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

Oligura- urine output less than 400ml/day



Anuria- Urine output less than 50ml/day



Higher specific gravity= MORE concentrated urine



Lower specific gravity= Dilute- more ‘watery’



Acute Renal Failure- Reversable- Sudden and almost complete loss of
kidney fxn over hours to days.


Increase in serum creatnine and BUN



3 Types ARF:





Pre-Renal- This is everything before the kidneys-ex.
Hypovolemia/dehydration, hemorrhage, renal losses-diuretics,
vomiting, diarrhea, prolonged fever (sepsis), n/v, hypotension,
decreased c.o., MI, diabetes type 1 and type 2. Is the result of
impaired blood flow that leads to hypoperfusion of the kidney
and a decrease in the GFR.



Intra-renal- Also called ARF or ATN-this is when there is
damage to the kidney that causes a nephritic infection. Ex.
Medications such as nephrotoxic episodes, (gentimyacin,
NSAIDS), transfusion reaction, hypercalcemia, and trauma..



Post-renal- This is after the kidneys and is usually the result of
an obstruction somewhere distal to the kidney. Pressure rises in
the kidney tubules and eventually, the GFR decreases. Ex:
infection in the ureters or bladder such as stones, obstruction,
tumor or stricture, BPH, or a blood clot.

Phases of ARF:




Initiation phase- (onset)- Begins with the initial insult and ends
when oliguria develops.


increase in BUN and Creatinine that can last hours to
days.



Urine output is 30 ml or less per hour- 50% of the pts. Are
noted to be oliguric

Oliguric phase- Decrease in urine output approx. 100-400
ml/24 hours. It doesn’t respond to fluid challenges and diuretics.


increase in creatinine, BUN, Potassium, and Magnesium.









Decrease in bicarb and calcium, and GFR.



F&E abnormalities, and metabolic acidosis.



Can last from 1-2 weeks.



Uremic symptoms first appear and life-threatening
conditions such as hyperkalemia develop.

Diuretic phase-Occurs when the source of the obstruction has
been removed but there is residual scarring and edema of the
renal tubules remains.


A gradual increase in u.o. which signal that GFR has
started to recover. The pt. will have a lot of urine in this
phase-about 4 L in 24 hours. pt. just can’t concentrate
their urine (Increased Specific gravity).



Gradual onset-(2-6 weeks) after the oliguric phase.



Electrolyte losses because they are putting out so much
urine.



Monitor them for dehydration-administer crystalloids
(D5W or NS) to prevent dehydration.



Monitor their BUN and creatinine levels-these will level off
at a lower level and plateau up and plateau down.



GFR will be increased (this increase contributes to the
passive loss of electrolytes which requires the admin of IV
crystalloids), u.o. will be 2-4 L per day, and the

Recovery period phase-This phase can last up to a year.


Edema decreases



Renal tubules begin to function adequately



F&E balance are restored.



GFR has returned to 70% to *0% of normal.

Non-oliguirc phase- May take the place of oliguric phase.


Urine output remains near normal. The pt. still puts out
urine but their kidneys are just not working.







Decreased renal function with increasing nitrogen
retention, yet actually excrete normal amounts of urine.



This occurs predominantly after exposure of the pt. to
nephrotoxic agents.

Prevention ARF


Assess S&S- fever, dehydration, and sustained hypotension.



Always monitor pt’s labs-if there is a decrease in urine-check
specific gravity-the kidney loses the ability to concentrate urine.



Monitor the pt’s fluid status-the best way to monitor this
is taking the pt’s weight!! Also take accurate I&O’s



Nephrotoxic meds- such as gentomyacin and tobimyocin,
immunoglycosides, contrast dyes. Dr. will take baseline BUN and
Creatnine before giving med- will recheck weekly.

Assessment/ Dx of ARF:


History: Ask about voiding (color, clarity, problems, etc).
Surgeries or trauma, blood transfusions, HTN or diabetes, meds
(otc and prescribed), allergies.




**One of the earliest manifestations of tubular damage is
the inability to concentrate urine.



Flat plate of abdomen x-ray

– Renal Scan



Renal ultrasound

– Renal Angiogram



CT and MAG3

– Renal Biopsy

Lab Values


Creatnine (0.6-1.2)- gradual increase over hours



BUN- (10-20)- value may reach as high as 80-100 within one
week



Serum Sodium- pre-renal= low serum Na; intra-renal= high;
post-renal= high or normal serum Na.



