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GLOMERULONEPHRITIS

IN SYSTEMIC LUPUS

ERYTHEMATOSUS

YOHANES SATRYA WIBAWA

030.09.275

INTRODUCTION

Systemic Lupus Erythemstosus (SLE) is a chronic systemic inflammatory disease that follows a course of alternating
Systemic Lupus Erythemstosus (SLE) is a
chronic systemic inflammatory disease that
follows a course of alternating exacerbations or
remissions. SLE is autoimmune disorder that
affects multiple organ systems including the
skin, kidneys, and brain. The exact cause of
SLE is unknown but genetic factors, ethnic
origin, environmental factors, and medications
may all be involved in its development.

EPIDEMIOLOGY

o Predominantly affects women of childbearing age (20 – 40 years) o Female to male ratio
o Predominantly affects women of childbearing
age (20 – 40 years)
o Female to male ratio of 9:1 to 15:1.
o Approximately 8% to 15% of SLE cases occurs
in children.
o Genetic and racial factors  African-American
women have a 3 to 4 times higher risk
prevalence of SLE than Caucasian women.

ETIOLOGY

A complex abnormal immune process (unknown)   Dysregulation of B- and T-lymphocytes production of autoantibodies
A complex abnormal immune process (unknown)
Dysregulation of B- and T-lymphocytes production of
autoantibodies  formation of immune complexes
Cytokines  key role
Environmental factors

PATHOPHYSIOLOGY

CLINICAL MANIFESTATION

Acute - insidious   Non spesific  fever, weight loss, severe fatique, and lymphadenopathy Every
Acute - insidious
Non spesific  fever, weight loss, severe fatique, and
lymphadenopathy
Every organ system may become involved
Common skin manifestations malar or butterfly rash,
with sun-induced macules or papules occurring on the
face
90%  joint inflammation
Renal complication (glomerulonephritis and
microvascular thrombosis)  common

GLOMERULUS

•Modified capillary network that delivers an unfiltrate of plasma to Bowman’s space •1.6 million glomeruli are
•Modified capillary network that delivers an unfiltrate of plasma to Bowman’s
space
•1.6 million glomeruli are present in two mature kidneys
 Filtration of plasma protein and blood cells  glomerular filtration barrier, composed of : 
Filtration of plasma protein and blood cells 
glomerular filtration barrier, composed of :
fenestrated glomerular endothelium;
basement membrane;
foot processes and slit diaphragms of visceral epithelial
cells (podocytes).
Glomerular injury  impairment of glomerular
filtration and/or inappropriate appearance of plasma
proteins and blood cells in the urine.

GLOMERULONEPHRITIS

Glomerular injury  Inflammation such as leukocyte infiltration,  antibody deposition, and complement activation Glomerular disease
Glomerular injury
Inflammation such as leukocyte infiltration,
antibody deposition, and complement activation
Glomerular disease :
Primary : the pathology is confined to the kidney and
any systemic features are a direct consequence of
glomerular dysfunction; usually idiopathic.
Secondary : part of a multisystem disorder.

GLOMERULONEPHRITIS IN

SLE

GLOMERULONEPHRITIS IN SLE

GLOMERULONEPHRITIS IN SLE

Commonest and most serious  75%  found at autopsy   Autoimmune disease the immune
Commonest and most serious
75%  found at autopsy
Autoimmune disease the immune system cannot tell
the difference between harmful substances and healthy
ones  attacks healthy cells and tissue
Damage different parts of the kidney  interstitial
nephritis, nephritic syndrome, and membranous
glomerulonephritis.
May rapidly worsen to kidney failure.

WHO CLASSIFICATION of LUPUS NEPHRITIS

WHO CLASSIFICATION of LUPUS NEPHRITIS WHO class I nephritis : no histologic abnormalities are detected WHO

WHO class I nephritis : no histologic abnormalities are detected WHO class II nephritis (mesangial lupus nephritis) WHO class III nephritis (focal segmental lupus glomerulonephritis) WHO class IV nephritis (diffuse proliferative lupus nephritis) WHO class V nephritis (membranous lupus nephritis)

WHO CLASSIFICATION of LUPUS NEPHRITIS WHO class I nephritis : no histologic abnormalities are detected WHO
WHO CLASSIFICATION of LUPUS NEPHRITIS WHO class I nephritis : no histologic abnormalities are detected WHO
WHO CLASSIFICATION of LUPUS NEPHRITIS WHO class I nephritis : no histologic abnormalities are detected WHO
WHO CLASSIFICATION of LUPUS NEPHRITIS WHO class I nephritis : no histologic abnormalities are detected WHO
WHO CLASSIFICATION of LUPUS NEPHRITIS WHO class I nephritis : no histologic abnormalities are detected WHO
WHO CLASSIFICATION of LUPUS NEPHRITIS WHO class I nephritis : no histologic abnormalities are detected WHO

CLINICAL FINDING

Hematuria  Proteinuria  Reduced renal function   In rare patients with proliverative glomerulonephritis, the
Hematuria
Proteinuria
Reduced renal function
In rare patients with proliverative
glomerulonephritis, the urinarylis may be
completely normal.

DIAGNOSIS

Detection of circulating antinuclear antibodies(ANA)  Confirmation : demonstrating antibodies that react with  native double-stranded
Detection of circulating antinuclear antibodies(ANA)
Confirmation : demonstrating antibodies that react with
native double-stranded DNA
Depressed C3 and C4 levels
Renal biopsy

TREATMENT

Medical and psychologic support  Immunosuppressive therapy :   Prednisone 1-2 mg/kg/day  for a
Medical and psychologic support
Immunosuppressive therapy :
 Prednisone 1-2 mg/kg/day  for a serologic
remission
 6 monthly i.v. infusions of Cyclophosphamide
500-1000mg/m 2  reduce the risk of progressive
renal dysfunction 4,5

PROGNOSIS

Unsatisfactory   Up to 25%  end stage renal failure in 10 years
Unsatisfactory
Up to 25%  end stage renal failure in 10
years

CONCLUSION

Systemic lupus erythematosus (SLE) is an autoimmune disorder that can affect several organ systems, including the
Systemic lupus erythematosus (SLE) is an autoimmune
disorder that can affect several organ systems, including
the kidney. Although renal involvement is common in
SLE, most studies showed that kidney disease
presented less commonly in late onset SLE compared
with younger patients. Better and earlier recognition of
SLE and more effective treatments have significantly
improved survival rates. The aim of the treatment is first
to stop disease progression, prevent reccurence, and
minimizing the adverse effects. More specifically with
lupus nephritis, the aims of treatment are to reduce the
risk of end stage renal disease, reduce renal and extra-
renal lupus activity of symptoms, and reduce the
mortality risk.