Angeles University Foundation

Angeles City

Case Analysis

Group 1

BSMT 3A

DIMLA, Mary Kimberly

PARTOLAN, Mark Jadrian
SALINAS, March Tracy
TORRES, Kristensen

January 7, 2010

CASE 2

From a rural hospital in Barangay Ilang-Ilang, this 71-year old woman was transferred to a
tertiary hospital complaining of shortness of breath and showing evidence of pulmonary
edema. There was no history of chest pains, nausea, vomiting or diaphoresis. Her
admission diagnosis was Congestive Heart failure (acute exacerbation), Myocardial
Infarction (subendocardial), DM and HTN. Medications included Lasix, morphine,
nitroglycerin, and Procardia. Laboratory tests were significant for increased CK, 544 U/L (21-
215) with a CKMB of 29.2 ng/mL (0-4), which is a relative index of 54. During the first few
days of her hospital stay, blood glucose ranged from 201 to 365 mg/dL (70-110); creatinine
ranged from 1.9 to 3.7 mg/dL (0.6-1.0); and BUN ranged from 31 to 46 mg/dL (5-25).
Admission urinalysis was significant for: glucose 100 mg/dL; blood moderate; protein >300
mg/dL (<90); WBCs 2-5/hpf; RBCs 10-20/hpf; epithelials/lpf few squamous, few renal;
casts/lpf 5-10 granular, 0-1 WBC. After aggressive treatment of the she received
intravenous nitroglycerin and insulin. The discharge diagnosis was status
postsubendocardial MI, triple-vessel cardiac disease, CHF, renal insufficiency, HTN, and DM.
She was scheduled to return to the hospital eventually for a triple vessel coronary bypass.
What renal condition do the urinalysis data suggest? Explain. Do the analyses on blood
correlate with this? Explain. What is the pathophysiology behind the renal condition in the
first question? Explain.

Gender: Female
Age: 71

Symptoms:

Shortness of breath
Pulmonary edema

*no chest pains

*no nausea
*no vomiting

Diagnosis:
CHF (Congestive Heart Failure)
MI (Myocardial Infarction)
HTN (Hypertension)
DM (Diabetes Mellitus)

Medications:
Lasix – CHF
Morphine –pain killer
Nitroglycerin –vasodilator
Procardia –antiaginal, antihypertensive
Insulin –DM

Blood Chemistry Results:

CK -554u/l
CKMB -29.2u/L
Glucose - 201 to 365 mg/dL (70-110)
Creatinine- 1.9 to 3.7 mg/dL (0.6-1.0)
BUN- 31 to 46 mg/dL (5-25)

Urinalysis Results:

Chemical:
Glucose: 100mg/dl
Blood (moderate)
Protein- >300 mg/dL (<90)

Microscopic:
RBC 10-20/hpf
WBC 2-5/hpfb
Epithelial. Cells (few)
Renal Cell (few)
Granular Cast (5-10/lpf)
Leukocyte Casts (0-1/lpf)

Patient Diagnosis:

Chronic Glomerulonephritis
Terminologies

Cardiac markers (CKMB) are biomarkers measured to evaluate heart function. They are
often discussed in the context of myocardial infarction, but other conditions can lead to an
elevation in cardiac marker level.

Blood urea nitrogen (BUN) test is a measure of the amount of nitrogen in the blood in the
form of urea, and a measurement of renal function.

Pulmonary edema is fluid accumulation in the lungs. It leads to impaired gas exchange and
may cause respiratory failure.

Congestive Heart failure (CHF) is a condition in which a problem with the structure or
function of the heart impairs its ability to supply sufficient blood flow to meet the body's
needs. The phrase is often wrongly used to describe other cardiac-related illnesses, such as
myocardial infarction (heart attack) or cardiac arrest.

Hypertension is a chronic medical condition in which the blood pressure is elevated. It is also
referred to as high blood pressure or shortened to HT, HTN or HPN. The word "hypertension",
by itself, normally refers to systemic, arterial hypertension.

Diabetes mellitus often referred to as diabetes—is a condition in which the body either does
not produce enough, or does not properly respond to, insulin, a hormone produced in the
pancreas.

Furosemide (INN) or frusemide (former BAN) is a loop diuretic used in the treatment of
congestive heart failure and edema. It is most commonly marketed by Sanofi-Aventis under
the brand name Lasix.

Morphine is an extremely potent opiate analgesic psychoactive drug, is the principal active
ingredient in Papaver somniferum, is considered to be the prototypical opioid. In clinical
medicine, morphine is regarded as the gold standard, or benchmark, of analgesics used to
relieve severe or agonizing pain and suffering.

Nitroglycerin is also used medically as a vasodilator to treat heart conditions, such as angina
and chronic heart failure.

Nifedipine (brand name Adalat, Nifedical, and Procardia) is a dihydropyridine calcium

channel blocker. Its main uses are as an antianginal (especially in Prinzmetal's angina) and
antihypertensive,

Guide Questions:

What renal condition do the urinalysis data suggest? Explain. Do the analyses on blood
correlate with this? Explain. What is the pathophysiology behind the renal condition in the
first question? Explain.

CHRONIC GLOMERULONEPHRITIS. Based on the urinalysis test results of the patient, there is
a high elevation of protein (proteinuria) and glucose level, a moderate amount of blood
(hematuria) has been also detected accompanied by granular and cellular cast. in which
these findings are assumed to be the primary urinalysis test result of this renal condition.

YES it correlates. According to the blood test assessment, the level of Blood Nitrogen Urea
(BUN) and creatinine are markedly increased, this may result to a decreased glomerular
filtration rate. When GFR is impaired, less creatinine is excreted by the glomerulus causing
serum levels to rise. While the concentration of urea nitrogen in the blood reflects
glomerular filtration and urine-concentrating capacity. Because urea is filtered at the
glomerulus, blood urea nitrogen (BUN) levels increase as glomerular filtra-tion drops.
Because urea is reabsorbed by the blood through the permeable tubules, the BUN rises in
states of dehydration and acute and chronic renal failure when passage of fluid through the
tubules is slowed. BUN also varies because of altered protein intake and protein catabolism
and therefore is a poor measure of GFR. The application of this principle is useful for
monitoring progressive changes in renal function. Serum creatinine and BUN are elevated in
chronic glomerulonephritis and other related renal conditions.

PATHOPHYSIOLOGY OF CHRONIC GLOMERULONEPHRITIS:

Chronic glomerulonephritis occurs when there is slow, progressive destruction of the
glomeruli of the kidney, with progressive loss of kidney function. Damage to the glomeruli
affects the kidney's ability to filter fluids and wastes properly. This leads to blood and
protein in the urine called microscopic hematuria and proteinuria. The inflammation causes
blood and protein to leak into the urine. As protein levels in the blood fall, excess fluid
accumulates in the body.

Tests show protein, blood cells, and kidney cells in the urine, while a high concentration of
the body's waste products of metabolism (such as urea and creatinine) may be found in the
blood.

Creatinine is a substance that is produced by muscle and released into the blood at a
relatively constant rate. Laboratory tests for serum creatinine provide an indicator or
glomerular filtration rate (GFR). When the GFR is damaged a reduced amount of creatinine is
being emit by the the glomerulus that causes the serum creatinine levels to increase.

BUN reflects the GFR, because the urea is being filtered to glomerulus, when the BUN
elevates the GFR drops, because the urea is being reabsorbed by the blood through the
permeable tubules, the BUN rises in chronic renal failure when passage of fluid through the
tubules is slowed. BUN also varies because of altered protein intake and protein catabolism
and therefore is a poor measure of GFR.

