LinkedIn emplea cookies para mejorar la funcionalidad y el rendimiento de nuestro sitio web, así como para ofrecer publicidad relevante. Si continúas navegando por ese sitio web, aceptas el uso de cookies. Consulta nuestras Condiciones de uso y nuestra Política de privacidad para más información.
LinkedIn emplea cookies para mejorar la funcionalidad y el rendimiento de nuestro sitio web, así como para ofrecer publicidad relevante. Si continúas navegando por ese sitio web, aceptas el uso de cookies. Consulta nuestra Política de privacidad y nuestras Condiciones de uso para más información.
Classification of glomerular disease
– Acute GN
• Post streptoccocal
• Non streptococal
Rappidly progressive GN
Minimal change GN
IgA nephropathy GN
Nephritis Caused by Circulating
the gromerulus is considered “innocent
bystander” because it does not incite the
The antigen is not of glomerular origin.
It may be endogenous, as in the GN
associated with SLE, or
it may be exogenous, as is probable in the
GN that follows certain bacterial, viral,
parasitic and spirochetal infections.
Often the inciting antigen is unknown, as
in most cases of membranous nephropathy.
Whatever the antigen may be,
antigen-antibody complexes are formed
in situ or in the circulation and are then
trapped in the glomeruli,
where they produce injury, in large
complement and the recruitment of
Regardless of the mechanism, the
glomerular lesions usually consist of
leukocytic infiltration into glomeruli and
variable proliferation of endothelial,
mesangial, and parietal epithelial cells.
Electron microscopy reveals the immune
complexes as electron-dense deposits
or clumps that lie at one of three sites:
in the mesangium,
between the endothelial cells and the
between the outer surface of the GBM
and the podocytes.
Seen in most cases of poststreptococcal
or acute infection-related GN.
Nephritis Caused by in Situ Immune
Membrance (GBM) Antibody
In this type of injury, antibodies
are directed against fixed antigens
in the GBM.
It has often been suggested that
sensitized T cells, formed during the
course of a cell-mediated immune
reaction, can cause glomerular injury.
In some forms of experimental GN
in rodents, the disease can be
induced by transfer of sensitized T
T cell-mediated injury may account for
the instances of GN in which either
there are no deposits of antibodies or
immune complexes or the deposits do
not correlate with the severity of
Mediators of Immune Injury
Glomerular damage, reflected
by loss of glomerular barrier
proteinuria and, in some instances,
by reduction in GFR.
A major pathway of antibody –
initiated injury is complementleukocyte-mediated
Activation of complemnt leads to the
generation of chemo tactic agents and
the recruitment of neutrophils and
Neutrophils release proteases, which
cause GBM degradation; oxygen-derived
free radicals, which cause cell damage;
and arachidonic acid metabolites, which
contribute to reduction in GFR.
This mechanism applies only to some
types of GN.
Some models suggest complementdependent but not neutrophil-dependent
injury, due to an effect of the C5 lytic
component of complement,
detachment and stimulates mesangial
and epithelial cells to secrete various
mediators of cell injury.
Thus giving rise to altered GBM
composition and thickening.
Other mediators of glomerular
(1)monocytes and macrophages,
which infiltrate the glomerulus in
reactions and, when activated,
biologically active molecules;
(2) platelets, which aggregate in the
prostaglandins and growth factors;
(3) Resident glomerular cells, which
can be stimulated to secrete
mediators such as cytokines
growth factors, nitric oxide, and
(4) fibrin-related products, which
cause leukocyte infiltration and
glomerular cell proliferation as a
consequence of intraglomerular
Other Mechanisms of Glomerular Injury
Two that deserve special mention are
podocyte injury and injury secondary to
This can be induced by antibodies to
visceral epithelial cell antigens; by
toxins, certain cytokines; or by still
poorly characterized factors, as in some
cases of focal and segmental
Such injury is reflected by
effacement of foot processes,
vascularization, and retraction and
detachment of cells from the GBM,
and functionally by proteinuria.
In most forms of glomerular
diaphrangms is key in the
development of proteinuria.
glomerular or otherwise, destroys
sufficient functioning nephrons to
reduce the GFR to 30% to 50% of
normal progression to end-stage
develop proteinuria, and their
These remaining glomeruli undergo
hypertrophy to maintain renal function.
This is associated with hemodynamic
changes, including increases in single
nephron, GFR, blood flow, and
These adaptations in the intact
glomeruli are ultimately maladaptive
and lead to further endothelial and
epithelial cell injury, increased
glomerular permeability to proteins,
and accumulation of proteins and lipids
in the mesangial matrix.
