Assessment of the Client

History

1. Has there been renal disease in the past?

2. Is there a family history of renal disease?
3. Age: developmental issues; incontinence and prostatic problems
4. Gender: incontinence increased in women; benign prostate hypertrophy
(BPH): older men

Manifestations

1. Pain (usually in acute conditions): flank radiating to upper thigh, testis, or

labium
2. Changes in voiding: hematuria, proteinuria, dysuria, frequency, urgency,
burning, nocturia, incontinence, polyuria, oliguria, anuria
3. Thirst, fatigue, edema (generalized)

Diagnostic Tests

A. Urinalysis
1. Specific gravity: 1.010-1.030
2. Color: yellow/amber
3. Negative glucose, protein, red blood cells and white blood cells
4. pH: 5-8
5. First voided morning sample preferred; 15 ml
6. Send to lab immediately or refrigerate
7. If clean catch, get urine for culture prior to starting antibiotics
a. Cleanse labia, glans penis
b. Obtain midstream sample

B. Renal Function Test

1. BUN (blood urea nitrogen): 10-20 mg/100 ml
2. Serum creatinine: 0-1 mg/dl
3. Creatinine clearance: 100-120 ml/minute; collect 24 hour urine
(refrigerate); blood drawn at start (measures glomerular filtration
rate)
4. Uric acid (serum): 3.5-7.8 mg/dl
5. Uric acid (urine): 250-750 mg/24 hour; 24 hour urine
6. Prostate-specific antigen (PSA): 0.85 ng/ml
C. Radiological Test
1. KUB (x-ray): shows size, shape and position of kidneys, ureters,
bladder; no preparation
2. Intravenous pyelography (IVP): visualization of urinary tract
a. Nursing Interventions
1. Obtain consent
2. Keep client NPO for 8-10 hours
3. Administer laxatives to clear bowel
4. Restrict fluids
5. Check for allergies to iodine or shellfish
6. Inform client that flushing, warmth, nausea, salty
taste may accompany injection of dye
7. Have emergency equipment available during
procedure
8. Push fluids after procedure to flush out dye

3. Renal angiography: visualization of renal arterial supply; contrast

material injected through a catheter
a. Nursing Interventions: Same as IVP plus
1. Shave proposed injection sites: groin or ankle
2. Locate and mark peripheral pulses
3. Have client void before procedure
4. Teach client: procedure takes ½ hour to 2 hour;
client will feel heat along vessel
b. Nursing Interventions (post procedure)
1. Maintain bed rest 4-12 hrs
2. Monitor vital signs until stable
3. Apply cold compresses to puncture site
4. Observe for swelling and hematoma
5. Palpate peripheral pulses/vascular checks
6. Monitor urinary output

D. Cystoscopy
1. Diagnostic uses: inspect bladder and urethra; insert catheters
into ureters; see configuration and position of urethral orifices
 2. Treatment uses: remove calculi from urethra, bladder and ureter;
treat lesions of bladder, urethra, prostate
3. Nursing Interventions (general preop care)
a. Maintain NPO if general anesthesia; liquids if local
anesthesia
b. Administer preop cathartics/enemas
c. Teach client deep breathing exercises to relieve bladder
spasms
d. Monitor for postural hypotension
e. Inform client that pink-tinged or tea-colored urine is
common following the procedure; bright red urine or clots
should be reported to physician
f. Inform client that post-procedural pain may be present
1. Leg cramps due to lithotomy position
2. Back pain and/or abdominal pain
3. Warm sitz baths comforting
g. Push fluids/analgesics
h. Monitor intake and output; make sure no obstruction

E. Needle Biopsy of Kidney

1. Nursing Interventions (pre-biopsy)
a. Obtain bleeding, clotting and prothrombin times
b. Obtain results of pre-biopsy x-rays of kidney, IVP
c. Inform pregnant client that ultrasound may be used
d. Keep client NPO 6-8 hours
e. Position client prone with pillow under abdomen,
shoulders on bed

2. Nursing Interventions (post-biopsy)

a. Keep client supine, bed rest for 24 hours
b. Monitor vital signs q 5-15 minutes for 4 hours, then
decrease if stable
c. Maintain pressure to puncture site 20 minutes
d. Observe for pain, nausea, vomiting, BP changes
e. Push fluids to 3,000 cc
f. Assess HCT and Hgb 8 hours after procedure
g. Measure output
h. Educate client to avoid strenuous activity, sports, and
heavy lifting for at least 2 weeks
Specific Disorders

