III.

Acute Kidney Injury

A. Description: the rapid loss of kidney function from renal cell damage.

2. Occurs abruptly and can be reversible

3. AKI leads to cell hypoperfusion, cell death, and decompensation of renal function.
4. The prognosis depends on the cause and the condition of the client.
5. Near-normal or normal kidney function may resume gradually.

Causes

1. Prerenal:

Outside the kidney; caused by intravascular volume depletion such as with blood
loss associated with trauma or surgery, dehydration, decreased cardiac output (as
with cardiogenic shock), decreased peripheral vascular resistance, decreased
renovascular blood flow, and prerenal infection or obstruction.

2. Intrarenal: Within the parenchyma of the kidney; caused by tubular necrosis,

prolonged prerenal ischemia, intrarenal infection or obstruction, and nephrotoxicity

2. Postrenal: Between the kidney and urethral meatus, such as bladder neck
obstruction, bladder cancer, calculi, and postrenal infection

Acute Kidney Injury: Phases and Laboratory Findings

Onset

▪ Begins with precipitating event

Oliguric Phase

▪ Elevated blood urea nitrogen (BUN) and serum creatinine levels

▪ Decreased urine specific gravity (prerenal causes) or normal (intrarenal causes) ▪
Decreased glomerular filtration rate (GFR) and creatinine clearance
▪ Hyperkalemia
▪ Normal or decreased serum sodium level
▪ Hypervolemia
▪ Hypocalcemia
▪ Hyperphosphatemia

Diuretic Phase

▪ Gradual decline in BUN and serum creatinine levels, but still elevated ▪ Continued
low creatinine clearance with improving GFR
▪ Hypokalemia
▪ Hyponatremia

▪ Hypovolemia

Recovery Phase (Convalescent)

▪ Increased GFR

▪ Stabilization or continual decline in BUN and serum creatinine levels toward normal

▪ Complete recovery (may take 1 to 2 years)

C. Phases of AKI and interventions

1. Onset: Begins with precipitating event

2. Oliguric phase
a. For some clients, oliguria does not occur and the urine output is normal; otherwise,
the duration of oliguria is 8 to 15 days; the longer the duration, the less chance of
recovery.

b. Sudden decrease in urine output; urine output is less than 400 mL/day.

c. Signs of excess fluid volume: Hypertension, edema, pleural and pericardial

effusions, dysrhythmias, heart failure, and pulmonary edema

d. Signs of uremia: Anorexia, nausea, vomiting, and pruritus

e. Signs of metabolic acidosis: Kussmaul’s respirations

f. Signs of neurological changes: Tingling of extremities, drowsiness progressing to
disorientation, and then coma

g. Signs of pericarditis: Friction

rub, chest pain with inspiration, and

low-grade fever
i. With early recognition or potential for

AKI, client may be treated with fluid challenges (IV boluses of 500 to
1000 mL over 1 hour).

j. Restrict fluid intake; if hypertension is present, daily fluid allowances may be 400
to 1000 mL plus the measured urinary output.

k. Administer medications such as diuretics, as prescribed to increase renal blood

flow and diuresis of retained fluid and electrolytes.

3. Diuretic phase

a. Urine output rises slowly, followed by diuresis (4 to 5 L/day).

b. Excessive urine output indicates that damaged nephrons are recovering their
ability to excrete wastes.
c. Dehydration, hypovolemia, hypotension, and tachycardia can occur.
d. Level of consciousness improves.
E.. Administer IV fluids as prescribed, which may contain electrolytes to replace
losses.

4. Recovery phase (convalescent)

a. Recovery is a slow process; complete recovery may take 1 to 2 years.

b. Urine volume returns to normal.
c. Memory improves.
d. Strength increases.
e. The older adult is less likely than a younger adult to regain full kidney function.
g. AKI can progress to chronic kidney disease (CKD).
The signs and symptoms of AKI are primarily caused by the retention of nitrogenous wastes,
the retention of fluids, and the inability of the kidneys to regulate electrolytes.

