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 doesnt 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 cant 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 pts labs-if there is a decrease in urine-check

specific gravity-the kidney loses the ability to concentrate urine.

Monitor the pts fluid status-the best way to monitor this

is taking the pts weight!! Also take accurate I&Os

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- 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 RBCs.

Phosphate binders-Amphojel, Renegel and Tums-these meds

are absorbed in the GI tract-they dont 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.

bodys 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 doesnt 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, pts 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 hyperphosphatemia.

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 pts.)

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 D leads to a decreased

absorption of calcium from the GI tract decreased serum calcium
level causes a release of PTH from the parathyroid gland-which
controls the amount of phosphorous excreted which causes a release
of calcium stored in the bones leads to an increased serum calcium
level 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 patients 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. cant 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- pts temp and heart rate will increase after dialysis.

Cardiac monitor- look at T-waves- cardiac issues- biggest cause of

death in pts

Assess electrolytes

DIALYSIS

Pts go to dialysis 3x/week.

Works by using passive transfer of toxins by diffusion. Some use

anticoagulation (Heparin)- newer machines dont.

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 pts 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 patients 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 pts not responding to tx.

If the K+ is 7 and not responding to tx such as kayexelate and they

cant 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 pts 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- 4.25 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.

Dont 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 pts 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,

pts 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 pts with ARF:

Continuous venovenous hemofiltration (CVH)

dont 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 pts 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 pts 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 dont 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- its 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 RBCs in urine,

increased K and phosphorous, decreased GFR, increased BUN
and creatinine, may be anemic because of epotien, metabolic
acidosis, decreased serum calcium

NIs- 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 pts 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 pts immune system so that transplant
rejection will not occur.

Pts are tx for dental cavities and gingival infections as well (make sure
you look in pts mouth).

It is preferred to avoid dialysis before transplant.

Meds after transplant:

Cyclosporine (immunosuppressive agent) are used with other

medications to prevent transplant rejection

Pts 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. Dont want to open if

pregnant.

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 WBCs-leukocytosis or leucopenia 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 pts urine output is. Check urine output every
1 to 2 hours and follow protocol. Keep the kidney good and hydrated!!!