constructive disorders, surgery, infec-
tion, contrast media
- impaired function of other organ systems from CV dis-
ease or DM can increase risk of AKI
- patients over 65 less key to recover from AKI
- but age should not be factored into deices about whether
to institute RRT- renal replacement therapy

43. Chronic Kidney - progressive, irreversible loss of kidney function


disease- - defines as either the presence of kidney damage or a
decreased GFR less than 60mL.min for longer than 3
months
- the last stage of kidney failure = end stage renal disease
occurs when GFR is less than 15mL.mi- at this point RRT-
dialysis or transplantation is required to maintain life

44. CKD causes - leading causes are diabetes 50% and hypertension 25%
- les common etiologies- glomerulonephritis, cystic dis-
eases, and urologic diseases
- CKD is much more common than AKI- partially attributed
to increasing in risk factors- aging population, rise in
obesity, and increased incidence of DM and hypertension
- mortality rate also increases
- because the kidneys are highly adaptive, kidney disease
is often not recognized until there has been considerable
loss of nephrons, frequently asymptotic CKD is under

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Acute Kidney Injury and Chronic Kidney
Disease
diagnosed and under under-treatment
70% of people with CKD are unaware
45. CKD Prognosis - highly variable depend on age and etiology
- some live normal active life, some rapidly progress to
stage 5
46. CKD Stages Stage 1- kidney disease with normal or increased GFR:
GFR >/= 90%
Stage 2- kidney damage with mild decrease GFR = 60-89
Stage 3- moderate decrease GFR- 30-59 mL/min
Stage 4 severe decrease GFR 15-29 Stage 5-
kidney failure <15 GFR or dialysis

47. Clinical Manifesta- tions: Uremia


Manifes- tations
CKD

48. CKD- Clini-


cal
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Acute Kidney Injury and Chronic Kidney
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- every body system fatigue, headache, sleep disturbances Ocular-
becomes affected hypertensive retinopathy
- including: urea, Pulmonary- pulmonary edema, uremic pleuritis, pneumo- nia
creatinine phenols, Integ- pruritus, ecchymosis, dry scaly skin Musculoskeletal-
hormones, elec- vascular and soft tissue calcifications, osteomalacia
trolytes and water Peripheral neuropathy
- uremia: syndrome electrolyte imbalances
in which kidney
function declines to - syndrome that incorporates all s/s seen in various sys- tems
the point that throughout the body
symptoms develop in - often occurs when GFR <10
multiple body sys-
tems- often occurs
when GFR <10
mL/min or less
Psychologic- anxiety
and depression
Cardiovas
cular-
hypertensi
on, HF,
CAD,
PAD GI-
anorexia,
n/v, GI
bleeds,
gastritis
Endocrine-
hyperparathyrodism,
thyroid
abnormalities, ED
Metabolic-
CHO
intolerance,
hyperlipidemia
Hematologic;:
anemia,
bleeding,
infection
Neurologic-
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Acute Kidney Injury and Chronic Kidney
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49. CKD- Clini- - as GFR decreases, BUN and serum creatinine levels
cal increase
Manifesta- - BUN increased not only by kidney failure but protein
tions: Waste Ac- intake, fever, corticosteroids, catabolism
cumulation - serum creatinine are more accurate

- caused by impaired glucose metabolism, resulting from


50. CKD- Clini- cellular insensitivity to the normal action of insulin
cal - mild to moderate hyperglycemia may occur
Manifesta- - patients with DM who develop uremia may require less
tions: altered insulin then before the onset of CKD because insulin which
CHO depends on kidneys for excretion, remains in cir- culation
metabolism longer- therefore patients who require insulin before starting
dialysis will be able to discontinue insulin therapy whey they
start dialysis and their dies disease progressives, monitor
insulin closely

51. CKD- Clini- - hyperinsulinemia stimulates hepatic production of


cal Manifesta- triglycerides
tions: - almost all patients with uremia develop dyslipdemia
elevated increased VLDL, increased LDL and decreased HDL-->
triglycerides CV disease
most CKD patients die from CV disease

52. CKD- Clini- - hyperkalemia happens


cal Manifesta- - fata dysrhythmias when reaches 7-8
tions: Potassium - results from decreased exception, food dietary supple-
ments IV infusions
53. CKD- Clini- may be elevated normal or low
cal Manifesta- - impaired sodium excretion, sodium and water are
tions: Sodium trained --> dilutional hyponatremia
- edema, hypertension HF
- generally restricted to 2g/day
54. CKD- Clini- - primarily excreted by the kidneys
cal Manifesta- - hyerpmagensia is generally not a problem unless patient
tions: Magne- digesting magnesium
sium

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Acute Kidney Injury and Chronic Kidney
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- absence of reflexes, decreased metal status, hypoten- sion =
s/s

55. CKD- Clini- - results from kidneys impaired ability to excrete the acid load
cal and from defective reabsorption and regeneration of bicarb
Manifesta- - acid usually buffered with bicarb
tions: - in kidney failure, bicarb falls 16-20
Metabolic
Acidosis - normocytic, normochromic anemia associated with CKD
- due to decreased production of erythropoietin in the
kidney --> dec RBC count
56. CKD- Clini- - for patients receiving maintenance hemodialysis, blood loss
cal in the dialer may also contribute to the anemic sate
Manifesta- - elevated PTH (produced to compensate for low serum
tions: Anemia calcium) can inhibit erythropoiesis shorten survival of RBC
--> more anemia

most common cause of bleeding is defect in platelet func-


tion
- impaired release of factor III
- alterations in coagulation system
57. CKD- Clini- - can usually be corrected with regular HD or PD
cal
Manifesta- - increased susceptibility to infection
tions: bleeding - both cellular and humoral immune response are sup-
tendencies pressed

-most common cause of death with CKD is CV disease


58. CKD- Clini- - MI, ischemic heart disease, PAD, HF, stroke
cal - CV disease may also be released to traditional and
Manifesta- NONtraiditional RF- vascular calcification, atrial stiffness,
tions: infection the calcium deposits in the vascular medial layer are
associated with stiffening of blood vessels
59. CKD- Clini- - vascular smooth muscle cells changing into chondro- cytes,
cal high total body calcium amount resulting from ab- normal
Manifesta- bone metabolism, impaired renal excretion, drug therapies
tions: Cardiovas- - hypertension is highly prevalent in CKD
cular system - DM are contributing factors

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Acute Kidney Injury and Chronic Kidney
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- CKD susceptible to cardiac dysrhythmias that result
from hyperkalemia and decreased coronary artery perfu-
sion
- uremic pericarditis can develop and occasionally
progress to pericardial effusion and cardiac tamponade-
friction rub, chest pain, low grade fever = pericarditis
60. CKD- Clini- - kussmaul breathing
cal Manifesta- - dyspnea may occur with fluid overhead, pulmonary ede-
tions: Respirato- ma, uremic pleuritic, respiratory infections like pneumonia
ry system

61. CKD- Clini- - stomatitis with exudate and ulcerations, metallic taste in
cal Manifesta- the mouth
tions: GI - uremic fetor- urinous odor of breath
- anorexia
- n/v
- conception
- fluid accumulates, nitrogenous waste is pulling fluid with
it

