Isbandiyah,dr,SpPD

GLOMERULUS
Schematic Representation of a Glomerular Lobe

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 Nomenclature
• Glomerulonephritis = glomerulopathy →
glomerular injury
• Glomerulonephritis: injury with evidence of
inflammation such as leukocyte infiltration,
antibody deposition, and or complement
activation
• Primary or secundary
• Acute (days or weeks), subacute or rapidly
progressive (weeks or few months) and chronic
(many months or years)
• Focal (<50%) or diffuse (> 50%) of glomeruli
 CLASSIFICATION OF
GLOMERULOPATHIES
• Nephrotic syndrome .
• Acute glomerulonephritis (acute nephritic
syndrome) .
• Rapidly progressive glomerulonephritis .
• Asymptomatic urinary abnormality
(haematuria, proteinuria or both) .
 Major Clinical Manifestations of Glomerular
Diseases
Acute nephritic syndrome
The nephrotic syndrome
Persistent urinary abnormalities with few or no
symptoms
Acute renal failure (RPGN)
Chronic glomerulonephritis
 ACUTE NEPHRITIC SYNDROME
Diseases commonly associated with
acute GN:
• Post streptococcal GN
• Non- streptococcal post-
infectious GN.
• Infective endocarditis
• Visceral abscess
• SLE
• Henoch-schonlein syndrome
• cryoglobulinemia
 Clinical Features of the Acute Nephritic
Syndrome
 haematuria is usually macroscopic with pink or brown urine
(like coca cola)
 oliguria may be overlooked or absent in milder cases
 oedema is usually mild and is often just peri-orbital- weight
gain may be detected
 hypertension common and associated with raised urea and
creatinine
 proteinuria is variable but usually less than in the nephrotic
syndrome
 Etiology of the Nephritic Syndrome

• Most common cause is acute post infectious

glomerulonephritis
• group A beta haemolytic streptococci of certain serotypes
important in NZ
• IgA disease and Henoch-Schonlein glomerulonephritis and
SLE can also present in thipurpura, crescentic s way
ETIOLOGY
Immune Glomerulonephritis:
 Pathology Immune complex disease
Complement-leukocyte- mediated Complement- dependent
mechanism
C₅- C₉ (MAC)
 Activation of the complement
pathway Recruitment of
neutrophils and monocytes Epithelial cell detachment.

 (+) epithelial & mesangial

cells to secrete damaging
 Neutrophils: chemical mediators.
Protease GBM degradation
O₂ free readicals cell damage Upregulates TGF receptors
AA metabolites ↓ GFR on epithelial cells, excessive
synthesis of extracellular
matrix which leads to
GBM thickening
Pathology of Acute glomerulunephritis

Diffuse proliferative GN
(PGN)
 proliferation of cells within
the glomeruli, accompanied
by leukocyte filtrate

 typical features of immune complex

disease :
- hypocomplimentemia
- granular deposits of IgG &
complement on GBM
Glomerular damage - patterns:
Glomerular diseases:
LIGHT MICROSCOPE
 CLINICAL FEATURES
 Abrupt onset of :
 glomerular haematuria
(RBC casts or dysmorphic
RBC).
 non-nephrotic range
proteinuria ( < 2 g in 24
hrs) .
 oedema ( periorbital,
sacral ).
 hypertension.
 transient renal impairment
(oliguria, uraemia).
 INVESTIGATIONS
Base line measurements:

- ↑ Urea

- ↑ Creatinine

- Urinalysis (MSU) :
a) Urine microscopy
(red cell cast)
b) proteinuria
Diagnostically useful tests :

 Culture (swab from throat or

infected skin)

 Serum anti-streptolysin-O
titre

 Hepatitis B surface antigen

Hepatitis C antibody

anti DNA , ANCA

 ↓C3,4

Renal biopsy
 COMPLICATIONS
• Nephrotic syndrome
• HTN
• AKI
• Volume overload
• Pulmonary edema
• Chronic glomerulonephritis and CKI
 Management & Prognosis
Post streptococcal GN
- Has a GOOD prognosis .
- Supportive measures until spontaneous
recovery.
- Control HTN.
- Fluid balance.
- Oliguric with fluid overload.
- GN complicating SLE or systemic
vasculitides : immunosuppression with
prednisolone, cyclophosphamide or
azathioprine