Serum Potassium- increased



Serum Phosphorous-increased
**Everything high





Serum Calcium-decreased
except for calcium



Serum Magnesium-increased
gasses**



Arterial Ph-decreased-è metabolic acidosis



arterial bicarbonate-decreased



arterial blood PaCO2-decreased



specific gravity-lower



glomerular damage-protein in urine



glucose in urine-ph of 5 or 6

and

Medications:


Cation Exchange Resins: Kayexalate and Sorbitol

Both can be given PO or rectally as an enema-the pt.
needs to hold onto it as long as possible.



If hemodynamically unstable (low BP, changes in mental
status, and dysrrythmias) – give IV D50, insulin, and
calcium replacements may be administered to shift
potassium back into the cells. They will give pt. 50%
dextrose and insulin IV-this pushes the K back into the
cells.



Vitamins and minerals- Folic acid and iron. Kidneys produce
erythropoietin (hormone that regulates RBC production)-if
kidneys are not producing this-pt. will need iron supp-pt. may be
anemic.



Biological Response Modifiers-Epogen and procrit-both of
these will increase the RBC’s.



Phosphate binders-Amphojel, Renegel and Tums-these meds
are absorbed in the GI tract-they don’t cause diarrhea like K.
They absorb Phosphate-so Ca levels will rise.



Stool softeners/laxatives-Colace and Dulcolax



Diuretics-Lasix-this is given to improve the renal blood flow-if
the pt. is oliguric they should not use it.











Nutrition: No protein- High-carb meals, because carbs have a protein
sparing effect; Restricted potassium and phosphorus


Foods containing potassium: Bananas, avacados, cantaloupe



Foods containing phosphorus: Bran cereal, whole-wheat bread,
almonds, nuts, beans

Nutrition in diuretic phase: High-protein and High-calorie

Chronic Renal Failure (ESRD)- Progressive, irreversible kidney injury where
kidney fxn DOES NOT recover.


body’s ability to maintain metabolic F&E balance fails, resulting in
uremia or azotemia.



Slow progression that it takes years before the pt. will have any S&S.

S/S CRF:


HTN-due to Na and H2O retention /Renin-angiotensin process (fluid
overload)



hyperlipidemia-the body doesn’t metabolize fats as it should



heart failure- because renal failure puts extra work on the heartanemia and fluid overload



pulmonary edema-d/t fluid overload



uremic pericarditis-due to the irritation of the pericardial lining by
uremic toxins-causes severe chest pain, SOB, increased HR, increased
temp, dysrythmias, and friction rub



dermatologic-severe itching and uremic frost-deposit of uremic crystals
on the skin, Skin will be yellow/gray topical color. Decreased skin turgor
and bruising. Give good skin care!!



GI-ulcers, bleeding, anorexia, n/v and hiccups, breath has odor of urine
(uremic halitosis)-if pt, has this may be the result of ineffective dialysis.



Altered LOC, muscle twitching, confusion, seizures, decreased attention
span.



Polyuria or alluric-urine will be dark and straw colored.

Azotemia- the buildup of nitrogenous wastes in the blood



Uremia- excess urea: s/s: metallic taste/ change in taste, itching, muscle
cramps, edema, sob.



*****#1 cause of CRF= diabetes**********


Other causes include HTN, glomerular nephritis, certain meds
over a long time



There has to be 95% damage to the millions of nephrons to be dx with CRF.



Normal GFR is 125 ml/min



Stages in CRF:





Stage 1-GFR > 90 ml/min-normal renal function



Stage 2-GFR 60-89 ml/min- mild decrease in GFR. No build up of waste
but nephrons are still working overtime, may have an increase in BP
which causes an increase in glomerular pressure on healthy nephrons.
There is no S&S of renal failure in this phase.



Stage 3-GFR 30-59 ml/min- moderate decrease in GFR. Will see a build
up of waste- Not enough healthy nephrons to prevent it. There is an
increase in BUN, creatinine, uric acid and phosphorous. An increase
managing fluid volume and an increase in BP and edema. There are
F&E changes. **If the pt. can manage their BP and diet, they can slow
down the progression.



Stage 4-GFR 15-29 ml/min-there is a severe decrease in GFR.