A. Cystitis
1. Definition: inflammation of the urinary bladder
2. Etiology: ascending infection after entry via the urinary meatus;
acute infections usually E. coli
a. More common in females
b. Benign prostate hypertrophy in men

3. Manifestations
a. Frequency and urgency
b. Dysuria
c. Suprapubic tenderness; pain in region of bladder or flank
pain
d. Hematuria
e. Fever/malaise/chills
f. Cloudy, foul-smelling urine

4. Nursing Interventions
a. Obtain urine for culture and sensitivity (before initiating
antibiotic therapy)
b. Give antimicrobial medications - sulfonamides are the
drugs of choice unless allergic; for example co-
trimoxazole, sulfamethoxazole-trimethoprim (Bactrim) and
nitrofurantoin microcrystal (Macrodantin)
c. Maintain acidic urine pH
d. Force fluids (greater than 3,000 cc per day)
e. Give analgesics - phenazopyridine (Pyridium)
f. Apply heat to perineum
g. Teach client: good perineal care, cotton underwear, avoid
bubble baths, high fluid intake

B. Glomerulonephritis
1. Definition: inflammatory disease involving the renal glomeruli of
both kidneys; thought to be an antigen-antibody reaction that
 damages the glomeruli of the kidney (usually in children); good
prognosis if treated
2. Etiology: group A beta-hemolytic streptococcal infection; usually
a history of pharyngitis or tonsillitis 2-3 weeks prior to
manifestations

3. Manifestations
a. Hematuria, proteinuria fever, chills, weakness, pallor,
nausea, vomiting
b. Edema (especially facial and periorbital/ascites)
c. Oliguria or anuria
d. Hypertension
e. Headache
f. Increased blood urea nitrogen (BUN); elevated BUN is
azotemia
g. Flank pain/abdominal pain
h. Anemia

4. Nursing Interventions
a. Goal: protect kidney; recognize and treat infection
b. Maintain bed rest
c. Administer penicillin for streptococcal infection
(substitute other antibiotics for clients with penicillin
allergy)
d. Reduce dietary protein and sodium; increase calories
e. Restrict fluids

C. Nephrotic Syndrome
1. Definition; clinical disorder associated with protein-wasting
secondary to diffuse glomerular damage
2. Etiology; unknown: kidneys become more permeable to protein
 3. Manifestations
a. Insidious onset of pitting edema (generalized edema is
anasarca)
b. Proteinura; hypoalbuminemia and hyperlipidemia
c. Anemia
d. Anorexia and Malaise
e. Nausea
f. Oliguria
g. Ascites

4. Nursing Interventions
a. Goal: preserve renal function
b. Maintain bed rest (during severe edema only)
c. Maintain low-sodium, low potassium, moderate-protein,
high calorie diet
d. Protect client from infection
e. Monitor intake and output
f. Weigh client daily
g. Measure abdominal girth

5. Drug Therapy
a. Loop diuretics: furosemide (Lasix)
b. Steroids: prednisone (Deltasone)
c. Immunosuppresive agents: cyclophosphamide (Cytoxan)

D. Urolithiasis
1. Definition: stones in the urinary system
2. Etiology
a. Obstruction and urinary stasis
b. Proteus infection
c. Dehydration
d. Immobilization
e. Hypercalcemia
f. More common in men 30-50
g. Tends to recur
 h. Most stones are calcium or magnesium with phosphate or
oxalate, although type of stone is commonly based on
alkalinity or acidity of urine

3. Manifestations
a. Pain: severe renal colic (ureter); dull, aching (kidney);
radiates to the groin
b. Nausea, vomiting, diarrhea, or constipation
c. Hematuria
d. Manifestations of urinary tract infection

4. Nursing Interventions
a. Goals: to eradicate the stone, determine stone type and
prevent nephron destruction
b. Force fluids: at least 3,000 cc/day (IV or PO)
c. Strain all urine
d. Give drugs as ordered (depends on type of stone)
e. Maintain proper urine pH (depends on stone type):
f. Implement diet therapy if stone type is known (see
Appendix B: Therapeutic Diets)
1. Antibiotics
2. Lithotripsy (crush stone through sound waves)
a. No surgery required but pain occurs
because of shock waves
b. Measure intake and output and strain all
urine post-procedure

