GLOMERULAR DISEASES ● U/A: gross hematuria, proteinuria, dysmorphic
Immune: immune complex RBCs, RBC cast, hyaline cast, granular casts,
● Associated with immune origin WBC
○ Immune origin: result to serologic disorders ● As the toxicity of the glomerular membrane wil
throughout the body including the kidney subside the urinalysis of patient will return to
● Since it is caused by immune disorder there is normal with the possible exception of microscopic
immune complexes (antigen-antibody binding) and hematuria because it will last until the membrane
usually trapped in the kidney damage has been repaired
○ When immune complex attached to the ● Blood: ↑ BUN during acute stages but will back to
parts of the body it will be attacked normal upon the recovery of the patient;
○ Immune complexes are formed as a result ○ Can also demonstrate elevated serum,
of immunologic reaction ASO titer - count the anti streptolysin O or
● Increase serum in IG such as igA that will circulate demonstrate the anti group A streptococca
in the bloodstream and deposited in glomerular enzyme test that will provide evidence that
membrane causing: the disease is of streptococcal origin
○ Cellular proliferation and infiltration ● Edema
○ Thickening of basement membrane ● Main effect: causative agent of strepto
Non-immune: toxins; amyloid ● Entry: oral cavity
● Exposure to chemicals and toxins that will affects ● Sometimes due to immune system and
the tubules leading to streptococcus pyogenes is not eliminated =
○ Disruption of electrical membrane charges produce antibodies against strep and may
○ Sometimes seen in nephrotic syndrome deposited in the kidney
● Deposition of amyloid materials from systemic
disorder that may involve chronic inflammation and
acute phase reactant and basement membrane
thickening associated with diabetic nephropathy
Changes:
● Cellular proliferation and infiltration
● Thickening of basement membrane
● Disruption of electrical membrane charges
● Hyalinization
Glomerular disease: PATHOPHYSIOLOGY
Rapidly Progressive / Crescentic Glomerulonephritis
● More serious AGN
● Has a much poorer prognosis often terminating in
renal failure
● Symptoms: inherited by deposition of immune
complexes in the glomerulus often as a
complication of another glomerulonephritis or
Immune systemic disorder (ex: systemic lupus
erythematosus)
(a) Normal glomerulus ; (b) glomerular disease ○ HAPPEN? There is damage caused by
macrophages to do capillary walls which
EXAMPLE OF glomerular diseases will release cells and plasma into the
Acute Post-Streptococcal Glomerulonephritis bowman's pace and production of
● Disease marked by sudden onset symptoms that crescentic formation that will contain
is consistent to the damage to glomerular macrophages, fibroblast, and polymerized
membrane fibrin that causes permanent damage to
● Symptoms: appear in children, young adults the capillary tuft
following respiratory infection caused by certain ● U/A: same as APSGN but become more abnorma
strain of group A streptococcus (s. pyogenes) that as this will progress
will contain M protein in the cell wall ● Includes markedly elevated protein levels and very
● All those contain protein in the cell wall will have a low glomerular filtration rate
post effect of post streptococcal glomerulonephritis
, ● Some forms may demonstrate increased fibrin
degradation products, cryoglobulins and
deposition of IgA immune complexes in
glomerulus
*since there is leakage of fluid so most of the time it will
IgA Nephropathy (BERGER’s disease)
lead to elevated protein levels in the blood and very low
● Mucosal infection
glomerular filtration rate
○ IgA deposition → thickening of membrane
Goodpasture Syndrome ● Common cause of glomerulonephritis
● Caused by cytotoxic antibody that can appear ● Patients has increased level of IgA (secretory Ab)
against the glomerular and alveolar basement caused by mucosal infection
membrane after viral respiratory infections ● Recovery from macroscopic hematuria is
● The attachment of the autoantibodies to the spontaneous however asymptomatic
basement membrane is followed by complement
microhematuria and elevated level of IgA will