Interventions
1. Monitor vital signs, especially for signs of hypertension, tachycardia, tachypnea,
and an irregular heart rate.
2. Monitor urine and intake and output hourly and urine color and characteristics.
3. Monitor daily weight (same scale, same clothes, same time of day), noting that an
increase of 0.5 to 1 lb/day (0.25 to 0.5 kg/day) indicates fluid retention.
4. Monitor for changes in the BUN, serum creatinine, and serum electrolyte levels.
5. Monitor for acidosis (may need to be treated with sodium bicarbonate).
6. Monitor urinalysis for protein level, hematuria, casts, and specific gravity.
7. Monitor for altered level of consciousness caused by uremia.
8. Monitor for signs of infection because the client may not exhibit an elevated
temperature or an increased WBC count.
9. Monitor the lungs for wheezes and rhonchi and monitor for edema, which can
indicate fluid overload.
10. Administer the prescribed diet, which is usually a low- to moderate-protein (to
decrease the workload on the kidneys) and high-carbohydrate diet; ill clients may
require nutritional support with supplements, enteral feedings, or parenteral
nutrition. 11. Restrict potassium and sodium intake as prescribed based on the
electrolyte level. 12. Administer medications as prescribed; be alert to the mechanism
for metabolism and excretion of all prescribed medications.
13. Be alert to nephrotoxic medications, which may be prescribed
14. Be alert to the PHCP’s adjustment of medication dosages for kidney injury.
15. Prepare the client for dialysis if prescribed; continuous renal replacement therapy
may be used in AKI to treat fluid volume overload or rapidly developing azotemia
and metabolic acidosis.
16. Provide emotional support by allowing opportunities for the client to express
concerns and fears and by encouraging family interactions.
17. Promote consistency in caregivers.
IV. Chronic Kidney Disease (CKD)

A. Description
1. CKD is a slow, progressive, irreversible loss in kidney function, with a GFR less than
or equal to 60 mL per minute for 3 months or longer.
2. It occurs in stages (with loss of 75% of functioning nephrons, the client becomes
symptomatic) and eventually results in uremia or end-stage kidney disease (with loss of
90% to 95% of functioning nephrons)
3. Hypervolemia can occur because of the kidneys’ inability to excrete sodium and
water; hypovolemia can occur because of the kidneys’ inability to conserve sodium and
water.

B. Primary causes
1. May follow AKI
2. Diabetes mellitus and other metabolic disorders
3. Hypertension
4. Chronic urinary obstruction
5. Recurrent infections
6. Renal artery occlusion
7. Autoimmune disorders
C. Assessment

Box 54-5

Key Features of Chronic Kidney Disease

Neurological Manifestations

▪ Asterixis
▪ Ataxia (alteration in gait)
▪ Inability to concentrate or decreased attention span ▪ Lethargy and daytime
drowsiness
▪ Myoclonus
▪ Paresthesias
▪ Seizures
▪ Slurred speech
▪ Tremors, twitching, or jerky movements
▪ Coma

Cardiovascular Manifestations

▪ Hypertension
▪ Heart failure
▪ Peripheral edema
▪ Cardiomyopathy
▪ Pericardial effusion
▪ Pericardial friction rub ▪ Uremic pericarditis
▪ Cardiac tamponade

Respiratory Manifestations

▪ Crackles
▪ Deep sighing, yawning ▪ Depressed cough reflex ▪ Shortness of breath
▪ Tachypnea
▪ Kussmaul’s respirations ▪ Pleural effusion
▪ Pulmonary edema

1872
▪ Uremic halitosis
▪ Uremic pneumonia

Hematological Manifestations

▪ Abnormal bleeding and bruising ▪ Anemia

Gastrointestinal Manifestations

▪ Anorexia, nausea, vomiting

▪ Changes in taste acuity and sensation
▪ Constipation
▪ Diarrhea
▪ Metallic taste in the mouth
▪ Stomatitis
▪ Uremic colitis (diarrhea)
▪ Uremic fetor
▪ Uremic gastritis (possible gastrointestinal bleeding)

Urinary Manifestations

▪ Polyuria, nocturia (early)

▪ Proteinuria
▪ Diluted, straw-colored appearance

▪ Hematuria
▪ Oliguria, anuria (later)

Integumentary Manifestations

▪ Decreased skin turgor ▪ Dry skin

▪ Yellow-gray pallor
▪ Ecchymosis
▪ Pruritus
▪ Purpura
▪ Soft tissue calcifications
▪ Uremic frost (late, premorbid)

Musculoskeletal Manifestations

▪ Bone pain

1873
▪ Muscle weakness and cramping ▪ Pathological fractures
▪ Renal osteodystrophy

Reproductive Manifestations

▪ Decreased fertility
▪ Decreased libido
▪ Impotence
▪ Infrequent or absent menses

