ACUTE GLOMERULONEPHRITIS

A. RISK FACTORS.
● Infectious
○ Streptococcal Infections
- The most common infectious cause of acute GN is infection by
Streptococcus​ species. It is generally accepted that acute
glomerulonephritis is a reaction that occurs as a byproduct of an
antecedent streptococcal infection with certain strains of the group
A -hemolytic streptococci, although other bacteria and viruses
have also been implicated
○ Viral Infection
- Having a condition which weakens the immune system and
increases the risk of chronic infection, and can be a risk factor of
glomerulonephritis
- Viral infections, such as the human immunodeficiency virus (HIV),
hepatitis B and hepatitis C, can trigger glomerulonephritis.
○ Bacterial Infection
- Strep Throat​. An excess of antibodies are produced to fight the
infection. This may cause or trigger an inflammation when they
settle in the kidneys.
- Bacterial endocarditis​. Bacteria occasionally can spread through
your bloodstream and lodge in your heart, causing an infection of
one or more of your heart valves. You're at greater risk of this
condition if you have a heart defect, such as a damaged or
artificial heart valve. Bacterial endocarditis is associated with
glomerular disease, but the connection between the two is
unclear.
○ Post Streptococcal Glomerulonephritis
- Glomerulonephritis may develop a week or two after recovery from
a strep throat infection or, rarely, a skin infection (impetigo). To
fight the infection, your body produces extra antibodies that can
eventually settle in the glomeruli, causing inflammation.
- Children are more likely to develop post-streptococcal
glomerulonephritis than are adults, and they're also more likely to
recover quickly.
● Immune
○ Goodpasture’s Syndrome
- A rare immunological lung disorder that can mimic pneumonia,
Goodpasture's syndrome that if it quickly progresses, you may
bleed from the lungs and cough up blood. It may also lead to
 inflamed kidneys (glomerulonephritis). It is not exactly known why
your antibodies begin to attack your own lungs and kidneys.
- Goodpasture's Syndrome may cause life-threatening bleeding in
the lungs, but does not usually cause long-term damage in that
area. The harm done to your kidneys, however, can result in
kidney failure.
○ Systemic Lupus Erythematosus (SLE)
- A chronic inflammatory disease, lupus can affect many parts of
your body, including your skin, joints, kidneys, blood cells, heart
and lungs.
- Systemic lupus erythematosus (SLE) that affects the kidneys is
called lupus nephritis. Lupus nephritis causes inflammation
(swelling or scarring) of the small blood vessels that filter wastes
in your kidney (glomeruli) and sometimes the kidneys, by attacking
them like they would attack a disease.
○ IgA Nephropathy (Berger’s Disease)
- IgA nephropathy, also known as Berger’s disease, is a disease
that causes damage to the tiny filters inside the kidneys. IgA is a
protein that helps you fight infections.
- In people with IgA nephropathy, these proteins build up and form
clumps inside the kidneys’ tiny filters (glomeruli). These clumps of
proteins damage the glomeruli. This damage can cause chronic
kidney disease and can lead to kidney failure/ESRD.
● Vasculitis
○ Polyarteritis
- Polyarteritis nodosa is a rare disease resulting from vasculitis, or
blood vessel inflammation.
- PAN can also affect the blood vessels to the kidney resulting in
high blood pressure​ and damage to kidney function.
○ Granulomatosis with polyangiitis
- Granulomatosis with polyangiitis (GPA), formerly known as
Wegener’s granulomatosis, is a disease that causes swelling and
irritation of blood vessels in the kidneys, nose, sinuses, throat and
lungs. Swollen blood vessels make it harder for blood to get to the
organs and tissues that need it, which can be harmful.
- GPA that affects the kidneys can lead to ​chronic kidney disease
and ​kidney failure.
● Conditions likely to cause scarring of the glomeruli
○ High blood pressure
- This can damage your kidneys and impair their ability to function
normally. Glomerulonephritis can also lead to high blood pressure
because it reduces kidney function and can influence how your
kidneys handle sodium.
 ○
Diabetic Kidney Disease (Diabetic Kidney Nephropathy)
- This can affect anyone with diabetes, usually taking years to
develop. Good control of blood sugar levels and blood pressure
might prevent or slow kidney damage.
○ Focal segmental glomerulosclerosis
- Characterized by scattered scarring of some of the glomeruli, this
condition can result from another disease or occur for no known
reason.
B. CLINICAL MANIFESTATIONS
C. ASSESSMENT AND DIAGNOSTIC
● Assessment
○ History
- Ask patient about recent infections, particularly of the skin or
upper respiratory tracts, and about recent travel or other possible
exposures to viruses, bacteria, fungi, or parasites.
- Recent illnesses, surgery or any invasive procedures that could
suggest infections
- Ask about family history of systemic lupus erythematosus, which
could cause acute GN.
○ Physical Assessment
- Inspect the patient’s skin for lesions or recent incisions (including
body piercings)
- Assess face, eyelids, hands and other areas for edema (present in
about 75% of the patients with acute GN)
- Assess for fluid overload and circulatory congestion
- Ask about any difficulty breathing or shortness of breath
- Ask about changes in urination pattern and urine color
- Weigh patient to assess for fluid retention
- Take patient’s blood pressure and compare it to baseline blood
pressure
- Ask patient if she/he has any fatigue, anorexia, nausea or vomiting
if severe kidney impairment is present.
● Diagnostic 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 Culture
- 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.

D. COMPLICATIONS

Rapidly progressive glomerulonephritis

The glomerular injury is accompanied by a rapid decline in glomerular function,

progressing to renal failure in a few weeks or months. Hematuria is common and may or
may not be accompanied by proteinuria, edema, or hypertension.