activation produces capillary destruction
● Upon activation of the complement it will also remain
attach the basement membrane of the kidneys ● Macroscopic hematuria is asymptomatic thus there
● The autoantibodies is referred to Antiglomerular is gradual progression to chronic
basement membrane antibodies (AGBM Ab) and glomerulonephritis (CGN) and end stage renal
Anti Alveolar basement membrane antibodies disease
● U/A: hematuria, proteinuria, RBC casts ● Present an episode of macroscopic hematuria
● Blood: Ab testing (to see AGBM Ab and
following an infection and straneus exercises
Antialveolar BM Ab)
Membranous Glomerulonephritis Wegener’s Granulomatosis
● IgG deposition → thickening ● Cause granuloma producing inflammation of smal
○ Predominant characteristic: thickening of blood vessels of kidneys and respiratory system
the glomerular basement membrane ● Key to diagnose: Antineutrophilic cytoplasmic
results from the deposition of igG AutoAb (ANCA) → granulomas in the lungs and
● Disorders associated: SLE, Sjogren’s syndrome, glomerulus
secondary syphilis and HBV ● Binding of these autoantibodies to neutrophils that
● Gold and mercury treatments and some are located to the vascular wall will initiate the
malignancies immune response and result to granuloma
● Many cases of unknown etiology have been formation
reported to cause membranous glomerulonephritis ● Patient presents first pulmonary symptoms and
and the disease will progress slowly with possible later develop renal involvement including
remission. However, frequent development of Hematuria, proteinuria, RBC cast
nephrotic syndrome will occur and there is ● Increase BUN and Creatinine
tendency towards thrombosis ● Ab testing
● UA: Hematuria and proteinuria (elevated urine
protein excretion that may reach concentration Nephrotic Syndrome
similar to nephrotic syndrome) ● Causes:
● Tests: ANA (antinuclear antibody), HBsAg (hepa ➢ Circulatory disruption- that will produce
B surface antigen), FTA-ABS (secondary syphilis) systemic shock that will decrease the
pressure and flow of blood to the kidneys
➢ Complication of other Glomerular
disorders
Immune: immune complex RBCs, RBC cast, hyaline cast, granular casts,
● Associated with immune origin WBC
○ Immune origin: result to serologic disorders ● As the toxicity of the glomerular membrane wil
throughout the body including the kidney subside the urinalysis of patient will return to
● Since it is caused by immune disorder there is normal with the possible exception of microscopic
immune complexes (antigen-antibody binding) and hematuria because it will last until the membrane
usually trapped in the kidney damage has been repaired
○ When immune complex attached to the ● Blood: ↑ BUN during acute stages but will back to
parts of the body it will be attacked normal upon the recovery of the patient;
○ Immune complexes are formed as a result ○ Can also demonstrate elevated serum,
of immunologic reaction ASO titer - count the anti streptolysin O or
● Increase serum in IG such as igA that will circulate demonstrate the anti group A streptococca
in the bloodstream and deposited in glomerular enzyme test that will provide evidence that
membrane causing: the disease is of streptococcal origin
○ Cellular proliferation and infiltration ● Edema
○ Thickening of basement membrane ● Main effect: causative agent of strepto
Non-immune: toxins; amyloid ● Entry: oral cavity
● Exposure to chemicals and toxins that will affects ● Sometimes due to immune system and
the tubules leading to streptococcus pyogenes is not eliminated =
○ Disruption of electrical membrane charges produce antibodies against strep and may
○ Sometimes seen in nephrotic syndrome deposited in the kidney
● Deposition of amyloid materials from systemic
disorder that may involve chronic inflammation and
acute phase reactant and basement membrane
thickening associated with diabetic nephropathy
Changes:
● Cellular proliferation and infiltration
● Thickening of basement membrane
● Disruption of electrical membrane charges
● Hyalinization
Glomerular disease: PATHOPHYSIOLOGY
Rapidly Progressive / Crescentic Glomerulonephritis
● More serious AGN
● Has a much poorer prognosis often terminating in
