NRS 457: GENITOURINARY AND ENDOCRINE
NURSING
CHRONIC KIDNEY DISEASE
GROUP 2
PREPARED BY:
1. NAZATUL IZZATI BINTI MOHD NOR ANGKASAH
2. PUTERI NURFARAH HANAN BINTI RAZAK
3. MAZNAH BINTI IBRAHIM
4. NUR FARZANA BINTI DAMANHURI
5. NURAIN NABILA BINTI HADI MUNIR
6. NURUL FARAH DALILA BINTI MOHD ASMADI
7. WAN DZUL ANEYS AQILAH BINTI WAN MOHD ZAKI
8. NOR RASYIDAH BINTI ABDUL RAHMAN
9. FARAH SYAZWANI BINTI RAZALI
10.NUR AIMUNI BINTI ZULKIFLEE
PREPARED TO:
PUAN FATIMAH BINTI SHAM
LEARNING OUTCOME
At the end of this lesson, students should be able
to :1. Define Chronic Kidney Disease (CKD).
2. Understand the pathophysiology of CKD.
3. Identify the etiology and risk factors of CKD.
4. Identify the clinical manifestations of CKD.
5. Identify the diagnostic tests for CKD.
6. Explain the management of clients with CKD.
DEFINITIONS
Chronic kidney disease (CKD) is defined by the
presence of kidney damage for three or more months
and the level of kidney function
(National Kidney Foundation [NKF], 2002)
End stage renal disease (ESRD) represents a
clinical state in which there has been an irreversible
loss of renal function.
#CKD often will lead to ERSD
DEFINITIONS
Uremia: The presence of excessive amounts of urea in the blood,
which may be a sign of kidney disease or failure.
Azotemia: An elevation of blood urea nitrogen (BUN) and
serum creatinine levels. The reference range for BUN is
8-20 mg/dL, and the normal range for serum creatinine
is 0.7-1.4 mg/dL.
Glomerular filtration rate (GFR) is the volume of plasma filtered in the
glomeruli per unit time, usually reported in mL/min.
(Medical Physiology: Principles for Clinical Medicine, 3rd edition, 2009)
PATHOPHYSIOLOGY
PATHOPHYSIOLOGY
Regardless of the primary cause of
nephron loss, some usually survive
or are less severely damaged
These nephrons then adapt and
enlarge, and clearance per nephron
markedly increases.
If the initiating process is diffuse,
sudden, and severe, such as in some
patients with rapidly progressive
glomerulonephritis (crescentic
glomerulonephritis), acute or subacute
renal failure may ensue with the rapid
PATHOPHYSIOLOGY
Focal glomerulosclerosis develops in
these glomeruli, and they eventually
become non-functional.
At the same time that focal
glomerulosclerosis develops, proteinuria
markedly increases and systemic
hypertension worsens.
This process of nephron adaptation has
been termed the "final common path."
Adapted nephrons enhance the ability of
the kidney to postpone uremia, but
ultimately the adaptation process leads to
the demise of these nephrons.
Adapted nephrons have not only an
PATHOPHYSIOLOGY
Uncontrolled diabetes
Glomerular hyperfitration- increase in GFR and
renal blood flow
Chronic hyperglycemia lead to diabetic
nephropathy
Systemic Hypertension
Elevated BP cause vascular and glomerular damagelead to tubular atrophy and chronic interstitial
nephritis tubular and glomerular loss and in the
end nephron loss
Nephrotoxins
Toxic agent or substance (NSAIDs) that inhibits,
damages or destroys the cells or tissues of the
kidneys.
Decreased perfusion (Blood flow)
From severe dehydration or episodes of shock.
Proteinuria
Presence of abnormal quantities of protein in the
urine, which may indicate damage to the kidneys.
Hyperlipidemia
High lipid levels can cause blockage in arteries
Hyperphosphatemia with calcium
phosphate deposition
Electrolyte disturbance, meaning abnormally
elevated level of phosphate in blood.