Casts (accumulations of cellular precipitates) originate in the renal tubules, from which they
take their shape. They are cylindrical with distinct borders. All casts have a precipitated
microprotein matrix and arise primarily from the ascending limb of the distal tubule.
Granular Cast, indicates that the patient occur glomerulonephritis. The type of cast
identified suggests the disease process occurring in the kidney.

White blood cells (WBCs) in the urine (a condition termed pyuria) are primarily indicative of
urinary tract infection, particularly when bacteria are present. Glomerulonephritis and
nephrotic syndrome also may demonstrate pyuria, but usually in combination with
proteinuria, red cells, and casts. The finding of WBC casts reflects a kidney infection,
because these casts are not formed in the bladder or prostate.

Chronic glomerulonephritis usually causes only very mild or subtle symptoms, it goes
undetected for a long time in most people. Edema may occur. High blood pressure is
common. The disease may progress to kidney failure, which can cause itchiness, fatigue,
decreased appetite, nausea, vomiting, and difficulty breathing.
Questions

Which of the following is not a symptom of Chronic Glomerulonephritis

hypertension
edema
oliguria
hypotension

All are types of immune mechanisms which contributes to glomerular injury except:
a. Deposition of circulating soluble antigen-antibody complexes
b. Formation of antibodies specific against the glomerular basement membrane
c. Streptococcal release of neuramidase, which alters IgG with binding of anti-IgG
to the glomerulus.
d. none of the above
Chronic Glomerulonephritis includes primary urinalysis results except:
a. hematuria
b. proteinuria
c. granular cast
d. oval fat bodies

Other significant test for Chronic Glomerulonephritis includes:

serum creatinine
creatinine clearance
both a and b
none of the above

Reduction in nephron mass from the initial injury reduces the GFR then leads to:
hypertrophy
hyperfiltration of the remaining nephrons
both a and b
none of the above

Which of the following best describes Chronic Glomerulonephritis:

Occurs primarily in children following viral respiratory infections.
Disruption of podocutes in certain areas of glomeruli associated with heroin and analgesic
abuse.
Deposition of IgA on the glomerular membrane resulting from increased levels of serum IgA
Marked decrease in renal function resulting from glomerular damage precipitated by other
renal disorder.

Which of the following is not a cause of Chronic glomerular injury:

Insulin-dependent diabetes mellitus
lupus erythematosus
Hypercholesterolemia
None of the above

Chronic Glomerulonephritis can be caused by:

mercury
non-steroidal anti-inflammatory analgesics
HIV
All of the above

First indicator of renal disorder is:

protein
glucose
blood
abnormal sediment

The most significant and the only one that can be found in a cast:
WBC
RBC
Renal epithelial
Squamous epithelial

Chronic glomerulonephritis
Chronic glomerulonephritis is the advanced stage of a group of kidney disorders, resulting in
inflammation and slowly worsening destruction of internal kidney structures called
glomeruli.
Causes, incidence, and risk factors:

Chronic glomerulonephritis occurs when there is slow, progressive destruction of the

glomeruli of the kidney, with progressive loss of kidney function. In some cases, the cause is
found to be a specific attack to the body's immune system, but in most cases, the cause is
unknown. Iit is generally thought that a still-unidentified abnormality of the immune system
is to blame.

Damage to the glomeruli affects the kidney's ability to filter fluids and wastes properly. This
leads to blood and protein in the urine.

This condition may develop after survival of the acute phase of rapidly progressive
glomerulonephritis. In about one-quarter of people with chronic glomerulonephritis there is
no prior history of kidney disease, and the disorder first appears as chronic kidney failure.

Glomerulonephritis is among the leading causes of chronic kidney failure and end stage
kidney disease. Causes include:

* Diabetic nephropathy/sclerosis
* Focal segmental glomerulosclerosis
* IgA nephropathy (Berger's disease)
* Lupus nephritis
* Membranous glomerulonephritis
* Mesangial proliferative disorder
* Nephritis associated with disorders such as amyloidosis, multiple myeloma, or immune
disorders, including AIDS

Symptoms:

This condition causes high blood pressure (hypertension) and chronic kidney failure.

Specific symptoms include:

* Blood in the urine (dark, rust-colored, or brown urine)

* Foamy urine

Chronic kidney failure symptoms that gradually develop may include the following:

* Decreased alertness
o Drowsiness, somnolence, lethargy
o Confusion, delirium
o Coma
* Decreased sensation in the hands, feet, or other areas
* Decreased urine output
* Easy bruising or bleeding
* Fatigue
* Frequent hiccups
* General ill feeling (malaise)
* Generalized itching
* Headache
* Increased skin pigmentation -- skin may appear yellow or brown
* Muscle cramps
 * Muscle twitching
* Nausea and vomiting
* Need to urinate at night
* Seizures
* Unintentional weight loss

Additional symptoms that may be associated with this disease:

* Blood in the vomit or stools

* Excessive urination
* High blood pressure
* Nosebleed

Signs and tests:

Because symptoms develop gradually, the disorder may be discovered when there is an
abnormal urinalysis during a routine physical or during an examination for another,
unrelated disorder. It may be discovered as a cause of high blood pressure that is difficult to
control.

Laboratory tests may reveal anemia or show signs of reduced kidney functioning, including
azotemia. Later, signs of chronic kidney failure may be apparent, including edema .

Tests that may be done include:

* Chest x-ray
* Kidney or abdominal CT scan
* Kidney or abdominal ultrasound
* IVP
* Urinalysis

A kidney biopsy may show one of the forms of chronic glomerulonephritis or scarring of the
glomeruli.

This disease may also alter the results of the following tests:

* Albumin
* Abdominal MRI
* Anti-glomerular basement membrane
* BUN
* Complement component 3
* Complement
* Creatinine clearance
* Renal scan
* Total protein
* Uric acid, urine
* Urine concentration test
* Urine creatinine
* Urine RBC
* Urine specific gravity
* Urine protein

Treatment:
Treatment varies depending on the cause of the disorder, and the type and severity of
symptoms. The primary treatment goal is control of symptoms. High blood pressure may be
difficult to control, and it is generally the most important aspect of treatment. Various
medications may be used to attempt to control high blood pressure.

Corticosteroids, immunosuppressives, or other medications may be used to treat some of

the causes of chronic glomerulonephritis.

Dietary restrictions on salt, fluids, protein, and other substances may be recommended to
help control of high blood pressure or kidney failure.

Dialysis or kidney transplantation may be necessary to control symptoms of kidney failure

and to sustain life.

The outcome varies depending on the cause. Some types of glomerulonephritis may get
better on their own.

If nephrotic syndrome is present and can be controlled, other symptoms may be controlled.
If nephrotic syndrome is present and cannot be controlled, end-stage kidney disease is
likely.

The disorder worsens at widely variable rates.

