Acute glomerulonephritis (GN) 

comprises a specific set of renal diseases in

which an immunologic mechanism triggers inflammation and proliferation of
glomerular tissue that can result in damage to the basement membrane,
mesangium, or capillary endothelium.

What is Acute Glomerulonephritis? 

.Acute glomerulonephritis (GN) comprises a specific set of renal diseases in
which an immunologic mechanism triggers inflammation and proliferation of
glomerular tissue that can result in damage to the basement membrane,
mesangium, or capillary endothelium.

 Acute GN is defined as the sudden onset of hematuria,

proteinuria, and red blood cell (RBC) casts in the urine.
 Acute GN is a condition that appears to be an allergic reaction to
a specific infection, most often group A beta-hemolytic
streptococcal infection.
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.
Statistics and Incidences
Acute Glomerulonephritis represents 10-15% of glomerular diseases.

 Acute GN has a peak incidence in children 6 to 7 years of age and

occurs twice as often in boys.
 Worldwide, IgA Nephropathy (Berger disease) is the most
common cause of GN.
 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.
 Acute GN predominantly affects males (2:1 male-to-female ratio).
Causes
The causal factors that underlie acute GN can be broadly divided into
infectious and noninfectious groups.

 Infectious. The most common infectious cause of acute GN is

infection by Streptococcus species (ie, group A, beta-hemolytic).
 Noninfectious. Noninfectious causes of acute GN may be divided
into primary renal diseases, systemic diseases, and miscellaneous
conditions or agents.
Clinical Manifestations
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.
Assessment and Diagnostic Findings
There are a lot of renal syndromes that may mimic the symptoms of acute GN,
so accurate assessment and diagnosis is essential.

 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.
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
The nurses’ role in the care of a child with AGN is crucial.
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 Diagnoses

Based on the assessment data, the major nursing diagnoses are:

 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.
Nursing Care Planning and Goals

Nursing care planning goals for a child with acute glomerulonephritis are:

 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

Nursing care of a child with AGN includes the following interventions:

 Activity. Bed rest should be maintained until acute symptoms

and gross hematuria disappear.
 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.
Evaluation

Goals are met as evidenced by:

 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.