Nancy Diaz
Prep questions- Renal
1. What are the pathophysiologic changes in acute streptococcal
glomerulonephritis?
Antibody-antigen complexes become lodged in the glomeruli, leading
to inflammation and obstruction. The glomerular membranes are
thickened and capillaries in the glomeruli are obstructed by damaged
tissue cells, leading to a decreased glomerular filtration rate. Vascular
permeability increases, allowing protein, red blood cells, and red cast
to be excreted. Sodium and water are retained, expanding the
intravascular and intestinal compartments and resulting in the
characteristic finding of edema.
2. What is the relationship between group A streptococcal infection and
glomerulonephritis?
The child with acute post infection glomerulonephritis (APIGN) usually
becomes ill after contracting a nephrogenetic strain of group A betahemolytic streptococcal infection of the upper respiratory tract or the
skin. Often the child contracts strep throat, recovers, and then
develops signs of APIGN after an interval of 10-21 days. Glomerular
damage occurs as a result of an immune complex reaction that
localizes on the glomerular capillary wall.
3. How is acute streptococcal glomerulonephritis diagnosed?
The serum BUN and Cr concentrations are elevated. Serum protein is
decreased (hypoalbuminemia) due to mild to moderate proteinuria.
WBC and erythrocyte sedimentation rate may be elevated. An
elevated antistreptolysin O (ASO) titer reflects the presence of
antibodies from a recent pharyngeal streptococcal respiratory
infection, ASO level associated with skin infection is low. The antiDNAase B titer is helpful for detecting antibodies associated with
recent skin infections. Most children have a reduced serum
complement (C3) level due to the initial infection.
Urinalysis reveals hematuria, proteinuria, and red and white cell cast.
Anemia is common in the acute phase, usually because extracellular
fluid dilutes the serum. Hgb and Hct levels reveal anemia, which is
common in the acute phase and is generally caused by dilution of the
serum by the extracellular fluid.