62. CKD- Clini- Expected as renal failure progresses


cal Manifesta- Attributed to
tions: Manifesta- tions: Muscu-
Neurologic

63. CKD- Clini-


cal

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Acute Kidney Injury and Chronic Kidney
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‘ imbalances Metabolic acidosis
Atrophy
N Demyelination of nerve fibers
i lethargy, cannot concentrate, irritable, seizures and coma
t Peripheral neuropathy is initially manifestations a slow- ing
r of nerve conduction- stage 5CKD may complain of restless
o leg syndrome described as bugs crawling inside the leg,
g parestesha expereinced --> muscle twitching and asterixis-
e hand flapping tumor
n - dialysis should improve general CNS manifestations
o however MOTOR neuropathy may not be reversible
u
s - CKD mineral and bone disorder develops
-as kidney function decreases, less vitamin D is converted to
w its active form resulting in decreased serum levels
a
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Acute Kidney Injury and Chronic Kidney
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loskeletal Sys- -activated vitamin D is necessary to optimize absorption
temCKD- Clinical of calcium from GI tract, thus low activ vitamin D results
Manifestations: in decreased serum calcium levels
- noramlly, serum calcium lees are tightly regulated by
PTH, when hypocalcemia occurs parathyroid secretes PTH
which stimulates bone demineralization releasing calcium
from the ones. phosphate is released as well, leading to
elevated serum phosphate
- hyperphosphatemia decreases serum calcium levels further
and reduces the kidneys ability to activate vitamin D
- lower serum calcium, elevated phosphate, decreased vitamin
D --> PTH which acts on bone remodeling causes a weakened
bone matrix and places patient at higher risk of FRACTURES
- normally plasma calcium is found ionized or free or
bound to protein
- in kidney failure, it is unusual for hypocalcemia to be
symptomatic- acidic state associated with renal failure more
calcium is in the ionized form and bout to protein, but low
ionized calcium --> tetany

= common complication of CKD and results in skeletal and


extra skeletal complications
64. CKD- Clinical - skeletal complications = osteomalacia, which results from
Manifestations: demineralization from bone turnover and defective
- CKD-MBD mineralization of newly formed bone and ostetits fibrosa-
decalcification of the bone replacement of bone tissue with
fibrous tissue
- extraskeletal complications- vascular calcifications- sig
contributing factor to CF disese- uremic red eye- caused by
irritation from calcium deposits in the eye

- Pruitus- kidney itch- from all of the uremia and at the


nitrogenous waste building up
65. CKD- Clini- -uremic frost
cal ---- very rare with urea crystallizes in the skin, BUN over
Manifesta- 200, if getting dialysis theory should never develop this
tions: Integu-
mentary

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Acute Kidney Injury and Chronic Kidney
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66. CKD- Clini- - infertility by both sexes and decreased lied
cal - women decreased estrogen, progesterone and leutinz- ing
Manifesta- hormone causing involution and menstrual changes, menses
tions: reproduc- and ovulation may return after dialysis is started
tive system - men lose testicular consistency, decreased testosterone
levels, low sperm counts
- sexual dysfunction may be caused by anemia- fatigue and
decreased libido
- may improve with dialysis
- pregnancy with transplantation is more common but still
considerable risk to mom and fetus

- personality, behavior changes, emotional lability, with-


67. CKD- Clini- draw, depression
cal Manifesta- - fatigue, lethargy
tions: - changes in body image
Psycho- logic - withdrawal
changes -emotional liability

- polyuria
- results from inability of kidneys to concentrate urine
68. CKD Clini- - occurs more often at night
cal - specific gravity fixed around 1.010
Manifesta-
tions: Urinary - oliguria occurs as CKD worsens
System - Anuria- urine output lower than 40mL per 24 hours
69. CKD Clini-
cal - protenuria is usual the FIRST indication of kidney dam-
Manifesta- age, CKD involves dipstick evaluation of protein in urine or
tions Oliguria evaluation for microalbuminuria, which is not detected on
routine urinalysis
70. CKD - a person with persistent proteinuria 1+ protein on dip- stick
Diagnostic testing two or more times over a 3 month period should have
Studies further assessment of RF and a diagnostic work of blood and
urine tests
- urine test for albumin to creatine ratio provides accu- rate
estimate of protein and albumin excretion rate- ratio
>300mg albumin/1g creatine = CKD
- a urinalysis can detect RBC, WBC, protein, casts and
23 /
Acute Kidney Injury and Chronic Kidney
Disease
glucose
- ultrasound of kidneys is done to detect obstructions and to
determine size
- can also use lipid profile, renal biopsy, hematocrit

71. Best indicator of many consider serum creatine but poorly reflect kidney
kidney function function use GFR for kidney function

72. CKD Care - preserve existing kidney function, follow up care stages 1-4
treat control then 5 is dialysis
- correction of fluid volume overload or deficit
- nutrition therapy
- erythopoetin therapy
- calcium supplements
- antihypertensives
- treat hyperlipidemia
- ACE or ARBs
- measure to lower potassium
- adjustment of dosages to degree of renal function Note
RF for exposure to nephrotoxic drugs- limit exposure and
give sodium bicarbonate last treatment

73. CKD Drug ther- - see previous for AKI


apy- Hyper- - IV glucose, IV 10% calcium glocnate
kalemia - teach patients to expect some diarrhea because con- tains
sorbitol- a sugar alcohol that has na osmotic laxative action
and ensure evacuation of potassium
- never give sodium polystyrene sulfonate to pa patient with
hypoactive bowel- paralytic ileus because fluid shifts could
lead to necrosis
- if EKG changes with hyperkalemia are present- peaked T,
widen QRS, dialysis may be required to remove excess
potassium
74. CKD Drug thera- - some can delay progression by controlling hypertension
py- - target = 130/80 for patients with CKD and 125/75 for
Hypertension patients with sig proteinuria
- treatment- weight loss, life style changes, diet recom-
mendations -DASH, administration of antihypertensive

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Acute Kidney Injury and Chronic Kidney
Disease
drugs
- diuretics, calcium channel blockers, ACE inhibitors,
ARBs
- ACE and ARBS used with diabetics and those with non
diabetic proteinuria- use cautiously in patients with elevated
BUN and creatine though?
- measure bP regularly

75. CKD - dryg - limiting dietary phosphorus, administrating phosphate


thera- py MBD binders, supplementing vitamin D and controlling hyper-
parathyrodisum
- phoshate intake is not restricted until patient requires RRT
- phosphate binders: calcium channel binders, calcium
carbonate- they bind phosphate in the bowel and are excrete
in the stool, the administration of calcium may increase
calcium load and place patient at increased risk for vascular
calcifications therefore consider changing to non calcium
based phosphate binder
- to be effective, administer phosphate binders with each
meal- constipation may be side effect use stool softness
- do NOT use magnesium containing antacids Maalox
because magnesium depends on kidneys for excretion
- if hypocalcemia persists even if the serum phosphate
levels are normal, supplemental calcium and vitamin D
should be given
- treatment for secondary hypoparthyrodism in ESKF re-
quires activated form of vitamin D because kidneys no longer
possess ability to activate it, active vitamin D is available as
oral or IV calcitriol
- if hypercalcemia occurs from supplements reduce or stop
the binders and supplements
- gold standard for diagnosis is bone biopsy for bone
disease
- exogenous erythropoietin EPO is used- available as
76. CKD Drug epoetin alfa IV or SubQ 2-3x per week
Thera- py - a sig increase in hemoglobin and hematocrit is not seen for
Anemia 2-3 weeks

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Acute Kidney Injury and Chronic Kidney
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- higher hemoglobin levels and higher doses of EPO are
associated with higher risk of thromoemboltic events and
increased risk of death
- use lowest dose possible EPO
side effect= hypertension
- uncontrolled hypertension= contraindication of EPO
may exacerbate individual's hypertension
- EPO side effect - iron deficiency from the increased
demand for iron to support erythroppesis, iron supple-
mentation is recommended if plasma ferritin is less than 100
- tell patient iron make the stool dark in color
- oral administration iron should NOT be taken at the same
time as phosphate binders because calcium binds to the iron,
preventing is absorption
- most patients receiving HD are prescribed IV iron su- crose,
supplemental folic acid usually given because it is needed for
RBC formation and is removed by dialysis
- blood transfusions should be avoided (increases the
potassium) in treatment of anemia unless patient experi-
ences acute blood loss or symptomatic anemia- undesir- able
effects of transfusions- increased sensitization and
development of antibodies