E. Acute Renal Failure

1. Definition: abrupt reversible cessation of renal function; may be
result of trauma, allergic reactions, kidney stones
2. Etiology: any condition that obstructs renal blood flow
a. Pre-renal: hemorrhage, dehydration, burns, anaphylaxis,
pulmonary emboli
b. Renal: acute tubular necrosis, trauma, hypokaliemia,
transfusion reaction
c. Post-renal: BPH, tumors, strictures, calculi, infection
 d. Hemolytic uremic syndrome (HUS): acute renal failure
following an acute gastroenteritis with bloody diarrhea;
usually related to ingestion of undercooked beef;
causative organism is E.coli O.57

3. Manifestations
a. Oliguric phase (8th-14th day): sudden onset, less than 400
cc/24 hours, edema, elevated BUN, creatinine and
potassium; decreased specific gravity
b. Period of diuresis (14th-24th day): dilute urine, 1,000
cc/24 hours, BUN and creatinine rise in early stage;
decrease in specific gravity
1. Recovery period: up to one year
2. Fluid and electrolyte imbalances

4. Nursing Interventions
a. Treat, eliminate or prevent cause
b. Prevent acidosis by maintaining fluid and electrolyte
balance
c. Monitor and treat increased potassium level
1. Kayexalate (an ion exchange resin given orally or
by enema)
2. IV glucose and insulin or calcium carbonate (causes
K+ to enter cells)
d. Implement diet
1. Oliguric phase: low-protein, high-carbohydrate,
restrict K+ intake to reverse glucogenesis
2. Diuresis phase: low-protein, high-calorie, restrict
fluids as indicated
e. Administer phosphate binding gels to increase calcium
levels; aluminum hydroxide (Amphojel)
f. Prevent infection
g. Weigh client daily
h. Monitor intake and output; replacement is usually based
on previous output
F. Chronic Renal Failure
1. Definition: a slower or progressive failure of the kidneys to
function that results in death unless hemodialysis or transplant is
performed; irreversible
2. Etiology
a. Chronic glomerulonephritis
b. Pyelonephritis
c. Uncontrolled hypertension
d. Diabetes mellitus
e. Congenital kidney disease
f. Renal vascular disease

3. Stages of renal failure

a. Diminished renal reserve (creatinine 1.6-2.0)
b. Renal insufficiency (creatinine 2.1-5.0)
c. Renal failure (creatinine >8.0)
d. Uremia: end stage (creatinine > 12.0)

4. Manifestations
a. Fatigue
b. Headache
c. Nausea, vomiting, diarrhea
d. Hypertension
e. Irritability
f. Convulsions/coma
g. Anemia
h. Edema
i. Hypocalcemia/hyperkalemia
j. Pruritus, uremic frost
k. Pallid, gray-yellow complexion
l. Metabolic acidosis/elevated BUN and creatinine

5. Nursing Interventions
a. Goal: help the kidneys maintain homeostasis
b. Maintain bed rest
 c. Implement renal diet: low-protein, low-potassium, high-
carbohydrate, vitamin and calcium supplements, low-
sodium, low-phosphate
d. Treat hypertension/give diuretics
e. Maintain strict I & O; fluid replacement: 500-600 cc more
than 24-hour urine output
f. Monitor electrolytes
g. Administer aluminum hydroxide gel (Amphojel); binds
phosphate to increase calcium
h. Do not administer any magnesium or phosphorus (for
example: M.O.M., Fleets Phospho-Soda)
i. Maintain dialysis
j. Administer diuretics
k. Provide skin care (collects kidney wastes)
l. Provide emotional support to client and family
m. Assess for and prevent bleeding tendencies
n. Evaluate need for Kayexalate orally to keep potassium
levels down
o. Care for anemia: administer epoetin alfa, erythropoietin
(Epogen) to stimulate red blood cell formation and
transfuse as necessary

Dialysis

1. Hemodialysis
a. Definition: process of cleansing the blood of accumulated waste
products; used for end-stage renal failure and those clients who
are acutely ill and require short-term treatment; uses diffusion,
osmosis, and filtration
b. Nursing Interventions
1. Weigh client before and after procedure
2. Monitor client continuously during procedure; BP may
"bottom out"
3. Provide care to access site to prevent clotting and
infection
4. Assess bruit and thrill; feel for patency
5. Provide adequate nutrition
6. Monitor for hypotension
7. Maintain fluid restrictions
8. Withhold regular morning medications prior to dialysis
9. Observe for psychological and physiological complications
 c. Goals
a. Remove end products of metabolism (urea and creatinine)
from the blood
b. Maintain a safe concentration of the serum electrolytes
c. Correction of acidosis and restoration of blood buffer
system
d. Removal of excess fluid from the blood

2. Peritoneal Dialysis
a. Definition: substitute for kidney function during failure that uses
the peritoneum as a dialyzing membrane; usually short term;
peritoneal catheter inserted by physician
b. Nursing Interventions
1. Have client void (if applicable) prior to procedure
2. Weigh client daily
3. Monitor vital signs, baseline electrolytes
4. Maintain asepsis
5. Keep accurate record of fluid balance
6. Procedure
a. Warm dialysate (1-2 liters of 1.5%, 2.5%, or 4.25%
glucose solution)
b. Allow to flow in by gravity
c. 5-10 minutes inflow time; close clamp immediately
d. 30 minutes of equilibration (dwell time)
e. 10-30 minutes of drainage (clear yellow)
7. Continue for 24-48 exchanges
8. Monitor for complications: peritonitis, bleeding,
respiratory difficulty, abdominal pain; bowel, or bladder
perforation

3. Continuous Ambulatory Peritoneal Dialysis

a. Definition: dialyzing method involving almost continuous
peritoneal contact with a dialysis solution for clients with end-
stage renal disease
b. Procedure (slightly different from peritoneal dialysis)
1. Permanent indwelling catheter into peritoneum
 2. Fluid infused by gravity (1.5-3 liters)
3. Dwell time: 4-10 hours
4. Dialysate drains by gravity: 20-40 minutes
5. Four to five exchanges daily, 3-7 days a week

c.
Advantages
1. More independence
2. Free dietary intake; better nutrition
3. Easy to use
4. Satisfactory control of uremia
5. Least expensive dialysis
6. Decreased likelihood of transplant rejection
7. Closely approximates normal renal function

Urinary Tract Surgery

1. Kidney Transplant
a. Indicated for individual with irreversible end-stage renal disease
b. Requires well-matched donor
1. Living donors: best donors are twin or family member
2. Cadaver donors
c. Preoperative management
1. Regain normal metabolic state
2. Tissue typing
3. Immunosuppressive therapy
4. Hemodialysis within 24 hours
5. Teaching and emotional support

2.
Urinary Diversion: remove bladder and transplant ureters into a pouch
under the abdominal skin; can be either continent or incontinent; care is
of a stoma plus general interventions
a. Nursing Interventions
1. Monitor vital signs (hemorrhage and shock are frequent
complications)
2. Provide pain control
3. Be alert for manifestations of paralytic ileus (very common)
4. Provide adequate fluid replacement
5. Weigh client daily
6. Maintain function and patency of drainage tubes
a. Indwelling catheter (dependent position, tape
tubing to thigh)
b. Nephrostomy tube
1. Never clamp
2. Irrigate only with order of 10 cc normal
saline
 3. Assess for leakage of urine
c. Ureteral catheters
1. Each one drains½ of the urinary system so
expect only ½ of the urinary output from
each one
2. Bloody drainage expected after surgery but
should clear
3. Never irrigate
4. Surgical implant; make sure secure
5. Aseptic technique required

Benign Prostatic Hyperplasia (BPH)

1. Definition: enlargement of the prostate

2. Etiology: unknown, usually accompanies aging process in the male
3. Manifestations
a. Difficulty starting stream/dribbling
b. Urinary tract infection
c. Nocturia; hematuria
d. Decrease in size and force of urinary stream
e. Differentiate from adenocarcinoma of the prostate with PSA test

When it comes to maintaining homeostasis, the kidneys may be the body's

most important organs. That's why kidney (or renal) failure so easily upsets the
body's chemical balance, sometimes with deadly consequences.
As you know, renal failure can be temporary or permanent. It occurs when
kidney structures are damaged by:

 A congenital disorder,
 An acute or chronic condition, such as cardiogenic shock or hypertension, or
 A nephrotoxic substance, such as an antibiotic

Now let's see how that knowledge applies to your patient who's receiving an antibiotic for
cellulitis.
As you review his laboratory test results, you notice that his blood urea
nitrogen and creatinine levels have increased dramatically. And when checking
his current drug list, you think that the aminoglycoside gentamicin may be the
cause.
But are you confident that you can spot the factors that place your patient at
risk for renal failure? Do you know how the disorder produces its signs,
symptoms, and complications? And can you tell what effects your
interventions are likely to have?
This video will answer all these questions. It will:

 Clearly explain the pathophysiology of acute and chronic renal failure,

 Show you how to identify the disorders, and
 Demonstrate ways to treat them and prevent their complications

Acute renal failure occurs when a disorder or nephrotoxic substance damages the kidneys
or interferes with kidney function. To understand renal failure, first remember how the
kidneys normally function.
The kidneys flank the spine in the lumbar area. Each one contains millions of
urine-producing units called nephrons. Each nephron contains a glomerulus, its
main filter, and a tubular system composed of proximal and distal convoluted
tubules and the loop of Henle. This U-shaped tubule, which has descending
and ascending limbs, concentrates urine. From the blood, nephrons filter
water, electrolytes, such as potassium and sodium, and toxins, such as urea.
Then they excrete these substances as urine.
Here's how the process works.
Through the renal arteries and their branches, the kidneys receive about one-
and-a-quarter liters of blood from the heart every minute. From the renal
arteries, the afferent arterioles carry unfiltered blood to the glomerular
capillaries, where it's filtered.  Then, it moves through the efferent arterioles
into the peritubular capillaries.

After urine is formed through glomerular filtration and tubular reabsorption

and secretion, it enters the collecting tubule. Eventually, urine moves to the
ureters. These muscular tubes transport urine to the bladder, where it's stored
until it's expelled through the urethra during urination.
Acute renal failure may be:

 Prerenal,
 Intrarenal, or
 Postrenal

Each type of renal failure is produced by a problem in a different part of the

renal system.

In prerenal failure, blood flow to the kidneys is reduced or interrupted. This

typically occurs when cardiac output falls below normal, such as in heart
failure. When blood flow is reduced, the kidneys try to compensate by
releasing renin.
This hormone triggers:

 The conversion of angiotensin I to angiotensin II in the lungs and kidneys, and

  The secretion of aldosterone from the adrenal cortex

Together, these substances constrict the arteries and raise intravascular volume, which
raises the blood pressure and improves blood flow to the kidneys. However, if this
compensation isn't sufficient, blood flow to the kidneys eventually decreases and may
cause ischemia.
When blood flow is decreased, the glomeruli can't filter blood efficiently,
which reduces the glomerular filtration rate (or GFR). When the GFR drops,
creatinine, urea, and other toxins build up in the blood, causing azotemia. In
the tubular system, ischemia damages the epithelial lining, causing it to slough
off in a syndrome known as acute tubular necrosis (or ATN).

In intrarenal failure, the tubules and other renal structures are damaged
directly, which often results in ATN. The damage may be caused by a disorder,
such as:

 Glomerulonephritis, or
 A nephrotoxic substance

These substances include:

 Antibiotics,
 Immunosuppressants,
 Heavy metals, and
 Contrast media

In this patient with ATN, the aminoglycoside gentamicin uniformly damaged

the epithelial layer of the proximal tubule in the loop of Henle. Then the
damaged epithelium let the filtered toxins (or filtrate) leak back into the blood,
causing azotemia.

In postrenal failure, urine flow from the kidneys is obstructed in the ureters,
bladder, or urethra.
Typically, this form of renal failure results from:

 Renal calculi,
 Blood clots,
 Tumors, or
 An enlarged prostate gland

The obstruction causes pressure to build behind it, which raises the pressure in
the glomeruli. This leads to glomerular dysfunction, reducing the GFR and
causing azotemia.
If you suspect acute renal failure, work quickly to assess your patient so you
can pinpoint its cause and begin treatment. Your assessment findings may vary
with the phase of acute renal failure.
If your patients in the oliguric phase, expect his urine output to fall sharply.
Normally, urine output exceeds 30 milliliters per hour. In the oliguric phase it
drops to about 15 milliliters per hour. This decreased urine output usually
occurs one to seven days after the causative event.
If the patient has severe tubular injury, he may develop anuria, with a urine
output of less than 50 milliliters in 24 hours. Urine output can fall because less
blood circulates to the kidneys to be filtered. Or it can fall because damaged
tubular epithelial cells collect and obstruct the tubules.

When your patient's urine output is low, look for signs of intravascular fluid
overload. First, measure his blood pressure, which may be high. Next, look for
signs of heart failure caused by fluid overload. These signs include:

 An S3 heart sound,
 Pulmonary crackles, and
 Jugular vein distention

Also assess for peripheral and central edema. They develop when intravascular
fluid leaks into the interstitial space.

