ACUTE

GLOMERULONEPHRITIS

PATHOPHYSIOLOGY
Glomerulonephritis

is an immunologic disorder that

cause inflammation and increased cells in the
glomerulus because the primary function of glomerulus
is to filter blood, most cases result when antigenantibody complexes produced by an infection elsewhere
in the body become trapped in the glomerulus. This
entrapment causes inflammatory damage and impedes
glomerular function, reducing the glomerular
membranes capacity for selective permeability. The
source of the antigens may be either exogenous (after
streptococcal infection) or endogenous (as in SLE).
Evidence also indicates that some antigen-antibody
complexes may form in the kidney itself.

CLINICAL MANIFESTATION
ACUTE

GLOMERULONEPHRITIS may develop

insidiously or suddenly, varying considerably with
the pathophysiology involved.
Classic manifestations of sudden onset includes:
Hematuria with red blood cell casts and proteinuria.
Fever
Chills
Weakness
Pallor
Anorexia
Nausea and vomiting will be present
Generalized edema (particularly facial expression
and periorbital swelling)
Headache and moderate to severe hypertension

 Visual

acuity may be reduced because of retinal edema

Abdominal or flank pain (probably because of kidney edema
and distention of the renal capsule)
Oliguria or anuria (may be present for several days; the longer
it persists, the more irreversible the kidney damage)
Vague weakness, anorexia, lethargy (mild client reports)
COMMON MANIFESTATIONS
Malaise
Weight loss
Edema
Increase irritability
Mental cloudiness
Digestive disturbances
CARDINAL MANIFESTATION
Is hypertension