STAGES OF CHRONIC KIDNEY DISEASE
STAGES OF CHRONIC KIDNEY DISEASE
ETIOLOGY
Diseases and conditions that often lead to CKD include :
Type 1 or type 2 diabetes
High blood pressure
Glomerulonephritis, an inflammation of the kidney's filtering
units (glomeruli)
Interstitial nephritis, an inflammation of the kidney's tubules and
surrounding structures
Polycystic kidney disease
Prolonged obstruction of the urinary tract, from conditions such
as enlarged prostate, calculi and some cancers
Vesicoureteral reflux, a condition that causes urine to back up
into your kidneys
RISK FACTORS
Factors that may increase the risk of chronic kidney
disease :
Diabetes
High blood pressure
Heart disease
Smoking
Obesity
High cholesterol
Family history of kidney disease
Age 65 or older
CLINICAL MANIFESTATIONS
Early Stage
Weakness
Decreased appetite
Nausea
Loin pain
Elevated BP
Change in
urination(nocturia,polyuria,frequen
cy)
Late Stage
General- Lassitude, fatigue, high BP,
decreased mental acuity
Skin- Pale due to anemia, dry, scaly,
bruises easily due to platelet
abnormalities, uremic frost.
Pulmonary- Dyspnea, pleural effusion,
pulmonary edema, uremic lung.
Cardiovascular- Pericardial friction rub,
pericarditis. congestive heart failure.
Gastrointestinal- Anorexia, nausea,
vomiting, weight loss, stomatitis,
unpleasant taste in the mouth (first
symptom for ESRD patient) ,GI bleeding
due to GI irritation.
Neuromuscular- Muscle cramps, restless
legs, sleep disorders, seizures, coma.
Central, peripheral and autonomic
neuropathy.
Endocrine- Elevated uric acid level(gout),
Sign/lab finding
Generalized
edema
Symptoms
Swelling
Mechanism
Water retention due to a loss of GFR leading to sodium and fluid retention.
Fluid moves into the extravascular space, due to increased hydrostatic
pressure, causing pitting edema in the lower extremity (fluid movement could
also be due to hypoalbuminemia, in some diseases, leading to a low oncotic
pressure).
Pulmonary
Shortness of breath
Fluid accumulation causes pulmonary edema and loss of air space causing
crackles
ventilation-perfusion mismatch. This leaves less area for oxygen diffusion form
the blood vessels.
Anemia
Fatigue, reduced
Erythropoietin (EPO), the major erythropoiesis stimulator, is released from the
exercise capacity, and kidneys; with renal failure, there is loss of EPO release.
pallor
Weight loss
Loss of lean body
Protein-energy malnutrition due to metabolic acidosis. Loss of kidney function
mass
results in impaired H+ secretion from the body.
Hyperkalemia
Malaise, palpitations Inability of the kidneys to secrete potassium in the urine leads to life
threatening arrhythmias.
Mechanisms of renal osteodystrophy
Hyperphosphatemi
Damaged kidneys fail to excrete phosphate.
a
Also secondary to high parathyroid hormone levels.
Hypocalcemia
Thought to be secondary to low Vitamin D3 levels. In early stages of CKD, low
levels of calcitriol are due to hyperphosphatemia (negative feedback). In the
later stages of CKD, low levels are hypothesized to be due to decreased
synthesis of 1-hydroxylase (enzyme that converts calcifediol to calcitriol in
the kidneys).
Secondary and
To compensate for the low calcium due to low Vitamin D levels, the
tertiary
parathyroid glands increase the parathyroid hormone secretion. This leads to a
hyperparathyroidis
high bone turnover, always attempting to normalize the low calcium levels in
m
the blood. Over time, this becomes maladaptive leading to extraosseous
calcification, and parathyroid hyperplasia develops (tertiary
DIAGNOSTIC TESTS
1.Urinalysis: fixed specific gravity 1.010 (low); excess protein, blood
cells, cellular casts
2. Urine culture; identify infection
3.BUN and serum creatinine; evaluate kidney function
Mild azotemia: BUN 20-50 mg/dl
Severe renal impairment: BUN > 100 mg/dl
Uremic symptoms: > BUN 200mg/dl
*Creatinine levels >4 mg/dl = serious renal impairment
(**better indicator than BUN of renal function); elevated BUN
responsible for neurological symptoms
4.Creatinine clearance: reflects GFR and renal function (most
accurate; need 24 hour urine collection)
5. *Serum electrolytes: monitored throughout course of CKD
6.CBC: moderately severe anemia with hematocrit 20-30%; low
hemoglobin; reduced RBCs and platelets
7. Renal ultrasonography: CKD; decreased renal size
MANAGEMENT ( attempt to delay onset of
ESRD)
1. Medications
General effects of CKD on medication effects
*Increased half-life and inc. plasma levels of meds
excreted by kidneys; monitor carefully
*Dosage may change when in renal failure; do not give
demerol to patients on dialysis (toxic); digitalis excreted
largely by kidney*
*Dec. drug absorption if phosphate-binding agents
administered concurrently
*Low plasma protein levels > lead to toxicity when proteinbound drugs are given
*Avoid nephrotoxic drugs (Aminoglycosides, penicillin in high
doses, carefully monitor vancomycin due to toxic accumulation);
Amphoteracin B very nephrotoxic ; also contrast-media induced
nephrotoxicity
Medications
Significance
Diuretics
eg. furosemide 20-80mg PO OD / 20-40mg
IV/IM once
To reduce extracellular fluid volume and
edema
Antihypertensive agents (ACE inhibitors
preferred)
eg. perindopril 4-8mg PO QID
To lower blood pressure
Antacids
To treat gastric irritation
No magnesium based, can cause
magnesium toxicity
to correct serum pH in metabolic acidosis
Alkalinizing agents
eg. sodium bicarbonate 325 to 2000 mg PO
OD to QID
Oral phosphorus binding agents
eg. calcium carbonate 1-1.2 g PO QID
Supplements and hormone replacement
Vitamin D
Folic acid and iron tablets
EPO inj.