High blood pressure

High blood pressure is a common complication of glomerulonephritis. This is because

your kidneys help regulate your blood pressure.

Acute kidney failure ​(decreased glomerular filtration)

Loss of function in the filtering part of the nephron can result in the rapid accumulation of
waste products.

Nephrotic syndrome ​(proteinuria, edema)

With this syndrome, too much protein in your urine results in too little protein in your
blood. Nephrotic syndrome can be associated with high blood cholesterol and swelling
(edema) of the eyelids, feet, and abdomen.

Pulmonary Edema
 E. MEDICAL MANAGEMENT
❖ Possible medications prescribed by the physician includes administering:
➢ Angiotensin-converting enzyme (ACE) inhibitors​ can be used to manage high
blood pressure. This type of medication widens the blood vessels which allows
to increase the amount of blood the heart pumps and lowers blood pressure and
the heart’s workload.
➢ Calcium channel blockers ​inhibit the movement of calcium ions across the cell
membrane, reducing calcium moving into cells of the heart and blood vessel
walls where it relaxes the blood vessel walls and the heart. Treatment for
hypertension.
➢ Loop diuretics ​decrease plasma volume and edema by causing diuresis where
there is an increase of urinary output and improve cardiovascular congestion.
➢ Antibiotic therapy​ such as penicillin, erythromycin is prescribed for acute
glomerulonephritis caused by streptococcal infection and when risk of
contamination is possible.

❖ Diet prescribed:
➢ Dietary protein intake is restricted ​by nutritionists when there is evidence of an
increase in nitrogenous wastes such as blood, urea, and nitrogen. It is also to
prevent hyperkalemia and uremia as a result of the elevated BUN.
➢ Low sodium and fluid restriction diet w ​ hen the patient has hypertension, edema,
and heart failure.

❖ Possible therapies:
➢ Dialysis ​may be needed in glomerulonephritis where the patient’s blood is
cleaned by a filtering machine to get rid of extra fluid and waste material when
uremic symptoms or fluid volume cannot be control

Sources:
Cheever, K., & Hinkle, J. (2018). Brunner and Sudddarths textbook of medical surgical nursing.
Philadelphia: Wolters Kluwer

Science Direct. (2020). Mesangial cell. Retrieved August 25, 2020 from
https://www.sciencedirect.com/topics/medicine-and-dentistry/mesangial-cell

National kidney foundation. (n.d). What is glomerulonephritis? Retrieved August 25, 2020 from
https://www.kidney.org/atoz/content/glomerul

Kanjanabuch, T., Kittikowit, W. & Ong, S. (2009). An update on acute postinfectious

glomerulonephritis worldwide. Retrieved August 25, 2020 from
https://pubmed.ncbi.nlm.nih.gov/19384327/
VandeVoorde, R. (2015). Acute postreptococcal glomerulonephritis: the most common acute
glomerulonephritis. Retrieved August 25, 2020 from ​https://pubmed.ncbi.nlm.nih.gov/25554106/

Research

An update on acute postinfectious glomerulonephritis worldwide

By Talerngsak Kanjanabunch, Wipawee Kittikowit and Somchai Eiam- Ong

Postinfectious glomerulonephritis is an immunologic response of the kidney to infection,

commonly triggered by streptococci, although many other organisms can cause the condition. In
recent decades, the prevalence of postinfectious glomerulonephritis has tended to decline in
most industrialized countries, but high rates persist in some developing communities.
Nowadays, patients in developed countries are usually adult and male, and those with
comorbidities such as diabetes and alcoholism are at increased risk of developing the disease.
The acute presentation ranges from nephritic syndrome to asymptomatic glomerulonephritis.
The exact pathophysiology of postinfectious glomerulonephritis is still unknown; however,
several possible pathologic antigens are under investigation. The majority of children and
patients with the epidemic form of postinfectious glomerulonephritis have an excellent
prognosis, which contrasts with the poor long-term outcome of sporadic cases. Therapy is
largely supportive unless renal function fails to recover after eradication of the causative
organism.

The Most Common Acute Glomerulonephritis

René G. VanDeVoorde

One of the oldest clinical observations in nephrology is the association of dark and scanty urine
after scarlet fever, which was first documented in the medical literature more than 200 years
ago. This postscarlatinal disorder was termed acute glomerulonephritis. Because it was later
discovered in the 1920s that scarlet fever was caused by an infection with β-hemolytic
streptococcus, the etiologically correct term poststreptococcal glomerulonephritis (PSGN)
became synonymous with acute glomerulonephritis, and the 2 terms are often used
interchangeably even today.
However, acute glomerulonephritis technically describes the pathologic process characterized
by inflammation and/or cellular proliferation of the glomeruli not caused by direct infection of the
kidneys. It classically manifests as an acute nephritic syndrome with hematuria, proteinuria, and
evidence of volume overload. However, it may also present as nephrotic syndrome (severe
proteinuria, hypoalbuminemia, and edema) or as a disorder characterized by particularly rapidly
progressive acute kidney injury. Of note, and much beyond streptococcal infection, there are
numerous different causes of glomerulonephritis, some being primary disorders only of the
kidneys and others representing multiorgan conditions with secondary renal involvement.

PSGN remains by far the most common glomerulonephritis in children worldwide. Its global
burden has been estimated at well more than 450,000 cases annually, with most cases
occurring in children. Most of these cases (97% in previous estimates) occur in developing
countries, where pyodermal infections, such as impetigo, are common. Despite a lower
incidence in developed countries, PSGN is still the most common glomerulonephritis in children
in the United States, and its epidemiology offers interesting insights into its prevention.

F. NURSING DIAGNOSIS
G. NURSING INTERVENTIONS
H. RESEARCH UPDATES