JMJ Marist Brothers

Notre Dame of Dadiangas University

College of Health Sciences

Nursing Department

AGN (Acute Glomerulonephritis)

In Partial Fulfilment of the Requirements in

NCM 109

For the Degree of Bachelor of Science in Nursing

JENN IAN DE CASTRO, RN, EMT

Clinical Instructor

Submitted by:

Shekainaneh R. Mondega, SN

Name of Student
 AGN (Acute Glomerulonephritis)

Introduction:

Acute glomerulonephritis (AGN) is a medical condition characterized by inflammation of

the glomeruli, which are tiny filters in the kidneys that remove excess fluid, waste
products, and toxins from the blood. AGN typically occurs as a complication of a
bacterial infection, most commonly caused by Streptococcus bacteria. The condition
can also be caused by autoimmune diseases, certain medications, or viral infections.

Incidence:

Acute glomerulonephritis (AGN) is more common in children than in adults. AGN is a

relatively rare condition in children, but it can be serious and may require hospitalization
and close monitoring. Prompt diagnosis and treatment can help to prevent
complications and improve outcomes.

● More common in male than females (2:1 male-to-female ratio).

● Most common in preschool and early school age children with a peak age of
onset of 6-7 years.
● Rare in children under two years of age.

● Accounts for about 90% of renal diseases in childhood

● Varies with the prevalence of nephritogenic strains of streptococci and the

likelihood of cross-infection.
● Statistics and Incidences
 ● Acute Glomerulonephritis represents 10-15% of glomerular diseases.

● In the United States, GN comprises 25-30% of all cases of end-stage renal

disease (ESRD).
● About one fourth of patients present with acute nephritic syndrome.

● Worldwide, IgA Nephropathy (Berger disease) is the most common cause of

GN.
● In Port Harcourt, Nigeria, the incidence of acute GN in children aged 3-16
years was 15.5 cases per year, with a male-to-female ratio of 1.1:1; the
current incidence is not much different.
● A study from a regional dialysis center in Ethiopia found that acute GN was
second only to hypovolemia as a cause of acute kidney injury that required
dialysis, accounting for approximately 22% of cases.
● Postinfectious GN can occur at any age but usually develops in children.

● Most cases occur in patients aged 5-15 years; only 10% occur in patients
older than 40 years.

Etiology
1. Presumed cause
a. antigen - antibody reaction secondary to an infection in the body.
2. Initial infection
a. Usually either an upper respiratory infection or a skin infection, usually one
to 3 weeks before the onset of symptoms
b. Most frequent causative agent - nephritogenic strains of group - A beta -
haemolytic streptococcus (type 12), acute post-streptococcal
glomerulonephritis (APSGN) is the most common.
c. Most cases are post infectious and have been associated with
i. Pneumococcal
ii. Viral infection
iii. Acute post streptococcal glomerulonephritis is the most common of
the post infectious renal disease in childhood. Streptococcal
pharyngitis is more common in the winter.
Pathophysiology
Acute Glomerulonephritis involves both structural changes and functional
changes.
● Structurally, cellular proliferation leads to an increase in the number of cells in the
glomerular tuft because of the proliferation of endothelial, mesangial, and
epithelial cells.
● The proliferation may be endocapillary (i.e., within the confines of the glomerular
capillary tufts) or extracapillary (ie, in the Bowman space involving the epithelial
cells).
● In extracapillary proliferation, proliferation of parietal epithelial cells leads to the
formation of crescents, a feature characteristic of certain forms of rapidly
progressive GN.
● Leukocyte proliferation is indicated by the presence of neutrophils and
monocytes within the glomerular capillary lumen and often accompanies cellular
proliferation.
● Glomerular basement membrane thickening appears as thickening of capillary
walls on light microscopy.
● Electron-dense deposits can be subendothelial, subepithelial, intramembranous,
or mesangial, and they correspond to an area of immune complex deposition.
● Hyalinization or sclerosis indicates irreversible injury.

● These structural changes can be focal, diffuse or segmental, or global.