Now observe your patient's breathing. He may have Kussmaul's respirations,

which are rapid, deep breaths caused by metabolic acidosis.
This complication occurs because the damaged tubular epithelial cells lose
their ability to synthesize ammonia (or NH3). Normally, ammonia combines
with hydrogen ions to form ammonium (or NH4), which is excreted in the urine.
By promoting hydrogen ion excretion, ammonia helps maintain a normal blood
pH.
Without ammonia, hydrogen ions accumulate in the blood, lowering the pH. At
first, bicarbonate (or HCO3) maintains a normal pH by combining with the
hydrogen to form carbonic acid (or H2CO3). Then carbonic acid breaks down
into carbon dioxide (or CO2) and water (or H2O).

Eventually, the bicarbonate supply is exhausted, and the damaged tubules

prevent the formation of new bicarbonate. These results in hydrogen ion
buildup and acidosis, to raise the pH, the body must remove more acid. So it
tries to exhale extra carbon dioxide, which is a weak acid. And this produces
the characteristic Kussmaul's respirations.
Next assess for neurologic effects, such as lethargy or confusion. These
findings may occur, when unexcreted urea and creatinine build up in the blood
and produce toxic effects on the central nervous system.

If your patient's in the diuretic phase of acute renal failure, you're likely to see
his urine output exceed 400 milliliters per hour. In this phase, urine output
increases because the glomeruli filter the blood, but the tubules can't
concentrate the urine. Urine output also rises because of osmotic diuresis,
which is caused by a high blood urea nitrogen (or BUN) level.
Because diuresis characterizes this phase, assess for signs of fluid and
electrolyte depletion. For example, check for dry skin and mucous membranes
and for arrhythmias.
Arrhythmias may result from an electrolyte imbalance, such as hypokalemia.

In the diuretic phase, large amounts of potassium and sodium are excreted in
the urine. So hypokalemia and hyponatremia are especially likely to occur. And
these electrolyte imbalances may trigger abnormal automaticity, causing an
arrhythmia.
If your patient's in the recovery phase expect his urine output to gradually
return to normal. This phase reflects tubule healing. It usually begins three to
four weeks after the injury and can last for six months to a year.

After assessing your patient, prepare him for diagnostic tests as ordered. First,
obtain blood samples and urine specimens for testing. When the test results
are ready, review them closely.
In the oliguric phase of acute renal failure caused by ATN, expect to find:

 A blood sodium level below 135 milliequivalents per liter, indicating hyponatremia,
 A blood potassium level above 4.5 milliequivalent per liter, indicating
hyperkalemia,
 A BUN level above 20 milligrams per deciliter, and
 A creatinine level above 1.2 milligrams per deciliter, indicating azotemia

In the diuretic phase, watch for the blood potassium level to fall as potassium is excreted
in the urine.
Expect urine tests to reveal:

 Low osmolality of dilute urine, indicating the tubules' inability to concentrate

urine,
 An elevated sodium level, reflecting sodium loss in urine, and
 Sediment that contains red blood cells and casts, reflecting blood cell leakage
through damaged glomeruli and tubules

Also, anticipate finding protein in the urine. Proteinuria occurs when damaged
glomerular capillaries let large protein molecules pass through to the urine.
If the cause of renal failure is unknown, prepare your patient for other tests,
such as a renal scan.
During a renal scan, a radioisotope is injected into the blood. Then the kidneys
are visualized through a scanner. A renal scan may show:

 Abnormal kidney structures, which may occur in renal infarction,

 Abnormal perfusion, which may occur in renal artery atherosclerosis, or

 Abnormal excretory function, which may occur in ATN

After acute renal failure is confirmed, provide treatment based on its cause. For a patient
like this one, immediately discontinue the nephrotoxic drug gentamicin, as prescribed.
And expect to replace it with a less nephrotoxic antibiotic, such as ceftazidime.
If prescribed, administer a loop diuretic, such as furosemide. Loop diuretics
increase water and sodium excretion, which helps relieve intravascular fluid
overload.
Also anticipate administering a low dose of intravenous dopamine. This drug
dilates the renal arteries, which increases blood flow to the kidneys. If your
patient has fluid overload and hyperkalemia, you may arrange for hemodialysis.
In hemodialysis, blood is filtered through a dialyzer, which contains a
semipermeable membrane. The membrane lets substances (such as urea,
creatinine, potassium, and phosphate) diffuse through so they can be removed
from the blood.

