1.

Acute Renal Failure

2. Chronic Renal Failure
3. Dialysis
4. Acute Glomerulonephritis (AGN)
5. Nephrotic Syndrome

After going through this topic, you will be able to:

• Discuss the etiology, risk factors, pathophysiology, clinical manifestations, medical management, and
nursing management for patients with renal disorders.
• Understand the nursing management of patients with chronic kidney disease and acute kidney injury.
• Compare and contrast the renal replacement therapies, including hemodialysis and peritoneal dialysis.
• Describe the nursing management of the patient on dialysis who is hospitalized.

The renal system helps regulate the body’s internal environment and is essential for the maintenance of
life. Nurses may encounter patients with various renal disorders and thus need to be knowledgeable about these
disorders. Comprehensive care of patients with renal disorders involves a full understanding of the full impact of the
disorders on the individual’s quality of life and his/her family. Nursing care plans need to address a person’s total

NCM 112
needs because the whole body is adversely affected when the kidneys are affected. Therefore, nurses should be
alert to indicators of pathology, since prognosis can be influenced by early diagnosis and treatment.
This study guide provides a brief discussion about acute and chronic renal failure, its causes, together with
management strategies to prevent damage and preserve renal function.

True/False
1. Diabetes is the primary cause of chronic kidney disease.
2. The glomerular filtration rate and the creatinine clearance decrease with end-stage kidney disease.
3. Peritonitis is the most common and the most serious complication of peritoneal dialysis.
4. Kidney transplantation has become the treatment of choice for most patients with end-stage kidney
disease.
5. The most striking clinical manifestation of Nephrotic Syndrome is proteinuria.

Fill-in-the-Blank

1. The most accurate indicator of fluid loss or gain in an acutely ill patient with a kidney disorder is
________ which must be assessed daily.

2. Any condition that damages the glomerular membrane and results in increased permeability to plasma
proteins is _______________ syndrome.

3. A widely accepted criterion for acute kidney injury is a 50% or greater increase in serum
________________ above baseline.

4. ________________ is the most immediate life threatening of the fluid and electrolyte imbalances that
occur in patients with kidney disorders.

5. _________________ is used when a patient is acutely ill until kidneys resume function and for long-
term replacement therapy for chronic kidney disease and end-stage kidney disease.

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in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise of any part of this document, without the prior written permission of UCU, is strictly prohibited.
 A sudden loss of kidney function that results in disturbances in fluid and electrolyte balance, acid-base
homeostasis, blood pressure regulation, erythropoiesis, and mineral metabolism. It is frequently associated with an
increase in BUN and creatinine, oliguria, hyperkalemia, and sodium and fluid retention.

Etiology
1. Prerenal- from decrease blood flow to the kidney
a. Hypovolemia (hemorrhage, dehydration, burns)
b. Cardiac disorders (MI, Heart failure)
c. Renal artery obstruction (stenosis)

2. Intrarenal- from injury to renal tissue (glomeruli or kidney

tubules)
a. Acute tubular necrosis (ATN) due to intratubular
obstruction, tubular back leak, and vasoconstriction.
b. Acute glomerulonephritis and pyelonephritis
c. Blood transfusion reactions
d. Nephrotoxins (aminoglycoside antibiotics, heavy metals,
NSAID, ACE inhibitors)

3. Postrenal- from obstruction or disruption to urine flow anywhere

along the urinary tract.
a. Ureteral obstruction (renal calculi, strictures, pregnancy,
blood clots)
b. Bladder obstruction (tumor, renal calculi, BPH)

Phases of Acute Kidney Injury

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1. Onset/Initiation: begins when the kidney is injured and ends when oliguria develops. It lasts from hours to
days.
2. Oliguric–anuric phase: last for 1-3 weeks
a. Urine volume is less than 400 mL/day.
b. Accompanied by a rise in serum concentration of elements usually excreted by the kidney (urea,
creatinine, and the intracellular cations like potassium and magnesium).
c. Volume overload
d. Uremia & metabolic acidosis

3. Diuretic phase: usually last for 1 week

a. A gradual increase in urine output, which signals that glomerular filtration has started to recover.
b. Urine output = 3-5 liters/day
c. Close monitoring of fluid volume and electrolytes is essential.
d. Electrolytes and acid-base problem begin to normalize

4. Recovery phase: usually lasts several months to 1 year.

a. Laboratory values return to the patient’s normal level
b. Complete recovery of renal function may occur or they may be some residual deficits because of
scarring of kidney tissue.
c. Avoiding secondary insults to the kidney, such as nephrotoxic drugs, contrast dye, hypotension, and
infection, is important to minimize permanent kidney damage.

Diagnostic Evaluation
1. Urinalysis reveals proteinuria, hematuria, casts, increased WBC (possible infection), glycosuria, and pH.
2. Rising serum creatinine and BUN levels.
3. Renal ultrasonography to estimate renal size, to evaluate for masses, and to exclude treatable obstructive
uropathy.
4. CT/MRI to evaluate for masses or vascular disorders and renal angiography to evaluate for renal artery
stenosis.

