3/26/2015

Glomerulonephritis & Nephrotic

syndrome
Ninuk DK

What is glomerulonephristis?
Glomerulonephritis is
is a kidney condition
that involves damage
/inflammation to the
glomeruli.

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Types of glomerulonephritis
Acute glomerulonephritis
- begins suddenly
Chronic glomerulonephritis
-develops gradually over
several years.

Glomeruli
Glomeruli The filters of the kidneys which
filter the blood and make urine.

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Etiology
Causes of glomerulonephritis include:
Streptococcal infection of the throat ( strep throat) or
skin ( impetigo)
Hereditary diseases
Immune diseases, such as lupus
diabetes
High blood pressure
Vasculitis (inflammation of the blood vessels)
Viruses ( HIV, hepatitis B virus, and hepatitis C virus)
Endocarditis (infection of the valves of the heart)

Streptococcal infection of the throat

( strep throat) or skin ( impetigo)

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Lupus

PATHOLOGY
glomerulonephritis are triggered by immunemediated injury.
The cellular immune response contributes to the
infiltration of glomeruli by circulating mononuclear
inflammatory cells (lymphocytes and macrophages)
and crescent formation in the absence of antibody
deposition.

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PATHOLOGY
The humoral immune response leads to immune
deposit formation and complement activation in
glomeruli.
Antibodies can be deposited within the glomerulus
when circulating antibodies react with intrinsic or
with extrinsic antigens that have been trapped within
the glomerulus.

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PATHOLOGY
Injury usually occurs as a consequence of the
activation and release of a variety of inflammatory
mediators.
Haemodynamic, and toxic stresses can also induce
glomerular injury.
A few glomerular diseases are due to hereditary
defects resulting in deformity of the glomerular
basement membrane.

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Pathophisiology Acute Glomerulonephritis

Sign and symptoms

Kidney pain normally happens in the flank

region, which is just below the bottom of rib
cage.

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Signs/Symptoms
Most common symptoms:
Hematuria (dark, brown, or
rusty colored,)
Foamy urine due to
Proteinuria
Swelling of the face, eyes,
ankle, feet, legs, abdomen
High blood pressure
(hypertension)
Fatigue/SOB from anemia or
kidney failure.

Signs/Symptoms
Symptoms which may also
appear include:
Abdominal pain
Cough
Diarrhea
Fever
Joint aches
Muscle aches
Loss of appetite
Shortness of breath

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Risk Factors

History of cancer
Blood or lymphatic disorders
Exposure to hydrocarbon solvents
Diabetes
Infections
Strep infections
Heart infections
Viruses

Diagnosis
Because symptoms develop gradually, the
disorder may be discovered when there is an
abnormal urinalysis during a routine physical
or examination for unrelated disorders.

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Tests and Clinical Procedures

Imaging tests:

Abdominal CT scan
Abdominal ultrasound
Chest x-ray
Intravenous Pyelogram (IVP)

Urinalysis and other urine tests:

Creatinine clearance
Urine concentration test
Urine specific gravity
Total protein

Glomerulonephritis
Nursing Care
Assessment: riwayat infeksi saluran nafas
dan kulit, pembedahan, prosedur invasif,
penyakit sistemik (SLE)

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Assessment

Kidney pain normally happens in the flank

region, which is just below the bottom of rib
cage.

Assessment
Most common symptoms:
Hematuria (dark, brown, or
rusty colored,)
Foamy urine due to
Proteinuria
Swelling of the face, eyes,
ankle, feet, legs, abdomen
High blood pressure
(hypertension)
Fatigue/SOB from anemia or
kidney failure.