Now suppose you're caring for this patient. She developed chronic renal failure
because her hypertension was undiagnosed, and untreated. Chronic renal
failure results from progressive, irreversible loss of kidney function. It has
several causes.
It can be produced by any disorder that permanently damages part of the
nephrons, such as hypertension, diabetes mellitus, or glomerulonephritis. For
this patient with hypertension, chronic renal failure probably resulted from the
sustained elevation of systemic arterial pressure.
This high blood pressure raises the pressure in the glomerular capillaries and
increases blood flow through the glomeruli. Over time, the increased blood
pressure and blood volume cause inflammation and fibrosis in one or more
glomeruli. Because these damaged glomeruli can't filter urea and other toxins,
the remaining nephrons must work harder to filter blood. Then these
overworked nephrons enlarge and eventually fail.

In most cases, renal function declines gradually. Generally, the GFR is

unaffected until more than 75 percent of the nephrons are damaged. When
only 25 percent of the nephrons are functioning, the patient has renal
insufficiency. At this stage, the BUN and creatinine levels begin to rise above
normal.
As renal failure progresses, the BUN level rises, producing uremic symptoms,
such as weakness and nausea. When only ten percent of the nephrons are
functioning, end-stage renal failure occurs.

If you're caring for a patient with chronic renal failure, be sure to perform a
complete and accurate assessment because this disorder can affect most body
systems and cause many complications. First, observe for a decreased level of
consciousness or alertness, which may reflect a neurologic complication.
In chronic renal failure, uremic toxin buildup depresses the central nervous
system, producing such symptoms as lethargy, weakness, and confusion. Now
measure your patient's blood pressure. Expect the reading to be higher than
normal. Because chronic renal failure causes sodium and water retention, it
increases the blood volume and leads to fluid overload. This, in turn, raises the
pressure on the arterial walls, and the blood pressure.
Chronic renal failure also increases blood pressure by activating the renin-
angiotensin-aldosterone system. This system triggers vasoconstriction and
sodium and water retention, which raises the blood pressure.
Next, evaluate the patient's respiratory rate, depth, and effort. Be alert for
Kussmaul's respirations, which are caused by metabolic acidosis. Also look for
labored respirations. These respirations develop when fluid overload and
hypoalbuminemia lead to fluid collection in the lungs.
When the glomerular capillaries are damaged, albumin and other plasma
proteins can pass through them and be excreted in the urine. This lowers the
blood albumin level. With less albumin in the blood, the intravascular oncotic
pressure falls below the interstitial oncotic pressure. This forces fluid into the
interstitial spaces, such as the alveoli and pleura.
So listen for pulmonary crackles, which are created by air moving through
fluid-filled alveoli. If fluid accumulates in the pleura, you may hear diminished
breath sounds caused by pleural effusion.

You may also note a pleural friction rub, which is a coarse squeaking or grating
sound that occurs late in inspiration or early in expiration. This adventitious
breath sound occurs when fluid with uremic toxins accumulates in the pleura.
These toxins inflame the lungs' visceral and parietal pleura. When the inflamed
pleural surfaces rub together during respiration, the characteristic rubbing
sound occurs.
Uremic toxins can also inflame the heart's pericardial layers, resulting in
pericarditis. If you suspect pericarditis, listen for a two or three component
pericardial friction rub. This rub is heard when the inflamed pericardial
surfaces slide over each other.
Next, assess your patient's skin. You're likely to detect pruritus, which occurs
when chronic uremia damages the cutaneous nerve endings. This causes
intense itching. You may also see uremic frost, a white crystal-like coating on
the skin. Uremic frost occurs when urea and other metabolic wastes pass
through capillary walls and are deposited on the skin with perspiration.

You may observe pallor caused by anemia. This disorder commonly occurs
because chronic renal failure reduces the production of erythropoietin, which
is formed in the kidneys' peritubular interstitial cells.
Normally, erythropoietin stimulates and regulates red cell production in the
blood. In chronic renal failure, the kidneys lose their ability to produce
erythropoietin. So red blood cell production declines. What's more, uremic
toxins in the blood decrease the red blood cells life span, causing them to die
sooner than normal.