Clinical Manifestations
1. The inability of the kidney to excrete metabolic waste products of protein through urine formation.
a. Oliguria
b. Increased BUN, serum creatinine (uremia)
c. Uriniferous odor breath
d. Stomatitis and G.I. bleeding due decomposition of urea back to ammonia on the oral cavity and
G.I tract which irritates the mucous membrane.
e. Destruction of RBC, WBC, platelets by the urea and nitrogenous waste
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 f.
Renal encephalopathy due to elevated levels of urea and nitrogenous waste
g.
Uremic frost due to accumulation of urates in the skin which causes severe pruritus and dryness
of the skin
h. Decreased libido, impotence, infertility caused by hormonal imbalances
2. The inability of the kidneys to maintain fluid-electrolyte, acid-base balance.
a. Edema due to retention of water
b. Hyperkalemia due to the inability of the kidneys to excrete potassium
c. Hyponatremia or hypernatremia due to the inability of the kidneys to regulate sodium balance
d. Hypermagnesemia due to the inability of the kidneys to excrete magnesium
e. Metabolic acidosis due to the inability of the kidneys to buffer hydrogen ions, unable to generate
bicarbonate, and unable to excrete waste products which are mostly acidic in nature
3. The inability of the kidney to secrete the hormone erythropoietin causes severe anemia.
4. The inability of the kidney to metabolize Vitamin D
a. Hypocalcemia due to decreased calcium absorption from the intestine.
b. Hyperphosphatemia due to decrease serum calcium levels
c. Renal osteodystrophy due to hypocalcemia
d. Hyperparathyroidism due to hypocalcemia that triggers the parathyroid gland to increase
secretion of parathormone
5. An altered biochemical environment like glucose intolerance that results in hyperglycemia

Medical Management
1. Correction of any reversible cause of acute renal failure
2. Fluid and electrolyte control
3. Drug therapy
a. Sodium polystyrene sulfonate (Kayexalate) for hyperkalemia
b. Sodium bicarbonate for metabolic acidosis
c. Aluminum hydroxide (Amphojel) for hyperphosphatemia
d. Calcium and Vitamin D supplement for hypocalcemia

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e. H2-receptor antagonist (cimetidine, ranitidine) for GI bleeding
f. Epoetin alfa (Epogen, Procrit) for anemia
4. Treatment of intercurrent disorders
a. Anemia
b. Gastrointestinal disturbance
c. Other conditions: hypertension, CHF, pulmonary edema, etc.
5. Dialysis

Nursing Diagnoses
1. Risk for imbalanced fluid volume related to the failure of the kidneys to maintain volume regulation and
excrete waste products
2. Risk for electrolyte imbalance related to kidney injury.
3. Potential for infection related to alterations in the immunologic system and host defenses.
4. Altered nutrition (less than body requirements) related to catabolic state, anorexia, and malnutrition
associated with acute renal failure.
5. Risk for bleeding related to GI mucosal irritation and altered platelet function.
6. Altered thought process (change in mental status) related to the effects of uremic toxins on the central
nervous system

Nursing Interventions
1. Correcting fluid volume deficit or overload
a. Watch for signs of hypovolemia like dry mucous membranes, poor skin turgor, hypotension; or
hypervolemia such as crackles on auscultation of lungs, engorged neck veins, periorbital edema,
ascites, edema of extremities, and elevated blood pressure.
b. Monitor urinary output and urine specific gravity; measure and record I & O.
c. Weigh the patient daily to provide an index of fluid balance
d. Adjust fluid intake to avoid volume overload and volume depletion.
➢ Fluid restriction is usually initiated in oliguric patients.
➢ During the oliguric-anuric phase, give only enough fluids to replace losses (usually 500
mL/day plus measured fluid losses).
➢ Fluid allowance should be distributed throughout the day.
➢ Restrict salt and water intake if there is evidence of extracellular excess.
2. Maintaining electrolyte and acid-base balance
a. Monitor and replace serum electrolytes ordered.
➢ Evaluate for signs and symptoms of hyperkalemia and notify the physician of value above
5.5 mg/L.
➢ Watch for ECG changes like tall T waves; wide QRS complex; depressed ST segment.
➢ Administer sodium bicarbonate or glucose and insulin to shift potassium into the cells, as
ordered.
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in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise of any part of this document, without the prior written permission of UCU, is strictly prohibited.
 Administer cation exchange resin (sodium polystyrene sulfonate [Kayexalate]) orally or
➢
rectally to provide more prolonged correction of elevated potassium, as ordered.
➢ Administer aluminum hydroxide for hyperphosphatemia
➢ Instruct patient about the importance of following the prescribed diet, avoiding foods high
in potassium.
➢ Prepare for dialysis when a rapid lowering of potassium is needed.
b. Monitor acid-base status as directed by checking the arterial blood gas (ABG)
➢ Prepare for ventilator therapy if severe acidosis is present.
➢ Administer oral alkalizing medications or IV sodium bicarbonate as ordered.
➢ Be prepared to implement dialysis for uncontrolled acidosis.
3. Preventing and monitoring for infection
a. Monitor for signs of infection.
b. Practice aseptic technique
c. Remove the bladder catheter as soon as possible; monitor for UTI.
d. Use intensive pulmonary hygiene since there is a high incidence of lung edema and infection.
e. Carry out meticulous wound care.
f. If antibiotics are administered, care must be taken to adjust the dosage for renal impairment.
4. Maintaining adequate nutrition
a. Work collaboratively with a dietitian to direct nutritional support.
b. Encourage a high carbohydrate, low protein, low potassium, and low sodium diet during the oliguric
phase.
c. Protein sources should be of high biologic value - rich in essential amino acids (fish, eggs, meat) so
that the patient does not rely on tissue catabolism for essential amino acids.
d. Encourage small frequent meals if the patient is experiencing nausea or reflux symptoms.
e. Weigh the patient daily.
f. Be aware that food and fluids containing large amounts of sodium, potassium, and phosphorus may
need to be restricted.
g. Tube feeding or total parenteral nutrition (TPN) if oral intake is not sufficient to meet requirements

