CASE 11. What is the significance of the present condition?

The present condition of the patient is representative disease ofacute 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 situdeposition 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 titerThe 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 21. 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 31. 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.