Complications:

* Nephrotic syndrome
* Acute nephritic syndrome
* Chronic renal failure
* End-stage renal disease
* Hypertension
* Malignant hypertension
* Fluid overload -- congestive heart failure, pulmonary edema
* Chronic or recurrent urinary tract infection
* Increased susceptibility to other infections

I. SUMMARY OF THE CASE

The 49 year old male presented in E.R. was complaining of abdominal pain accompanied by
nausea, vomiting, some coughing which is non-productive and a slightly erythematous rash
on the toes of both feet. He was experiencing these in the past 5 months and was getting
worst in the last two days. The patient medical history show the he was diagnosed with AIDS
last year, disseminated tuberculosis and was an intravenous drug abuser. On admission, the
patient is taking in some medications and this includes:
➢ INH (Isonicotinic Acid Hydrazide) - It is prescribed for prophylaxis for those who
have been exposed to tuberculosis and is used in combination with other agents
in the treatment of tuberculosis caused by mycobacteria sensitive to the drug.
Adverse effect: Rashes
➢ RIFAMPIN - an antituberculosis agent, it works by killing or stopping the growth of
tuberculosis bacteria. Adverse effects: reddish orange discoloration of body fluids
including urine,
➢ BACTRIM DS – antibiotic that treat different types of infection caused by bacteria,
used to treat ear infections, urinary tract infections, bronchitis, traveler's diarrhea,
and Pneumocystis carinii pneumonia. Adverse effects: nausea, vomiting, abdominal
pain and allergic skin reactions such as rash and urticaria, Cough and pulmonary
infiltrates
➢ He is also taking in Megace, Flucon, MS Contin, Morphine Elixir
The patient’s abdomen x-ray showed multiple air- fluid levels in the small bowel. The patient
was then admitted for observation and treatment of the ileus. The results Urinalysis are as
follows:
➢ Color- amber
➢ pH- 7.0
➢ Specific Gravity- 0.020
➢ Glucose- negative
➢ Bilirubin- negative
➢ Ketone- negative
➢ Blood- negative
➢ Nitrite and leukocyte esterase- negative
➢ Urobilinogen- normal
➢ Protein- 30mg/dl

He was discharged after 3 days in stable condition and continued taking in Bactrim DS, INH,
Rifampin and Diflucan.

I. ANSWER TO GUIDE QUESTIONS

1. Are there any significant findings in the urinalysis?

• Yes, the positive urine protein may indicate a renal disease. The result of the
Urinalysis of the patient is 30mg/dL which is trace to 1+. Normal urine contains
very little protein; usually, less than 10mg/dL or 100mg/24 hours is excreted and
clinical proteinuria is indicated at >30mg/dL.

1. How would you characterize the casts and cells that may be observed in the urine if
microscopic analysis was performed?
• Hyaline casts may appear + sulphonamide crystals due to administration of
Bactrim.

1. What pathophysiologic picture is illustrated by the urinalysis in this case?

• This is a possible case of Focal Segmental Gloerulosclerosis, secondary to narcotic
abuse. The patient’s urine protein which is 30mg/dL is considered normal since
clinical proteinuria is indicated at >30mg/dL of urine protein, but it still depends
upon the severity of the disease. We have concluded that this is a possible case
of FSGS probably because the disseminated tuberculosis of the patient was just
starting to affect the urinary system that is why only trace up to 1+ protein is
present.
• AMBER COLORED URINE is due to Rifampin, while nausea, vomiting,
abdominal pain and allergic skin reactions such as rash and urticaria are the
most common adverse effects of Bactrim DS associated with the Gastrointestinal
Tract. Cough and pulmonary infiltrates are also adverse effect of Bactrim DS
related with Respiratory. Side effects generally are more common and more
severe in patients with AIDS. Side effects generally are more common and more
severe in patients with AIDS. Hypersensitivity reactions may be more likely in
patients with HIV infection, with opportunistic infections.
• ILEUS; an obstruction of the intestine can cause ABDOMINAL PAIN due to
contractions of intestinal muscle and distension of intestine. This Abdominal Pain
may worsen due to COUGHING. Patients with ILEUS may also report NAUSEA
AND VOMITING. One probable cause of ileus is the USE OF CERTAIN DRUGS,
such as NARCOTIC PAIN DRUGS or high blood pressure medicine.
• DISSEMINATED TUBERCULOSIS (TB) is a contagious bacterial infection that
has spread from the lungs to other parts of the body through the blood or lymph
system. Disseminated disease develops in the small number of infected people
 whose immune systems do not successfully contain the primary infection. Since
the patient was diagnosed with ADIS, therefore he is immune compromised.

I. SAMPLE TEST PAPER

1. This is the most indicative of renal disease among the routine chemical tests
performed on urine:
a) Protein d) Blood
b) Glucose
c) pH

1. Normal levels of protein present in urine daily:

a) 5mg/dL c) 15mg/dL
b) 10mg/dL d) 20mg/dL

1. The amber color urine was caused by which of the following medications that the
patient is taking in?
a)
b) INH
c) Bactrim DS
d) Rifampin
e) Flucon

1. With the given Physical and Chemical results, Microscopic Analysis should be
requested.
a) Statement is TRUE
b) Statement is FALSE

1. What Renal disorder is related to the case of the patient?

a)
b) Acute Glumerulonephritis
c) Focal Segmental Glomerulosclerosis
d) Alport Syndrome
e) Good Pasture Syndrome

1. Among which of the following Renal Disease may resemble with your answer in
number 5?
a)
b) Nephrotic Syndrome
c) Minimal Change Disease
d) Either
e) Neither

1.
2. Focal Segmental Glomerulosclerosis is often associated with the following conditions
seen in the patient except:

a) Cough d) NIL
b) AIDS
c) Narcotic abuse of drugs
 1. What are the cast or cells that may be present if Microscopic Analysis is performed?
a) Fatty Cast
b) Hyaline Cast
c) Waxy Cast
d) RBC Cast

1. The cause of proteinuria based on the origin of Protein:

a)
b) Pre renal
c) Renal
d) Post Renal
e) NIL

1. Clinical proteinuria is indicated in which of the following protein levels in urine?

a)
b) >10mg/dL
c) >20mg/dL
d) >30mg/dL
e) >40mg/dL

ANSWERS:
1. A) Protein
2. B) 10mg/dL
3. C) Rifampin
4. A) TRUE
5. B) Focal Segmental Glomerulosclerosis
6. C) Either
7. A) Cough
8. B) Hyaline Cast
9. B) Renal
10. B) >30mg/dL

I. PERTINENT INFORMATION
FOCAL SEGMENTAL GLOMERULOSCLEROSIS

FSGS affects only certain numbers and areas of glomeruli, and others remain normal.
Symptoms may be similar to the nephritic syndrome and minimal change disease owing to
damaged podocytes. Immune deposits, primarily immunoglobulins M and C3, are a frequent
finding and can be seen in undamaged glomeruli. FSGS is often seen in association with
abuse of heroin and analgesics and with AIDS. Moderate to heavy proteinuria and
microscopic hematuria are most consistent urinalysis findings.
Focal Segmental Glomerulosclerosis is a disease that attacks the kidney’s filtering system
(glomeruli) causing serious scarring. FSGS affects only certain numbers and areas of
glomeruli, and others remain normal. Symptoms may be similar to the nephritic syndrome
and minimal change disease owing to damaged podocytes. FSGS is often seen in association
with abuse of heroin and analgesics and with AIDS. Moderate to heavy proteinuria and
microscopic hematuria are most consistent urinalysis findings.

Primary UA results: Other Significant test:

Proteinuria Drugs of abuse
Microscopic hematuria HIV tests
Macroscopic or microscopic hematuria Genetic testing
Etiology:
Disruption of podocytes in certain areas of glomeruli associated with heroin and analgesic
abuse and AIDS.

