NEPHRITIC SYNDROME.pptx

8/11/2019 NEPHRITIC SYNDROME.pptx

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NEPHRITIC SYNDROME

Literally means 'inflammation of

glomeruli'


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abrupt onset of glomerular

haematuria (RBC casts or

dysmorphic RBC)

non-nephrotic range proteinuria

Oedema

hypertension

transient renal impairment.


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This is due to the immunologic response

which triggers inflammation and proliferation

of glomerular tissue that results in damage to

the glomerular layers.


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Post-streptococcal glomerulonephritis

Non-streptococcal post-infectious glomerulonephritis, e.g.staphylococcus, pneumococcus, Legionella, syphilis, mumps,varicella, hepatitis B and C, echovirus, EpsteinBarr virus,toxoplasmosis, malaria, schistosomiasis, trichinosis

Infective endocarditis

Shunt nephritis

Visceral abscess Systemic lupus erythematosus

HenochSchnlein syndrome

Cryoglobulinaemia


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Disease Most Frequent

Clinical

Presentation

Pathogenesis Age Group

Affected

Treatment and

Outcome

Acute (Post-

Streptococcal)Glomerulo

nephritis

Acute

nephritis Abrupt

oliguria,

hematuria,

facial

edema,

hypertension.

Immune-complex

mediated Occurs after

Streptococcal

pharyngitis or

Hepatitis-B

High ASO-titer,

low

C3

Common

renaldisease

in

childhood

-Return to

normalin 8 weeks.

Complete

recovery

without

treatment

(especially in

kids) within 3

years.


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Clinical

Presentation


Affected

Treatment

and

Outcome

Focal

SegmentalGlomerulo

nephritis

IgA

Nephropathy(Berger's

Disease):

Most common

primary

Glomerulonephritis

Circulating IgA +

fibronectin (due tochronic liver

disease)

Young men

15-30


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Clinical

Presentation


Affected

Treatment

and

Outcome

Endocarditis S. Aureus Subepithelialimmune deposits Kidneydisease

resolves

when

infection is

cured.

Rapidly

Progressive

Crescentic

Glomerulonephritis

Wegener's:

kidney +

upper

respiratorytract.

Anuria

Oliguria

Inflamed

glomerular

capillaries

ANCA (+)

Must be

treated or it

will go to

renal failurewithin weeks.


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POSTINFECTIOUS ACUTE

GLOMERULONEPHRITIS

is due to immune attack on the infecting organism inwhich there is cross-reactivity between an antigen ofthe infecting organism and a host antigen.

Lancefield group A -haemolytic streptococcus of a

nephritogenic type. The result is deposition of immune complexes and

complement in glomerular capillaries and themesangium.

Symptoms and signs typically occur 710 days afteronset of the acute pharyngeal or cutaneous infectionand resolve over weeks after treatment of theinfection.


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This is diagnosed by evidence of a recent

streptococcal infection (culture of the

organism, raised ASO titre) and low

complement C3 levels that return to normal

after 3-4 weeks.

Long-term prognosis is good.


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Renal function begins to improve spontaneously

within 10-14 days, and management by fluid and

sodium restriction and use of diuretic and

hypotensive agents is usually adequate. Remarkably, the renal lesion in almost all children

and most adults seems to resolve completely

despite the severity of the glomerularinflammation and proliferation seen

histologically.


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GENERAL MEASURES

Fluid balance : strict input/output if oliguria ispresent, daily weight measurement.

Diet : restriction of sodium intake in allchildren with edema or hypertension,restriction of foods high in potassium until

oliguria resolves Bed rest: if hypertension, edema or cardiac

failure are present


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A small number of adults develop hypertensionand/or renal impairment later in life.

Therefore in older patients, an annual bloodpressure check and measurement of serumcreatinine are required.

Evidence in support of long-term penicillinprophylaxis after the development ofglomerulonephritis is lacking.

In non-streptococcal post-infectiousglomerulonephritis, prognosis is equally good ifthe underlying infection is eradicated.


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RAPIDLY PROGRESSIVE

GLOMERULONEPHRITIS

RPGN is a syndrome with glomerular haematuria (RBC casts or

dysmorphic RBCs), rapidly developing acute renal failure over

weeks to months and focal glomerular necrosis with or without

glomerular crescent development on renal biopsy.

The crescent is an aggregate of macrophages and epithelial cells

in Bowmans space .

RPGN can develop with immune deposits (anti-GBM or immune

complex type, e.g. SLE) or without immune deposits

(pauciimmune, e.g. anti-PR3 and or anti-MPO-ANCA positivevasculitides).

It can also develop as an idiopathic primary glomerular disease or

can be superimposed on secondary glomerular diseases such as

IgA nephropathy, membranous GN and postinfective GN.


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plasma exchange is used to remove circulating antibodies, steroids

to suppress inflammation from antibody already deposited in the

tissue, and cyclophosphamide to suppress further antibody

synthesis.

The prognosis is directly related to the extent of glomerular

damage (measured by percentage of crescents, serum creatinine

and need for dialysis) at the initiation of treatment.

When oliguria occurs or serum creatinine rises above 600700

mol/L, renal failure is usually irreversible.

Once the active disease is treated, this condition, unlike other

autoimmune diseases, does not follow a remitting/ relapsing

course.

Furthermore, if left untreated, autoantibodies diminish

spontaneously within 3 years and autoreactive T cells cannot be

detected in the convalescent patients.

Di M F P h i A G T d


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Clinical

Presentation


Affected

Treatment and

Outcome

SLE

Nephropathy

Degree of

kidneyinvolvement

correlates with

prognosis in

SLE.

Anti ds-DNA

antibodies.


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NEPHRITIC SYNDROME.pptx