77. CKD drug thera- - staitins used to lower LDL


py dyslipdemia - however, simvastatin is associated with higher rate of
myopathy then switch to atorvastitin- minimal renal clear-
ance less cause of myopathy
- goal lower LDL below 100
lower triglycerides below 200

78. CKD Drug - many are partially or totally excreted by the kidneys
Thera- py - delayed and decreased elimination leads to drug toxicity
complications potential
- adjust!
- NSAIDS- no Motrin
- drugs of most concern = digoxin, diabetic agents (met-
formin) antibodies, and opioid medications

79. 79.
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Acute Kidney Injury and Chronic Kidney
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CKD Nutrition 1. Protein Restriction
Therapy 2. Water restriction
3. sodium and potassium restriction
4. phosphate restriction
80. CKD Nutrition - in pre-end stage kidney disease restrict to 0.6-
Therapy- 1.0g/kg/day - low protein
protein - if hemodialysis 1.2g/kg/day
- peritoneal dialysis: 1.2-1.3g/kg/day
- undergoing dialysis, not normally restricted
- many patients find it difficult and many clinicians encour-
age a diet with normal protein intake
- hwoever teach patients to avoid high protein diets and
supplemetns- overseers the diseased kidneys
- during PD protein intake must be high enough to com-
pensate for the losses so that the nitrogen balance is
maintained
- for patients with malnutrition commercially prepared
products that are high in protein but low in sodium and
potassium are avilable

- water and other fluids are not routinely restricted in


81. CKD Nutrition patients with CKD stages 1-5 who are not on HD
Therapy- - in an effort to reduce fluid retention, dialysis is used
water - for those receiving HD as their urine output diminishes,
fluids are restricted general 600mL/day + urine outputs
- foods that are liquid at room temperature- gelatin, ice
cream should be counted as fluid intake
- patients advised to limit fluid intake so the weight gains are
no more than 1-3kg between dialysis

vary from 2-4 g a day see chart


-do not equate sodium and salt because the sodium
82. CKD Nutrition content in 1g of sodium chloride = 400mg of sodium
Therapy- - instruct patient to avoid high sodium foods- cured meats,
sodium and pickled foods, canned soups, cold cuts, soy sauce, salad
potassium dressings
- potassium restriction depends kidneys ability to excrete
potassium

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Acute Kidney Injury and Chronic Kidney
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- most salt subtitles should be avoided big been instructed
to restrict potassium because they contain potassium
chloride
**patients with PD do NOT need potassium restrictions
because of the loss potassium with dialysis exchange-
may need replacement
83. CKD Nutrition - as kidney function decreases, phosphate elimination by
Therapy- Phos- kidneys is diminished --> hyperphosphatemia
phate - by time reaches ESKD, phosphate should be limited to
1g/day
- foods high include meat, dairy products
- many foods high in phosphate are also high in protein
- since patients on dialysis are encourage to eat a diet
containing high protein, phosphate binders are ESSEN-
TIAL to control phosphate

84. High potassium - apricot, avocado, banana, cantaloupe, dried fruits, or-
foods ange, OJ, rasins, baked beans, squash, black beans,
raw carrots, potatoes, spinach, tomatoes, veggies juices,
bran, chocolate, milk, granola, nuts and seeds, PB, slat
substitutes, yogurt, salt free-broth

85. CKD health pro- - identify those at risk


motion - people with DM have urine checked for microalbuminuria
if routine urinalysis is negative for protein- report changes
in urine

86. CKD Acute inter- - most outpatient basis, hospital required for complica-
vention tions

87. CKD- Home Care - teach diet drugs and follow up


- pill organizer
- any OTH is risk needs to be asked even acetaminophen
taken in large doses
- avoid certain OTh- NSAIDS and aluminum and magne-
sium based laxatives and antacids
- teach to take daily BP, deitnfiy s/s of fluid overload,
hyperkalemia, electrolyte imbalances
- evaulation for transplant

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Acute Kidney Injury and Chronic Kidney
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- most patients require dialysis- PD or HD- most chose
HD
- discuss opportunity for home HD
- alternate ways at reducing thirst- ice chips, hard candy,
lemon
DRUG side effects
1. Phospate binders including calcium supplements
should be taken with meals
2. calcium supplements should be taken on an empty
stomach but NOT same time as iron supple,tents
3. iron supplements- should be taken between meals

88. CKD- what - Weight gain >4 lb 2kg


should patient - increasing BP
report - SOB
- Edema
- Increasing fatigue or weakness
- confusion or lethargy

89. Dialysis the movement of fluid and moecuels across a semimper-


meable membrane form one compartment to another
- clinically dialysis is a technique in which substances
move from the blood through a semipermeable mem-
brane and into a dialysis solution- dialystate
- used to correct fluid and electrolyte imbalances, and to
remove waste products in kidney failure
- also usde to treat drug overdose

90. Methods of Dial- 2


ysis 1. Peritoneal Dialysis PD
- the peritoneal membrane acts as the semipermeable
membrane
2. Hemodialysis HD
- an artificial membrane usually made out of cellu-
lose-based or synthetic materials is use as the semiper-
meable membrane and is in contact with patents blood

91. When is dialysis - when the patient's uremia can no longer be adequately
done? treated with medical management

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Acute Kidney Injury and Chronic Kidney
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- generally when GFR is <15 ml/min
- criteria varies with clinicians

92. What indicates - encephalopathy


immediate - Neuropathies
dialy- sis? - Uncontrolled hyperkalemia
- Pericarditis
- Accelerated hypertension

93. Why are most 1. lack of donated organs


pa- tients with 2. some patients are not suite for transplantation
ESKD treated 3. some do not want transplants
with dial- ysis - some receive maintenance dialysis note
** a persons chronologic age is NOT a factor in determin- ing
candidacy for dialysis
- factors that ARE important are patients ability to cope and
support system

94. Peritoneal Advantages:


Dialy- sis +/- - immediate initiation in almost any hospital
- less complicated the HD
- portable system with CAPD
- Fewer dietary restriction
- Relatively short training time
- USABLE in patient with VASCULAR ACCESS problems
- less cardiovascular stress
- home dialysis is POSSIBLE
- PREFERABLE FOR DIABETIC PATIENT
Disadvantages
- bacterial or chemical peritonitis
- protein loss into dialysate
- exit site and tunnel infections
- self-image problems with catheter placement
- Hyperglycemia
- Surgery to catheter placement
- Contraindicated in patients with- multiple abdominal
surgeries, trauma, unprepared hernia
- requires completion of education program

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Acute Kidney Injury and Chronic Kidney
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- catheter can migrate
- best instituted with willing partner
95. Hemodialysis +/- Advantages
- rapid fluid removal
- rapid removal of urea and creatinine
- effective potassium removal
- less protein loss
- lowering of serum triglycerides
- home dialysis possible
- temporary access can be placed at bedside
Disadvantages
- vascular access problems
- diet and fluid restrictions
- heparinization may be necessary
- extensive equipment necessary
- hypotension during dialysis
- added blood loss that contributes to anemia
- specially trained personnel necessary
- surgery for permanent access placement
- self image problem with permanent access

