Nursing College

1. Chronic Renal Failure
Dr. Hayder Ali Hussein
Adult Nursing Phd

2. CHRONIC RENAL FAILURE
(END-STAGE RENAL DISEASE)
Chronic renal failure, or ESRD, is a progressive,
irreversible deterioration in renal function in which the
body’s ability to maintain metabolic and fluid and
electrolyte balance fails, resulting in uremia or azotemia
(retention of urea and other nitrogenous wastes in the
blood).
The incidence of ESRD has increased by almost 8% per
year for the past 5 years, with more than 300,000 patients
being treated in the United States .

3. ↓Blood
volume
or ↓BP
Volume receptor
Atria and great veins
Hypothalamus
↓
Posterior
pituitary gland
Osmoreceptors in
hypothalamus
↑Osmolarity
↑ADH Kidney
tubules
↑H2O
reabsorption
↑vascular
volume and
↓osmolarity
Narcotics, Stress,
Anestheticagents, Heat,
Nicotine, Antineoplastic
agents, Surgery
ANTIDIURETIC HORMONE REGULATION MECHANISMS

4. Angiotensinogen in
plasma
Juxtaglomerular
cells-kidney
↓Serum Sodium
↓Blood volume
Angiotensin I
Kidney tubules
Angiotensin II
Adrenal Cortex
↑Sodium
resorption
(H2O resorbed
with sodium);
↑ Blood
volume
RENIN
Angiotensin-
converting enzyme
ALDOSTERONE
Intestine, sweat
glands, Salivary
glands
Via vasoconstriction of arterial smooth muscle
ALDOSTERONE-RENIN-ANGIOTENSIN SYSTEM

5. ESRD may be caused by systemic diseases, such
as
diabetes mellitus (leading cause); hypertension; chronic
glomerulonephritis; pyelonephritis; obstruction of the
urinary tract; hereditary lesions, as in polycystic kidney
disease; vascular disorders; infections; medications; or
toxic agents.

6. • Stage 1
• Kidney damage with normal or ↑ GFR
• GFR ≥ 90 ml/min/1.73 m2
• Stage 2
• Kidney damage with mild ↓ GFR
• GFR 60-89
• Stage 3
• Moderate ↓ GFR
• GFR 30-59
• Stage 4
• Severe ↓ GFR
• GFR 15-29
• Stage 5
• Kidney failure
• GFR <15 (or dialysis)
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7. Pathophysiology of ESRD
• As renal function declines, the end products of
protein metabolism accumulate in the blood.
Uremia develops and adversely affects every
system in the body. The greater the buildup of
waste products, the more severe the symptoms.
• ESRD occurs when there is less than 10%
nephron function remaining. All of the normal
regulatory, excretory, and hormonal functions
of the kidney are severely impaired.
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8. Pathophysiology of ESRD (Continued….)
• The rate of decline in renal function and
progression of chronic renal failure is related
to the underlying disorder, the urinary
excretion of protein, and the presence of
hypertension. The disease tends to progress
more rapidly in patients who excrete
significant amounts of protein or have elevated
blood pressure than in those without these
conditions.
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9. Clinical Manifestations of ESRD
• Cardiovascular: These are hypertension (due to
sodium and water retention), heart failure and
pulmonary edema (due to fluid overload), and
pericarditis (due to irritation of the pericardial lining
by uremic toxins).
• Dermatologic symptoms: Severe itching (pruritus)
• Other systemic manifestations: GI signs and
symptoms (anorexia, nausea, vomiting, and hiccups)
are common. Neurologic changes (altered levels of
consciousness, inability to concentrate, muscle
twitching, and seizures) were reported. It is generally
thought that the accumulation of uremic waste
products is the probable cause.
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10. Investigations and Diagnostic Test
1-Blood urea
2-Serum Creatinine
3- Blood Urea Nitrogen
4-Uric acid

11. Assessment and Diagnostic Findings
• Glomerular filtration rate: GFR is decreased
resulting in a decrease in creatinine clearance,
whereas the serum creatinine and BUN levels
increase. Serum creatinine is the more sensitive
indicator of renal function because of its constant
production in the body.
• Sodium and water retention: In ESRD, some
patients retain sodium and water, increasing the risk
for edema, heart failure, and hypertension. Other
patients may lose salt and run the risk of developing
hypotension and hypovolemia.

