NURSING NOTES
PEDIATRIC NURSING
Acute Glomerulonephritis
Acute glomerulonephritis (AGN) is a significant renal disorder that
demands vigilant nursing care and prompt intervention. This condition, characterized by
inflammation of the glomeruli in the kidneys, can lead to impaired kidney function and potential
complications.
This nursing note aims to explore the multifaceted aspects of AGN, including its causes, clinical
manifestations, diagnostics, medical management, and nursing interventions.
What is Acute Glomerulonephritis?
Hippocrates originally described the natural history of acute glomerulonephritis (GN), writing of
back pain and hematuria followed by oliguria or anuria. Richard Bright (1789-1858) described acute
GN clinically in 1827, which led to the eponymic designation Bright disease. With the development of
the microscope, Theodor Langhans (1839-1915) was later able to describe the pathophysiologic
glomerular changes.
• 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.
• 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.
• 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 are essential.
• Initial blood tests. A CBC is performed; a decrease in the hematocrit may demonstrate
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 the 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 includes:
• 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:
PEDIATRIC NURSING
Acute Glomerulonephritis
Acute glomerulonephritis (AGN) is a significant renal disorder that
demands vigilant nursing care and prompt intervention. This condition, characterized by
inflammation of the glomeruli in the kidneys, can lead to impaired kidney function and potential
complications.
This nursing note aims to explore the multifaceted aspects of AGN, including its causes, clinical
manifestations, diagnostics, medical management, and nursing interventions.
What is Acute Glomerulonephritis?
Hippocrates originally described the natural history of acute glomerulonephritis (GN), writing of
back pain and hematuria followed by oliguria or anuria. Richard Bright (1789-1858) described acute
GN clinically in 1827, which led to the eponymic designation Bright disease. With the development of
the microscope, Theodor Langhans (1839-1915) was later able to describe the pathophysiologic
glomerular changes.
• 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.
• 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.
• 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 are essential.
• Initial blood tests. A CBC is performed; a decrease in the hematocrit may demonstrate
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 the 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 includes:
• 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:
