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Glomerulonephritis
Glomerulonephritis
Nephrotic syndrome.
Acute glomerulonephritis (acute
nephritic syndrome).
Rapidly progressive
glomerulonephritis.
Asymptomatic urinary abnormality
(haematuria, proteinuria or both).
Proteinuria asymptomatic
Haematuria asymptomatic
Hypertension
Nephrotic syndrome
Nephritic syndrome
Acute renal failure
Rapidly progressive renal failure
End stage renal failure
Complement-leukocyte- mediated
mechanism
Activation of the complement
pathway Recruitment of
neutrophils and monocytes
Neutrophils:
Protease
GBM
degradation
O free readicals cell damage
AA metabolites
GFR
Complement- dependent
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
Named according to
etiology
microscopic findings
clinical syndrome
acute nephritic syndrome
nephrotic syndrome
hematuria
HT
increased urea & creatinine
low urine output
edema
Unknown causes or
secondary to
poststreptococcal
glomerulonephritis
Autoimmune
aka crescentric
glomerulonephritis
Some present as acute
nephritic syndrome &
others as renal failure
Caused by deposition of
An-Ab complexes
All but a few progress to
renal failure
Autoimmune
Most common
cause of nephrotic
syndrome in adults
About 10% proceed
to renal failure
within 10 yrs, 25%
recover
completely, most
progress slowly
with proteinuria,
HTN, loss of renal
function
Vascular disease
atherosclerosis
HTN
vascultitis
Infectious
Streptococcal
Nonstreptococcal postinfectious
glomerulonephritis
Bacterial
Viral
Parasitic
Noninfectious
Fever
Headache
Malaise
Anorexia
Nausea and vomiting
High blood pressure
Pallor due to edema and/or anemia
Confusion
Lethargy
Loss of muscle tissue
Enlargement of the liver
proper hygiene
prompt medical assessment for necessary
antibiotic therapy should be sought when
infection is suspected
prophylactic immunizations
Antimicrobial therapy
Diet:
Post streptococcal GN
- Has a GOOD prognosis.
- Supportive measures until spontaneous
recovery.
- Control HT.
- Fluid balance.
- Oliguric with fluid overload.
- GN complicating SLE or systemic vasculitides:
immunosuppression with prednisolone,
cyclophosphamide or azathioprine/MMF.
fusion of
podocytes on electron
microscopy
Segmental
areas of glomerular
sclerosis,
hyalinization of
glomerular capillaries
thickened BM, IF
+ve for IgG & C3 and
subepithelial deposits
on EM
Uremia-specific findings
Edemas
Hypertension
Jugular venous distension (if severe volume
overload is present)
Pulmonary rales (if pulmonary edema is present)
Pericardial friction rub in pericarditis
Tenderness in the epigastric region or blood in the
stool (possible indicators for uremic gastritis or
enteropathy)
Decreased sensation and asterixis (indicators for
advanced uremia)
Urinalysis
Urinary protein excretion
Serum chemistry
Renal ultrasonogram
Kidney biopsy
Mesangiocapillary GN
Treatment: None is of proven benefit.
Prognosis: 50% develop ESRF.
Membranous nephropathy
If renal function deteriorates, consider
corticosteroids and chlorambucil.
Prognosis: Untreated, 15% complete
remission, 9% ESRF at 25yrs and 41%
at 15yrs.
Mesangial proliferative GN
Antibiotics, diuretics, and
antihypertensives as necessary. Dialysis is
rarely required.
Prognosis: Good.
Rapidly progressive
glomerulonephritis (RPGN) is a
disease of the kidney that results in a
rapid decrease in the glomerular
filtration rate of at least 50% over a
short period, from a few days to 3
months.
More than 80% of patients with pauciimmune RPGN were subsequently found
to have circulating antineutrophil
cytoplasmic antibodies (ANCA), and thus,
this form of RPGN is now termed ANCAassociated vasculitis.
The link between ANCA and the
pathogenesis of ANCA-associated disease
is unknown, but it is postulated that
neutrophils and mononuclear phagocytes
are directly activated by ANCA and these
activated cells, in turn, attack vessel
walls, producing injury similar to that
produced by anti-GBM antibodies or
immune complexes.
Renal biopsy
specimens show a
diffuse, proliferative,
necrotizing
glomerulonephritis with
crescent formation. The
main pathologic finding
is fibrinoid necrosis
(>90% of biopsy
specimens); extensive
crescent formation is
present in at least 50%
of glomeruli.
High-dose corticosteroids;
cyclophosphamide plasma exchange/
renal transplantation. Prognosis: Poor if
initial serum creatinine >600mol/L.