12. Assessment and Diagnostic Findings (Continued…)
• Metabolic acidosis: This condition develops as the
kidney cannot excrete increased loads of acid.
Decreased acid secretion primarily results from
inability of the kidney tubules to excrete ammonia
(NH3) and to reabsorb sodium bicarbonate
(CHNaO3).
• Anemia: Anemia results from inadequate
erythropoietin (stimulates bone marrow to produce
RBCs) production by kidneys, the shortened life span
of RBCs, nutritional deficiencies, and blood loss
during hemodialysis.
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14. Medical Management
• Pharmacologic therapy:
– Antacids: Hyperphosphatemia and hypocalcemia are
treated with aluminum-based antacids that bind dietary
phosphorus in the GI tract. To avoid the potential long-term-
toxicity of aluminum and its association with neurologic
symptoms, calcium carbonate is prescribed.
– Antihypertensive and Cardiovascular Agents:
Hypertension is managed by intravascular volume control (via
dietary salt restriction) and a variety of antihypertensive
agents. Heart failure and pulmonary edema may also require
treatment with fluid restriction, low-sodium diets, diuretic
agents, and dialysis.
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15. • Pharmacologic therapy (Continued……):
•
– Antiseizure Agents: Neurologic abnormalities
such as seizures are controlled via intravenous
diazepam (Valium) or phenytoin (Dilantin). The side
rails of the bed should be padded to protect the
patient.
– Erythropoietin: Anemia associated with chronic
renal failure is treated with recombinant human
erythropoietin (Epogen).. Epogen is administered
either intravenously or subcutaneously three times a
week, and it may take 2 to 6 weeks for the
hematocrit to rise.
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16. • Nutritional therapy:
– Protein is restricted because urea, uric acid, and
organic acids accumulate rapidly in the blood. The
allowed protein must be of high biologic value
(dairy products, eggs). Usually, the fluid allowance
is 500 to 600 mL more than the previous day’s 24-
hour urine output. Calories are supplied by
carbohydrates and fat to prevent wasting. Vitamin
supplementation is necessary because a protein-
restricted diet does not provide the necessary
complement of vitamins. Additionally, the patient
may lose water-soluble vitamins from the blood
during dialysis.
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17. • Hemodialysis:
– Hyperkalemia is usually prevented by ensuring
adequate dialysis treatments with potassium
removal and careful monitoring of all medications
for their potassium content. The patient is placed
on a potassium-restricted diet. Dialysis is usually
initiated when the patient cannot maintain a
reasonable lifestyle with conservative treatment.
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18. Nursing Care Plan of a Patient With ESRD
•Assess fluid status (Daily weight, intake and output
balance, skin turgor and presence of edema, distention of
neck veins, blood pressure, pulse rate, and rhythm,
respiratory rate and effort).
➢ Limit fluid intake to prescribed volume.
➢Provide oral and written information as appropriate about
renal function and failure, fluid and dietary restrictions,
medications, reportable problems, signs, and symptoms,
follow-up schedule, community resources, and treatment
options.
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19. Nursing Care Plan of a Patient With ESRD (Cont…)
Assess nutritional status (weight changes, serum
electrolyte, BUN, creatinine, protein, transferrin, and
iron levels).
➢Provide patient’s food preferences within dietary
restrictions.
➢ Promote intake of high biologic value protein foods .
Assess factors contributing to fatigue (anemia, fluid and
electrolyte imbalances, retention of waste products,
depression)
➢ Promote independence in self-care activities as
tolerated; assist if fatigued.
➢ Encourage alternating activity with rest.
➢ Encourage patient to rest after dialysis treatments.
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20. THANKK
YOU FOR
YOUR
ATTENTION