Stage 5-the GFR is less than 15 ml/min. Will see S&S and kidney
failure. ESRF will result from severe F&E imbalances.

Diagnostic findings of CRF:


GFR- The lower the GFR, the more kidney damage is done.



Electrolytes-Na and K-early chronic renal failure-hyponatremic. In the
later stages, pt’s are hypernatremic and K will go up.



Acid-base balance-as nephrons die-acid builds up and the pt. gets
metabolic acidosis.



Hematological-the pt. is anemic because of a decrease in
erythropoietin and RBC







Effects on phosphate:


phosphate retention àhyperphosphatemia.



Binding of phosphate with calcium. This decreases the serum calcium.
The pt. is not making good ca because of low Vitamin D. (High
phosphate levels=low Ca levels.)



The parathyroid gland releases PTH-the parathyroid gland controls the
amount of phosphate excreted. In CRF, the parathyroid gland is not
doing its job. So, the more the body secretes PTH, the more Ca is
released from the bones. So this gives you an increased serum Ca level
which will cause binding of phosphate with calcium and cause
metastatic calcification. With increased serum ca levels-crystals can
lodge in your heart, brain etc., so it puts you at risk for metastatic
calcification(crystal like clots-detrimental to pt’s.)

Effects on calcium




Calcium and phosphorous-these lab values go hand in hand. The
lower the Ca values, the more at risk the pt. is for sucking Ca out of the
bone and increasing the serum Ca

There is a decreased production of vitamin Dà leads to a decreased
absorption of calcium from the GI tractà decreased serum calcium
levelà causes a release of PTH from the parathyroid gland-which
controls the amount of phosphorous excretedà which causes a release
of calcium stored in the bonesà leads to an increased serum calcium
levelà So there is binding of phosphorous with calcium

Meds for CRF ***KNOW***






Calcium and phosphate binders:

**Give both with food**



If calcium is LOW- give Oscal (calcium carbonate) and Phos-lo



If calcium is HIGH – give Renegel

Antihypertensive and CV agents


Lanoxin, Dobutamine, and diuretics



These prevent heart failure and pulmonary edema and control
BP

Antiseizure agents


Valium and Dilantin





Give to patient in ESRF



Watch if patient’s sodium is low

Erythropoietin






Epogen- give 3x a week- SQ or IV

Nutrition with CRF


Protein-restricted; complete proteins only (dairy products, eggs, meats
only)



Fluids – 500-600ml more thank the previous days 24-hour urine output



No potassium



No sodium



Vitamin supplements

Nursing Interventions with CRF


Accurate I&O



daily weight- assess for manifestations of volume excess-assess by pt.
weight. 1 kg of extra weight=1 liter of fluid. Weigh the pt. at the same
time, with the same clothes on the same scale.



fluid restriction-assess the pt. for fluid excess-crackles-they will start at
the base of the lungs. The more fluid the pt. retains the more the
crackles will move up the lung. S/S include restlessness, agitation,
anxious- feels like pt. can’t breathe.



When pt. goes to dialysis hold all meds. Will get meds when they get
back from dialysis..



Meticulous/ preventative skin care- due to uremic frost and itching
(keep nails cut short)



Inspection of vascular access site



Monitoring of v/s- pt’s temp and heart rate will increase after dialysis.



Cardiac monitor- look at T-waves- cardiac issues- biggest cause of
death in pt’s



Assess electrolytes

DIALYSIS


Pt’s go to dialysis 3x/week.



Works by using passive transfer of toxins by diffusion. Some use
anticoagulation (Heparin)- newer machines don’t.



Arteriovenous fistula- the preferred method of permanent access that is
created surgically.





Join an artery to a vein usually an anastomosis between the radial
artery and cephalic vein.



Most of the time, they will start the pt’s off with a fistula.

Arteriovenous graft- Can be created subcutaneously interposing a biologic
(silicone tube) graft material between an artery and vein.








Usually created when the patient’s vessels are not suitable for creation
of a fistula.

Acute dialysis- used for QUICK fluid changes


High potassium

– Increasing acidosis



Fluid overload

– Pericarditis



Pulmonary Edema

– Severe confusion

Chronic or Maintenance dialysis


ESRD
– fluid overload not responsive to
diauretics and fluid restrictions



Presence of uremic S/S affecting all body systems (N/V)



Hyperkalemia

– pericardial friction rub

Hemodialysis- Used to extract toxic nitrogenous substances from the blood
and to remove excess water.