renal failure
● Symptoms: inherited by deposition of immune
complexes in the glomerulus often as a
complication of another glomerulonephritis or
Immune systemic disorder (ex: systemic lupus
erythematosus)
(a) Normal glomerulus ; (b) glomerular disease ○ HAPPEN? There is damage caused by
macrophages to do capillary walls which
EXAMPLE OF glomerular diseases will release cells and plasma into the
Acute Post-Streptococcal Glomerulonephritis bowman's pace and production of
● Disease marked by sudden onset symptoms that crescentic formation that will contain
is consistent to the damage to glomerular macrophages, fibroblast, and polymerized
membrane fibrin that causes permanent damage to
● Symptoms: appear in children, young adults the capillary tuft
following respiratory infection caused by certain ● U/A: same as APSGN but become more abnorma
strain of group A streptococcus (s. pyogenes) that as this will progress
will contain M protein in the cell wall ● Includes markedly elevated protein levels and very
● All those contain protein in the cell wall will have a low glomerular filtration rate
post effect of post streptococcal glomerulonephritis
, ● Some forms may demonstrate increased fibrin
degradation products, cryoglobulins and
deposition of IgA immune complexes in
glomerulus
*since there is leakage of fluid so most of the time it will
IgA Nephropathy (BERGER’s disease)
lead to elevated protein levels in the blood and very low
● Mucosal infection
glomerular filtration rate
○ IgA deposition → thickening of membrane
Goodpasture Syndrome ● Common cause of glomerulonephritis
● Caused by cytotoxic antibody that can appear ● Patients has increased level of IgA (secretory Ab)
against the glomerular and alveolar basement caused by mucosal infection
membrane after viral respiratory infections ● Recovery from macroscopic hematuria is
● The attachment of the autoantibodies to the spontaneous however asymptomatic
basement membrane is followed by complement
microhematuria and elevated level of IgA will
activation produces capillary destruction
● Upon activation of the complement it will also remain
attach the basement membrane of the kidneys ● Macroscopic hematuria is asymptomatic thus there
● The autoantibodies is referred to Antiglomerular is gradual progression to chronic
basement membrane antibodies (AGBM Ab) and glomerulonephritis (CGN) and end stage renal
Anti Alveolar basement membrane antibodies disease
● U/A: hematuria, proteinuria, RBC casts ● Present an episode of macroscopic hematuria
● Blood: Ab testing (to see AGBM Ab and
following an infection and straneus exercises
Antialveolar BM Ab)
Membranous Glomerulonephritis Wegener’s Granulomatosis
● IgG deposition → thickening ● Cause granuloma producing inflammation of smal
○ Predominant characteristic: thickening of blood vessels of kidneys and respiratory system
the glomerular basement membrane ● Key to diagnose: Antineutrophilic cytoplasmic
results from the deposition of igG AutoAb (ANCA) → granulomas in the lungs and
● Disorders associated: SLE, Sjogren’s syndrome, glomerulus
secondary syphilis and HBV ● Binding of these autoantibodies to neutrophils that
● Gold and mercury treatments and some are located to the vascular wall will initiate the
malignancies immune response and result to granuloma
● Many cases of unknown etiology have been formation
reported to cause membranous glomerulonephritis ● Patient presents first pulmonary symptoms and
and the disease will progress slowly with possible later develop renal involvement including
remission. However, frequent development of Hematuria, proteinuria, RBC cast
nephrotic syndrome will occur and there is ● Increase BUN and Creatinine
tendency towards thrombosis ● Ab testing
● UA: Hematuria and proteinuria (elevated urine
protein excretion that may reach concentration Nephrotic Syndrome
similar to nephrotic syndrome) ● Causes:
● Tests: ANA (antinuclear antibody), HBsAg (hepa ➢ Circulatory disruption- that will produce
B surface antigen), FTA-ABS (secondary syphilis) systemic shock that will decrease the
pressure and flow of blood to the kidneys
➢ Complication of other Glomerular
disorders