96. Principles of - solutes and water move across the semipermeable


Dialysis membrane from the blood to the dialystate or from the
dialystate to trebled
1. Diffusion- movement of solutes from an area of greater
concetration to lesser concetration
- in Kidney failure, urea, creatinine, uric acid, and elec-
trolytes- potassium, phosphate move from the BLOOD to the
dialystate- net effect = lowering of their concetration in the
blood
- RBC, WBC, and plasma proteins are too large to diffuse
through pores of the membrane
- small molecular weight substances can pass from the
dialystate into a patients blood, so the purity of water used for
dialysis is controlled
2. Osmosis- movement of fluid from lesser concetration to
greater concetration of solutes
- glucose is added to dialystate and creates an osmotic

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Acute Kidney Injury and Chronic Kidney
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gradient, pulling excess fluid from the blood
- excess fluid is removed by creating a pressure differen- tial
between the blood and dialystate solution
3. Ultrafiltration= water and fluid removal and results when
there is an OSMOTIC gradient or pressure gradient across the
membrane
- in PD exces fluid is removed by increasing the osmolality of
the dialystate (osmotic gradient) with the ADDITION OF
GLUCOSE
- In HD, the gradient is created by increasing pressure in the
blood compartment (positive press) or decreasing pressure in
the dialystate compartment (negative pres-
sure)- ECF moves into dialystate because of the pressure
gradient

97. PD: Catheter Note 12% of US patents receiving dialysis treatments are PD
Placement - Peritoneal access is obtained by inserting a catheter
through the anterior abdominal wall
- catheter is about 60cm long and has one or two Dacron cuffs
on its subcutaneous and peritoneal portions- the cuffs act as
anchors and prevent the migration of microor- ganisms down
the shaft of the skin
- within a few weeks, fibrous tissue grows into the Dacron
cuff, holding the catheter in place and preventing bacterial
penetration into the peritoneal cavity
- the tip of the catheter rests in the peritoneal cavity and has
many perforations spaced along the distal end of the tubing
allowing fluid of flow in and out of the catheter
- may instill prophylactic antibiotics
- waiting period before use 7-14 days
*Note its called a tenckhoff catheter with Darcon cuffs
- one of biggest complications peritonitis-

varies
98. PD Catheter - possible to place at bedside
Placement - usually doe via surgery so placement can be visualized
Tech- nique - preparation: emptying the bladder and bowel, weight the
patient AND consent form signed

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Acute Kidney Injury and Chronic Kidney
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99. When can PD - after placement, PD may be initiated immediately with
begin? restric- LOW volume exchanges, or delayed of 2 weeks pending
tions? healing and sealing of the exit site
- once catheter incision is healed, the patient may shower and
then pat the catheter exit site dry
- daily care varies
- some patients wash with soap and water and go without a
dressing- some require daily dressing changes
- teach all patients to examine their catcher for signs of
infection
100. PD what method Shower
of bathing is
pre- ferred

101. PD: Cycles - PD is accomplished by putting dialysis solution into the


peritoneal space
3 phases
1. Inflow (fill)
2. Dwell (equilibration)
3. Drain
102. PD Cycle- Inflow - a prescribed amount of solution, usually 2L is infused
through an established catheter over about 10 minutes
- the flow rate may be decreased if the patient has PAIN
- after the solution has been infused, the inflow flow clamp is
closed before air enters the tubing

103. PD cycle Dwell + = Equilibration


WHAT AND - diffusion and osmosis occur between patient's blood and
HOW peritoneal cavity
- 20-30 minutes up to 8+ hours depending on the method
- depends on osmotic forces, with glucose being most
effective osmotic agent used
- dextrose remains the most commonly sused PD solu- tion-
safe and inexpensive
- but also has high rates of peritoneal glucose absorption
--> hypertriglyceredmia, hyperglycemia
1.5%, 2.5%. 4.25%- warmed to body temperature- if too cold
--> cramping and pain
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Acute Kidney Injury and Chronic Kidney
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104. PD cycle- drain - takes 15-30 mins


- may be facilitated by gently massaging the abdomen or
changing positions
- the cycle starts again with the infusion of another 2L
solution
- for manual PD a period of aout 30-50 minutes is required for
complete exchange

105. PD Dialysis vary


solu- tions - determined by size of peritoneal cavity
- larger person may tolerate 3L without difficulty, small
person usually tolerates 2L
- smaller volumes used for smaller bodies, pulmonary
compromise or inguinal hernias
106. Alternatives to - icodextrin and amino acid solutions
PD glucose - Icodextrin is a commercially available isoomolar prepa-
dex- trose ration and induces ultrafiltration by oncotic effect
solutions - amino acid solutions are available and primarily used for
patients REQUIRING NUTRITIONAL SUPPLEMEN-
TATION

- most popular form of PD


107. Automated - allows patient to do dialysis while they sleep
Peri- toneal - automated device called a cylinder is used to deliver the
Dialysis dialystate for APD
- cycler times and controls the fill, dwell, and drain phases
- the machine cycles 4+ exchanges per night with 1-2
hours per exchange
- alarms and minors are built in to make it safe
- patient disconnects from the machine in the morning and
leaves fluid in the abdomen during the day
- difficult to achieve the required solute and fluid clearance
solely with nighttime APD
- therefore 1-2 daytime manual exchanges may be re-
quired
- cyclers are size of DVD player and have longer tubing for
greater mobility

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Acute Kidney Injury and Chronic Kidney
Disease
108. Continuous - done while the patient is awake during the day
Am- bulatory - exchanges are carried out manually be exchanging
Peri- toneal 1.5-3L of peritoneal dialystate at least 4x a day with dwell
Dialysis- CAPD timings emerging 4 hours
- disposable plastic tube
-in CAPD the bag and line can be disconnected after the
instillation of fluid
- after the equilibration period, the line is reconnected to
the catheter and the dialystate is drained from the
peritoneal cavity, and a new 2-3L bag of dialystate is
infused
109. In PD it is CRITI- maintain aseptic technique to avoid peritonitis
CAL to - one of biggest benefits is can do at home
- tube is in stomach- not vascular, not in venous or arterial
system!
110. Complications - Exit site infection
of Peritoneal - Peritonitis
Dialy- sis List - Hernias
- lower back problems
- bleeding
- pulmonary complications
- protein loss
111. Contraindica- - history of multiple abdominal surgical procedures or
tions of PD her severe abnormal pathology
list - recurrent abdominal wall or inguinal hernias
- excessive obesity with large abdomen wall and fat de-
posits
- pre-existing vertebral disease- chronic back problems
- severe obstructive pulmonary disease
112. Complications - most commonly caused by staphylococcus aureus or
of Peritoneal epidermis- from skin flora
Dialy- sis-Exit - redness, tenderness, draininage
site in- fection - generally resolved with antibiotics
- if not treated immediately --> tunnel infections --> ab- scess
formation --> peritonitis -> catheter removal neces- sary

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Acute Kidney Injury and Chronic Kidney
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113. Complications - results form contamination or from progression of an exit


of Peritoneal site or tunnel infection
Dial- ysis- - most frequently, occurs because of improper technique in
Peritonitis making or breaking connections for exchanges
+ MANIFESTA- - can also (less common) result for bacteria in intestine
TIONS crossing over to peritoneal cavity- S/ aureus or S. epider- mis
Manifestations
-abdominal pain, cloudy peritoneal effluent with a WBC count
greater than 100cells/ul- more than 50% neu- trophils or
demonstration of bacteria by gram stain culture
- GI manifestations- diarrhea, vomiting, abdominal disten-
tion, hyperactive bowel sounds, may or may not be a fever
- cultures, gram stains, and WBC differential used to
confirm diagnosis
- antibiotics can be given orally, IV or intraperionteally
- most often treated outpatient
- repeated infections may require removal of catheter and
termination of PD