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5. Monitoring for and preventing gastrointestinal bleeding
a. Examine all stools and emesis for gross and occult blood.
b. Administer H2-receptor antagonist (cimetidine, ranitidine) as directed as prophylaxis for gastric
stress ulcers. If an H2- receptor antagonist is used, care must be taken to adjust the dose for the
degree of renal impairment.
c. Prepare for endoscopy when GI bleeding occurs.
6. Monitoring cognition and orientation
a. Speak to the patient in simple orienting statements, using repetition when necessary.
b. Monitor for and report mental status changes - somnolence, lassitude, lethargy, and fatigue
progressing to irritability, disorientation, twitching, seizures.
c. Encourage and assist the patient to turn and move, as drowsiness and lethargy may prevent activity.
d. Use seizure precautions - padded side rails and airway and suction equipment
e. Prepare for dialysis, which may help prevent neurologic complications.

(End-Stage Renal/Kidney Disease)

Gradual, progressive deterioration of renal function, which ends fatally in uremia (an excess of urea and
other nitrogenous wastes in the blood) and its complications. The treatment for end-stage renal disease (ESRD) is
dialysis or kidney transplantation.

Etiology
1. Prolonged and severe hypertension
2. Diabetes mellitus
3. Glomerulopathies
4. Interstitial nephritis
5. Hereditary renal disease
6. Obstructive uropathy

Stages of Chronic Kidney Disease

1. Stage 1: GFR ≥90 mL/min
➢ Kidney damage with normal or increased GFR
2. Stage 2: GFR = 60–89 mL/min
➢ Mild decrease in GFR
3. Stage 3: GFR = 30–59 mL/min
➢ Moderate decrease in GFR
4. Stage 4: GFR = 15–29 mL/min

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in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise of any part of this document, without the prior written permission of UCU, is strictly prohibited.
 ➢ Severe decrease in GFR
5. Stage 5: GFR <15 mL/min
➢ End-stage kidney disease or chronic renal failure

Pathophysiology
➢ In chronic renal failure, the end product of protein metabolism accumulates in the blood instead of being
excreted in the urine. Retention of sodium and water leads to edema, congestive heart failure, and
hypertension. Conversely, episodes of diarrhea and vomiting may lead to sodium and water depletion,
exacerbating uremia, and producing hypotension and hypovolemia.
➢ Metabolic acidosis results from the kidney’s inability to excrete hydrogen ions, decrease bicarbonate ion
reabsorption, and the generation and retention of acid end-products of metabolism.
➢ Decrease GFR results in electrolyte imbalances leads to:
a. Increase serum phosphate
b. Decrease serum calcium
c. Increase parathormone but depleted bone calcium, leading to bone changes
d. Increase serum magnesium
➢ Erythropoietin production by the kidney decreases, resulting in anemia
➢ Uremia affects the CNS (uremic encephalopathy), which, if left untreated, can result in neurologic
complications like altered mental functioning, personality, and behavioral changes, convulsions, and coma

Clinical Manifestations

1. Gastrointestinal: anorexia, uremic fetor, metallic taste in the mouth, nausea, vomiting, diarrhea,
constipation, ulceration of GI tract, and hemorrhage.
2. Cardiovascular: hypertension, pericarditis, pericardial effusion, pericardial tamponade.
3. Respiratory: pulmonary edema, pleural effusions, pleural rub, Kussmaul’s respiration

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4. Neuromuscular: fatigue, sleep disorders, headache, lethargy, muscular irritability, peripheral neuropathy,
seizures, coma.
5. Metabolic and endocrine: changes in insulin metabolism, decreased vitamin D3 levels (resulting in decreased
calcium absorption), secondary hyperparathyroidism (high parathyroid hormone levels), hyperlipidemia, sex
hormone disturbances causing decreased libido, impotence, amenorrhea.
6. Electrolyte and acid-base disturbances: metabolic acidosis, hyperkalemia, hypermagnesemia, and
hypocalcemia
7. Dermatologic: pallor, pruritus, ecchymosis, uremic frost (deposits of urate crystals on the skin from
untreated ESRD).
8. Skeletal abnormalities: bone demineralization from renal osteodystrophy.
9. Hematologic: anemia, impaired platelet function causing increased bleeding tendencies, and white blood cell
dysfunction, resulting in a state of immunosuppression.
10. Psychosocial functions: personality and behavior changes, alteration in cognitive processes.