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Assessment
Symptoms which may also
appear include:
Abdominal pain
Cough
Diarrhea
Fever
Joint aches
Muscle aches
Loss of appetite
Shortness of breath

Physical assessment:

Dispnea
Ceackles/gallop
Neck vein distention
Elevated blood pressure

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Diagnosing, Planning, & Implementing

Excess Fluid Volume
Fatigue
Risk for Infection
Ineffective Role Performance

Intervention
Managing infection
Preventing complication
Appropriate patients education

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Management of infection
Anti biotic
Stress personal hygiene

Prevent complications
Fluid overload: diuretic, sodium + water
restriction
Antihipertensive drugs
Potassium and protein intake restriction
Conserve energy: maintain restfull
environment

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Pts edu

Drugs
Diet & fluid restriction
Measure weight and BP daily
Peritoneal dialysis: teach how to prevent
infection and how to do it at home

Patients education:
Lifestyle Changes
Restrict salt and water intake.
Restrict intake of potassium,
phosphorous, and magnesium.
Cut down on protein in the diet.
Maintain a healthy weight through diet
and exercise.
Take calcium supplements.

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Treatments
Treatment varies depending the type and
severity of symptoms.
High blood pressure may be difficult to control,
and it is generally the most important aspect of
treatment.
Medicines that may be prescribed include:
Blood pressure medications are often needed to
control high blood pressure.
Medications that suppress the immune system may
also be prescribed, depending on the cause of the
condition.

Therapeutic management

Corticosteroids (prednisone)
Dietary management
Restriction of fluid intake
Prevention of infections
Monitoring for complications: infections,
severe GI upset, ascites, or respiratory distress

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Physiotherapy treatment
Patient education
Endurance Exercise
Walking test
walking, swimming, bicycling, aerobic dancing
Circulatory exercise

Exercise
program during
dialysis

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Prognosis
Glomerulonephritis may be a temporary and
reversible condition, or it may get worse.
Progressive glomerulonephritis may lead to
chronic kidney failure and end-stage kidney
disease.

AGN
Treatment and nursing care:
Bed rest may be recommended during the
acute phase of the disease
A record of daily weight is the most useful
means for assessing fluid balance

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Nursing care specific to the child with AGN

Allow activities that do not expend energy

Diet should not have any added salt
Fluid restriction, if prescribed
Monitor weights
Education of the parents

Nursing diagnosis for the child with

glomerulonephritis
Fluid volume excess r/t to decreased plasma
filtration
Activity intolerance r/t fatigue
Altered patterns of urinary elimination r/t
fluid retention and impaired filtration
Altered family process r/t child with chronic
disease, hospitalizations

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A case study
Jung-Lin Chang is a 23-year-old graduate
student in biology. He presents at the
university health center, brown and foamy
urine. The physician there admits him to the
infirmary and orders a throat culture,ASO
titer,CBC,BUN, serum creatinine, and
urinalysis.

Assessment

Connie King, the nurse admitting Mr. Chang, notes that his history is essentially
negative for past kidney or urinary problems. He relates having had a pretty bad
sore throat a couple of weeks before admission. However, it was during midterms,
so he took a few antibiotics he had from a previous bout of strep throat, increased
his fluids, and did not see a doctor. The sore throat resolved, and he felt well until
noticing the change in his urine. He admits that his eyes seemed a little puffy, but
he thought this was due to lack of sleep and fatigue. He has eaten little the past 2
days, but was not alarmed because his food intake is irregular most of the time.
Physical assessment findings include: T 98.8 F (37.1 C) PO, P 98, R 18, and BP
136/90. Weight 165 pounds (75 kg), up from his normal of 160 (72.5 kg). Moderate
periorbital edema and edema of hands and fingers noted. Throat culture is
negative, but the ASO titer is high. CBC essentially normal. BUN 42 mg/dL, serum
creatinine 2.1 mg/dL. Urinalysis reveals the presence of protein, red blood cells,
and RBC casts.A subsequent 24-hour urine protein analysis shows 1025 mg of
protein (normal 30 to 150 mg/24 hours). The physician diagnoses acute
poststreptococcal glomerulonephritis and places Mr. Chang on bed rest with
bathroom privileges. He orders fluid restriction (1200 mL/day) and a restricted
sodium and protein diet.

