Name: Angel Jacob Reyes Guzi
Section: N1-B
ANATOMY
AND
PHYSIOLOGY
Acute Glomerulonephritis
Introduction to the Disease
Glomerulonephritis is inflammation of the tiny filters in your kidneys (glomeruli).
Glomeruli remove excess fluid, electrolytes and waste from your bloodstream and pass
them into your urine. Glomerulonephritis can come on suddenly (acute) or gradually
(chronic).
Glomerulonephritis occurs on its own or as part of another disease, such as lupus or
diabetes. Severe or prolonged inflammation associated with glomerulonephritis can
damage your kidneys. Treatment depends on the type of glomerulonephritis you have.
Signs and Symptoms
Signs and symptoms of glomerulonephritis depend on whether you have the
acute or chronic form and the cause. Your first indication that something is wrong might
come from symptoms or from the results of a routine urinalysis.
Glomerulonephritis signs and symptoms include:
Pink or cola-colored urine from red blood cells in your urine (hematuria)
Foamy urine due to excess protein (proteinuria)
High blood pressure (hypertension)
Fluid retention (edema) with swelling evident in your face, hands, feet and
abdomen
Causes
Many conditions can cause glomerulonephritis. Sometimes the disease runs in families
and sometimes the cause is unknown. Conditions that can lead to inflammation of the
kidneys' glomeruli include:
Infections

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.
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.
Viral infections. Viral infections, such as the human immunodeficiency virus
(HIV), hepatitis B and hepatitis C, can trigger glomerulonephritis.
Immune diseases
Lupus. A chronic inflammatory disease, lupus can affect many parts of your
body, including your skin, joints, kidneys, blood cells, heart and lungs.
Goodpasture's syndrome. A rare immunological lung disorder that can mimic
pneumonia, Goodpasture's syndrome causes bleeding in your lungs as well as
glomerulonephritis.
IgA nephropathy. Characterized by recurrent episodes of blood in the urine, this
primary glomerular disease results from deposits of immunoglobulin A (IgA) in
the glomeruli. IgA nephropathy can progress for years with no noticeable
symptoms.
Vasculitis
Polyarteritis. This form of vasculitis affects small and medium blood vessels in
many parts of your body, such as your heart, kidneys and intestines.
Granulomatosis with polyangiitis. This form of vasculitis, formerly known as
Wegener's granulomatosis, affects small and medium blood vessels in your
lungs, upper airways and kidneys.
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 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.
Infrequently, chronic glomerulonephritis runs in families. One inherited form, Alport
syndrome, also might impair hearing or vision.
In addition to the causes listed above, glomerulonephritis is associated with certain
cancers, such as multiple myeloma, lung cancer and chronic lymphocytic leukemia.
Pathophysiology
Glomerular lesions in acute GN are the result of glomerular deposition or in situ
formation of immune complexes. On gross appearance, the kidneys may be enlarged
up to 50%. Histopathologic changes include swelling of the glomerular tufts and
infiltration with polymorphonucleocytes. Immunofluorescence reveals deposition of
immunoglobulins and complement.
In PSGN, involvement of derivatives of streptococcal proteins has been reported. A
streptococcal neuraminidase may alter host immunoglobulin G (IgG). IgG combines with
host antibodies. IgG/anti-IgG immune complexes are formed and then collect in the
glomeruli. In addition, elevations of antibody titers to other antigens, such as
antistreptolysin O or antihyaluronidase, DNAase-B, and streptokinase, provide evidence
of a recent streptococcal infection.
GN associated with staphylococcal infection occurs in the setting of an active
infection. Immunofluorescence microscopy of kidney biopsy specimens in these cases
show deposits that stain in a dominant or co-dominant fashion for IgA and the C3
component of complement.
