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