D. Interventions
1. Same as the interventions for AKI.
2. Administer a prescribed diet, which is usually a moderate-protein (to decrease the
workload on the kidneys) and high-carbohydrate, low-potassium, and low-
phosphorus diet.
3. Provide oral care to prevent stomatitis and reduce discomfort from mouth sores.
4. Provide skin care to prevent pruritus.
5. Teach the client about fluid and dietary restrictions and the importance of daily
weights.
6. Provide support to promote acceptance of the chronic illness and prepare the client
for long-term dialysis and transplantation, or explain to the client about her or his
choice to decline dialysis or transplantation; with elderly clients, provide
information that kidney function is declining and in time may reach end-stage renal
disease and require dialysis; encourage healthy lifestyle and discuss choices.
2. Anemia
a. Fatigue results from anemia and the buildup of wastes from the diseased kidneys.
b. Provide adequate rest periods.
c. Teach the client to plan activities to avoid fatigue.
d. Mild central nervous system (CNS) depressants may be prescribed to promote rest.

a. Anemia results from the decreased secretion of erythropoietin by damaged

nephrons, resulting in decreased production of red blood cells.
b. Monitor for decreased hemoglobin and hematocrit levels.
c. Administer hematopoietics such as epoetin alfa or darbepoetin alfa, as prescribed
to promote maturity of the red blood cells.
d. Administer folic acid as prescribed.
e. Administer iron orally as prescribed, but not at the same time as phosphate
binders.
f. Administer stool softeners as prescribed because of the constipating effects of iron.
g. Note that oral iron is not well absorbed by the GI tract in CKD and causes nausea
and vomiting; parenteral iron may be used if iron deficiencies persist despite folic
acid or oral iron administration.
h. Administer blood transfusions; prescribed only when necessary (acute blood loss,
symptomatic anemia), because they decrease the stimulus to produce red blood cells.

i. Blood transfusions also cause the development of antibodies against human

tissues, which can make matching for organ transplantation difficult.

3. Gastrointestinal bleeding
a. Urea is broken down by the intestinal bacteria to ammonia; ammonia irritates the
GI mucosa, causing ulceration and bleeding.
b. Monitor for decreasing hemoglobin and hematocrit levels.
c. Monitor stools for occult blood.
d. Avoid the administration of acetylsalicylic acid, because it is excreted by the
kidneys; if administered, aspirin toxicity can occur and prolong the bleeding time.

Place the client with kidney disease on continuous telemetry. The client can develop
hyperkalemia, resulting in the risk for dysrhythmias.

4. Hyperkalemia
a. Monitor vital signs for hypertension or hypotension and the apical heart rate; an
irregular heart rate could indicate dysrhythmias.
b. Monitor the serum potassium level; an elevated serum potassium level can cause
decreased cardiac output, heart blocks, fibrillation, or asystole
c. Provide a low-potassium diet
e. Administer prescribed medications:
50% dextrose and regular insulin IV may be prescribed to shift potassium into the
cells; calcium gluconate IV may be prescribed to reduce myocardial irritability from
hyperkalemia; and sodium bicarbonate IV may be prescribed to correct acidosis.
f. Administer prescribed loop diuretics to excrete potassium.
g. Avoid potassium-retaining medications such as spironolactone and triamterene,
because these medications will increase the potassium level
h. Prepare the client for peritoneal dialysis (PD) or hemodialysis as prescribed.

5. Hypermagnesemia
a. Results from decreased renal excretion of magnesium.
b. Monitor for cardiac manifestations such as bradycardia, peripheral vasodilation,
and hypotension.
c. Monitor CNS changes, such as drowsiness or lethargy.
d. Monitor neuromuscular manifestations, such as reduced or absent deep tendon
reflexes or weak or absent voluntary skeletal muscle contractions.
e. Administer loop diuretics as prescribed to excrete magnesium.
f. Administer calcium as prescribed for resulting cardiac problems.
g. Avoid medications that contain magnesium, such as antacids; some laxatives and
enemas may also contain magnesium.
h. During severe elevations, avoid foods that increase magnesium levels

6. Hyperphosphatemia
a. As the phosphorus level rises, the calcium level drops; this leads to the stimulation
of parathyroid hormone, causing bone demineralization.
b. Treatment is aimed at lowering the serum phosphorus level.
c. Administer phosphate binders as prescribed with meals to lower serum phosphate
levels.
d. Administer stool softeners and laxatives as prescribed, because phosphate binders
are constipating.
e. Teach the client about the need to limit the intake of foods high in phosphorus