Used for pt’s not responding to tx.



If the K+ is 7 and not responding to tx such as kayexelate and they
can’t get the K+ down, they will start the pt. on dialysis.



If the BUN is too high they will also start dialysis.



If pt. has ARF- this dialysis tx will be short-term







Cath. will be in subclavian or jugular with an inflow/outflow lumen



If pt. only has dialysis 1 or 2 times, will put cath. in femoral artery- not
used longterm d/t risk for infection and kinking.

Peritoneal Dialysis- used to remove toxic substances and metabolic wastes
and to re-establish normal F&E balance.


May be used for pt’s with renal failure who are unable to undergo
hemodialysis or renal x-plant.



Will put dialysate into the abdomen- let it sit and well- then the
drainage tube is unclamped and fluid drains from the peritoneal cavity.
Uses a Tenkoff catheter



Usually takes 36 to 48 hours to achieve what Hemodialysis
accomplishes in 6-8 hours.



High risk for peritonitis- infection comes from insertion site- STERILE
technique is used.



Dialysate is warmed prior to administration to prevent discomfort and
abdominal pain and to dilate the vessels of the peritoneum to decrease
urea clearance.

3 Phases of peritoneal dialysis:


Infusion: 2-3 Liters – takes 5-20 minutes. The docs can add different
things to dialysate (ex: insulin, antibiotics, or dextrose- 4.25à the
higher the dextrose concentration, the more water will be removed.



Dwell- solution sits in the abd. Cavity for 20-30 mins



Drain- should look colorless, pale, straw with a little blood.




Don’t want to see cloudy fluid- Indicates infection **exam**

Two types of peritoneal dialysis:


Continuous ambulatory PD: 5 different exchanges per day.


Can be done at home-it allows more flexibility and remains in
the ab for 4 to 5 hours.



Less extreme fluctuations in the pt’s lab values occur because
dialysis is constantly in progress.



Because of protein loss with CAPD, the pt. needs to eat high
protein, and increase daily fiber to help prevent constipation,

which can impede the flow of dialysate into or out of the
peritoneal cavity.








May be asked to limit their carb intake to avoid excessive wt.
gain. Potassium, sodium, and fluid restrictions are not normally
needed

Continuous cycle PD: This combines overnight intermittent
peritoneal dialysis with a prolonged dwell time during the day


Need a very stable pt. to do this.



The peritoneal cath is connected to a cycler machine every
evening and the pt receives 3 to 5 exchnages during the night.
In the morning the pt. caps off the cath after infusing 2 to 3 L of
fresh dialysate. This dialysate remains in the ab cavity until the
tubing is reattached to the cycler machine at bedtime

Complications of Peritoneal Dialysis:


Peritonitis/ Infection-this is the most common-due to connection
contamination. Characterized by cloudy dialysate, drainage, diffuse
abdominal pain, and rebound tenderness. Can teat this by using
dextrose alone to clear system and then add ATBX if not helping take
out TEEKOFF cath and get rid of catheter.



pain- usually goes away with time. Heat/warm dialysate-wrap in
heating pad and then infuse it.



poor dialysate flow-make sure bag is lower, no kinks or blocks in
tubing. Constipation can also cause this. Have a good bowel regimen
and stool softener. Also have pt. turn from side to side. The catheter
should never be pushed further into the peritoneal cavity.



dialysate leakage-this is common at the beginning of dialysis. 1 to 3
L exchange. Body has a hard time adapting to large amounts of
volume. Leakage can be avoided by using small volumes (500 ml) of
dialysate and then gradually increasing the volume.



Blood tinged drainage is common-if yellow like urine color-pt could
have bladder perforation; if brown-pt could have bowel perforation.

Nursing Interventions during PD


always evaluate baseline v.s., weight and lab values before and after
treating the pt.



continue to monitor the pt for resp distress, pain and discomfort



always monitor prescribed dwell time and initiate outflow



observe the outflow for amount and pattern of fluid.-document I&O,
pt’s response to tx, how long it took the fluid to go in, color that came
out, how much fluid came out.



Want to see more fluid come out than you instill (ex: if you put in 3L- you
want to see 4L come out). Can use a stronger dextrose solution if you need to
pull more fluid off.



