CASE 1

1. What is the significance of the present condition?

The present condition of the patient is representative disease of
acute nephritic syndrome in which inflammation of the glomerulus is
manifested by proliferation of cellular elements secondary to an
immunological mechanism. Acute poststreptococcal glomerulonephritis
(APSGN) results from infection by nephritogenic streptococci. It s a renal
disease characterized by inflammation of the glomeruli, or small blood
vessels in the kidneys.

2. What is the significance of the past medical history?

The past medical history shows that a patient had sore throat
and
pyodermas. And this could have predisposed the patient to develop
Acute poststreptococcal glomerulonephritis. Acute poststreptococcal
glomerulonephritis is the result of an infection, not of the kidneys, but of
a completely different area, such as the skin or throat, with a specific
type of Group A beta hemolytic streptococcus bacteria.

3. Describe the histologic changes particularly in the glomerulus in this

condition
The basic process in AGN is deposition or in situ
deposition of immune complexes in the glomeruli. Cellular pathology
reveals swelling of the glomerular tufts and infiltration with
polymorphonucleocyte. Kidneys then enlarge and may increase in size
until they are twice that of a normal kidney.
The development of acute post-streptococcal glomerulonephritis
is
that nephritogenic streptococci produce proteins with unique antigenic
determinants. These antigenic determinants have a particular affinity for
sites within the normal glomerulus.Following release into the circulation,
these antigens bind to these sites within the glomerulus. Once bound to
the glomerulus, they activate complement directly by interaction with
properdin. Glomerular-bound streptococcal antibodies also serve as
fixed antigens and bind to circulating anti-streptococcal antibodies
forming immune complexes. Complement fixation via the classical
pathway leads to generation of additional inflammatory mediators and
recruitment of inflammatory cells. The 2 major nephritogenic antigens
that have been identified are zymogen, a precursor of exotoxin B called
SPEB and nephritis plasmin binding protein. Bound plasmin can cause
tissue destruction by direct action on the glomerular basement
membrane or by indirect activation of pro-collagenases and other matrix
metalo-proteinases. Also, the in situ–formed and circulating immune
complexes can readily pass through the altered glomerular basement
membrane and accumulate on the sub-epithelial space as humps.

4. How does this pathology affect glomerular filtration?

In Acute poststreptococcal glomerulonephritis there is
reduced glomerular filtration. GFR is compromised by the presence of
inflammation in the glomerulus. APSGN damage the glomeruli, letting
 protein and sometimes red blood cells leak into the urine. Sometimes a
glomerular disease also interferes with the clearance of waste products
by the kidney, so they begin to build up in the blood. Glomerular
inflammation reduces glomerular filtration without a coexistent decrease
in total renal blood flow.

5. Interpret the findings in the urinalysis, serum C3, ASO titer

The urinalysis reveals that the patient has dark colored urine
which is caused by hemolysis of red blood cells that have penetrated the
glomerular basement membrane and have passed into the tubular
system. The turbidity is hazy because of presence of many solutes like
protein and RBC. The specific gravity reveals that the patient’s urine is
concentrated. There is proteinuria and hematuria which means that
protein and red bloods cells passes through the glomerulus.
There is decreased C3 levels which means that the
complement
system is depress. This is brought about by decreased protein in the
blood (because it is excreted in the urine), The complement system is a
group of proteins that move freely through your bloodstream. The
proteins work with your immune system and play a role in the
development of inflammation.
ASO test help determine whether a person has had a recent
streptococcal infection. ASO antibodies are produced about a week to a
month after an initial strep infection. ASO levels peak at about 4 to 6
weeks after the illness and then taper off but may remain at detectible
levels for several months after the strep infection has resolved. The ASO
level of the patient indicates that the patient had recent streptococcal
infection.

6. Can RBC be found in the urine without any pathology in filtering

membrane?
No, because the RBC is a macromolecule, which means that, it
is so
large that, it cannot pass through the glomerular membrane.

7. Do you expect to find glucose in the urine if the filtration barrier is

damaged?
Yes, because the glucose can freely pass through the damaged
glomerular membrane.

CASE 2
1. How will this condition affect the following?
a. renal blood flow – decreased, can be brought about by
internal bleeding (damage to blood vessels) cause by trauma
b. glomerular filtration rate - decreased, because of decrease
renal blood flow
c. plasma colloidal osmotic pressure – none, because it is only
determine by plasma proteins.
d. Bowman’s capsular pressure - increase, due to decrease in
GFR
 2. What is the significance of a 5cc/kg/hr urine output?
The patient has oliguria, this is brought about by the decrease in
the function of the kidneys especially the glomerulus where in there is
decrease glomerular filtration rate and also the tubules are not
functioning well.

3. What is the significance of elevated creatinine and blood urea

nitrogen?
This means that there is decreased renal functional which could
be
brought about by decrease renal perfusion. The nephrons becomes
ischemic there by decreasing there functional especially its ability to
excrete waste product.

CASE 3
1. How does the presence of the ureteral stone affect the following?
a. renal blood flow – decrease, due to increasing pressure in
the tubules
b. glomerular filtration – decrease, due to increase in bowman’s
capsular pressure
c. tubular pressure – increase, due to the presence of
obstruction
d. pressure in the pelvico-calyceal system – increase, due to
fluid/urine accumulation

2. If the urteroliathiasis persist, what structural changes do you expect in

the:
a. Ureter – the ureter may become inflamed due to mucosal
irritation brought about by presence of stone. The stone
could also damage the mucosal lining (by scratching it)
b. pelvico- calyceal system – there could be fluid accumulation
in this region cause by obstruction in the ureter.
c. renal pyramids - there will be distention of the renal pelvis
because the urine are not emptied.

3. What is the significance of the RBC in the urine?

There could be bleeding the ureter due to the presence of stone.
The bleeding could be cause by damage in the lining of the ureter, as
the ureter tries to expel the stone this cause injury to the mucosa.