Diagnostic Evaluation
1. CBC for anemia
2. Elevated serum creatinine or BUN, potassium, and phosphorus
3. Decrease serum calcium, bicarbonate, and proteins, especially albumin
4. Low blood pH

Medical Management
1. Detection and treatment of reversible causes of renal failure (e.g., glycemic control, optimal blood pressure
management).
2. Dietary regulation- low protein diet supplemented with essential amino acids to minimize uremic toxicity.
Other dietary restrictions include sodium, potassium, and phosphorus restrictions and possible fluid
restriction.
3. Treatment of associated conditions to improve renal dynamics
a. Anemia: erythropoiesis-stimulating agents, such as epoetin alfa and darbepoetin; PO or IV iron
administration.
b. Acidosis: replacement of bicarbonate stores by oral administration of sodium bicarbonate.
c. Hyperkalemia: restriction of dietary potassium; administration of cation exchange resin.

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 d. Phosphate retention and hypocalcemia: dietary PO4 restriction (chicken, milk, legumes, carbonated
beverages), administration of phosphate-binding agents; IV or PO vitamin D3.

4. Prevent fluid overload through sodium and fluid restriction.

5. Maintenance dialysis or kidney transplantation when symptoms can no longer be controlled with
conservative management.

Nursing Diagnoses
1. Fluid volume excess related to the disease process.
2. Altered nutrition (less than body requirements) related to anorexia, nausea, vomiting, and restricted diet.
3. Impaired skin integrity related to changes in oil and sweat glands.
4. Altered elimination (constipation) related to fluid restriction and ingestion of phosphate-binding agents.
5. Risk for Injury because of hemodynamic instability, increased bleeding tendency, and altered cognition.
6. Altered thought process (change in mental status) related to the effects of uremic toxins on the central
nervous system.

Nursing Interventions
1. Achieving fluid and electrolyte balance
a. Weigh patient daily to assess fluid balance
b. Blood pressure measurement to assess vascular volume status
c. Adjust fluid intake to maintain adequate urinary volume and to avoid dehydration
d. Restrict salt and water intake if there is extracellular excess
e. Monitor for acidosis
2. Maintain nutrition
a. Provide a low-protein diet supplemented with essential amino acids and vitamins
b. High carbohydrate intake, low sodium, and potassium diet
c. Monitor body weight
3. Maintain skin integrity

NCM 112
a. Provide tepid, cool baths and use mild soap
b. Apply emollient lotions
c. Keep nails short and trimmed to prevent excoriation
d. Administer antihistamines for relief of itching
4. Relieving constipation
a. Encourage a high fiber diet
b. Stool softener as prescribed
c. Increase activity as tolerated.
5. Prevent Injury
a. Inspect patient’s gait, range of motion, and muscle strength.
b. Increase activity as tolerated to avoid immobilization because it increases bone demineralization.
c. Check orthostatic blood pressures.
d. Monitor for signs and symptoms of bleeding.
6. Preventing or reducing cognitive distortion
a. Speak to the patient in simple orienting statements, using repetition when necessary
b. Use close contact, nurturing voice, eye contact, and touch to establish rapport
c. Maintain predictable routine and keep change to a minimum

Patient Education: Teach the following:

1. Weigh every morning to avoid fluid overload.
2. Drink limited amounts only when thirsty.
3. Measure allotted fluids & save some for ice cubes; sucking ice is thirst-quenching.
4. Use lemon wedges, hard candy, chewing gum to moisten the mouth.

Refers to the diffusion of solute molecules through a semipermeable membrane, passing from the side of
higher concentration to that of lower concentration. The purpose of dialysis is to maintain fluid, electrolyte, and
acid-base balance and to remove endogenous and exogenous toxins. It is a substitute for some kidney excretory
functions but does not replace the kidneys’ endocrine functions.

Physiologic principle: Diffusion, Osmosis, and Ultrafiltration

➢ Diffusion: movement of solutes (toxins & waste products) from an area of higher concentration in the blood
to an area of lower concentration in the dialysate. The dialysate is a solution that circulates through the
dialyzer, made up of all the electrolytes in their ideal extracellular concentrations.

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in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise of any part of this document, without the prior written permission of UCU, is strictly prohibited.
 ➢ Osmosis: movement of water through a semipermeable membrane from an area of lower solute
concentration to an area of higher solute concentration. This is the way that excess fluid is removed from
the blood, in which water moves from an area of low concentration potential (the blood) to an area of high
concentration potential (the dialysate bath).

➢ Ultrafiltration: a process whereby water is removed from the blood using a pressure gradient between the
patient’s blood and the dialysate. That is fluid moves under high pressure to an area of lower pressure. This
process is much more efficient than osmosis for fluid removal and is accomplished by applying negative
pressure or a suctioning force to the dialysis membrane.