Treatment of choice in pt’s with ARF:






Continuous venovenous hemofiltration (CVH)

don’t have arterial access-



only removes fluid – very slowly



is tolerated better by the patient



It is done in the ICU setting. It is used to manage acute renal
failure.



This provides continuous slow fluid removal. Therefore
hemodynamic effects are mild and better tolerated by pt’s with
unstable conditions.

Continuous Venovenous Hemodialysis ***EXAM***


You will see this used in ******UNSTABLE PATIENTS****



It removes fluid and uremic waste.



Blood is pumped from a double-lumen venous catheter through
a hemofilter and returned to the patient through the same
catheter.



In addition to the benefits of filtration, CVVHD uses a
concentration gradient to facilitate the removal of uremic toxins
and fluid. No arterial access is required.

Short term catheters are placed at the bedside and are used for 1-week
because of infection. Veins used are subclavian, internal jugular or femoral
vein.



Perm caths can last longer. There is a notch/cuff which is used for infection.
This helps micro-organisms from entering the wound. Want the notch to be
inside the pt.



Complications of dialysis ***EXAM***





atherosclerotic cardiovascular disease-caused by disturbances of lipid
metabolism



heart failure



coronary artery disease



anginal pain/chest pain-occur in pt’s with anemia or arteriosclerotic
heart disease



stroke



peripheral vascular insufficiency



hypotension-n/v, diaphoresis, tachycardia, dizziness-all S&S of
hypotension



painful muscle cramping-this occurs usually late in dialysis as F&E
rapidly leave the extra-cellular space



exsanguinations- occurs if blood lines separate or dialysis needle
become dislodged



air embolism



****Dialysis disequilibrium-cerebral fluid shifts-this can cause cerebral
edema. S&S include headache, n/v, restlessness, LOC changes
(1st symptom), seizures, and death. Can prevent this by having shorter
dialysis treatment with lower blood volume shifts. Can cause Increased
ICP.

Complications of having a vascular access device, fistula or graft?
***EXAM***


Thrombus- **most common** Due to reduced blood flow- due to the
muscles in the vein thickening up. They will use decreased doses of
TPA to treat.



Infection-usually cause by staph aurus-use sterile technique when
accessing a graft.







Aneurysms-repeated needle sticks can weaken the vein/fistula



Ischemia-this is a rarer complication. There is decreased arterial blood
flow. See diminished pulses, discoloration, cool skin-this can progress
to gangrene if you don’t catch it in time.

Safety measures when a pt. undergoes dialysis


No BP, no blood draws, no IV fluids through fistula



No tight dressings, restraints, or jewelry



Assess bruit or thrill over the site at least every 8 hours-absence may
indicate clot or blockage



Assess site for infection-pts with renal disease are more prone to
infection-they have low WBC counts, low RBC counts, and impaired
platelet function.

Weight is taken before and after dialysis- it’s is a good indication of how
dialysis worked.


Drop in weight and drop in blood pressure is good sign- showed it
worked.



Glomerulonephritis- inflammation of the capillaries of the glomerulus



2 types:


Acute: -see more in children


if severe it can progress to acute renal failure.



Most common cause is strep throat. You see this about 2-3
weeks after the infection.



The kidney becomes large, edematous, and congested.



Can also see this after viral infections but not as common.



S/S: hematuria-blood in urine-coca cola urine, proteinuria-protein
in urine, edema-will see this in orbital area, face and handswatch out for fluid overload and SOB, HTN, Azotemia-this is the
build up of urea and nitrogenous waste



Labs: Decreased GFR, blood and protein in urine, increased BUN
and creatinine, hypoalbumin-pt. losing all protein, urine output

will decrease-may do renal biopsy to make a definitive
diagnosis, anemia may be present




Tx: infection management-treat the pt. with ANTBX-penicillin,
arythromycin, zithromycin-use good hygiene to prevent spread
of this. May also use steroids and immunosuppressants. Prevent
complications with diuretics(get rid of protein-prevent fluid
overload-also helps with HTN and edema); Na, H2O, K and
protein restrictions(pt. needs a diet high in carbs-give energy
and decrease the catabolism (break down) of protein; dialysis
and plasmapheresis(usually if pt. has fluid overload and uremic
symptoms-take off fluid and antibodies if immunosuppressive
component);pt. education-teach diet and nutrition-teach that if
the pt. has a sore throat then he needs to take an ANTBX.