Act as binding agent to lower phosphate
level
As calcium supplement
Improve calcium absorption
To combat anemia
MANAGEMENT
2. Dietary restrictions
*Early in CRF: diet modification-slow kidney failure
avoid uremic symptoms
Restrict proteins (40gm/day) of high biologic value
Increase carbohydrate intake (35kcal/kg/day)
Limit fluid to 1-2 L per day; limit sodium to 2 g/day
(usual guideline is 500-600 ml more than previous days
24 urine output)
Restrict potassium to (60-70 mEg/day; no salt
substitutes); avoid bananas, prunes, raisins, orange juice,
tomatoes, deep green and yellow vegetables
Restrict phosphorus food (especially milk, ice cream,
MANAGEMENT
3. Renal replacement therapies
*Used when medications and diet are no longer effective
Haemodialysis (AV fistula or
graft)
the most common type of
dialysis.
During the procedure,a tube is
attached to a needle in your
arm.Blood passes along the
tube and into an external
machine that filters it, before
it's passed back intothe arm
along another tube.
MANAGEMENT
Peritoneal dialysis
uses the inside lining of abdomen (the peritoneum) as the filter, rather
than a machine. Like the kidneys, the peritoneum contains thousands of
tiny blood vessels, making it a useful filtering device.
1. Warmed sterile dialysate instilled into peritoneal cavity via
catheter inserted into peritoneal cavity
2. Metabolic waste products and excessive electrolytes diffuse into
dialysate while it remains in abdomen
3. Water diffusion controlled by glucose (dextrose) concentration in
the dialysate which acts as an osmotic agent
4. Amount of solution removed determined by glucose
concentration of the dialysate!
Excess fluid/solutes removed more gradually; less risk for unstable
client
5. Fluid drained by gravity into sterile bag at set interval-removing
waste products/ excess fluid
TYPES OF PERITONEAL DIALYSIS
a.CAPD:
. most common
. continuous
ambulatory peritoneal
dialysis
. exchanges 4-5 times a
day
. treatments-ongoing 24
hours a day; 7 days a
week
. 2 liters solution in
peritoneal cavity except
during drain time;
independent treatment
b. CCPD:
continuous cycler peritoneal
dialysis;
uses delivery devise
(cycler) during nighttime
hours and continuous dwell
during day
Peritoneal Dialysis
No vascular access & heparin (except
placement peritoneal catheter)
No rapid fluctuation of in extracellular
fluid; continuous process
Diet liberalized; more protein,
personal adjustment of fluid intake by
increasing amount of dextrose in
dialysate (osmosis to cause loss of
fluid) *still should control Na, Mg,
Phosphorous intake & fluid
May require less insulin; add insulin to
dialysate
Potential increased risk for infection
(peritonitis)
Hemodialysis
Requires vascular access and heparin
Rapid fluid/electrolyte shift; done only 3-4
times a week; 3-5 hours
Diet more restrictive; only means to
control fluids is by dialysis 3-4 times week
and personal regulation fluid intake
Onset of dialysis may allow control of
diabetes to improve
Still at risk for infection; blood borne due
to dialysis and vascular access (Hepatitis,
HIV)
Slower process; less effective in waste Rapid improvement in fluid and electrolite
elimination
status
Increased serum triglycerides
Improved control of serum triglycerides
Altered body image; weight gain
Minimal body image change
DIALYSIS
Kidney
Transplant
involves surgically
placing a healthy
kidney from a donor
into body
can come from
deceased or living
donors.