- because of increased intraabdominal pressure sec- ondary to


dialystate infusion, hernias can develop in pre- disposed
114. Complications individuals- multiparous - a women having born more than 1
of Peritoneal child women and older men
Dialy- sis- - most times after hernia repaid, PD can be resumed and keep
Hernias patient supine

- increased intraabdominal pressure --> LBP


- orthopedic binders and regular exercise programs for
strengthening back muscles can help
115. Complications
of Peritoneal
Dial- ysis- low - After Tenckhoff catheter placement, not uncommon for PD
back problems drained after the first few exchanges to be PINK
or SLIGHTLY BLOODY secondary to trauma associated
116. Complications with insertion
of Peritoneal - HOWEVER, body effluent over several days or the NEW
Dialy- sis- appearance of blood in the effluent can indicate active
bleeding intraperitoneal bleeding- if this occurs check BP

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Acute Kidney Injury and Chronic Kidney
Disease
and hematocrit
- blood may also be present in the effluent of women who
are menstruating or ovulation and this requires NO
intervention

117. Complications - atelectasis, pneumonia and bronchitis may occur from


of Peritoneal repeated upward displacement of diaphragm, resulting in
Dial- ysis- decreased lung expansion
Pulmonary - longer the dwell time, greater chance
complications - frequent repositioning and deep-breathing exercises can
help
- when lying on bed elevate head

- peritoneal membrane is permeable to plasma proteins,


118. Complications amino acids, and polypeptides- and are lost in dialystate fluid
of Peritoneal - amount loss is usually 0.5g/L of dialystate draininage but can
Dialy- sis- be as high as 10-20g/day
Protein Loss - may increased to 40g/day lost during peritonitis (mem-
brane is more permeable)
- unresolved peritonitis is associated with exaggerated
protein loss that can result in malnutrition and may indi-
cated termination PD temp or permanently

- learning the self-management skills required to do PD


takes 3-7 day training program
- mortality rates are - between in center HD patients and PD
119. Effectiveness of patients for first few years, or even a little lower for PD
Chronic PD Pa- - yet, after 2 years mortality rates for patients on PD are
tient higher, especially for DM patient or CV disease
- primary advantage is simplicity, home based, none for
special water systems and equipment set up
- especially induced for the individual with vascular ac-
cess problems, or responds poorly to hemodynamic stress
of HD
* fewer dietary restrictions
- major disadvantage= peritonitis
- ideally urinate
- must do every day if not compliant --> failure

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Acute Kidney Injury and Chronic Kidney
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120. HD: General - vascular access is most difficult problem associated with HD
- to perform HD, a very rapid blood flow is required, and
access to a large blood vessel is essential
types of vascular access
1. Arteriovenous fistulas- AVFs
2. Arteriovenous grafts AVG
3. Temporary vascular access

121. Arteriovenous - a subcutaneous arteriovenous fistula is usually created in the


Fistulas forearm or upper arm with an anastomosis between an artery
and a vein- usually cephalic or basilica
- the fistula allows arterial blood to flow through the vein
- the vein becomes- arterialized with a larger caliber and
thicker walls
- the arterial blood flow is essential to provide the rapid
blood flow required for HD
- as the arterialized vein matures, it is more amendable to
repeated venipuncture
- maturation may take 6 weeks- months
- AVF should be placed at least 3 months before need to
initiate HD
- best patency need to wait 3 months so use temporary
device
122. AVF what is im- - normally a thrill can be felt by palpating the area of
portant to note anastomosis and a bruit can be heard with stethoscope
for - the bruit and thrill are cared by arterial blood moving at a
assessment? high velocity through the vein
*AVFs are more difficult to create in patients with history of
severe peripheral vascular disease, prolonged IV drug use,
obese women --> synthetic graft

- made of synthetic materials and form a bridge between the


123. Arteriovenous arterial and venous blood supply
Grafts - grafts are placed under the skin and are surgically
anastomosed between an artery usually brachial and a vein
usually antecubital
- an interval of 2-4 weeks is necessary to allow the graft

38 /
Acute Kidney Injury and Chronic Kidney
Disease
to heal, some earlier
- because make of artificial material, they are MORE likely
that AVFS to become INFECTED,a nd tendency to be
thrombogenic
- when AVG infections occur, they may require surgical
removal
- surgical creation of AVG has several risks- development of
distal ischemia (steal syndrome) and pain because too much
of the arterial blood is being shunted from the distal
extremity- s/s= pain distal to the access site, numbness or
tingling of fingers that may worsen during dialysis and poor
capillary refill, aneurysms can also develop in AV access and
can lead to rupture if left utnreated

124. What should NEVER perform BP measurements, insertion of IV lines and


you never do venipuncture in the extremity with vascular access
with HD? - to prevent infection and clotting

125. HD: Temporary - in some situations, when immediate vascular access is


vascular required catheterization if the internal jugular or femoral even
access is performed- best is right internal jugular straight shot right
to superior vena cava (left has to cross over can get
kinked)***
- a flexible Teflon, silicone rubber or polyurethane catheter is
inserted at the bedside into one of these large veins and
provides access to the circulation without surgery
- the catheters usually have a double external lumen with an
internal septum separating the two internal segments
- one limen is used for blood removal and one for blood
return
-not recommend that patients not to be discharged from the
hospital with temporary catheter- high rates of infec- tion,
dislodgment and malfunction

- long-term cuffed HD catheters are often used for tem-


porary vascular access- they provide temporary access while
the patient is waiting for fistula placement or a long term
access when other forms have failed- this type of catheter
exits on the upper chest wall and is tunneled

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Acute Kidney Injury and Chronic Kidney
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subcutaneously to the internal or external jugular vein- and
the catheter tip rests in the right atrium. It has 1
or 2 Dacron cuffs that prevent infection and anchor the
catheter- eliminating the need for sutures
126. HD: Dialyzers - the HD dialyzer is a long plastic cartilage that contains
thousands of parallel hollow tubes or fibers
- the fibers are semipermeable membranes made of cel-
lulose-based or other synthetic materials
- the blood is pumped into the top of the cartilage and is
dispersed into all of the fibers
- dialysis fluid (dialystate) is pumped into the bottom of the
cartridge and baths the outside fibers
- ultrafiltration, diffusion and osmosis occur across the
pores of this semipermeable membrane
- when the dialyzed blood reaches the end of the thou- sands
of semipermeable fibers, it converges into a single tube that
returns it to the patient
- dialyzers differ in SA, membrane composition, thick-
ness, clearance

127. Nursing- 129. Medications to hold for dialysis


prepare a
patient for dial-
ysis her slide

128. Nursing Post


dialysis her
slide

40 /
Acute Kidney Injury and Chronic Kidney
Disease
- hold medications
- plan for blood
transfusions
- weight patient
- CBC and electrolytes
- VS prior

- VS Q15 min x 1 hr
- hypotension
- cramping
- nausea
- exhaustion
- bleeding
- medications
- post weight
Lots of complications
after dialysis has
ended: hypoten- sion,
nausea, exhaustion,
bleeding, exhaustion

- any meds that effect HR


and BP
example Coreg
(carvedilol)- it is a beta
blocker would not

41 /
Acute Kidney Injury and Chronic Kidney
Disease
take hemodynamic medication
- Digoxin- Lanoxin do NOT take that
- cannot take motrin, but can take tylenol, tylenol is a liver
drug
- can take anemia drugs, vitamin D drugs, calcium car-
bonate, colace, benadryl

130. Her questions: The metabolic rate is increased when a patient has surgery
James Bean is and is healing. The increased metabolic wastes accumulate in
67 years of age the patient with renal failure and the patient develops
and a male pa- symptoms of uremia more quickly and needs daily dialysis to
tient who is get rid of the increased wastes.
three days
postopera- tive
after a coro-
nary artery by-
pass graft op-
eration. The pa-
tient has a his-
tory of hyperten-
sion, type 1 di-
abetes, coronary
artery disease,
and end-stage
renal disease,
which is treated
with hemodialy-
sis three times
per week. The
pa- tient has a
left atriovenous
(AV) shunt.
The patient is or-
dered to have
daily dialysis.
What is the
ratio- nale for
this or- der?