7. Hypertension
a. Caused by failure of the kidneys to maintain BP homeostasis.
b. Monitor vital signs for elevated BP.
c. Maintain fluid and sodium restrictions as prescribed.
d. Administer diuretics and antihypertensives as prescribed.
8. Hypervolemia
a. Monitor vital signs for an elevated BP.
b. Monitor intake and output and daily weight for indications of fluid retention.
c. Monitor for periorbital, sacral, and peripheral edema.
d. Monitor the serum electrolyte levels.
e. Monitor for hypertension and notify the PHCP if there are sustained elevations.
f. Monitor for signs of heart failure and pulmonary edema, such as restlessness,
heightened anxiety, tachycardia, dyspnea, basilar lung crackles, and blood-tinged
sputum; notify the PHCP immediately if signs occur.

g. Maintain fluid restriction.

h. Avoid the administration of large amounts of IV fluids.
i. Administer diuretics as prescribed
j. Teach the client to maintain a low- sodium diet.
k. Teach the client to avoid over-the- counter medications without checking with the
PHCP.

9. Hypocalcemia
a. Results from a high phosphorus level and the inability of the diseased kidney to
activate vitamin D
b. The absence of vitamin D causes poor calcium absorption from the intestinal tract.
c. Monitor the serum calcium level.
d. Administer calcium supplements as prescribed.
e. Administer activated vitamin D as prescribed.

Protein and Potassium:

 Protein is needed to help build muscle and heal from injury and infection
 Too much protein can cause waste buildup in the blood.
 The goal is to eat enough protein but avoid eating too much. 40-65 g/day
 Need more high value protein

Potassium:
 Important role in your nerve and muscle fx, including heart
 Kidney may not be able to remove enough K+ from your blood which can be
dangerous.
 K+ found naturally in foods: fruits, vegetables, nuts, and daiy products
  Don’t restrict K+ unless ordered by your doctor

Higher K+ foods to avoid:

-dairy, oranges, bananas, nuts, seeds, potatoes, tomatoes, avocados

Lower Potassium:
-apples, grapes, berries, non-dairy drinks (enriched milk, almond milk), non-
dairy sorbets, popsicles

Avoid Salt substitutes: sodium chloride is replaced w/ potassium chloride

-be aware that some “low sodium” products are replacing sodium with
potassium.

10. Hypovolemia

a. Monitor the vital signs for hypotension and tachycardia.

b. Monitor for decreasing intake and output and a reduction in the daily weight.
c. Monitor for dehydration.
d. Monitor electrolyte levels.
e. Provide replacement therapy based on the serum electrolyte level values.

11. Infection

a. The client is at risk for infection caused by a suppressed immune system, dialysis
access site, and possible malnutrition.
b. Monitor for signs of infection.
c. Avoid urinary catheters when possible; if used, provide catheter care per protocol.
d. Provide strict asepsis during urinary catheter insertion and other invasive
procedures.
e. Instruct the client to avoid fatigue and avoid persons with infections.
f. Administer antibiotics as prescribed, monitoring for nephrotoxic effects.

12. Metabolic acidosis

a. The kidneys are unable to excrete hydrogen ions or manufacture bicarbonate,
resulting in acidosis.
b. Administer alkalizers such as sodium bicarbonate as prescribed.
c. Note that clients with CKD adjust to low bicarbonate levels and as a result do not
become acutely ill.

13. Muscle cramps

a. Occur from electrolyte imbalances and the effects of uremia on peripheral nerves
b. Monitor serum electrolyte levels.
c. Administer electrolyte replacements and medications to control muscle cramps as
prescribed.
d. Administer heat and massage as
prescribed.
4. Neurological changes

a. The buildup of active particles and fluids causes changes in the brain cells and
leads to confusion and impairment in decision-making ability.
b. Peripheral neuropathy results from the effects of uremia on peripheral nerves.
c. Monitor the level of consciousness and for confusion.
d. Monitor for restless leg syndrome, which is also common during dialysis
treatments.
e. Teach the client to examine areas of decreased sensation for signs of injury.

IV. Hemolytic-Uremic Syndrome

A. Description
1. Hemolytic-uremic syndrome is thought to be associated with bacterial toxins,
chemicals, and viruses that cause acute kidney injury in children.

2. It occurs primarily in infants and small children 6 months to 5 years old.

3. Clinical features include acquired hemolytic anemia, thrombocytopenia, kidney
injury, and central nervous system symptoms.