Stamatiades et al determined that in PSGN and other type III hypersensitivity reactions,
vascular endothelial cells in the kidney actively transport circulating immune complexes
from the capillaries to the peritubular interstitial space, where they are detected and
scavenged by resident macrophages. Uptake of these immune complexes by the
resident macrophages triggers the release of pro-inflammatory cytokines, which in turn
results in recruitment of monocytes and neutrophils into the kidney from the circulation.
Structural and functional changes
Acute GN 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 (ie, 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. On electron microscopy, this may appear as the result of thickening of
basement membrane proper (eg, diabetes) or deposition of electron-dense material,
either on the endothelial or epithelial side of the basement membrane. 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.
Poststreptococcal glomerulonephritis
Streptococcal M-protein was previously believed to be responsible for PSGN, but the
studies on which this belief was based have been discounted. Nephritis-associated
streptococcal cationic protease and its zymogen precursor (nephritis-associated
plasmin receptor [NAPlr]) have been identified as a glyceraldehyde-3-phosphate
dehydrogenase that functions as a plasmin(ogen) receptor.
Immunofluorescence staining of renal biopsy tissues with anti-NAPlr antibody revealed
glomerular NAPlr deposition in early-phase acute PSGN, and glomerular plasmin
activity was almost identical to NAPlr deposition in renal biopsy tissues of acute PSGN
patients. These data suggest that NAPlr may contribute to the pathogenesis of acute
PSGN by maintaining plasmin activity. However, the unique glomerular staining
patterns of NAPlr and plasmin activity have also been reported in patients with other
glomerular diseases in which a preceding streptococcal infection was suggested. [7]
Antibody levels to nephritis-associated protease (NAPR) are elevated in streptococcal
infections (group A, C, and G) associated with GN but are not elevated in streptococcal
infections without GN, whereas anti-streptolysin-O titers are elevated in both
circumstances. These antibodies to NAPR persist for years and perhaps are protective
against further episodes of PSGN. In a study in adults, the two most frequently identified
infectious agents were streptococci (27.9%) and staphylococci (24.4%)
Risk Factors
The cause is often unclear, but there are risk factors that can affect the likelihood
of glomerulonephritis.
Post-streptococcal glomerulonephritis can result from streptococcal infections of
the throat or, in rarer cases, impetigo, a skin infection. Improved treatments for most
streptococcal infections mean that this is now less common.
Infectious diseases, such as tuberculosis (TB) and syphilis, can lead to
glomerulonephritis. This is also true of bacterial endocarditis, an infection of the heart
valves. Viral infections, such as HIV, hepatitis B, and hepatitis C also increase the risk.
Acute glomerulonephritis may develop into chronic, or long-term, glomerulonephritis.
Genetic factors can play a role, but people with glomerulonephritis do not
normally have a family member who also has the condition.
Long-term use of certain medications, including non-steroidal anti-inflammatory
drugs (NSAIDS), such as ibuprofen or aspirin, can increase the risk.
People with Hodgkin’s, sickle cell disease, and systemic diseases, especially
diabetes are at higher risk.
Complication
Glomerulonephritis can damage your kidneys so that they lose their filtering ability. As a
result, dangerous levels of fluid, electrolytes and waste build up in your body.
Possible complications of glomerulonephritis include:
Acute kidney failure. Loss of function in the filtering part of the nephron can
result in rapid accumulation of waste products. You might need emergency
dialysis — an artificial means of removing extra fluids and waste from your blood
— typically by an artificial kidney machine.
Chronic kidney disease. Your kidneys gradually lose their filtering ability.
Kidney function that deteriorates to less than 10 percent of normal capacity
results in end-stage kidney disease, which requires dialysis or a kidney
transplant to sustain life.
High blood pressure. Damage to your kidneys and the resulting buildup of
wastes in the bloodstream can raise your blood pressure.
Nephrotic syndrome. 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.
Citations:
https://www.medicalnewstoday.com/articles/167252#scarring
https://www.mayoclinic.org/diseases-conditions/glomerulonephritis/symptoms-causes/syc20355705
https://emedicine.medscape.com/article/239278-overview#a6