● Functional changes include proteinuria, hematuria, reduction in GFR (ie, oliguria

or anuria), and active urine sediment with RBCs and RBC casts.
● The decreased GFR and avid distal nephron salt and water retention result in
expansion of intravascular volume, edema, and, frequently, systemic
hypertension.

Signs and Symptoms:

Presenting symptoms appear 1 to 3 weeks after the onset of a streptococcal infection.

● Hematuria. Usually the presenting symptom is grossly bloody urine; the

caregiver may describe the urine as smoky or bloody.
 ● Periorbital edema. Periorbital edema and/or pedal edema may accompany or
precede hematuria.
● Fever. Fever may be 103°F to 104°F at the onset but decreases in a few days to
about 100°F.
● Hypertension. Hypertension occurs in 60% to 70% of patients during the first 4
or 5 days.
● Oliguria. Oliguria (production of a subnormal volume of urine) is usually present,
and the urine has a high specific gravity and contains albumin, red and white
blood cells, and casts.
● Fluid overload. Observe for periorbital and/or pedal edema; edema and
hypertension due to fluid overload (in 75% of patients); crackles (ie, if pulmonary
edema); elevated jugular venous pressure; ascites and pleural effusion
(possible).
● Cerebral symptoms. Cerebral symptoms consisting mainly of headache,
drowsiness, convulsions, and vomiting occur in connection with hypertension in a
few cases.

Diagnosis
● Ineffective breathing pattern related to the inflammatory process.

● Altered urinary elimination related to decreased bladder capacity or irritation

secondary to infection.
● Excess fluid volume related to a decrease in regulatory mechanisms (renal
failure) with the potential of water.
● Risk for infection related to a decrease in the immunological defense.

● Imbalanced nutrition less than body requirements related to anorexia, nausea,

vomiting.
● Risk for impaired skin integrity related to edema and pruritus.

● Hyperthermia related to the ineffectiveness of thermoregulation secondary to

infection.
● Fluid volume excess related to altered renal function (or) diminished glomerular
filtration increased Na* retention.
 ● Activity intolerance related to edema.

● Altered skin integrity related to edema

● Altered nutritional, less than body requirement, related to albuminuria and GI

disturbances.
● Fear and anxiety related to disease processes.

● Knowledge deficit regarding care of the child with renal disease and continuation
of care at home.

Treatment:
Medical Management
Treatment of acute glomerulonephritis (AGN) is mainly supportive, because there is no
specific therapy for renal disease.
● Diet. Sodium and fluid restriction should be advised for treatment of signs and
symptoms of fluid retention (eg, edema, pulmonary edema); protein restriction for
patients with azotemia should be advised if there is no evidence of malnutrition.
● Activity. Bed rest is recommended until signs of glomerular inflammation and
circulatory congestion subside as prolonged inactivity is of no benefit in the
patient recovery process.
● Long term monitoring. Long-term studies on children with AGN have revealed
few chronic sequelae.

Pharmacologic Management
The goals of pharmacotherapy are to reduce morbidity, to prevent complications, and to
eradicate the infection.

● Antibiotics. In streptococcal infections, early antibiotic therapy may prevent

antibody response to exoenzymes and render throat cultures negative, but may
not prevent the development of AGN.
● Loop diuretics. Loop diuretics decrease plasma volume and edema by causing
diuresis. The reductions in plasma volume and stroke volume associated with
diuresis decrease cardiac output and, consequently, blood pressure.
● Vasodilators. These agents reduce systemic vascular resistance, which, in turn,
may allow forward flow, improving cardiac output.
 ● Calcium channel blockers. Calcium channel blockers inhibit the movement of
calcium ions across the cell membrane, depressing both impulse formation
(automaticity) and conduction velocity.

Nursing Management
Nursing Assessment
Assessment of a child with AGN include:
● Physical examination. Obtain complete physical assessment

● Assess weight. Monitor daily weight to have a measurable account on the

fluid elimination.
● Monitor intake and output. Monitor fluid intake and output every 4 hours to
know progressing condition via glomerular filtration.
● Assess vital signs. Monitor BP and PR every hour to know progression of
hypertension and basis for further nursing intervention or referral.
● Assess breath sounds. Assess for adventitious breath sounds to know for
possible progression in the lungs.