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Acute Kidney Injury and Chronic Kidney
Disease
131. 131.

43 /
Acute Kidney Injury and Chronic Kidney
Disease
The patient is The nurse should hold the carvedilol (Coreg), which is a beta
go- ing to blocker antihypertensive.
hemodial- ysis
at 9 am
on an odd day.
Which medica-
tion or medica-
tions should the
nurse hold be-
fore sending the
patient?
-The nurse should place a sign over the left side of the bed
132. Her list nurs- that states "No BP or venipuncture in the left arm."
ing manage- -Assess the AV fistula every 8 hours for patency and for signs
ment considera- of infection and report any problems to the physi- cian.
tions related to Inspect the arm to ensure that there is no jewelry or any
the above constrictive clothing on the arm.
exam- ple - Assess vital signs as ordered and report hypotension
patient promptly and receive orders to help increase the blood
pressure so that the AV fistula does not clot off.
- When administering IV fluids, always use a volumetric
infusion pump and make sure that the fluid does not contain
potassium. (IV fluid, such as lactated Ringer's, has potassium
in the mixture.) - -- - Assess medications to ensure that the
medications DO NOT CONTAIN MAG- NESIUM as well.
-Assess lungs for crackles, which is a sign of fluid over-
load.
-Monitor for complications: Pericarditis
-Monitor electrolytes closely and report abnormalities.
-Weigh patient daily to monitor fluid status.
- Monitor appetite and diet intake. Monitor serum albumin
level as ordered.
- Provide pain medications as ordered for postoperative pain.
- Provide comfort measures for complications related to end-
stage renal disease.
- Use mild super fatted soap or bath oil to cleanse skin and
apply lotion to decrease dry skin.

44 /
Acute Kidney Injury and Chronic Kidney
Disease
- Provide diphenhydramine hydrochloride (Benadryl) as
ordered for itching.
- Assess and report signs of infection at incisions, includ- ing
fever, redness, edema, or purulent drainage.
- Maintain strict aseptic technique when handling any
invasive lines or when performing dressing changes be- cause
the patient is at increased risk to develop an infec- tion.
-Provide the patient with opportunity to vent feelings and
reactions to treatment.
133. Procedure for HD - needles are large bore, usually 14-16 age inserted into
fistula or graft
- once need is placed to pull blood from the circulation toe
HD machine, and the other needle is used to return the
dialyzed blood to the patient- needles are attached via tubing
- if a patient has a catheter, the 2 blood lines are attached to
the two catheter laments
- the needle closer to the fistula is used to pull the blood
FOM the patient and send it to the dialyzer with the
assistance of blood pump
*Heparin is added to the blood as it flows into the dialyzer
because any time blood contacts a foreign substance, it has a
tendency to clot- blood is returned from dialyzer to the patient
with second needle usually blue first is red
- a dialysate delivery monitoring system is also used- this
system pumps the dialystate through the dialyzer
countercurrent to the blood flow- dialysis is terminated by
flushing the dialyzer with saline solution- then removed and
firm pressure applied until bleeding stops

134. Before HD - complete assessment that includes fluid status- weight, BP,
Treat- ment peripheral edema, lung and heart sounds
- condition of vascular access
- temperature
- general skin condition
- the difference between the last post dialysis weight and the
present pre dialysis weight determine the ultrafiltration

45 /
Acute Kidney Injury and Chronic Kidney
Disease
or the amount to weight to be removed
- while ON dialysis take VS at least every 30-60 minutes
because rapid BP changes may occur
- most facilities use reclining chairs that allow for elevation of
the feet if hypotension develops- most people sleep, red talk
watch TV etc.

135. Settings and - community-based center and dialyzes for 2-4 hours 3
schedules for HD days per week
- other schedule option for HD are short daily and long
nocturnal HD
- short dail- dialyzes for 2.5-3hrs per session 5-6 days per
week- usually done at HOME
- in center HD programs have adapted their dialysis schedules
so patients can be free during the day- the patient receiving
long nocturnal HD has advantage of sleeping while dialyzing-
each nocturnal treatment is 6-8 hours 6x per week
- patients who chose daily or nocturnal dialysis tend to feel
better, in more control of their lives, require fewer
medications and tend to have fewer dialysis side effects like
hypertension and cramps
- home HD is also available- depends on family support-
greater freedom 2% population

136. HD: Complica- - hypotension


tions List - muscle cramps
- loss of blood
- hepatitis
137. HD: Complica- -results from rapid removal of vascular volume, de- creased
tions- cardiac output, decreased systemic vascular re- sistance
hypoten- sion - the drop in BP during dialysis --> light headless, nausea,
vomiting, seizures, vision changes and chest pain from
cardiac ischemia
treatment- decreasing volume of fluid being removed and IV
NS

138. 138.

46 /
Acute Kidney Injury and Chronic Kidney
Disease
HD: Complica- -poorly understood why
tions- muscle - factors- hypotension, hypovolemia, high ultrafiltration
cramps rate, low sodium dialysis solution
- more often seen in first month after invitation
- treatment- reducing ultrafiltration rate and fluids
- hypertonic saline is NOT recommended
- hypertonic glucose is preferred
139. HD: Complica- - results from blood not being completely rinsed from
tions- loss of dialyzer, accidental separation of blood tubing, dialysis
blood membrane rupture or bleeding after the removal f needle
- if patient has received too much heparin or has clotting
problems, can be sig
- essential to rinse back all blood to closely monitor he-
parinization and to hold nonexclusive pressure on sites until
bleeding has stopped
140. HD: Complica- - incidence today of hep B is low, used to be v high
tions- Hepatitis - lower transfusion requirements, screening, and recom-
mendations for vaccinations have lowered the incidence
- yet hepatitis B still occurs, since transmission is attrib-
uted to breaks in infection control practices
- to prevent CDC recommend all patients in dialysis units
receive hepatitis B vaccine
- currently, hepatitis C virus is responsible for majority of
hepatitis on dialysis
- no vaccine is available for C precautions
- note the liver can get hepatitis from damage and RBC
- also have complication of sepsis
and disequilibrium syndrome- very rapid changes in com-
position of ECF-->cerebral edema

141. Effectiveness - cannot fully replaced the normal functions of the kidneys
of HD - can easy symptoms of CKD and if started early can
prevent certain complications
- does NOT alter accelerated rate of development of CF
disease is the related high mortality rate
- the yearly death rate of patents receiving maintenance
dialysis 19-24% majority caused of CD disease- stroke,

47 /
Acute Kidney Injury and Chronic Kidney
Disease
MI
-initially patient feel positive about dialysis because it makes
them feebler but then ambivalence to make sure it is
worthwhile, dependent on a machine is their reality

142. CRRT- Contin- - alternative or adjunctive method for AKI


uous Replace- - provides a means by which uremic toxins and fluids are
ment Renal removed while acid base status and electrolytes are adjusted
Ther- apy slowly and continuously in a hemodynamically unstable
patient- cannot handle large fluid shifts, ICU
- usually patients who do not respond to dietary interven-
tions and drug therapy
- principle is to dialyze patients in more physiologic way over
24 hours just like the - long time to correct abnormal- ity