Chronic-This will progress to renal failure.


The cause includes repeated episodes of acute glomerular
nephritis, hypertensive nephrosclerosis (hardening of renal
arteries) hyperlipidemia and other causes of glomerular
damage.



The pt. may be without symptoms for years.



S/S: first symptoms-sudden nose bleed, stroke or seizure,
swollen feet at night, gradual weight loss, decreased strength,
increased irritability, confusion, nocturis-getting up more at
night to go to the bathroom, complain of HA and dizziness, will
look poorly nourished, skin-yellow.grayish color, orbital edema,
s&s of heart (or renal) failure



Labs: decreased urine output, protein and RBC’s in urine,
increased K and phosphorous, decreased GFR, increased BUN
and creatinine, may be anemic because of epotien, metabolic
acidosis, decreased serum calcium



NI’s- slow the progression of the disease, prevent complications
through management of symptoms-if pt has hypertensionreduce BP with sodium and water restrictions, high carbs and
good complete proteins (eggs and dairy products), restrict K and
Na, have pt. limit fluid intake-monitor it along with weight daily,
the pt. may or may not use diuretics as drug therapy. Will be on
anti-HTN meds, dialysis and transplant is needed for the pt. to
survive.



Nephrotic Syndrome: Increased glomerular permeability that allows larger
molecules to pass through the membrane into the urine and be removed from
the blood.


An immune or inflammatory response (ex. Lupus, multiple myloma).



Cluster of findings r/t this syndrome including proteinuria (severe loss
of protein in urine), hypoalbumemia, edema and hyperlipidemia.



Without treatment this will lead to ESRD



S/S: massive proteinuria, hypoalbuminia, lipiduria-protein and lipids in
urine, edema-periorbital and in dependent areas



Tx: use immunosuppressive agents-steroids. ACE inhib and loop
diuretics to decrease proteinuria-takes about 6 weeks to be effective.
Heparin-.this reduces protein in urine and reduces the risk of renal
insufficiency. Diet changes-if the pt. is not hyperkalemic-decrease Na
and increase K in diet. This helps get rid of Na and help edema-use
ONLY if K is not high! The pt. should be on a low protein diet. Mild
diuretics.



Teach Importance of following all medication and dietary regimens so
that their condition can remain stable as long as possible.

Kidney Transplant


Treatment of choice for pt’s with ESRD



Live /related donor-pt. will have good urine output after surgery.




If kidney from cadaver-may take 2 weeks for kidney to wake up. If
kidney does not produce urine output after surgery, pt may need to go
on dialysis until the kidney wakes up.

Make sure pt is free from infection before transplant. Meds are prescribed
after surgery to immunosuppress the pt’s immune system so that transplant
rejection will not occur.
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Pt’s are tx for dental cavities and gingival infections as well (make sure
you look in pt’s mouth).

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It is preferred to avoid dialysis before transplant.

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Meds after transplant:

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Cyclosporine (immunosuppressive agent) are used with other
medications to prevent transplant rejection


Pt’s receiving cyclosporine may not exhibit the ususal signs and
symptoms of acute rejection.



The pt. is closely monitored for infection because of
susceptibility to impaired healing and infection r/t
immunosuppressive therapy and complications of renal failure.

Tacrolimus (Prograf) similar to cyclosporine and about 100 times
more potent. Given in smaller doses than cyclosporine.

Mycophenolate (CellCept)- immunosuppressive. Don’t want to open if
pregnant.

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Sirolimus (Rapamune)



Doses are gradually reduced- but the pt is required to take
immunosuppressives for the rest of their life.



Risks of meds: *nephrotoxicity*, HTN, hyperlipidemia, hirsutism-excessive
hair, tremor, several types of cancer



S/S transplant rejection: fever (one of the first signs), oliguria, edema,
increasing BP, weight gain, swelling or tenderness over the transplanted
kidney



S/S Infection: shaking chills, fever, rapid heartbeat, tachypnea, increase or
decrease in WBC’s-leukocytosis or leucopeniaà need freq. urine cultures.



Chase Urine: ***EXAM*** The pts. will need a lot of IV fluids. Need to adjust
the IV fluids based on what the pt’s urine output is. Check urine output every
1 to 2 hours and follow protocol. Keep the kidney good and hydrated!!!