Renal Failure Notes

Oliguria 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:
Reversible- Sudden and almost complete loss of kidney fxn over hours to
days.
Increase in serum creatinine 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.
o increase in BUN and Creatinine that can last hours to days.
o 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.
o Increase in creatinine, BUN, Potassium, and Magnesium.
o Decrease in bicarb and calcium, and GFR.
o F&E abnormalities, and metabolic acidosis.
o Can last from 1-2 weeks.
o 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.
o 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).
o Gradual onset-(2-6 weeks) after the oliguric phase.
o Electrolyte losses because they are putting out so much urine.
o Monitor them for dehydration-administer crystalloids (D5W or NS)
to prevent dehydration.
o Monitor their BUN and creatinine levels-these will level off at a
lower level and plateau up and plateau down.
o 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

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

o Edema decreases
o Renal tubules begin to function adequately
o F&E balance are restored.
o GFR has returned to 70% to *0% of normal.

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

o Urine output remains near normal. The pt. still puts out urine but
their kidneys are just not working.
o Decreased renal function with increasing nitrogen retention, yet
actually excrete normal amounts of urine.
o This occurs predominantly after exposure of the pt. to nephrotoxic
agents.

PREVENTION OF ARF
Assess S&S- fever, dehydration, and sustained hypotension.
o Always monitor pts labs-if there is a decrease in urine-check
specific gravity-the kidney loses the ability to concentrate urine.
o Monitor the pts fluid statusthe 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 * everything high except for calcium and gasses

Creatinine (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
Serum Calciumdecreased

Serum Magnesiumincreased
Arterial pH- decreased- metabolic acidosis
Arterial bicarbonatedecreased
Arterial blood PaCO2-decreased
Specific gravitylower
Glomerular damage protein in urine
Glucose in urinepH of 5 or 6

MEDICATIONS:
Cation Exchange Resins:
o 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 dysrhythmias) 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:

o 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:

o Epogen and procrit-both of these will increase the RBCs.

Phosphate Binders:
o 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
o Colace and Dulcolax

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

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

Foods containing potassium: Bananas, avocados, 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 heart-anemia
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, dysrhythmias, and friction rub

dermatologic-severe itching and uremic frost-deposit of uremic crystals

on the skin, Skin will be yellow/gray topical color.
o Decreased skin turgor and bruising. Give good skin care!!

GI-ulcers, bleeding, anorexia, n/v and hiccups, breath has odor of urine
(uremic halitosis)
o 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
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
o 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
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:

o **Give both with food**
o If calcium is LOW- give Oscal (calcium carbonate) and Phos-lo
o If calcium is HIGH give Renegel

Antihypertensive and CV agents

o Lanoxin, Dobutamine, and diuretics
o These prevent heart failure and pulmonary edema and control BP

Antiseizure agents
o Valium and Dilantin
o Give to patient in ESRF
o Watch if patients sodium is low

Erythropoietin
o Epogen- give 3x a week- SQ or IV

Nutrition with CRF

o Protein-restricted; complete proteins only (dairy products, eggs,
meats only)
o Fluids 500-600ml more thank the previous days 24-hour urine
output
o No potassium
o No sodium
o 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 diuretics 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 long-term 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 exchanges 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)o dont have arterial access

o only removes fluid very slowly
o is tolerated better by the patient
o It is done in the ICU setting. It is used to manage acute renal failure.
o 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 infectionthey 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
o if severe it can progress to acute renal failure.
o Most common cause is strep throat. You see this about 2-3 weeks
after the infection.

o The kidney becomes large, edematous, and congested.

o 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 hands-watch 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 decreasemay 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, skinyellow.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 hypertension-reduce 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:

o Cyclosporine (immunosuppressive agent) are used with other
medications to prevent transplant rejection
o Pts receiving cyclosporine may not exhibit the ususal signs and
symptoms of acute rejection.
o The pt. is closely monitored for infection because of susceptibility to
impaired healing and infection r/t immunosuppressive therapy and
complications of renal failure.
o Tacrolimus (Prograf) similar to cyclosporine and about 100 times
more potent. Given in smaller doses than cyclosporine.
o Mycophenolate (CellCept)- immunosuppressive. Dont want to
open if pregnant.
o Sirolimus (Rapamune)
Doses are gradually reduced- but the pt is required to take
immunosuppressive 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!!!

Drugs-detail

Antibiotics/Antimicrobials
o Must check culture and sensitivity
o If not there, check your drug book and it will tell you the organism it
treats.
o What if it says stop Zosyn, start azithromycin because they started
an antibiotic before the c/s came back to get a jump start.
o Look at WBC and LOOK at the patient and see how they are feeling
from the start of the therapy
o The drug MUST penetrate the tissue that it penetrates
Whats it life, peak etc.
o What else might determine the type of microorganism they have?
HACP
CAP
House? Nursing home? These are TWO completely different
sets of organisms because each region has it own set of inhouse organisms and they all mean something.
When youre taking care of people you want to know if they
were admitted from the nursing home because that give you
a wealth of information.