Clinical course:
May resemble nephritic syndrome or minimal change disease

The individual components of the name refer to the appearance of the kidney tissue on
biopsy: FOCAL—only some of the glomeruli are involved (as opposed to diffuse)
SEGMENTAL—only part of an entire glomerulus is involved (as opposed to global)
GLOMERULOSCLEROSIS—refers to scarring of the glomerulus (a part of the nephron)
The important risk of intravenous drug use as a pathogenic factor of renal disease and
shows a rarity of renal disease in homosexual or bisexual men with AIDS.
The patient’s complaint matches the side effects of the Bactrim DS he is taking which is
more common in AIDS patients. This includes vomiting, nausea, urticaria, rashes and
systemic lupus erythematous. There are no significant findings in the urinalysis; amber
colored urine may be due to his medications. If microscopic analysis is performed,
crystalluria may be observed as a side effect. If crystalluria is observed in the urinalysis, the
patient will experience irritation of the kidney. However, crystals observed in urinalysis are
usually insignificant.
Kidney damage under a microscope showed diffuse glomerular membrane increased, with
minimal glomerular sclerosis. The number of occurrence ranging from segmental glomerular
sclerosis, which is characterized by a thick cytoplasm containing vacuoles of epithelial cell
proliferation, capillary wall collapse, or because of protein deposition (hyaline degradation)
and to the capillaries disappear, cavity foam cells (lipid filled with mononuclear cells).
Glomerular cysts are usually expanded, tubular damage is extensive.
Focal Segmental Glomerulosclerosis (FSGS) is a disease that attacks the kidney’s filtering
system (glomeruli) causing serious scarring. FSGS is one of the many reasons of a disease
known as Nephrotic Syndrome, which occurs when valuable protein in the blood leaks into
the urine (proteinuria).
II. REFERENCES
Susan King Strasinger, Urinalysis and Body Fluids, 2008
Amy M. Karch, Lippincott’s Nursing Drug Guide, 2009
http://www.drugs.com/sfx/bactrim-side-effects.html
www.medicinenet.com/abdominal_pain/article.htm
en.wikipedia.org/wiki/Abdominal_pain
http://www.medcohealth.com/medco/consumer/ehealth/ehsarticle.jsp?
packageTemplate=HE+article+XML+template&ltSess=y&currentPage=%2Fconsumer
%2Fehealth%2Fehsarticle.jsp&com.broadvision.session.new=Yes&articleID=97666
en.wikipedia.org/wiki/Bowel_obstruction
www.answers.com/topic/ileus
www.health-care-clinic.com/family-health/i/ileus.htm
www.health-care-clinic.com/family-health/i/ileus.htm
http://en.wikipedia.org/wiki/Focal_segmental_glomerulosclerosis
http://www.ich.ucl.ac.uk/gosh_families/information_sheets/focal_segmental_glomeruloscleros
is/image1.jpg
http://www.91sqs.com/attachments/2007/07/2446_200707141110261.jpg
http://www.nephcure.org/fsgs-facts.htm
http://www.tcmwell.com/TCM_News/hiv/The-performance-of-HIV-infection---Urinary-
system.html

Angeles University Foundation

Angeles City
College of Allied Medical Professions
Medical Technology Department
Post Prelim Conference in Clinical Microscopy
Case 7

Submitted By:
GROUP 10
Torres, Chelzylyn M.
Bacani, Fernando,
Ocampo, Toni Jerico
Savellano, Lara Mikee

Submitted To:
Ms. Crizelda Liwanag, RMT
Mrs. Eloisa Q. Singian, RMT

7 January 2010

Angeles University Foundation

Angeles City

Group 7

Dimaun, Joy
Sandoval, Noel
Santos, Marjorie
Soliman, Lea

Case
Jessica is a 20-year old woman admitted to R/O appendicitis, pancreatitis, pyelonephritis,
abdominal abscess, or ruptured viscus. She came to the ER complaining of severe
abdominal pain or what is called an “acute abdomen”. Because she was 36 weeks’
(estimated) IUP, a low C-section was performed and the child was delivered. Her appendix
was found to be ruptured and it was removed at the same time. Blood cultures were
positive for E.coli, sensitive to Cefotan (cefotetan disodium) and to gentamicin, which she
was given. The urinalysis, obtained two days postsurgery, was as follows: glucose negative,
bilirubin small; ketones 40 mg/dL; specific gravity 1.025; blood negative; pH 6.5; protein 30
mg/dL; urobilinogen 1.0 EU/dL; nitrite negative; leucocyte esterase trace; color orange;
WBCs 5-10/hpf; RBCs 0-2/hpf; epithelial cells 1+/hpf; bacteria 1+/hpf; bacteria 1+; casts 1-5
granular. Ictotest negative. C&S was not requested on this urine.

Questions:
1. What aspects of the urinalysis do you find significant?
Microorganisms (bacteria, trichomonads, yeast)
In health, the urinary tract is sterile; there will be no microorganisms seen in the urine
sediment. Microorganisms are usually reported as "none," "few," "moderate," or "many"
present per high power field (HPF). Bacteria from the surrounding skin can enter the urinary
tract at the urethra and move up to the bladder, causing a urinary tract infection (UTI).
Leukocyte esterase: Normally negative. Leukocytes are the white blood cells (or pus cells).
This looks for white blood cells by reacting with an enzyme in the white cells. White blood
cells in the urine suggests a urinary tract infection.
WBC up to 5/HPF are commonly accepted as normal. Greater numbers (pyuria) generally
indicate the presence of an inflammatory process somewhere along the course of the
urinary tract (or urogenital tract in voided specimens).
Granular casts almost always indicate significant renal disease. However, granular casts
may be present in the urine for a short time following strenuous exercise. Granular casts
that contain fine granules may appear grey or pale yellow in color. Granular casts that
contain larger coarse granules are darker. These casts often appear black because of the
density of the granules.
2. What pathophysiologic aspects of this case are illustrated by the urine microscopic
examination?

The acute pyelonephritis of the patient is the result of the bacterial invasion (e.coli) from the
ruptured appendictis of the patient