- life threatening manifestations of uremia


143. When is - hyperkalemia, pericarditis
CRRT contraindi- - can be used in conjunction with HD
catioed note nurse must be 1:1 in ICU labor in time

144. Types of CRRT - various


most common is venvenous hemofiltration CVVH
145. CVVH- continuous venovenous hemofiltration
- removes BOTH fluid and solutes
- replacement fluid is required
- vascular access achieved through double lumen catheter as
used in HD placed in JUGULAR or FEMORAL vein
- a blood pump is used to propel the blood through the
circuit
- a highly permeable hollow fiber hemofiliter removes
plasma water and nonprotein solutes- ultra filtrate
- the ultrafiltration rate may range from 0-500mL/hr
- under the influence of hydrostatic pressured osmotic
pressure, water and nonprotein solutes pass out of the filter
--> extracapaillary space and drain through ultra filtrate port
into drainage bag
- remaining fluid continues

48 /
Acute Kidney Injury and Chronic Kidney
Disease
CRRT

146. What is needed


with CRRT

147. Features that


differ
between
CRRT and HD

148. Ultrafiltration
flu- id in CRRT

149. Nursing Inter-


ventions
49 /
Acute Kidney Injury and Chronic Kidney
Disease
- when the ultra filtrate required) in addition to osmosis and diffusion
drains out of - causes less hemodynamic instability- hypotension
hemofiliter, fluid and - does NOT require constant monitoring by a specialized HD
electrolyte nurse but DOES require a trained ICU nurse
replacements can be - it dos NOT require complicated equipment, but a blood
infused into the pump is needed
infusion port- designed - can be continuous as long as 30-40 days but the he-
to replace volume and mofiliter should be changed every 24-48 hours because of
solutes- sodium, loss of filtration efficacy and potentil for clotting
chloride, bicarbonate,
glucose - should be clear yellow
- also further dilutes - specimens may be obtained for evaluation of serum
intravascular fluid, chemistries
decreasing con- - if it becomes BLOODY or blood TINGED a possible
centration of rupture in the filter membrane should be suspected and
unwanted solutes like treatment is suspended immediately to prevent blood loss and
BUN, creatinine and infection
potassium
- obtaining weights and assess and document lab values to
- anticoagulation to ensure adequate fluid and electrolyte balance
prevent blood clotting - hourly I/O
- heparin may be
infused as a bolus at
the initiation of CRRT
or through heparin
infusion port before the
hemofil- iter

CCRT IS
- continuous rather than
intermittent
- large volumes of
fluid can be removed
over days 24 hours
to more than 2 weeks
vs. 3-4 hours- slower
fluid shifts
- solute removal can
occur by convection
(no dialystate
50 /
Acute Kidney Injury and Chronic Kidney
Disease
- VS
- hemodynamic status
***** Reductions in central venous pressure and pul- monary
artery pressure are EXPECTED there should be little change
in mean arterial pressure or cardiac output
- patency of CRRT system is assessed and maintained and
assess for infection
- treatment is discontinued and needles are removed once
patients AKI is resolved or decision to withdraw
treatment

150. Kidney - by far best treatment option for ESKD fewer than 4%
Trans- plant receive it because high disparity between supply and
general demand
- most die while waiting
- transplantation from a deceased donor usuallyy requires
prolonged waiting period depending on age, gender, race
- average weight time is 2-5 years
- very succesful, 1 year survival rates over 90% for de-
ceased donor transplant and 95% for live transplant
- reverses many pathophysiologic changes associated with
renal failure also eliminate dependence on dialysis and
accompanying dietary and lifestyle restrictions
- also less expensive then dialysis after the first year

- some programs exclude patients who are morbidly


151. Kidney Trans- obese or who continue to smoke
plant- Recipient - careful evaluation to minimize potential complications
selection - those with CV risk and diabetes are high risk and most be
closely monitored after transplant
- for a small number of patients who are approaching ESKD,
a preemptive transplant (before dialysis is re- quired) is
possible if they have a living donor- this ap- proach is most
advantageous for patients with DM who have much higher
mortality rate on dialysis than nondia- beteics
- family cannot find out where organs came form Class
Notes-- In stage 5 or end stage renal failure with
NO infection, other comorbidities are very well controlled

51 /
Acute Kidney Injury and Chronic Kidney
Disease
then candidates for kidney transplant - careful evaluation
must be done
If approaching end stage can get onto list before on dialysis
Most advantages are for someone who has DM

- disseminated malignances
152. Contraindica- - refractory or untreated cardiac disease
tions for - chronic respiratory failure
kidney - extensive vascular disease
transplant - conrhonc infection
- psychologic disorders- nonadherence ot medical regi-
ments, alcoholism, drug addition
- at one time HIV people were denied opportunity, now
centers have included HIV patients
- the presence of hepatitis B or C is NOT a contraindica- tion
Note
- sometimes surgical procedures are required before
transplantation- coronary artery bypass or angioplasty may
be indicated etc.
*in general, the recipient's own kidneys do not need to be
removed before he or she receive transplant

153. Donor sources - can be compatible blood type deceased donors, blood
relatives, emotionally related living donors, or friends
- another option is paired organ donation- where one do
not/recipent pair who are incompatible or poorly matched find
another donor/pair with whom they can exchange kidneys-
thus a soups person A wants to donate to wife, person B but
can't so find another pair in the same situa- tion
154. Live Donors - undergo extensive multidisciplinary evaluation to be cer-
tain in good health
-psychosocial and financial evaluations are done
- crossmatches are done at time of evaluation and a week
before transplant to ensure NO antibodies to the donor are
present or that the antibody titer is below allowed level

52 /
Acute Kidney Injury and Chronic Kidney
Disease
- advantages over live= better patient and graft survival
regardless of match, immediate organ availability, imme-
diate function because of minimal cold time (kidney out of
body and not getting blood supply)
- potential donor sees nephrologist for complete history and
physical examination and lab- 24 hour urine study for
creatinine clearance, total proteins, CBC, electrolytes, hepatic
B and C, HIV, ECG and chest X-ray done, CT done
- transplant social worker determines if the individual is
emotional style to deal with the issues- must no risks
- kidney donation is considered SAFE without any long
term consequences
- cost of evaluation and surgery covered by insurance, no
compensation is available for lost wages during posthos-
pitalation recovery- can take 6+ weeks

paired donor exchange is viable alternative


155. What happens - or to use plasmapheresis to remove antibodies from the
when there is an recipient after transplant patient undergoes additional
ABO incompati- plasmapheresis treatment
bility between a
donor and
recipi- ent

156. Decased Donors - cadaver kidney donors are relatively healthy individuals
who have suffered irreversible brain injury= brain dead
-must have effective CV function and be supported on a
ventilator to preserve the organs
- must be free of active IV drug use, severe hypertension,
long standing DM, malignancies, sepsis, communicable
diseases- HIV, hepatitis B, C, syphaliss TB
- *even if the donor carried a singed donor cad, permis- sion
from the donor's legal next of kill is REQUIRED after breath
death is determined
- kidneys are removed and preserved for up to 72 hours- but
most surgeons prefer to transplant kidneys before cold time
reaches 24 hours- increases acute tubular necrosis