Cystitis/urethritis
o Cleansing front to back
o Cranberry

o
o

Health of that vaginal tissue, meatus tissue.

Vaginal topical estrogen works for post-menopausal women

S/S relief: Bladder spasm/pain

o AZO PYRIDIUM, PHENAZOPYRIDINE (stain) Analgesic

CAUSATIVE
o UTI

ORGANISMS

STREP GRAM + AND

ENTEROCOCCUS GRAM +
ECOLI GRAM + **** MOST COMMON COMMUNITY
NOT most common in hospital/nursing home
Proteus
GRAM POSITIVE
Cephalosporins ( first generation)
Small amount of fluoroquinolone
How are antibiotics excreted in the urine?
Almost completely unchanged because its coming through
when they come in so theyre good for renal issues. The two
above antibiotics are better because they hang in the
kidneys longer.

Urethritis
o Trichomonas

 metronidazole
DO NOT USE WITH ETOH will act as anabuse
CHLAMYDIA
Doxycycline or Azithromycin
Gonorrhea
Rocephin
Candida
Fluconazole

o
o
o

NITROFURANTOIN AND DOXYCICLINE

o STAY OUT OF SUN

Steven Johnson Syndrome***

FLUROQUINOLONE
o Enter cell through porins; fragment DNA= cell death **
o CLASS EFFECT: QT interval prolongation
Torsade de pointes
V-tach
Dont give to people younger than 18 because of
tendon rupture

 CEPHALOSPORINS
o Beta lactam group
1st generation
sensitivity to penicillins
ACUTE UTI TX
o Cipro first, low dose short term but cant use this with people with
repeated infections
Can try Bactrim (d/s) double strength
UTI GONE BIG PYELONEPHRITIS
o Infection of the renal parenchyma
Organism
Enterobacter, e.coli, enterococcus, pseudomonas
Older people generate a fever due to pyelonephritis
If you cant treat it can cause urosepis
Can cause pneumonia and pneumonia can cause
pyelonephritis
High WBCeven if UTI is the issue, still Going to do
CXR
If they look sick, fever, etc probably go to hospital
o Aminoglycosides
GRAM
GENTAMYCIN shot IM at office
Fluoroquinolone follow up with this for 7 days

Nephrosclerosis control of HTN for tx

NEPHROTIC SYNDROME
Immune response, need immunosuppressant
Take with food, absorbed through skin
Takes special prep/gloves IMURAN
Why do we use it? It suppresses the body attacking renal
function
Some people are on this drug for a long time, used for
renal transplant to knock down immune system to
keep patient from rejecting
REPLACE PROTEIN BECAUSE OF HYPOALBUMENIA
( you will see edema)
If GFR is low, cant give too much
Give heparin because they are hyper-coag
Why give them an ACE Inhibitor
To suppress aldosterone
Why lipid lowering?
Hyperlipidemia
Diuretic
Lasix
Metolazone
o Probably most powerful diuretic

 UROLITHIASIS
o Treat:
PAIN, OBSTRUCTION, INFECTION
The type of stone determines treatment approach
Struvite common in women
Calcium oxalate
o Cholestyramine
Uric acid stonewith gout
o Allopurinol
Inhibits purine production
Cysteine stones
o Captopril
GRANDPA OF ALL ACE INHIBITOR
FIRST EVER

US or CT
What is it that you are looking for?
Obstruction
o What happens?
HYDRONEPHROSIS

Post-OP

PREVENT HEMORRHAGE
Prevent infection

GLOMERULONEPHRITIS
o INFECTION STREPT**
Tx ORGANISM with Antibiotics
Beta Lactam: What is the purpose
*LOOK AT DRUG LIST
macrolides and flouroquinolones QT INTERVAL WIDENED
Gram + ATYPICAL
AtypicalMYCOPLASMA PNEUMONEA
o Hydralazine
DIRECT ARTERIAL DILATOR
S/E: LUPUS

Look for topic

o Anticholinergic
Blocks acetylcholine
Constipation, dry mouth
Who would you not want to give this to?
****
Glaucoma?

Paroxentin paxil increase level

Paroxin decrease

AKI and CKD

o Hyperkalemia > 5.3 mEq/L
o Tx:
Minoxidil
o Hypertrichosis
o Vasodialate
o Rogain

CKD

Why give them Epogen?responds to o2 levels, H/H, Rbc, VD

o Preventing issues

Epogen
o HTN, HA- adjust to HTN patient
o Increase with CV problems in patients with kidney disease

Ferric gluconate
Contraindations
o Generic blood disorders