Appendicitis
Appendicitis is a condition characterized by inflammation of the appendix. Reginald Fitz first described
acute and chronic appendicitis in 1886, and it has been recognized as one of the most common causes of
severe acute abdominal pain worldwide.
Symptoms
Signs and symptoms of acute appendicitis can be classified into two types, typical and
atypical. The typical history includes pain starting centrally (periumbilical) before localizing
to the right iliac fossa (the lower right side of the abdomen); this is due to the poor localizing
property of visceral nerves from the mid-gut, followed by the involvement of somatic nerves
as the inflammation progresses. The pain is usually associated with loss of appetite and
fever, although the latter isn't a necessary symptom. Nausea or vomiting may occur, as well
as drowsiness and malaise.
Atypical symptoms may include pain beginning and staying in the right iliac fossa, diarrhea
and a more prolonged, smoldering course. If an inflamed appendix lies in contact with the
bladder, there is frequency of urination. With post-ileal appendix, marked retching may
occur. Tenesmus or "downward urge" (the feeling that a bowel movement will relieve
discomfort) is also experienced in some cases.
Causes
On the basis of experimental evidence, acute appendicitis seems to be the end result of a
primary obstruction of the appendix lumen. Once this obstruction occurs the appendix
subsequently becomes filled with mucus and swells, increasing pressures within the lumen
and the walls of the appendix, resulting in thrombosis and occlusion of the small vessels,
and stasis of lymphatic flow. Rarely, spontaneous recovery can occur at this point. As the
former progresses, the appendix becomes ischemic and then necrotic. As bacteria begin to
leak out through the dying walls, pus forms within and around the appendix (suppuration).
The end result of this cascade is appendiceal rupture (a 'burst appendix') causing peritonitis,
which may lead to septicemia and eventually death.
Pyelonephritis
Pyelonephritis is an ascending urinary tract infection that has reached the pyelum (pelvis) of
the kidney (nephros in Greek). If the infection is severe, the term "urosepsis" is used
interchangeably (sepsis being a systemic inflammatory response syndrome due to
infection). It requires antibiotics as therapy, and treatment of any underlying causes to
prevent recurrence. It is a form of nephritis. It can also be called pyelitis.
Diagnosis
The presence of nitrite and leukocytes (white blood cells) on a urine dipstick test in patients
with typical symptoms are sufficient for the diagnosis of pyelonephritis, and are an
indication for empirical treatment. Formal diagnosis is with culture of the urine; blood
cultures may be needed if the source of the infection is initially doubtful.
Causes
Most cases of "community-acquired" pyelonephritis are due to bowel organisms that enter
the urinary tract. Common organisms are E. coli (70-80%) and Enterococcus faecalis.
Hospital-acquired infections may be due to coliforms and enterococci, as well as other
organisms uncommon in the community (e.g. Klebsiella spp., Pseudomonas aeruginosa).
Most cases of pyelonephritis start off as lower urinary tract infections, mainly cystitis and
prostatitis.
Pathology
Acute pyelonephritis is an exudative purulent localized inflammation of the renal pelvis
(collecting system) and kidney. The renal parenchyma presents in the interstitium abscesses
(suppurative necrosis), consisting in purulent exudate (pus): neutrophils, fibrin, cell debris
and central germ colonies (hematoxylinophils). Tubules are damaged by exudate and may
contain neutrophil casts. In the early stages, glomeruli and vessels are normal. Gross
pathology often reveals pathognomonic radiations of hemorrhage and suppuration through
the renal pelvis to the renal cortex. Chronic infections can result in fibrosis and scarring.
Sample Test Paper
It is an infection of the kidney, and the ureters, the ducts that carry the urine away from the
kidney?
Appendicitis
Pyelonephritis
Kidney stone
NOTA
Exams and test for pyelonephritis?
Blood cultures
Urine culture
Both
nota
Medications for pyelonephritis?
amoxicillin
cephalosporin
Both
nota
The following are other possible complication of pyelonephritis, exept?
Kidney failure
perinephric abscess
Sepsis
nota
The following are symptoms of pyelonephritis except?
Back pain
Abdominal apin
Fatigue
aota
These are urination problems of pyelonephritis?
Blood in the urine
Cloudy or abnormal urine color
Increased urinary frequency or urgery
AOTA
What is the probable cause of acquiring pyelonephritis in this case?
E. coli
Staphylococcus
Both
NOTA
Positive results for pyelonephritis?
Leukocyte
Bacteria
Both
Nota
A positive bilirubin and urobilinogen may lead to?
liver damage
heart failure
convulsion
aota

Presence of WBC in the urine indicates what?

Infection
Heart problems
No need to worry
nota
References:
http://library.med.utah.edu/WebPath/TUTORIAL/URINE/URINE.html
http://en.wikipedia.org/wiki/Urinary_cast
http://en.wikipedia.org/wiki/Appendicitis
http://en.wikipedia.org/wiki/Pyelonephritis

group 4
 [Type the document
[Year] [Type the company address]
Clinical Microscopy

title]
[Type the document subtitle]
Robin Christian G. Cao
Johanna Selina D. Lim
Jennie Q. Lingad
Anna Kamille C. Suyat
 Group 4
Cao, Robin Christian G.
Lim, Johanna Selina D.
Lingad, Jennie Q.
Suyat, Anna Kamille C.
Case 6
With a medical history of HTN, IDDM and CHF, this 57-year old woman was attending
a social event until the early morning hours, had been walking around complaining of
shortness of breath, and suddenly collapsed with a blood-tinged discharge coming from her
mouth. She was rushed to the ER in a private car and on arrival was unresponsive to verbal
or painful stimuli, and showed agonal respirations with a weak radial pulse. The impression
was respiratory arrest, acute pulmonary edema, R/O MI. Subsequent laboratory work did
not support the diagnosis of acute MI, suggesting instead acute pulmonary edema. Her
admission urinalysis produced the following results:

Urinalysis Results

Physical Examination

Color Amber

Appearance Hazy

pH 5.5

Specific Gravity 1.010

Chemical Examination

Protein 100 mg/dL

Glucose 250 mg/dL

Bilirubin and Ketones Negative

Urobilinogen Normal

Nitrite and Leukocyte

Negative
Esterase

Microscopic Examination

White Blood Cell 20-50/hpf

Red Blood Cell 0-2/hpf

Epithelial Cell Few/hpf

Bacteria 1+/hpf

TNTC
Casts
granular/lpf

Blood Small

Questions:

What urinalysis results do you find significant?

What pathophysiology of this case is most closely related to the urinary sediment
findings?
Answers:

Significant Findings

○ Color : Amber

○ Protein:100 mg/dL

○ Glucose : 250 mg/dL

○ WBC : 20-50/hpf

○ Bacteria :1+/hpf

○ Cast :Granular TNTC/LPF

This is a case of pulmonary edema secondary to left sided heart failure base on the
patient signs and symptoms and history of IDDM, CHF and Hypertension.

Pathophysiology
○ The decreased in cardiac output in heart failure patients results in an
"unloading" of high-pressure baroceptors in the left ventricle, carotid sinus,
and aortic arch. This unloading leads to the generation of afferent signals to
the central nervous system that stimulate cardioregulatory centers in the
brain which stimulate the release of anti-diuretic hormone from the posterior
pituitary. Antidiuretic hormone (ADH) is a powerful vasoconstrictor that
increases the permeability of the renal collecting ducts, leading to the
reabsorption of free water. These afferent signals to the CNS also activate
efferent sympathetic nervous system pathways that innervate the heart,
kidney, peripheral vasculature, and skeletal muscles. Sympathetic stimulation
of the kidney leads to the release of renin, with a resultant increase in the
circulating levels of angiotensin II and aldosterone. The activation of the renin-
angiotensin-aldosterone system promotes salt and water retention and leads
to vasoconstriction of the peripheral vasculature, myocyte hypertrophy,
myocyte cell death, and myocardial fibrosis. While these neurohormonal
mechanisms facilitate short-term adaptation by maintaining blood pressure,
and hence perfusion to vital organs, these same neurohormonal mechanisms
are believed to contribute to end-organ changes in the heart and the
circulation, and to the excessive salt and water retention in advance heart
failure.
In summary the cause of the concentrated urine which causes the amber color
is the release of Anti-diuretic hormone by the posterior pituitary and the
activation of renin-angiotensin-aldosterone pathway which lead to water
reabsorption.
Amber Urine
○ Amber colored urine is normal in the presence of dehydration this is due to
the increase in the concentration of urobilinogen which is a pigment that gives
the urine its color. When a person is well hydrated this urobilinogen is diluted
resulting to a yellow or sometimes colorless color of the urine. In our case
where there is no presence of fluid loss (dehydration) the principle that cause
the amber colored urine is the same (that it is due to a concentrated urine)
but the mechanism that cause this is different (no fluid loss or dehydartion).
This mechanism is best explained with the understanding of the
pathopysiology of heart failure (disease of the patient)
Proteinuria
○ The presence of proteinuria is caused by the hypertension that is caused by
the vasoconstricting effect of angiotensin II and sodium retention by the
aldosterone. Hypertension causes proteinuria by altering the glomeruli and
post glomeruli structure this is due to ischemia or direct damage to this
structure because of the increase in pressure. These changes in turn allow the
protein to pass through resulting to proteinuria.
Glucosuria
 ○ Glucosuria is caused by the patient IDDM. Glucosuria occurs when the
concentration of glucose in the urine is greater in the amount of glucose that
the kidney can reabsorb back in the circulation.
Pyuria and Bacteria +1
○ Pyuria and bacteria +1 may signify urinary tract infection. Since the patient is
a female and has history of IDDM she is most prone to the development of
UTI.
Granular Casts
○ The presence of granular cast that is TNTC signify that this patient has a long
standing UTI. This is due to the fact that granular cast are found on patient
with pyelonephritis, viral infection, and chronic lead poisoning. Since the
patient doesn’t have history of viral infection and chronic lead poisoning the
most probable cause of the granular cast are pyelonephritis (type of UTI).
○ Granular cast may also be pathologic or non pathologic. The origin of the
granules in nonpathologic conditions appears to be from the lysosomes
excreted by RTE cells during normal metabolism. Increased cellular
metabolism occurring during strenuous exercise accounts for the transient
increase of granular casts. In disease states, granules may represent
disintegration of cellular casts and tubule cells or protein aggregates filtered
by the glomerulus.