need to take
medications for the
rest of life to keep
NURSING CARE PLAN
ing Diagnosis : Risk for Ineffective Renal Perfusion
Nursing Interventions
Monitor intake and output, vital
signs including orthostatic blood
pressures and weight
Restrict fluids as ordered
Rationale
To identify changes in fluid volume
Report manifestations of electrolyte
imbalances
To determine further action
Time activities and procedures to
allow rest periods
To prevent patient from having
others complication such as fatigue
Administer medications as
prescribed by doctor
To treat electrolyte imbalances
To promote elimination of excess
fluid
NURSING CARE PLAN
Nursing Diagnosis : Imbalanced Nutrition related
to disease process
Nursing Interventions
Rationale
Monitor food and nutrient intake
To determine the adequacy of intake
Assist with mouth care prior to
meals and at bedtime
To improve taste and stimulate
appetite
Serve small meals and provide
between-meal snacks
To prompt nausea and help improve
food intake
Encourage family members to bring
food as dietary restrictions allow
To provide preferred foods within
restrictions promotes intake
Administer antiemetic agents as
ordered by doctor 30 to 60 minutes
before eating
To prevent nausea and vomiting with
foo intake
NURSING CARE PLAN
Nursing Diagnosis : Risk for Infection related
to disease process
Nursing Interventions
Rationale
Monitor temperature and vital signs
To detect low-graded fever and
at least every 4 hours
prevent it from getting worse
Use standard precautions and good
hand hygiene technique all times
To prevent the transfer of organisms
Culture urine, peritoneal dialysis fluid To verify the presence of pathogens
and other drainage as indicated
Teach patient coughing and deep
breathing exercise
Teach the patient and family
members about the risk for infection
To improve clearance of respiratory
secretions
To reduce the spread of infection
COMPLICATIONS
COMPLICATIONS
1. Anemia
.Anemia is a reduction in one or more of the major red
blood cell measurements: hemoglobin concentration,
hematocrit, or red blood cell count.
.A hemoglobin level less than 13 g/dL in men and postmenopausal women, and less than 12 g/dL in premenopausal women.
(World Health
Organization)
.The significant mechanism of anemia in CKD:
-Insufficient production of EPO by the diseased kidneys.
*In CKD, tubular atrophy generates tubulointerstitial fibrosis,
COMPLICATIONS
2. CKD-associated mineral and bone disorders.
. CKD-associated mineral and bone disorders comprises
abnormalities in bone and mineral metabolism and/or
extra-skeletal calcification secondary to CKD
pathophysiology
. Four types of bone phenotypes (renal osteodystrophy)
can be diagnosed in CKD patients:
o osteitis fibrosa cystica (high bone turnover with secondary
hyperparathyroidism),
o osteomalacia (low bone turnover and inadequate mineralization,
primarily related to diminished vitamin D synthesis)
o adynamic bone disorder (low bone turnover from excessive suppression
of the parathyroid glands)
o mixed osteodystrophy (with elements of both high and low bone
COMPLICATIONS
3. Cardiovascular Risk
.Hypertension is the most common complication of CKD and
ESRD.
.It may develop early during the course of hypertension in
uremia.
.Volume overload is the major cause of hypertension in uremia.
.Rarely, patient may develop malignant hypertension.
4. Gastrointestinal and Nutritional Abnormalities
.Gastrointestinal symptoms (abdominal pain, nausea, vomiting)
usually may the first symptom for ESRD patients.
.Urimic toxins is associated with an unpleasant metallic taste in
ESRD patient.
.Gastritis, peptic disease are common in ESRD patient.
COMPLICATIONS
5. Dyslipidemia
A major risk factor for cardiovascular
morbidity and mortality, and is very
common in CKD.
Lipid profiles in CKD patients reflect the
level of kidney function and the degree of
proteinuria.
Prevalence of hyperlipidemia , as renal
function
.
The degree of hypertriglyceridemia and
elevation of LDL cholesterol is proportional to
severity of renal impairment.
REFERENCE
Chronic Kidney Disease, (2015), Medscape, accessed on 25/9/2015,
http://emedicine.medscape.com/article/238798-overview#a3
About Chronic Kidney Disease, (2015), National Kidney Foundation,
accessed on 25/9/2015, https://www.kidney.org/kidneydisease/aboutckd
LeMone, P., & Burke, K. (2011). Nursing Care of Patients with Kidney
Disorders. In Medical-surgical nursing: Critical thinking in patient care (5th
ed.). Upper Saddle River, N.J.: Pearson.
Thomas, N. (2014). Chronic Kidney Disease. In Renal nursing (Fourth ed.,
pp. 116-133). London: Wiley Blackwell.
THANK YOU