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Acute Kidney Injury and Chronic Kidney
Disease
157. United Network - distributes donor kidneys using an objective computer- ized
for Organ point system
Shar- ing - ABO group, HLA typing, aline, antibody level and length of
time entered into national computer
- when available all patients are given points for how close
HLA match is, time waiting, antibody level is high and if
younger than 19 years old
- extra points for high anitbody levels because this can
severely limit the number of donors with the patient has a
match
- kidney is offered to the recipient with the MOST points in
the local area
- if no patients in the load area are suitable then the region the
the nation
*Only expecting if patient needs emergency transplant or if a
donor and recipient match on all six HLA antigens- 0 antigen
mismatch- goes to top of list better survival rates
158. Surgical proce- - 27% of all transplants in US
dure- Live donor - donor nephrectomy is performed by urologist or trans-
plant surgeon donors surgery begins 1-2 hours before
recipient's
- Laparoscopic donor nephrectomy- most comment tech-
nique for living donor
- after kidney has been removed it is flushed with a chilled,
sterile electrolyte solution and prepared for immediate
transplant to recipient- minimal invasive with fewer risks and
shorter recover time than open procedure- dec hos- pital stay,
pain, blood loss, time off work
- open conventional nephrectomy- donor is placed in LAT-
ERAL DECUBITUS position on table so flank is exposed
laterally, incision made at 11th rib- rib may have to be
removed to see kidney

159. Kidney Trans- - usually placed extraperiotneally in the iliac fossa


plant Recipient - the right iliac fossa is preferred to facilitate anastomoses of
Surgery the blood vessels and ureter to minimize the occur- rence of
paralytic ileus
- before any incisions are made, urinary voter is placed

54 /
Acute Kidney Injury and Chronic Kidney
Disease
into bladder- an antibiotic solution is installed to distend the
bladder and decrease risk of infection
- a present shaped incision is made extending from iliac crest
to symphysis pubis
- rapid revascuarlization is critical to prevent ischemic
injury the kidney
- the donor artery is anastomosed to the recipient's inter- nal
iliac or external iliac artery
- the donor vein is anastomosed to the recipient's external iliac
vein
- when the anastomoses are complete, the clamps are
released and BF to kidney is reestablishes
- kidney should become firm and pink
- urine may begin to flow from ureter immediately
- the honor ureter in most cases is tunneled through the
bladder submucosa before entering the bladder cavity and
being sutured in place= ureternecystostomy- allows the
bladder wall to compress the ureter as it contracts for
mictruciation preventing reflux
- transplant surgery takes 2-4 hours

160. Nursing kidney - emotional and physical prep fr surgery


transplant pre - stress that there is chance the kidney may NOT function
op care immediately and dialysis MAY be required for days to weeks
- review need for immunosuppressive drugs and mea-
sures to prevent infections
- ensure patient is in optimal physical condition for
surgery- ECG< chest X-ray, lab studies
- dialysis may be required before surgery for any sig
problems like fluid overload or hyperkalemia
- a patient on PD must empty peritoneal cavity of all
dialsyte solution
- vascular access for dialysis must be maintained extrem- ity
should be labeled "dialysis access no procedures to prevent
BP blood drawing or IV
presence of cancer and infection are contraindications

161. 161.

55 /
Acute Kidney Injury and Chronic Kidney
Disease
Nursing Post op - donor post op is similar to open or laaroscopi
care: Live donor - monitor renal function to assess for impairment and
monitor hematocrit
- donors experience MORE pain after open
- generally donors have more pain then recipients
- donors who had open discharge in 4-5 days and
can return to work in 6-8 weeks
- laparoscopic stay in hospital 2-4 days and return work 4-6
weeks
- donor is seen by surgeon 1-2 weeks after discharge
-
162. Nursing Post - fluid and electrolyte balance
op- Kidney - 12-24 hours in ICU
recipient - very large volume of urine may be produced soon after
blood supply is reaestabilsihsed diuresis due to- new kidneys
ability to filter BUN, abundance of fluids adminis- tered
during operation, initiation renal tubular dysfinction
- urine output may be as high as 1L/hr and gradually
decrease as BUN and creatinine return to normal
- urine output is replaced with fluids
- central venous pressure readings are essential
- delation must be avoided
- electrolyte monitor for hyponatremia and hypokalemia-
treat with potassium supplements or NS
- acute tubular necrosis can occur because of prolonged cold
times causing ischemia- dialysis is require then- dialysis is
discontinued when urine output increases, and serum creatine
and BUN are normalizing
- a sudden decrease in urine output in early postop =
CONCERN- may be due to dehydration, rejection, leak or
obstruction- blood clot in urinary catheter, catheter patency
must be maintained, catheter remains in bladder 3-5 days to
allow it to heal. if blood clots are suspected gentle catheter
irrigation can be used to get patency
- hospital average stay 4-5 days distal teaching is v impor- tant

163. 163.
56 /
Acute Kidney Injury and Chronic Kidney
Disease
Transplat- -goal to adequately suppress the immune response to prevent
immunosuppres- rejection of transplanted kidney while maintaining sufficient
sive therapy immunity to prevent overwhelming infection
164. Complications - rejection
of - infection
transplantation - CVD
list - malignancies
- recurrence of original kidney disease
- corticosteroid related complications
165. Complications one of major problems
of - can by acute or chronic
transplantation- - should be put on transplant list hope can be retransplant- ed
rejection before dialysis is required
166. Complications sig cause of dying after
of - because of suppression of boys normal defense mecha-
transplantation- nisms by surgery, immunosuppressive drugs and effects of
infection ESKD
- underlying illness like DM, malnutrition, older age can
further complicate -
- most common observed in first month- pneumonia,
wound infection, IV lien drain infections, UTI
- fungal and viral are not uncommon because immunsp-
resed state
- fungal difficult to treat
- viral- CMV, Epstein Barr, herpes
- CMV is one most common viral- if recipient has never had
CMV and receives an organ from a donor with history CMV
antiviral prophylaxis will be administered
167. Complications - transplant recipients have increased incidence of ather-
of osclerosis vascular disease
transplantation- - hypertension, dyslipdemia SM rejection --> CV disease
cardiovascular - immunosuppressants can worsen hypertension and
disease dyslipdemia
168. Complications - greater then general population because immunosup-
of pressive therapy
57 /
Acute Kidney Injury and Chronic Kidney
Disease
transplantation- - most common basal squamous cell carcinoma of skin,
malignancies Hodgkin's and NHL
- screening for cancer is important
169. Complications - occurs in some
of - most common with glomerulonephritis, immunoglobin A
transplantation- nephropathy, diabetic nephropathy
recurrence of - must be advice is can happen
original kidney
disease

170. Complications - aseptic necrosis of hips, knees and other joints can
of result form chronic corticosteroid therapy
transplantation- - or peptic ulcer
corticosteroid - in first year after transplantation, corticosteroid doses are
complications usually decreased 5-10mg/day
- many transplant programs have initiated corticosteroid free
drug regiments because of problems
171. Gerontologic - diminished cardiopulmonary function
considerations - bone loss
CKD - immunodeficiency
- altered protein synthesis
- impaired cognition
- altered drug metabolism
- when conservative therapy for CKD is no longer effec-
tive, need to reevaulate
-PD allows patient to be more mobile and enjoy some
control
- PD causes less hemodynamic instability than HD but does
require self care assistance from other person, may not be
available
- most 65+ select HD in center treatment because of lack of
assistance and difficult technology
- establishing vascular access for HD may be hard be-
cause atherosclerotic changes
- less likely to be candidate fro transplant- living donor is
preferred
- most common cause of death in ESKD is CV disease

58 /
Acute Kidney Injury and Chronic Kidney
Disease
and removal from dialysis
- if a competent patient decides to withdraw from dialysis it is
essential to support the patient and family
- dialysis especially PD has been successfully used in older
adults, QOL is improving with dialysis
there is NO justification for excluding older adults form
dialysis!

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