TYPES OF GLOMERULONEPHRITIS:There are different types of GN
It may involve either the nephrotic
syndrome or nephritic syndrome
Diagnosis made by C/F or by renal
Types of glomerulonephritis (ACUTE NON
Minimal change disease
Is a benign disorder
Frequent cause of nephrotic
syndrome in children
Here the glomeruli shows a diffuse
effacement of podocyte foot
1. MINIMAL CHANGE DISEASE
It is a begin disorder.
Frequence cause of nephrotic
Different affacement of
pocodeyti foot processes (they
Systemic disease (hodgkins disease, HIV
infection) & drug therapy (NSAID)
Protenuria has been attributed to T cell
derived factor that cause podoeyte
enjury & affacement.
C/F:- Protein Loss
Prognosis – good, Rx is corticosteroids
Focal & segmental to slecrosis :
Characterized by sclerosis
affecting some but not all the
Associated with HIV infection
Maladaptation after nephron loss
Congenital malformation in
Investigators have said that FSGS
and MCD are continuous – MCD
may transform into PSGS
Not responding to corticosteroids
Recurs after transplantation
3. MEMBRANOUS NEPHROPATHY
Occurs between 30 & 50 years.
Causing thickening of the capillary wall.
idiopathic secondary to
Infections (chronic hepatitis, syphillis,
Malignant tumors of lung & colon
SLE & other auto immune disorders
Does not respond to
They may respond to prednisolone.
30% may have spontaneous
Menbranoproliferative FN:Alteration in the GBM &
Proliferation of glomerular cell
Mesengial cells are found between
the endothelium & GBM
Immune deposits are found in
(bacterial endocardites, HIV,
Is autoimmune disease called
IgG autoantibodies called c3
Causing lipodystrophy loss of
subcutaneous fat from the upper
half of the body.
IGA NEPHROPATHY :
Associated with gross hematuria
Associated with loin pain
Here there is deposition of IgA is
mesangium (due to IgA production
& clearance abnormal)
It is due to some infection is to
respiratory or GI tract.
These activates the alternative
Red blood cell cast on urine
Antigen (group A seta – hemolylic
Antigen – antibody products
Deposition of antigen – antibody
complexes in glomerulers
Increase production of epithelial
cells lining the glonerulus
Luekocyte infiltration of
Thickening of the GF membrane
Scarring and loss of glomerular
Decreased glomerular filtration rate
Abdominal or flank pain
Fever, chills, weakness, pallor,
anorexia, nausea and vomitting
may be present.
Elderly patient may experience
circulattory ocurroal, with dyspnea,
engorged nec ceeins, cardionegely
and pulmonary edema.
DIAGNOSTIC STUDIES: History and physical examination
BUN, seum creatinine and albunmin
Complement levels and ASO titre
Signs of overload
Edema and hypertension due to overload
Elevated jugular venous pressure
Twenty-four hours urine test for
Anti sterptolysin O titre
Renal biopsy: cellular infiltration,
granular deposits of
Penicillin 500000 IU q6 q8 hourly
Edema: 40-80mg to 20- 40mg 6th
Hypertension: 20- 40mg bid PO bid
0.5-8mcg/kg/mim IV infusion
Sodium and fluid restriction
Protein restriction 0.6 – 0.75g/kg/wt
Water restriction to 600ml plus the
previous days urine output.
Sodium restriction; 2 to 4g
depending on the degree of edema.
Avoid high sodium food.
Acute GN (repeated episodes)
Cause hardening of renal arteries
Reducing the size
Scar tissue formation (numerous
glomerulus and branches of renal
arteries are thickened)
Severe glomerular damage
End stage renal failure
Edema of the optic disc
General symptoms like malaise,
weight loss, edema, mental
Gallop rhythm, distended neck
veins, symptoms of heart failure.
Mucous membrain pale because of
Urine analysis shows hematuria,
protienuria, scanty, dark, smoky,
Nephrotic syndrome is a cluster of
clinical findings, including
Marked increase in protein
(particularly albumin) in the urine
Decreased in albumin in the blood
Edema, hypercholesterolemia &
normal renal function.
The causes can be classified also
Minimal change disease
Drugs. (heavy metal compounds
like gold & mercury, heroin
Bee sting, snake bite, poison ivy
Toxemia of pregnancy
VII. Circulatory disturbance
Renal vein thrombosis
VIII. Hereditary diseases
Nail patella syndrome
Damage to the glomerular capillary
Loss of plasma protein
decreased oncotic press