Reference:
○ Robbins and Cotrans Pathologic Basis of Disease 7th Edition
○ Harrisons Principle of Internal Medicine 17 Edition
○ Henry’s Clinical Diagnosis and Management by Laboratory methods 21st
Edition
○ Oxford handbook of Clinical diagnosis 1st Edition
Case #5:

An 82 year old woman with an history of HTN treated with Vasotec (enapril maleate), and of NIDDM, was
seen in the outpatient clinic complaining of a blister on her lower lip that she said she had been
developing slowly over a year. The blister was diagnosed as a mucocele (a mucus cyst), and an
appointment was made to have it biopsied and excised at a future date. In the course of her examination,
a routine urinalysis (without the microscopic) was requested and the urine was found to be significant for
nitrite positive; and leukocyte esterase moderate. The results prompted the request for a urine C&S. The
urine C&S subsequently indicated a colony greater than 100,000 CFU/ml with an identification of E. coli.

• What aspect of the urine sediment do you find significant?

- Pus cells and bacteria (Caused the Nitrite and Leukocytes Esterase test in the urine to be
positive.)
• There are certain types of bacteria (e.g. E. coli) which have the ability to reduce nitrate, a
normal constituent of urine, to nitrite, which does not normally appear in the urine.
Therefore, Nitrites in the urine can be an early warning that a urinary tract infection might
exist.
• A positive LE test result is most frequently accompanied by the presence of bacteria.
The LE detects the presence of esterase in the granulocytic white blood cells
(neutrophils, eosinophils, and basophils) and monocytes. Neutrophils are the leukocytes
most frequently associated with bacterial infections.

• What diagnosis would you give this case?

- Urinary tract infection
• The presence of a single type of bacteria (E. coli) growing at high colony counts (greater
than 100,000 colony forming units (CFU)/ml) indicates a Urinary Tract Infection.

• What type of treatment do you think this patient was given for the condition shown here
- Antibiotic therapy with the correct dosage relating to her age.

Antibiotic Age Route Dosage

Trimethoprim-Sulfamethoxazole Adult ORAL or IV 160 mg-800 mg/

(TMP-SMX 12 hours for 10 to 14 days
8 to 10 mg/kg/day

Nitrofurantoin (Furadantin, Adult ORAL 50 to 100 mg four times daily for

Macrodantin seven days

Amoxicillin Adult ORAL 250 mgs/ 8 hrs or 500 mgs/12

hours.

• What results will be expected upon performing the microscopic examination of the patient's
urine?
- Urine microscopic exam will be, pus cells ranging from many to TNTC (too numerous to count)
and bacteria.

References:
http://www.labtestsonline.org/understanding/analytes/urine_culture/test.html

http://www.testsymptomsathome.com/TEC06.asp

http://adam.about.com/reports/000036_7.htm

http://kidney.niddk.nih.gov/kudiseases/pubs/utiadult/

http://adam.about.com/reports/000036_7.htm

http://www.labtestsonline.org/understanding/analytes/urine_culture/test.html
http://www.testsymptomsathome.com/TEC06.asp

http://kidney.niddk.nih.gov/kudiseases/pubs/utiadult/

http://www.drugs.com/mtm/sulfamethoxazole-and-trimethoprim.html

http://en.wikipedia.org/wiki/Nitrofurantoin

http://www.drugs.com/pdr/amoxicillin.html

http://www.rxlist.com/vasotec-drug.htm

Angeles University Foundation

College of Allied Medical Professions

Department of Medical Technology

In Partial Fulfillment of the requirement in

Clinical Microscopy

(Case Analysis)
 Submitted by:

Group 5

Garcia, Vixienne Geia

Natividad, Justine Lorenz

Nicdao, Jan Kevin

BSMT III-A

Submitted to:

Ms. Crizelda Liwanag

Submitted on:

January 7, 2010

Sample Test Paper:

1. NIDDM stands for:

a. Non-Identifiable Diabetes Mellitus
b. Non-Insulin Dependent Diabetes Mellitus
c. Non-Insulin Deficient Diabetes Mellitus
2. In the case, the old woman was complaining of a blister on her lower lip, which was later
diagnosed as a mucocele. A mucocele is a/an:
a. Allergy
b. Mucus cyst
c. Mole
3. An excision and a/an ____ were scheduled on a future date for the mucocele.
a. Chemotherapy
b. Biopsy
c. Aspiration
4. Which of the following was used to treat the patient’s history of HTN?
a. Vasotec
b. Amoxicillin
c. Nitrofurantoin
5. The significant results of the requested Routine Urinalysis is/are:
a. Leukocyte esterase (many); nitrite (+)
b. Leukocyte esterase (few); nitrite (-)
c. Leukocyte esterase (moderate); nitrite (+)
6. The results in #5 prompted for a/an:
a. C&S
b. Repeat test
c. None; the tests were sufficient in diagnosis
7. Women tend to have higher LE values due to:
a. Vaginal contamination
 b. Difference in sexual activity
c. Men and women have same range values
8. In the nitrite reaction, which is normally found in the urine?
a. Nitrite
b. Nitrate
c. Both
9. The C&S results indicated:
a. >100,000 CFU/ml of E.coli
b. <100,000 CFU/ml of E.coli
c. 100,000 CFU/ml of E.coli
10. The diagnosis of the case was:
a. HTN
b. UTI
c. NIDDM

Answer Key:

1. NIDDM stands for:

a. Non-Identifiable Diabetes Mellitus
b. Non-Insulin Dependent Diabetes Mellitus
c. Non-Insulin Deficient Diabetes Mellitus
2. In the case, the old woman was complaining of a blister on her lower lip, which was later
diagnosed as a mucocele. A mucocele is a/an:
a. Allergy
b. Mucus cyst
c. Mole
3. An excision and a/an ____ were scheduled on a future date for the mucocele.
a. Chemotherapy
b. Biopsy
c. Aspiration
4. Which of the following was used to treat the patient’s history of HTN?
a. Vasotec
b. Amoxicillin
c. Nitrofurantoin
5. The significant results of the requested Routine Urinalysis is/are:
a. Leukocyte esterase (many); nitrite (+)
b. Leukocyte esterase (few); nitrite (-)
c. Leukocyte esterase (moderate); nitrite (+)
6. The results in #5 prompted for a/an:
a. C&S
b. Repeat test
c. None; the tests were sufficient in diagnosis
7. Women tend to have higher LE values due to:
a. Vaginal contamination
b. Difference in sexual activity
c. Men and women have same range values
8. In the nitrite reaction, which is normally found in the urine?
a. Nitrite
b. Nitrate
c. Both
 9. The C&S results indicated:
a. >100,000 CFU/ml of E.coli
b. <100,000 CFU/ml of E.coli
c. 100,000 CFU/ml of E.coli
10. The diagnosis of the case was:
a. HTN
b. UTI
c. NIDDM

Research Information:

Hypertension is a chronic medical condition in which the blood pressure is elevated. It is also
referred to as high blood pressure or shortened to HT, HTN or HPN. The word "hypertension", by itself,
normally refers to systemic, arterial hypertension. Hypertension can be classified as either essential
(primary) or secondary. Essential or primary hypertension means that no medical cause can be found to
explain the raised blood pressure. It is common. About 90-95% of hypertension is essential hypertension.
Secondary hypertension indicates that the high blood pressure is a result of (i.e., secondary to) another
condition, such as kidney disease or tumours (adrenal adenoma or pheochromocytoma). Persistent
hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysm, and is
a leading cause of chronic renal failure. Even moderate elevation of arterial blood pressure leads to
shortened life expectancy. At severely high pressures, defined as mean arterial pressures 50% or more
above average, a person can expect to live no more than a few years unless appropriately treated.
Beginning at a systolic pressure (which is peak pressure in the arteries, which occurs near the end of the
cardiac cycle when the ventricles are contracting) of 115 mmHg and diastolic pressure (which is minimum
pressure in the arteries, which occurs near the beginning of the cardiac cycle when the ventricles are
filled with blood) of 75 mmHg (commonly written as 115/75 mmHg), cardiovascular disease (CVD) risk
doubles for each increment of 20/10 mmHg.
VASOTEC® (Enalapril Maleate) is the maleate salt of enalapril, the ethyl ester of a long-acting
angiotensin converting enzyme inhibitor, enalaprilat. Enalapril maleate is chemically described as (S)-1-
[N-[1-(ethoxycarbonyl)-3-phenylpropyl]-L-alanyl]-L-proline, (Z)-2-butenedioate salt (1:1). Enalapril maleate
is a white to off-white, crystalline powder with a molecular weight of 492.53. It is sparingly soluble in
water, soluble in ethanol, and freely soluble in methanol. Enalapril is a pro-drug; following oral
administration, it is bioactivated by hydrolysis of the ethyl ester to enalaprilat, which is the active
angiotensin converting enzyme inhibitor. VASOTEC is indicated for the treatment of hypertension. It is
effective alone or in combination with other antihypertensive agents, especially thiazide-type diuretics.
The blood pressure lowering effects of VASOTEC and thiazides are approximately additive.
Diabetes mellitus type 2 or type 2 diabetes (formerly called non-insulin-dependent
diabetes mellitus (NIDDM), or adult-onset diabetes) is a disorder that is characterized by high blood
glucose in the context of insulin resistance and relative insulin deficiency. Traditionally considered a
disease of adults, type 2 diabetes is increasingly diagnosed in children in parallel to rising obesity rates
due to alterations in dietary patterns as well as in life styles during childhood. Unlike type 1 diabetes,
there is very little tendency toward ketoacidosis in type 2 diabetes, though it is not unknown. One effect
that can occur is nonketonic hyperglycemia which also is quite dangerous, though it must be treated very
differently. Complex and multifactorial metabolic changes very often lead to damage and function
impairment of many organs, most importantly the cardiovascular system in both types. This leads to
substantially increased morbidity and mortality in both type 1 and type 2 patients, but the two have quite
different origins and treatments despite the similarity in complications.
An oral mucocele, is a clinical term that refers to two related phenomena: mucus extravasation
phenomenon, and mucus retention cyst. The former is a swelling of connective tissue consisting of
collected mucin due to a ruptured salivary gland duct usually caused by local trauma, in the case of
mucus extravasation phenomenon, and an obstructed salivary duct in the case of a mucus retention cyst.
The mucocele is a bluish translucent color, and is more commonly found in children and young adults.
A urinary tract infection (UTI) is a bacterial infection that affects any part of the urinary tract.
The main causitive agent is Escherichia coli. Although urine contains a variety of fluids, salts, and waste
products, it usually does not have bacteria in it. When bacteria get into the bladder or kidney and multiply
in the urine, they cause a UTI. The most common type of UTI is a bladder infection which is also often
called cystitis. Another kind of UTI is a kidney infection, known as pyelonephritis, and is much more
serious. Although they cause discomfort, urinary tract infections can usually be quickly and easily treated
with a short course of antibiotics.

Angeles University Foundation

Angeles City, Pampanga

Clinical Microscopy

Case Study Analysis

Group 6
Alagdon, Edsel
Gomez, Paul Arvin
Laus, Abigail

BSMT 3-A

Ms. Crizelda Liwanag

January 7, 2010

Case 10:
A 32-year old woman with a long history of IDDM has been checking her blood sugar at
home daily and administering her own insulin. On a rainy Sunday night, she was admitted
through the ER after 2 days of vomiting, upper abdominal pain, and right jaw pain. Her
admission diagnosis was Diabetic Ketoacidosis and dehydration. The admission urinalysis
(no microscopic) was significant for glucose >1000 mg/dL and ketones >80 mg/dL. Her
condition was resolved with fluid and electrolyte therapy and insulin drip.

Guide Questions and Answers:

1. What urinalysis results correlate with the diagnosis of DKA?

Color Colorless
Odor Strong, sweet smell
pH Decreased
Protein Increased
Glucose Increased
Specific Gravity Increased
Ketones Present

2. Explain.
The color of the urine appears to be diluted, but the specific gravity is high due to the
increased glucose content. Excretion of ketone bodies in the urine is responsible for the
sweet smell of the urine. The production of ketone bodies increases the acidic nature of the
urine. The presence of sugar in the blood leads to its excretion in to urine. Ketones in the
urine mean the body is burning fat to get energy.
3. What results should be expected from the microscopic examination?
In patients with diabetes mellitus, fatty casts are observed during microscopic examination
of the urine.

10-item Sample Test Paper:

1. The urinalysis was significant because of:
a. Increased amount of glucose
b. Decreased amount of ketones
c. Presence of low specific gravity
d. Increased pH
2. What sediment constituents may be seen from the microscopic examination?
a. RBC casts
b. WBC
c. Fatty casts
d. Bacteria
3. What may be the cause of the woman having diabetic ketoacidosis on her case?
a. Failure to administer insulin
b. High insulin intake
c. Drinking lots of electrolytes
d. Low glucose level
4. Which will show a correct urinalysis results for Diabetic ketoacidosis?
a. Odor – normal; pH – 7; protein – increased; glucose – normal; spec. gravity – normal;
ketones – negative
b. Odor –strong sweet; pH – decreased; protein – increased; glucose –increased; spec.
gravity –increased; ketones - present
c. Odor – normal; pH – decreased; protein – increased; glucose –increased; spec. gravity
– normal; ketones - negative
d. Odor –foul; pH – decreased; protein – increased; glucose – increased; spec. gravity –
normal; ketones - negative
e.
5. In the patient’s case, insulin level is low with type 1 Diabetes. What is the other name
for this type?
a. Insulin Sufficient Diabetes mellitus
b. Adequate insulin diabetes mellitus
c. Non-insulin dependent diabetes mellitus
d. Insulin dependent diabetes mellitus
6. The insulin level of the patient is low because of:
a. Excessive urination and sweating
b. Her immune system destroys some beta cells in the pancreas
c. Her kidney is swelling
d. High glucose level
7. What organ of the body is responsible for the insulin problem in type 1 diabetes?
a. Kidney
b. Pancreas
c. Spleen
d. gallbladder
8. In the absence of glucose, most cells use this to produce ATP for energy production:
a. Fatty acids
b. Sucrose
c. Protein
d. Cells don’t use energy at all
9. Fatty acid breakdown causes:
a. Bad cholesterol production
b. Release of glucose
c. Fatty acid accumulation
d. Ketone production and accumulation
10. It is a condition among Diabetes patients wherein insulin deficiency or resistance
causes the pulling of fluid body tissues leading to polyuria and dehydration
a. Hyperglucosemia
b. Polyuria
c. Hyperglycemia
d. Metabolic acidosis

