ACUTE POSTINFECTIUOS - University of Babylon
Transcript of ACUTE POSTINFECTIUOS - University of Babylon
ACUTE
POSTINFECTIUOS
BABYLON UNIVERSITY-COLLAGE OF MEDCINE
Dr.Hadi AL-Moswi
ACUTE POSTINFECTIUOS (POSTSTREPTOCOCCAL)GN
Pathogenesis:
It is generally that immune complex deposition is involved
The relevant antigens are probably streptococcal proteins
Primary injury result from complement activation, resulting in
diffuse proliferation and swelling of glomerular cells and
frequent infiltration of leukocytes.
Similar proliferative GN are seen in other endogenous and
exogenous antigens??
Clinical course: the onset is abrupt, proceed by malaise, slight
fever, nausea and nephritic syndrome, oliguria, azotemia, and
hypertension, gross haematuria
Morphology:
Uniformly increased cellularity, of the glommerular tufts result
from proliferation and swelling of endothelial and mesangial
cells and by neutrophilic and monocytic infiltrate
IgA Nephropathy(Berger Disease)
Pathogenesis:
It is associated with an abnormality in IgA production and
clearance, is at low lvels in normal individual but increased in
50% of patients with IgA nephropathy, studies suggest an
abnormality in glycosylation of the IgA immunoglobulin this
will led to reduce plasma clearance of IgA thus fovring
deposition in the mesangium, IgA nephropathy occurs with
increased frequnciy with celiac disease
Clinical course: often affects childdern and young adults,
often with gross haematuria after an infection of the
respiratory or??, 30-40% have only micrscopic haematuria, 5-
10% develop acute nephritic syndrome , haematuria last for
few days and then subside and return every few months
Morphology
:variable , may show mesangial widening or mesangial
proliferation
Rapidly progressive (Crescentic) GN:
Pathogenesis:TypeI (anti-GBM antibody cresentic G.N is characterized by linear deposits of
IgG, some time associated with with pulmonary hemorrhage called Goodpasture
syndrome
TypeII immune complex –mediated Cresentic GN
Idiopathic, SLE, Henoch-Scholein purpura
TypeIII Pauci –immune Cresentic GN: there are antineutrophil cytoplasmic Abs
in the serum, idiopathic, wegner granulomatosis, microscopic angitis
Morphology: the distinctive lesions of proliferation are called crescents due to
their shape as they fill Bowmans space, the crescents are formed by both by
proliferation of partial cells and by migration of monocytes, small number of
leukocytes
Clinical course:
The patients present with nephritic syndrome the prognosis releated to number
of crescent if less than 80% of the glomeruli have better prognosis
Chronic GN
It is an important cause of end stage renal disease
Morphology:
There is obliteration of the glomeruli, there is marked
interstial fibrosis, thick wall of small and medium sized
arteries , lymphocytic infiltration are present in the fibrotic
interstial tissue
Acute pyelonephiritis
Is suppurative inflammation of the kidney and the renal pelvis
is caused by bacterial infection
Pathogenesis:There are two routs by which bacteria can reach the kidney
A- through bloodstream
B- from lower urinary tract : is the most important and
common route, there are adhesion of the bacteria to mucosal
surface , follwed by colonization of the distal urthera, the
organisms must gain access to the bladder this occur during
urtheral instrumentation ,
2-obstruction at the level of the urinary bladder results in
incomplete emptying and increase residual volume of urine as
with BPH and uterine prolapse
3- in DM because neurogenic bladder dysfunction
4- incompetence of the vesicoureteral orifice leading to VUR
5- female
Morphology:Grossly characteristically discrete , yellowish raised abscesses
, histiologically is suppurative necrosis or abscess formation
within the renal parenchyma
Clinical course;
The onset is usually sudden with pain at the costoverterbral
angle , chills, fever and malaise pyuria , dysuria, frequency
and urgency