CHRONIC RENAL FAILURE reduced renal reserve, renal insufficiency, and

 Renal failure results when the kidneys cannot ESRD.

remove the body’s metabolic wastes or perform GFR categories in CKD
their regulatory functions. Category GFR Terms Clinical
 The substances normally eliminated in the urine presentations
G1 ≥90 Normal or high Markers of kidney
accumulate in the body fluids as a result of damage (nephrotic
G2 60-89 Mildly decreased syndrome, nephritic
impaired renal excretion, leading to a disruption syndrome, tubular
in endocrine and metabolic functions as well as syndrome, urinary
tract symptoms,
fluid, electrolyte, and acid-base disturbances. asymptomatic
urinalysis
 Renal failure is a systemic disease and is a final abnormalities,
common pathway of many different kidney and asymptomatic
radiologic
urinary tract diseases. abnormalities,
hypertension due to
AZOTEMIA kidney disease)
 Defined as excess of urea and nitrogenous G3a 45-59 Mildly to Mild to severe
moderately complications:
compounds in blood. decreased -anemia
-mineral and bone
 Due to breakdown of protein G3b 30-44 Moderately to disorder (elevated
severe decreased
 (Metabolism of carbohydrates and fats yields parathyroid
G4 15-29 Severely hormone)
water and CO2) decreased -cardiovascular
disease
 If symptoms, use term “uremia” (hypertension, lipid
Chronic renal failure, or ESRD, is a abnormalities, low
serum albumin)
progressive, irreversible deterioration in renal G5 <15 Kidney failure -includes all of
function in which the body’s ability to maintain the above in
metabolic and fluid and electrolyte balance fails, addition
-uremia
resulting in uremia or azotemia (retention of urea
and other nitrogenous wastes in the blood).
STAGES OF RENAL FAILURE
ESRD may be caused by systemic disease, such
What happen?
as diabetes mellitus (leading cause); hypertension;
There are no specific symptoms, but kidney
chronic glomerulonephritis; pyelonephritis;
function can slowly decline.
obstruction of the urinary tract; hereditary lesions,
Kidney function is very low, and treatment
as in polycystic kidney disease; vascular disorders:
for kidney failure may be needed soon.
infections; medications; or toxic agents.
Kidneys can no longer keep up with
Dialysis or kidney transplantation eventually
removing waste products and extra water. This is
becomes necessary for patient survival. Dialysis is an
called kidney failure. Although there is no cure,
effective means of correcting metabolic toxicities at
treatment options are available.
any age, although the mortality rate in infants and
Stage Description GFR,
young children is greater than adults in the presence ml/min/1.73 m2
of other, nonrenal diseases and in the presence of At increased risk ≥ 60
anuria or oliguria. 1 Kidney damage ≥90
with normal or
PATHOPHYSIOLOGY increased GFR
 As renal function declines, the end products of 2 Kidney damage 60-89
protein metabolism (which are normally excreted with mild
in urine) accumulate in the blood. Uremia decreased GFR
3 Moderately 30-59
develops and adversely affects every system in decreased GFR
the body. 4 Severely 15-29
 The greater the buildup of waste products, the decreased GFR
more severe the symptoms. There are three well- 5 Kidney failure <15 (dialysis)
recognized stages of chronic renal disease;
CLINICAL MANIFESTATION
 Because virtually every body system is affected
by the uremia of chronic renal failure, patients
exhibit a number of signs and symptoms depends
in part on the degree of renal impairment, other
underlying conditions, and the patient’s age.
CARDIOVASCULAR MANIFESTATION
 Hypertension (due to sodium and water retention
or from activation of the renin-angiotensin-
aldosterone system), heart failure and pulmonary
edema (due to fluid overload), and pericarditis
(due to irritation of the pericardial lining by
uremic toxins) are among the cardiovascular
problems manifested in ESRD.
 Strict fluid volume control has been found to
normalize hypertension in patients receiving
peritoneal dialysis.
DERMATOLOGIC SYMPTOMS
 Severe itching (prutitus) is common. Uremic
frost, the deposit of urea crystals on the skin, is
uncommon today because of early and
aggressive treatment of ESRD with dialysis.
OTHER SYSTEMIC MANIFESTATIONS
 GI signs and symptoms are common and include
anorexia, nausea, vomiting and hiccups.
 Neurologic changes, including altered levels of
consciousness, inability to concentrate, muscle
twitching, and seizures, have been observed.
 It is generally thought, however, that the
accumulation of uremic waste products is the
probable cause.
GLOMERULAR FILTRATION RATE
 Decreased GFR can be detected by obtaining a
24-hour urinalysis for creatinine clearance.
 As glomerular filtration decrease (due to
nonfunctional glomeruli), the creatinine
clearance value decreases, 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
 The kidney cannot concentrate or dilute the urine
normally in ESRD.
 Some patients retain sodium and water,
increasing the risk for edema, heart failure, and
hypertension.
 Hypertension may also result from activation of
the renin-angiotensin-aldosterone axis and the
concomitant increased aldosterone secretion.
 Episodes of vomiting and diarrhea may produce
sodium and water depletion, which worsens the
uremic state.
ACIDOSIS
 With advanced renal disease, metabolic acidosis
occurs because 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 (HCO3-).
ANEMIA
 Anemia develops as a result of inadequate
erythropoietin production, the shortened life span
of RBCs, nutritional deficiencies, and the
patient’s tendency to bleed, particularly from the
GI tract.
 Erythropoietin, a substance normally produced
by the kidney, stimulates bone marrow to
produce RBCs.
 In renal failure, erythropoietin production
decreases and profound anemia results,
producing fatigue, angina, and shortness of
breath.
CALCIUM AND PHOSPHORUS IMBALANCE
 Serum calcium and phosphate levels have a
reciprocal relationship in the body: as one rises,
the other decreases.
 With decreased filtration through the glomerulus
of the kidney, there is an increase in the serum
phosphate level and a reciprocal or
corresponding decrease in the serum calcium
level.
 The decreased serum calcium level causes
increased secretion of parathormone from the
parathyroid glands. In renal failure, however, the
body does not respond normally to the increased
secretion of parathormone; as a result, calcium
leaves the bone. Often producing bone changes
and bone disease.
COMPLICATIONS
 Potential complications of chronic renal failure
that concern the nurse and that necessitate a
 collaborative approach to care include the  Usually, the fluid allowance is 500-600 mL more
following: than the previous day’s 24-hour urine output.
o Hyperkalemia –due to decreased (give 1L of water to patient good for 1 day)
excretion, metabolic acidosis, DIALYSIS
catabolism and excessive intake (diet,  Hyperkalemia is usually prevented by ensuring
medications, fluids). adequate dialysis treatments with potassium
o Pericarditis –pericardial effusion, and removal and careful monitoring of all
pericardial tamponade due to retention medications, both oral and intravenous, for their
of uremic waste products and potassium content. The patient is placed on a
inadequate dialysis potassium-restricted diet.
o Hypertension –due to sodium and water  The patient with increasing symptoms of chronic
retention and malfunction of the renin- renal failure is referred to a dialysis and
angiotensin-aldosterone system. transplantation center early in the course of
o Anemia –due to decreased progressive renal disease.
erythropoietin production, decreased  Dialysis is usually initiated when the patient
RBC life span, bleeding in the GI tract cannot maintain a reasonable lifestyle with
from irritating toxins, and blood loss conservative treatment.
during hemodialysis. ASSESS FLUID STATUS:
o Bone disease and metastatic a. Daily weight
calcifications due to retention of b. Intake and output balance
phosphorus, low serum calcium levels, c. Skin turgor and presence of edema
abnormal vitamin D metabolism, and d. Distention of neck veins
elevated aluminum levels. e. Blood pressure, pulse rate, and rhythm
MEDICAL MANAGEMENT f. Respiratory rate and effort
 The goal of management is to maintain kidney FLUID RESTRICTION
function and hemostasis for as long as possible. L –limit fluid intake to prescribed volume
 All factors that contribute to ESRD and all E –explain to patient and family rationale for
factors that are rerversible (e.g., obstruction) are restriction
identified and treated. A –assist patient to cope with the discomforts
 Management is accomplished primarily with resulting from fluid retention.
medications and diet therapy, although dialysis P –provide or encourage frequent oral hygiene.
may also be needed to decrease the level of ASSESSMENT:
Assess possible risk factors To obtain baseline data
uremic waste products in the blood.
Monitor and record vital To obtain baseline data
PHARMACOLOGIC THERAPY signs
 Complications can be prevented or delayed by Assess patient’s appetite To note for presence of
administering prescribed antihypertensives, nausea and vomiting
erythropoietin (Epogen), iron supplements, Note amount/rate of fluid To prevent fluid overload
intake from all sources and monitor intake and
phosphate-binding agents, and calcium output
supplements. Compare current weight To monitor fluid retention
NUTRITIONAL THERAPY gain with admission or and evaluate degree of
previous stated weight excess
 Dietary intervention is necessary with
Auscultate breath sounds For presence of crackle or
deterioration of renal function and includes congestion
careful regulation of protein intake, fluid intake Record occurrence of To evaluate degree of
to balance fluid losses, sodium intake to sodium dyspnea excess
Note presence of edema To determine fluid retention
losses, and some restriction of potassium.
Measure abdominal girth May indicate increase in
FLUID INTAKE for changes fluid retention
Evaluate mentation for May indicate cerebral
confusion and personality edema
changes
Observe skin mucous
membrane
Change position of client
timely
Review lab data like BUN,
creatinine, serum electrolyte
Restrict sodium and fluid
intake if indicated
Record I&O accurately and
calculate fluid volume
balance
Weigh client
Encourage quiet, restful
atmosphere
Promote overall health
measure
To evaluate degree of fluid
excess
To prevent pressure ulcers
To monitor fluid and
electrolyte imbalances
To lessen fluid retention
and overload
To monitor kidney function
and fluid retention
Weight gain indicated fluid
retention or edema
To conserve energy and
lower tissue oxygen
demand
To promote wellness