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DIAGNOSIS
Ms. King develops the following nursing diagnoses
for Mr. Chang:
Excess fluid volume related to plasma protein
deficit and sodium and water retention
Risk for imbalanced nutrition: Less than body
requirements related to anorexia
Anxiety related to prescribed activity restriction
Risk for ineffective therapeutic regimen
management related to lack of information about
glomerulonephritis and treatment

EXPECTED OUTCOMES
The expected outcomes are that Mr. Chang will:
Maintain blood pressure within normal limits.
Return to usual weight with no evidence of edema.
Consume adequate calories following prescribed
dietary limitations.
Verbalize reduced anxiety regarding ability to continue
studies.
Demonstrate an understanding of acute
glomerulonephritis and prescribed treatment regimen.

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PLANNING AND IMPLEMENTATION

Ms. King plans the following nursing interventions for Mr. Chang.
Vital signs every 4 hours; notify physician of significant changes.
Weigh daily; intake and output every 8 hours.
Schedule fluids allowing 650 mL on day shift, 450 mL on evening shift, and
100 mL on night shift.
Arrange dietary consultation to plan a diet that includes preferred foods as
allowed.
Provide small meals with high-carbohydrate between-meal snacks.
Encourage Mr. Chang to talk about his condition and its potential effects.
Assist with problem solving and exploring options for maintaining studies.
Enlist friends and family to listen and provide support.
Teach Mr. Chang and his family about acute glomerulonephritis and
prescribed treatment.
Instruct in appropriate antibiotic use

EVALUATION
Mr.Chang is released from the infirmary after 4
days.He decides to return to his parentshome for
the 6 to 12 weeks of convalescence prescribed by
his doctor. Mr. Changs renal function gradually
returns to normal with no further azotemia and
minimal proteinuria after 4 months. He verbalizes
understanding of the relationship between the
strep throat, his inappropriate use of antibiotics,
and the glomerulonephritis. He says,I may not
always remember to take every pill on time in the
future, but I sure wont save them for the next
time again!

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Critical Thinking in the Nursing Process

1. How did Mr. Changs use of a few previously
prescribed antibiotics to treat his sore throat
affect his risk for developing poststreptococcal
glomerulonephritis?
2. What additional risk factors did Mr. Chang have
for developing glomerulonephritis?
3. The initial manifestations of acute
poststreptococcal glomerulonephritis and
rapidly progressive glomerulonephritis are very
similar. What diagnostic test would the physician
use to make the differential diagnosis?

Nephrotic Syndrome
Chronic renal disorder in which the basement
membrane surfaces of the glomeruli are
affected, cause loss of protein in the urine.

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Nephrotic syndrome is a condition where there

is a change in renal function, which is
characterized by:
hypoproteinemia
edema
hyperlipidemia
proteinuri
ascites
decrease in urine output

Etiology

Primary renal parenchymal disease

Acute post-streptococcal glomerulonephritis
Idiopathic Glomerular
Systemic Diseases
DM, renal abnormalities that are characteristic of diabetes is
diabetic nephropathy
Amyloidosis / associated with chronic diseases such as
tuberculosis, chronic osteomiliti, lung abscess, ulcerative colitis
and neoplasms.
SLE is known as lupus nephritis. SN is a clinical manifestation of
SLE
Mechanical circulatory disorders
Renal vein thrombosis
The increase in renal venous pressure can lead to increasing the
basal membrane permeability resulting in leakage of plasma
Right heart syndrome
Proteinurin to congestive heart disease.