Goals of Dialysis therapy

1. Removed the end products of protein metabolism, such as urea and creatinine, from the blood
2. Maintain a safe concentration of serum electrolytes
3. Correct acidosis and replenish the blood’s bicarbonate buffer system
4. Removed excess fluid from the blood

Methods
A. Hemodialysis
A process of cleaning the blood of accumulated waste products. Involves diverting toxin-laden blood from
the person into a dialyzer and then returning the clean blood to the person. Treatment time approximately 4 hours,
three times weekly.

Underlying Principles
1. Heparinized blood passes down a concentration gradient
through a semi-permeable membrane by dialysis to the
dialysate fluid. The dialysis fluid is delivered by a
mechanical proportion pump to flow on the other side of
the membrane.

NCM 112
2. The dialysate is designed to approximate the normal
electrolyte structure of plasma and extracellular water.
Dialysis solution consists of highly purified water to which
sodium, potassium, calcium, magnesium, chloride, and
dextrose have been added.
3. Through the process of diffusion, the blood component
equilibrates with those in the dialysate. Noxious
substances (urea, creatinine, uric acid, phosphate, and
other metabolites) are transferred from the blood to the
dialysate so that they can be discarded. Small pores of the
membrane hold back desirable blood components.
4. Excess water is removed from the blood (ultrafiltration)
5. The body’s buffer system is maintained by the addition and diffusion of acetate from the dialysate into the
patient; it is metabolized to form bicarbonate to achieve the proper pH balance.
6. Purified blood is returned to the body through one of the patient’s veins.
7. At the end of the treatment, most poisonous wastes have been removed, electrolytes and water balances
have been restored, and the buffer system has been replenished.

Methods of Access to the Patient’s Circulation

1. Arteriovenous fistula (AVF): the creation of a vascular
communication by suturing a vein directly to an artery.
a. Usually, radial artery and cephalic vein are anastomosed
in the non-dominant arm
b. Following the procedure, the superficial venous system
of the arm dilates.
c. Using 2 large-bore needles, inserted into the dilated
venous limb, blood may be obtained and passed through
the dialyzer. The arterial end is used for arterial flow and
the distal end for reinfusion of dialyzed blood.
d. Healing of AVF requires several weeks (at least 6 to 8
weeks); a central vein catheter is used in the interim.
2. Arteriovenous graft (AVG): type of surgically created vascular
access for dialysis by which a piece of biologic, semi biologic, or
synthetic graft material connects the patient’s artery to a vein.
3. Central vein catheters (CVC): direct cannulation/catheterization
of veins (subclavian, internal jugular, or femoral) is used for temporary dialysis access. CVC access is the
least preferred permanent access because of the increased risk of clotting and infection.

Complications related to vascular access

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in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise of any part of this document, without the prior written permission of UCU, is strictly prohibited.
 1. Partial or complete obstruction (clotting, stenosis or thrombosis of AVF/AVG, central vein thrombosis or
stenosis)
2. Infection; bleeding; aneurysm

Nursing Interventions in Hemodialysis

1. Practice Arm precaution
2. Assess for patency: auscultate for bruit, palpate for thrill
3. Tourniquet be always available if A-V shunt is present
4. Facilitate fluid and electrolyte balance
a. Preventing hypovolemic shock
i. Administer blood transfusion as ordered
ii. Omit dose of the hypertensive drug on dialysis days to avoid hypotension.
b. Prevent disequilibrium phenomenon
i. Initial hemodialysis be done for 30 minutes only
ii. Disequilibrium syndrome is caused by more rapid removal of waste products from the blood
than from the brain. This is due to the presence of the blood-brain barrier. Cerebral edema
causes signs & symptoms of increased ICP. Signs and symptoms include headache, nausea
and vomiting, restlessness, decreased level of consciousness, and seizures.
c. Preventing blood loss because exsanguination may occur if bloodlines separates or dialysis needles
become dislodged.
5. Surveillance for complications
a. Hypertriglyceridemia due to disturbance of lipid metabolism leading to arteriosclerotic cardiovascular
disease, heart failure, coronary heart disease, stroke.
b. Infections, systemic, or localized.
c. Anemia
d. Gastric ulcers from the physiologic stress of chronic illness, medication, and preexisting medical
conditions (e.g., diabetes).

NCM 112
e. Bone problems (renal osteodystrophy) from alterations in mineral metabolism that can result in
bone pain and fractures, interfering with mobility
f. Hypotension may occur during the treatment as fluid is removed.
g. Hypervolemia/pulmonary edema often occur as fluid accumulates between dialysis treatments.
6. Promoting comfort by providing hygienic measures
7. Maintaining activity and nutrition

B. Peritoneal Dialysis
Involves repeated cycles of instilling dialysate into the peritoneal cavity, allowing time for substance
exchange, and then removing the dialysate.

The major advantages of peritoneal dialysis

1. It provides a steady state of blood chemistries.
2. The patient can dialyze alone in any location without the need for machinery.
3. The patient can readily be taught the process.
4. The patient has few dietary restrictions, because of loss of CHON in dialysate, the patient is usually placed
on a high CHON diet.
5. The patient has much more control over daily life.
6. Peritoneal dialysis can be used for hemodynamically unstable patients.

