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

Nephrotic syndrome .
Acute glomerulonephritis (acute nephritic
syndrome) .
Rapidly progressive glomerulonephritis .
Asymptomatic urinary abnormality
(haematuria, proteinuria or both) .
CLASSIFICATION OF
GLOMERULOPATHIES
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
Diseases commonly associated with
acute GN:
Post streptococcal GN
Non- streptococcal post-
infectious GN.
Infective endocarditis
Visceral abscess
SLE
Henoch-schonlein syndrome
cryoglobulinemia


ACUTE NEPHRITIC SYNDROME
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 purpura, crescentic
glomerulonephritis and SLE can also present in this way
ETIOLOGY
Immune Glomerulonephritis:
Pathology
Immune complex disease
Neutrophils:
Protease GBM degradation
O free readicals cell damage
AA metabolites GFR
Complement- dependent Complement-leukocyte- mediated
mechanism

Activation of the complement
pathway Recruitment of
neutrophils and monocytes


C- C (MAC)
Epithelial cell detachment.

(+) epithelial & mesangial
cells to secrete damaging
chemical mediators.

Upregulates TGF receptors
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
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).

CLINICAL FEATURES
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
Nephrotic syndrome
HTN
AKI
Volume overload
Pulmonary edema
Chronic glomerulonephritis and CKI

COMPLICATIONS
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