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Pathophysiology

In nephrotic syndrome, type III hypersensitivity reaction occurs in which the immune
complex precipitated in the tissue.
Activation of the complement system also stimulates vaksoaktive amines (including
histamine) and this substance causes retraction of endothelial cells thus increasing
vascular permeability.
Changes in membrane glomerolus, causing increased permeability, allowing the
proteins (especially albumin) out through the urine (proteinurine).
Decreased oncotic pressure causing albumin moves from intra vascular space into
interstitiel.
Transfer of proteins to the interstitial cavity causing lipoproteinemia.
It stimulates the liver to compensate by increasing the production of lipoproteins and
increased concentrations of blood fats (hyperlipidemia).
When the liver is not able to compensate for damage in fat and protein metabolism.
Transfer of protein exit the vascular system, causing fluid to move into the space plasma
interstitisel resulting edema and hypovolemia.
Decrease in vascular volume stimulates renin angiotensin system, which allows the
secretion of aldosterone and antidiuretic hormone (ADH).
Aldosterone stimulates increased reabsorsi distal tubules of the sodium and water,
leading to increased edema.

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Contrast of normal gloumerular activity with

changes seen in Nephrotic Syndrome

Pathogenesis of Proteinuria:

Increase glomerular permeability for proteins due to loss of negative

charged glycoprotein

Degree of protineuria:Mild less than 0.5g/m2/day

Moderate 0.5 2g/m2/day
Sever more than 2g/m2/day

Type of proteinuria:A-Selective proteinuria: where proteins of low molecular weight .such as

albumin, are excreted more readily than protein of HMW
B-Non selective :
LMW+HMW are lost in urine

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pathogenesis of hypoalbuminemia

*Due to hyperproteinuria----- Loss of plasma

protein in urine mainly the albumin.
*Increased catabolism of protein during acute
phase.

pathogenesis of hyperlipidemia:*Response to Hypoalbuminemia reex to liver -- synthesis

of

generalize protein ( including lipoprotein ) and lipid in the

liver ,the lipoprotein high molecular weight no loss in urine
hyperlipidemia

*Diminished catabolism of lipoprotein

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pathogenesis of edema: *Reduction plasma colloid osmotic

pressure secondary to
hypoalbuminemia Edema and hypovolemia
*Intravascular volume antidiuretic
hormone (ADH ) and aldosterone(ALD)
water and sodium retention Edema
*Intravascular volume glomerular
filtration rate

(GFR) water and sodium retention

Edema

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How many pathological types

causes nephrotic syndrome?

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Clinical Manifestation

weight increased
anorexia
edema anasarca
abdominal pain
swelling of the face, especially around the eyes
voleme urine decreased, sometimes colored thick and
foamy
pale skin
the child becomes irritable, tiredness / lethargy
celulitis, pneumonia, peritonitis or sepsis
azotemia
blood pressure is usually normal / up slightly

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Assessment
Four most common characteristics:
1. Massive proteinuria
2. Hypoalbuminemia (K+ normal, BP normal)
3. Edema usually starts in periorbital area and
dependent areas of the body and progresses to
generalized, massive edema. Pitting edema of 4+.
Caused by hypo albumin which causes shift of fluids
to extracellular space. *There is an insidious weight
gain- shoes don't fit, etc
4. Hyperlipidemia
* Of note is that there is no
hematuria or hypertension

Focus Assessment
Urinary System (oliguric, urine retention,
proteinurin and urine discoloration).
Fluid and electrolyte balance (excess fluid,
edema, ascites, weight gain, dehydration)
Circulation (increased blood pressure)
Neurology (decreased level of consciousness due
to dehydration)
Breathing (shortness of breath, tachypnea)
Mobility (redness, malaise)

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Other signs and symptoms

Fatigue
Anorexia
Weight gain
Abdominal pain from large amount of fluid in abdominal

Treatment of nephrotic syndrome

Varies with degree of severity

Treatment of the underlying cause
Prognosis depends on the cause
Children usually have the minimal change
syndrome which responds well to treatment

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Nursing Diagnosis
Impaired Urinary Elimination related to Na
and water retention.
Excess Fluid Volume related to edema
Imbalanced Nutrition Less Than Body
Requirements related to damage protein
metabolism
Ineffective Breathing Pattern related to
suppression of the diaphragm due to ascites

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