Types of Peritoneal Dialysis

1. Intermittent Peritoneal Dialysis (IPD): involves dialyzing for a total of approximately 40 hours per week.
The time period is divided into segments and is done three to seven times per week, usually at night; the
abdomen is left empty between dialysis sessions.

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 2. Continuous Ambulatory Peritoneal Dialysis (CAPD): is a practical self-
dialysis method that involves almost constant peritoneal contact with the
dialysis solution for patients with end-stage renal disease.
a. A permanent indwelling catheter is implanted into the peritoneum.
b. A connecting tube is attached to the external end of the peritoneal
catheter, and the tube is inserted into a sterile plastic bag of
dialysate solution.
c. The dialysate bag is raised to the shoulder level and infused by
gravity into the peritoneal cavity (approximately 10 minutes for a
2-L volume).
d. Then the plastic bag attached to the connecting tube is folded and
placed in a pouch at the waist, under the patient’s clothing.
e. At the end of the dwelling time (approximately 4 hours) the bag is
removed from the pouch, unfolded, and placed near the floor to
allow the dialysate to drain by gravity over a 10-20 minutes period.
f. The patient performs 4-5 exchanges daily, 7 days/week with an
overnight dwell allowing uninterrupted sleep.

➢ Advantages Over Hemodialysis

o Physical and psychological freedom and independence.
o More liberal diet and fluid intake.
o Relatively simple and easy to use.
o Satisfactory biochemical control of uremia
➢ Patient Education
a. The use of CAPD as a long-term treatment depends on the prevention of recurring peritonitis.
b. Use strict aseptic technique when performing bag exchanges. All persons in the room, including the
patient, must wear a mask any time connecting or disconnecting the transfer set to or from another

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system.
c. Perform bag exchanges in a clean, closed-off area without pets and other activities.
d. Wash hands before touching the bag.
e. Inspect bag and tubing for defects and leaks.
f. Do not omit bag changes—this will cause inadequate control of renal failure.
g. Some weight gain may accompany CAPD—the dialysate fluid contains a significant amount of
dextrose, which adds calories to daily intake.
h. Report signs and symptoms of peritonitis like cloudy peritoneal fluid, abdominal pain or tenderness,
malaise, fever.

3. Continuous Cycling Peritoneal Dialysis (CCPD) – uses automated peritoneal dialysis machine overnight with
prolonged dwell time during the day.
a. The patient is connected to a cycler machine every evening, receiving 3-5 exchanges during the
night. In the morning, after infusing fresh dialysate, the catheter is capped.
b. Permits freedom from the exchange during the day.

( )

Inflammation of the glomerular capillaries of the kidney because of an immunologic mechanism.

Etiology: Occurs after an infection elsewhere in the body or may develop secondary to systemic disorders.

Pathophysiology
Antigen (group A beta-hemolytic streptococcus)
↓
Antigen-Antibody Reaction produces immune complexes
↓
Infiltration & trapping of circulating antigen-antibody complexes within the glomeruli
↓
Inflammation & degeneration of renal tissue
↓
Thickening of the glomerular filtration membrane
↓
Scaring & loss of filtering surface
↓
Decrease glomerular filtration rate (GFR)
↓
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 Renal Failure

Clinical Manifestations
1. History of a precipitating streptococcal infection, usually pharyngitis or impetigo from group A streptococcus
2. Proteinuria
3. Hematuria or cola-colored urine → Anemia
4. Oliguria for several days
a. Edema particularly periorbital and facial swelling; edema of the extremities
b. Uremia (Azotemia)
c. Hypertension, headache
5. Anorexia, fatigue, and weakness

Diagnostic Evaluation
1. Urinalysis for gross hematuria and proteinuria; scanty in amount
2. Blood - elevated BUN & serum creatinine level, low total protein (albumin) level, increased antistreptolysin
titer (from reaction to the streptococcal organism)
3. Needle biopsy of the kidney reveals obstruction of glomerular capillaries from the proliferation of endothelial
cells.

Medical Management
1. Antibiotics to eliminate the infection
2. Diuretics & antihypertensives for volume overload and hypertension
3. Digitalis if circulatory overload develops
4. Plasmapheresis (plasma exchange) and corticosteroids to reduce the inflammatory response
5. Dialysis if a severe renal problem develops

Nursing Diagnoses
1. Excess fluid volume related to sodium retention and decreased glomerular filtration rate.

NCM 112
2. Imbalanced nutrition: less than body requirements related to a catabolic state, anorexia, and malnutrition-related
to acute glomerulonephritis.

Nursing Interventions
1. Improving fluid balance
a. Monitor vital signs, I & O and replace fluids according to patient’s fluid losses (urine, feces, insensible
loss if rapid breathing or sweating) and weights
b. Recognize common complications such as congestive heart failure: distended neck veins,
tachycardia, enlarge and tender liver, crackles at the base of the lungs.
c. Monitor for hypertension; observe for hypertensive encephalopathy and any evidence of seizure
activity.
2. Dietary restrictions
a. High carbohydrates
b. Low protein (if BUN & serum creatinine is elevated)
c. Low Na intake
d. Fluid restriction

A type of renal failure characterized by a marked increase of protein in the urine (proteinuria), decrease in
albumin in the blood (hypoalbuminemia), edema, and excess lipids in the blood (hyperlipidemia). These occur as a
consequence of excessive leakage of plasma proteins into the urine because of increased permeability of the
glomerular capillary membrane.