B. Assessment
1. Triad of anemia, thrombocytopenia, and kidney failure
2. Proteinuria, hematuria, and presence of urinary casts

3. Blood urea nitrogen and serum creatinine levels elevated; hemoglobin and hematocrit
levels decreased
Assessment Findings in Hemolytic-Uremic Syndrome

▪ Vomiting
▪ Irritability
▪ Lethargy
▪ Marked pallor
▪ Hemorrhagic manifestations: bruising, petechiae, jaundice, bloody diarrhea

▪ Oliguria or anuria
▪ Central nervous system involvement: seizures, stupor, coma

C. Interventions

1. Hemodialysis or peritoneal dialysis may be prescribed if a child is anuric (dialysate

solution is prescribed to meet the child’s electrolyte needs).
2. Strict monitoring of fluid balance is necessary; fluid restrictions may be prescribed if
the child is anuric.
3. Institute measures to prevent infection.
4. Provide adequate nutrition.
5. Other treatments include medications to treat manifestations and the administration
of blood products to treat severe anemia (administered with caution to prevent fluid
overload).
VI. Hemodialysis an irregular heart rate.
2. Monitor serum electrolyte levels.
3. Monitor intake and output and for oliguria.
4. Provide a limited but high-quality protein diet as prescribed.
5. Provide a limited sodium, nitrogen, potassium, and phosphate diet as prescribed.
6. Assist the client to cope with body image disturbances caused by uremic syndrome.
Hemodialysis

A. Description

1. Hemodialysis is an intermittent renal replacement therapy involving the process of

cleansing the client’s blood.
2. It involves the diffusion of dissolved particles from 1 fluid compartment into
another across a semipermeable membrane; the client’s blood flows through 1 fluid
compartment of a dialysis filter, and the dialysate is in another fluid
compartment.inability to filter out these waste products.

B. Functions of hemodialysis
1. Cleanses the blood of accumulated waste products

2. Removes the byproducts of protein metabolism such as urea, creatinine, and uric
acid from the blood
3. Removes excess body fluids
4. Maintains or restores the buffer system of the body

5. Corrects electrolyte levels in the body

E. Interventions

1. Monitor vital signs before, during, and after dialysis; the client’s temperature may
elevate because of slight warming of the blood from the dialysis machine (notify the
PHCP about excessive temperature elevations because this could indicate sepsis,
requiring blood cultures to be collected).
2. Monitor laboratory values, specifically the BUN, creatinine, and complete blood
cell counts before, during, and after dialysis.
3. Assess the client for fluid overload before dialysis and fluid volume deficit
following dialysis.
4. Weigh the client before and after dialysis to determine fluid loss. Note that the
client will not urinate or will urinate small amounts (may be less than 30 mL/hr).
5. Assess the patency of the blood access device before, during, and after dialysis.
6. Monitor for bleeding; heparin is added to the dialysis bath to prevent clots from
forming in the dialyzer or the blood tubing.
7. Monitor for hypovolemia during dialysis, which can occur from blood loss or
excess fluid and electrolyte removal.
8. Provide adequate nutrition; the client may eat before or during dialysis.
9. Identify the client’s reactions to the treatment and support coping mechanisms;
encourage independence and involvement in care.

Withhold antihypertensives and other medications that can affect the BP or

result in hypotension until after hemodialysis treatment. Also withhold
medications that could be removed by dialysis, such as water-soluble
vitamins, certain antibiotics, and digoxin.

IX. Peritoneal Dialysis

A. Description
1. The peritoneum acts as the dialyzing membrane (semipermeable membrane) to
achieve dialysis, and the membrane is accessed by insertion of a PD catheter through
the abdomen.
2. PD works on the principles of osmosis, diffusion, and ultrafiltration; PD occurs via
the transfer of fluid and solute from the bloodstream through the peritoneum into the
dialysate solution.
3. The peritoneal membrane is large and porous, allowing solutes and fluid to move
via osmosis from an area of higher concentration in the body to an area of lower
concentration in the dialyzing fluid.
4. The peritoneal cavity is rich in capillaries; therefore, it provides a ready access to
the blood supply.

B. Contraindications to PD

1. Peritonitis
2. Recent abdominal surgery
3. Abdominal adhesions
4. Other GI problems such as diverticulosis
X. Complications of Peritoneal Dialysis

Infection is a concern with PD; sites of infection are either the

catheter insertion site or the peritoneum, causing peritonitis.

CCRT
 Stage 5: some form of replacement therapy, hemodialysis, transpants
needed
 Used in crtically ill patients 24 hrs/day
 Goal: remove toxins, excess fluid, and balance electrolytes
 Disadvantage: need for prolonged anticoagulation, sophisticated
monitoring

 Earliest manifestation of tubular damage is inability to concentrate urine

 Dilute urine is a warning sign
 Treating secondary infections (major cause of death)
 Hemodialysis or CRRT maybe indicated when theres a buildup of nitrogen
wastes and fluid & electrolyte imbalance cant be kept under control