Nursing Care Planning and Goals

● Excretion of excessive fluid through urination.

● Demonstration of behaviors that would help in excreting excessive fluids in the

body.
● Improvement of distended abdominal girth.

● Improvement of respiratory rate.

● Participation and demonstration of various ways to achieve effective tissue

perfusion.

Nursing Interventions
● Activity. Bed rest should be maintained until acute symptoms and gross
hematuria disappears.
● Prevent infection. The child must be protected from chilling and contact with
people with infections.
 ● Monitor intake and output. Fluid intake and urinary output should be carefully
monitored and recorded; special attention is needed to keep the intake within
prescribed limits.
● Monitor BP. Blood pressure should be monitored regularly using the same arm
and a properly fitting cuff.
● Monitor urine characteristics. The urine must be tested regularly for protein
and hematuria using dipstick tests.
● Monitor Fluid balance: Regular measurement of vital signs, body weight and
intake and output is essential to monitor the disease's progress and detect
complications that may appear at any time during the course of the disease.
o A record of daily weight is the most useful means to assess fluid balance
and should be kept for children treated at home and for those who are
hospitalized. Sodium and water restriction is useful when the output is
significantly reduced (<2 to 3 dl/24hr.)
o In these children the water allowed is equivalent to the calculated
insensible loss plus the volume of urine excreted.

How is AGN Diagnose:

Diagnostic Findings: Tests
● Initial blood tests. A CBC is performed; a decrease in the hematocrit may
demonstrate a dilutional anemia; in the setting of an infectious etiology,
pleocytosis may be evident; electrolyte levels are measured (particularly the
serum potassium), along with BUN and creatinine (to allow estimation of the
glomerular filtration rate [GFR]); the BUN and creatinine levels will exhibit a
degree of renal compromise and GFR may be decreased.
● Complement levels. Differentiation of low and normal serum complement levels
may allow the physician to narrow the differential diagnosis.
● Urinalysis. The urine is dark; its specific gravity is greater than 1.020; RBCs and
RBC casts are present; and proteinuria is observed.
● Streptozyme tests. The streptozyme tests test includes many streptococcal
antigens that are sensitive for screening but are not quantitative, such as
DNAase, streptokinase, streptolysin O, and hyaluronidase; the antistreptolysin O
(ASO) titer is increased in 60-80% of patients; increasing ASO titers or
streptozyme titers confirm recent infection.
 ● Blood and tissue cultures. Blood culture is indicated in patients with fever,
immunosuppression, intravenous (IV) drug use history, indwelling shunts, or
catheters; cultures of throat and skin lesions to rule out Streptococcus species
may be obtained.

Family Teaching Plan

● Teach the mother to report signs of fluid overload, vision changes, headaches,
edema, or seizures.
● Explanation of the disease: Explain to the family what acute glomerulonephritis
is, its causes, symptoms, and the treatment plan.
● Medications: Inform the family about the prescribed medications, how they
should be taken, and their possible side effects. Explain the importance of taking
the medications as prescribed, and the consequences of missing doses.
● Diet: Instruct the family about the importance of a balanced diet, and how to limit
sodium, protein, and potassium intake. Educate them about the importance of
hydration, and encourage them to encourage the patient to drink plenty of fluids.
● Lifestyle modifications: Encourage the family to help the patient to reduce their
stress levels, get adequate rest, and avoid contact with individuals with
infections.
● Monitoring of symptoms: Explain to the family how to monitor the patient's
symptoms, including changes in urine output, blood pressure, and any signs of
infection.
● Follow-up appointments: Schedule follow-up appointments with the healthcare
provider and instruct the family on the importance of keeping these
appointments.
● Prevention of complications: Inform the family about the possible complications
of acute glomerulonephritis, and how to prevent them. Encourage the family to
seek medical attention immediately if they notice any signs of complications.
● Emotional support: Provide emotional support to the patient and their family, and
connect them to available resources like support groups and counseling services.
● Overall, it's important to provide the family with clear and concise information,
encourage them to ask questions, and involve them in the patient's care plan.
This will help them to feel more confident in caring for their loved one and
improve the patient's overall outcomes.