Etiology: seen in any conditions that seriously damage the glomerular capillary membrane such as infection (chronic
glomerulonephritis); Diabetes Mellitus, Systemic Lupus Erythematosus; circulation problem; pregnancy
(preeclampsia); and viral infections (human immunodeficiency)

Pathophysiology

Damage of cell in glomerular capillary membrane

↓
Increase membrane porosity/permeability of glomerular capillaries to protein
↓
Proteinuria or Hypoalbuminemia
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 Decrease Oncotic pressure Increase liver synthesis of protein & lipids
↓ ↓
Fluid moves from intravascular to Hyperlipidemia
Extracellular compartment ↓
↓ Accelerated atherosclerosis
Decrease Plasma volume
↓
Hypovolemia
↓
Release of renin & angiotensin Decrease Blood pressure
↓ ↓
Increase Aldosterone secretion Release of ADH
↓ ↓
Na and H2O retention Reabsorption of H2O

Edema

Clinical Manifestations
1. Insidious onset of edema; easily pitting edema
a. Puffiness around eyes in the morning
b. Ascites
c. Sacrum, ankles, and hands (dependent areas)
2. Fatigue, headache, malaise, irritability
3. Marked proteinuria leading to depletion of body proteins.
4. Hypercholesterolemia (increased cholesterol and triglycerides) may lead to accelerated atherosclerosis

NCM 112
Diagnostic Evaluation
1. Urinalysis shows marked proteinuria
2. Twenty-four-hour urine for protein (increased) and creatinine clearance (maybe decreased).
3. Needle biopsy of the kidney for histologic examination of renal tissue to confirm the diagnosis.
4. Serum chemistry: decreased total protein and albumin, normal or increased creatinine, increased
triglycerides, and altered lipid profile

Medical Management
1. Treatment of causative glomerular disease.
2. Drug therapy
a. Corticosteroids and ACE inhibitors to decrease proteinuria.
b. Antibiotics for bacterial infection
c. Diuretics in edematous stage
d. Lipid-lowering agents.
e. IV albumin infusion

Nursing Diagnoses
1. Risk for deficient fluid volume intravascularly related to the disease process.
2. Risk for infection related to treatment with immunosuppressive agents.

Nursing Management
1. Increasing circulating volume and decreasing edema
a. Monitor daily weight, intake and output, and abdominal girth
b. Assess for vital signs especially BP, and heart rate to detect hypovolemia.
c. Monitor serum BUN and creatinine to assess renal function.
d. Bed rest (if with severe edema) however, some ambulation is necessary to reduce the risk of
thromboembolic complications.
e. Dietary regimen to counteract hypoproteinemia
i. High protein and carbohydrate diet
ii. Low sodium and fluid restriction if edema is severe
iii. Diet low in saturated fats
2. Preventing infection both illness and drug therapy increase susceptibility
a. Monitor for signs and symptoms of infection like an elevation of body temperature.
b. Monitor CBC as ordered.
c. Protect from others who are ill
d. Limit invasive procedures but if it is inevitable, use aseptic technique for all invasive procedures and
educate the patient on the importance of strict handwashing.
All information contained in this module are property of UCU and provided solely for educational purposes. Reproduction, storing in a retrieval system, distributing, uploading or posting online, or transmitting
in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise of any part of this document, without the prior written permission of UCU, is strictly prohibited.
 3. Maintain skin integrity
a. Avoid IM injections
b. Turn frequently
4. Monitor for signs and symptoms of blood clots due to leakage of proteins that prevent clot formation
a. Pulmonary embolism shows an increased RR, dyspnea, decrease O2 Saturation, increase HR, and chest
pain
b. Deep Vein Thrombosis shows redness, swelling, warmth, and tenderness in the legs and arms.

Written Assignment: Prepare a short-written report on the causes of acute kidney injury and ways to
prevent it.
Group Assignment: Discuss the signs and symptoms to assess for end-stage kidney disease.
Web Assignment: Review the Internet for information on kidney transplantation. Summarize your findings.