Because uremic toxins can also inflame the gastrointestinal mucosa, assess for
signs of GI complications. To do this, ask about:

 Anorexia,
 Nausea, and
 Vomiting

Also inspect the oral mucosa for ulcerations, which occur when inflammation
progresses to erosion.

After examining your patient, prepare her for diagnostic tests. When the
results are available, review them closely. For your patient with chronic renal
failure, blood tests are likely to reveal high levels of uremic toxins, such as
BUN and creatinine. They also may show severe electrolyte imbalances,
including:

 Hyperkalemia,
 Hyperphosphatemia, and
 Hypermagnesemia

These imbalances occur because the kidneys can't excrete potassium, phosphate, and
magnesium in the urine. Surprisingly, test results may point to:

 Hypocalcemia, and
 Hyponatremia
Hypocalcemia occurs because the kidneys can't activate vitamin D. Normally, the GI tract
requires activated vitamin D for calcium absorption. Hyponatremia occurs because the
blood retains sodium, which attracts water. The extra water dilutes the blood, producing a
false-low blood sodium level, known as dilutional hyponatremia.
Also look for the complete blood count (or CBC) to show a low red blood cell
count, hemoglobin level, and hematocrit. These test results reflect reduced
erythropoietin production and red blood cell damage by uremic toxins.
If your patient undergoes arterial blood gas analysis, expect to find low blood
pH and bicarbonate levels. These abnormal levels are caused by the kidneys'
inability to secrete hydrogen ions and by insufficient bicarbonate reabsorption
and production in the body.

In a patient with chronic renal failure, urinalysis may detect:

 Protein,
 Casts,
 Red blood cells, and
 Low-to-normal specific gravity

To identify the cause of your patient's renal failure, she may undergo a renal biopsy. In
this procedure, the physician inserts a needle into the kidney to remove a small piece of
tissue for analysis. The renal biopsy may reveal characteristic tissue changes that confirm
the underlying disorder, such as systemic lupus erythematosus or amyloidosis.

After chronic renal failure is confirmed, begin your patient's treatment which usually starts
with dietary changes.
Expect to provide a diet that's low in:

 Protein,
 Potassium,
 Sodium, and
 Phosphorus

Also plan to restrict your patient's fluid intake to about 500 milliliters more
than her daily urine output.

To treat anemia, administer recombinant erythropoietin, as prescribed. This

drug mimics endogenous erythropoietin and increases red blood cell
production. To correct hyperkalemia, administer sodium polystyrene sulfonate
orally or rectally. This resin absorbs potassium ions through the GI mucosa in
exchange for sodium ions. Or administer I.V. glucose and insulin. This drug
combination shifts intravascular potassium into the cells, lowering the blood
potassium level.
To treat hyperphosphatemia, expect to provide a phosphate binder, such as
aluminum hydroxide gel. In the intestines, aluminum hydroxide binds with
phosphate to form aluminum phosphate. Because the intestines can't absorb
aluminum phosphate, it's excreted in the stool. This lowers the blood
phosphate level.

Despite these treatments, your patient may develop a life-threatening

complication, such as severe fluid overload or hyperkalemia. If so, prepare for
hemodialysis or peritoneal dialysis. Your patient with chronic renal failure may
need hemodialysis, at least three times a week to remove uremic toxins,
electrolytes, and excess intravascular fluid.
Or she may need peritoneal dialysis. This procedure requires the surgeon to
insert a flexible catheter into the peritoneal space. To perform dialysis, infuse a
hypertonic dialysate into the peritoneal cavity. Because the peritoneal
membrane is semipermeable, it allows electrolytes and uremic toxins to diffuse
into the dialysate. After the prescribed dwell time, remove the dialysate
through the catheter.
If necessary, prepare your patient with end-stage renal failure for kidney
transplantation. In this procedure, the surgeon implants a kidney from a
compatible donor into the patient's abdominal cavity. If the transplant is a
success, the new kidney takes over the failed kidneys function, which usually
prevents the need for dialysis.

Whenever you're caring for a patient with acute or chronic renal failure,
individualize your nursing care based on the patient's condition. But be sure to
perform these general nursing interventions:

 Measure your patient's blood pressure and other vital signs at least once every
four hours,
 Monitor your patient's weight every day to detect any weight gain,
 Provide a diet that's low in fluid, protein, and potassium and other electrolytes, as
prescribed, and
 Perform skin care and other interventions to reduce distressing symptoms, such
as pruritus