Acute renal failure is a sudden, rapid decrease in renal function that is potentially reversible. Whereas,
chronic renal failure is a progressive and irreversible condition that eventually requires lifesaving treatment
measures such as dialysis or a kidney transplant in end-stage disease. Dialysis is a technique for cleaning and
filtering the blood; there are two different methods: hemodialysis and peritoneal dialysis
Renal dysfunction may be due to a primary disease within the kidney or maybe a secondary disorder
elsewhere in the body when the kidney function is impaired, dysfunction of extrarenal systems ultimately develops;
similarly, primary dysfunction in other systems may readily affect renal function.
Dialysis is the diffusion of solute molecules through a semipermeable membrane, passing from the side of
higher concentration to that of lower concentration. The purpose of dialysis is to maintain fluid, electrolyte, and

NCM 112
acid-base balance and to remove endogenous and exogenous toxins.
Glomerulonephritis is inflammation of the tiny filters in your kidneys (glomeruli). Glomeruli remove excess
fluid, electrolytes, and waste from your bloodstream and pass them into your urine. Severe or prolonged
inflammation associated with glomerulonephritis can damage your kidneys.
Nephrotic syndrome is a kidney disorder that causes your body to pass too much protein in your urine.
Nephrotic syndrome is usually caused by damage to the clusters of small blood vessels in your kidneys that filter
waste and excess water from your blood. The condition causes swelling, particularly in your feet and ankles, and
increases the risk of other health problems.
We have gone through acute and chronic renal failure in this unit. I do hope that you have learned a great
deal which must have equipped you with the necessary knowledge and skills to care for your future patients.

Lippincott Manual of Nursing Practice 11th Edition. Nettina et al., 2019

Textbook of Medical-Surgical Nursing-13th Edition. Brunner & Suddarth, 2014
Medical-Surgical Nursing 8th Edition. Joyce Black, 2014
Mosby’s Comprehensive Review of Nursing 20th Edition. Nugent et al., 2014
Assessment & Management of Clinical Problems 9th Edition. Lewis et al., 2014
Medical-Surgical Nursing 2nd Edition. Udan, 2009
Anatomy and Physiology. Tortora. 2008.
Pathophysiology Review. Marlene Hurst, 2008

https://tinyurl.com/y2wpom34 (Acute Renal Failure)

https://tinyurl.com/y43ycmdp (Chronic Renal Failure)
https://tinyurl.com/y6ogqr76 (Nephrotic Syndrome vs Glomerulonephritis)

All information contained in this module are property of UCU and provided solely for educational purposes. Reproduction, storing in a retrieval system, distributing, uploading or posting online, or transmitting
in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise of any part of this document, without the prior written permission of UCU, is strictly prohibited.
Patient Profile: John, a patient 66 years of age, is 4 days postoperative after a coronary artery bypass graft
operation. The patient has a history of hypertension, type 1 diabetes, coronary artery disease, and end-stage kidney
disease, which is treated with hemodialysis three times per week. The patient has a left arteriovenous (AV) shunt.
The patient is taking the following medications:
• Sevelamer (Renagel): 2 capsules with each meal
• Vitamin D, B12, and iron supplements with meals
• Calcium carbonate (OS-Cal): 3 tablets with each meal
• Procrit (epoetin alfa): 100 U/kg/dose subcutaneously every Monday, Wednesday, and Friday (dialysis days)
• 70/30 NPH and regular insulin 30 U twice daily (Fingerstick blood sugars are taken before meals and at
bedtime and regular insulin given per sliding scale.)
• Coreg (carvedilol): 12.5 mg twice daily
• Lanoxin: 0.125 mg (every other day, on even days)
• Acetaminophen with Codeine No. 3: 1 to 2 tablets every 6 hours
• Diphenhydramine hydrochloride (Benadryl): 25 mg every 8 hours PRN for itching
• Docusate sodium (Colace): 100 mg b.i.d.

Critical Thinking and Discussion Questions:

Using a separate sheet of paper, answer the following questions:
1. The patient is ordered to have daily dialysis. What is the rationale for this order?
2. The patient is going to hemodialysis at 8 am on an odd day. Which medication or medications should the
nurse hold before sending the patient?
3. What nursing management considerations should be made for this patient?

❖ Renal Failure, Acute

➢ Main Problem: Abrupt reversible cessation of renal function as a result of trauma, allergy, and kidney stones
➢ Initial Manifestation: Oliguria (U.O., 400 ml/24 hours)
➢ Laboratory data: elevated BUN and creatinine

NCM 112
➢ Nursing Diagnosis: Alteration in Urinary Elimination
Fluid and electrolyte imbalance
➢ Interventions: Monitor Intake and output
Maintain a low protein, high carbohydrate, low sodium diet and fluid restricted during the oliguric phase
and high protein, high calorie, and fluid replacement during the diuretic phase

❖ Renal Failure, Chronic

➢ Main Problem: Irreversible slow or progressive failure of the kidneys to function that results in death unless treatment is
instituted
➢ Initial manifestation: GI manifestations like anorexia, nausea, and vomiting
➢ Laboratory Data: Elevated serum creatinine level and low urine creatinine clearance
➢ Nursing Diagnosis: Alteration in urinary elimination
Fluid Volume Excess
➢ Interventions: Maintain low protein, low sodium, low potassium diet
Prepare patient for hemodialysis/peritoneal dialysis and monitor for complications
Monitor for signs and symptoms of anemia
Administer Epogen, diuretics, and antihypertensive drugs as ordered

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 NCM 112

All information contained in this module are property of UCU and provided solely for educational purposes. Reproduction, storing in a retrieval system, distributing, uploading or posting online, or transmitting
in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise of any part of this document, without the prior written permission of UCU, is strictly prohibited.