Answer Key:
1. A
2. C
3. A
4. B
5. D
6. B
7. B
8. A
9. D
10. C

Pertinent Information:
Autoimmune diseases are diseases that occur because of the body’s immune system
attacking its own cells and rendering a function useless as is the case in diabetes. In
diabetes, the killer T cells of the body attack the insulin producing cells of the pancreas;
thereby, shutting down the production of insulin. When the production of insulin is affected,
the body cannot control the amount of sugar in the blood and this sugar is even excreted in
the urine. The liver then starts to produce ketone bodies as a response to the low insulin
level, which the body is fooled into thinking that, it is because of a low intake of glucose. The
production of ketone bodies then increases the acidic nature of the blood, because ketones
are created from fatty acids and the adipose stores in the liver. At a certain pH level that
indicates high acidity, the tissues of the body start to die and the breath of diabetes patient
has a sweet, alcoholic smell that emergency room doctors immediately recognize as the
symptom of diabetic ketoacidosis. This condition is potentially fatal if not treated on time.

The presence of sugar in the blood leads to its excretion into urine, which is due to the
overloading of certain binding proteins in the kidneys that send back glucose into the blood
in normal circumstances. Urine that usually contains glucose and sugars has a sweet, fruity
smell. However it is an indication that you need to rush to the emergency room before
ketoacidosis occurs and a possible coma.
References:
Diabetes Mellitus: A Guide to Patient Care by Lippincott Williams and Wilkins
Nutrition and Diagnosis-related Care by Sylvia Escott-Stump
Urinalysis and Other Body Fluids by Susan King Strasinger
Handbook of Disease by Lippincott Williams and Wilkins
Principles of Anatomy and Physiology by Gerard Tortora

Angeles University Foundation

AY 2009 – 2010

Clinical Microscopy:
Case Study No. 3

Group 2
Garcia, Tiffany Verzil
Geronimo, Jerome
Nogoy, Princess May
Ramos, Jayson
BSMT 3 – A

Ms. Crizelda D. Liwanag/Eloisa Q. Singian

Instructors

January 7, 2010
Summary

Patient: Man, 46 years old

Urinalysis results: Blood Chemistry Results:

Bilirubin: large Total Bilirubin: 32.1 mg/dL (0-1.5)
Color: amber Conjugated Bilirubin 22.2 mg/dL (0-0.4)
Casts: granular, 1-5/lpf ALP: 299 U/L (37-107)
WBC: 1-5/hpf AST: 302 U/L (8-42)
Ictotest: positive ALT: 46 U/L (3-96)
LD: 272 U/L (100-190)
Total Protein: 4.9 g/dL (6.4-8.2)
Albumin: 2.1 m/dL (3.4-5.0)
Accompanied Signs and Symptoms:
Diarrhea (entire previous month)
Gas and Nausea (previous 3 wks)
Jaundice

Patient Diagnosis:
Liver Cirrhosis
Hepatocellular Carcinoma
Obstructive Jaundice

Guide Questions:

What urine results correlate with the diagnosis? Explain.

• Color: amber
○ The patient’s urine color is caused by the presence of the abnormal pigment
Bilirubin due to the blockage of the hepatic portal vein which carries the bile
pigment to the GIT. The presence of this pigment in the urine, significantly in
an increased level coincides with the diagnosis of the patient’s liver diseases
such as that of jaundice, cirrhosis and hepatocellular carcinoma.

• Ictotest: positive
○ Indicates the presence of Bilirubin which is correlated with liver damage and
jaundice. This test is requested to further identify if the amber colored urine is
caused by early stages of liver diseases.

• Bilirubin: large
○ Bilirubin resulted in high level in the urinalysis result due to the damaged
integrity of the liver and the blockage of the porta of hepatis (the liver’s portal
vein), thus, the blood containing the pigment cannot reach the
gastrointestinal tract. The patient, having been diagnosed to have liver
cirrhosis at first - which is the onset of his history of alcoholism, wherein the
liver is injured due to massive alcohol consumption by blocking the normal
metabolism of protein, fats and carbohydrates – and further became
hepatocellular carcinoma due to malignancy and severe damage of the liver
cells is confirmed to possess these diseases.

How do the blood analyses correlate with this? Explain.

• Total Bilirubin and Conjugated Bilirubin – high

○ Due to the blocked portal vein of the patient, direct bilirubin aggregated,
escaped from the liver, and ended up in the blood. Increased direct bilirubin
usually means that the liver is obstructed, thus, correlated to hepatic
carcinoma and jaundice.
○ Total Bilirubin is also increased due to cirrhosis of the patient.
Liver Enzymes:

• ALP: 299 U/L (37-107)

○ Alkaline Phosphatase, high. Elevated ALP detects diseases involving the biliary
system of our body. Since the patient has a liver disease, this enzyme is
expected to rise because of the damage of the oragan’s cells. This marker is
intended to be sensitive upon the deterioration of the liver’s cells, as in
cirrhosis and carcinoma, wherein it is leaked out in the blood.
 ○ It is elevated due to the excessive alcohol consumption, which indicates
shedding of the liver, cirrhosis – the patient showed history of alcoholism.

• AST: 302 U/L (8-42) - high

○ Aspartate Amino Transferase (Serum Glutamate Oxaloacetate Transferase)
showed high level. As a liver enzyme, it is increased in the blood due to its
leakage from the destructed cells of the liver. But, as an enzyme involved in
other organs such as the heart, and skeletal muscles, it is more sensitive than
specific. Still, due to the dramatic increase of ALP, it is confirmed that its
increase is due to the lowering profile of the liver. Thus, correlating to the
patient’s diagnosis of jaundice and hepatocellular carcinoma.

• ALT: 46 U/L (3-96)

○ Alanine Amino Transferase is, by contrast, normally found largely in the liver.
This is not to say that it is exclusively located in liver, but that is where it is
most concentrated, making it specific than only sensitive. It is released into
the bloodstream as the result of liver injury. It therefore serves as a fairly
specific indicator of liver status of the patient.

• LD: 272 U/L (100-190)

○ Isoenzyme Fractionation detects any LD increase in the serum. Since this
enzyme is not that correlated with most of the hepatic disorders, due to its
sensitivity, there can be a strong possibility of liver damage. As the patient’s
liver disease in the case is already chronic, great increase in LD suggests that
the diagnosis is highly correlated with the result.

• Total Protein and Albumin – low

○ Value of the total protein decreases in the serum is due to the decrease in the
level of albumin, globulin or both. Albumin is low due to the damage in the
patient’s liver, wherein the low values indicate the poor capability of the organ
to synthesize proteins due to the concluded hepatic profile of the patient.

Pathophysiology:

In this case, a long term history of the patient signifies the outcome of the diagnosis. Due to
severe alcohol abuse, the liver develops a scar tissue that replaces normal parenchyma,
blocking the portal flow of blood through the organ and disturbing normal function. Thus, if
the portal vein is clogged, the blood containing the pigment from the disintegration of the
hemoglobin will not be able to enter the ducts of the bile and will not be able to reach the
GIT, making it a single way directed to the urinary system producing darker color urine and
pale colored stool. The pigment that creates the amber color of the patient’s urine is known
to be bilirubin, which is not considered a normal constituent. Blockage of the portal vein will
result to a pressure into the liver obstructing it and damaging its cells, thus creating
jaundice.
The patient’s alcohol abuse led to the prior diagnosis of cirrhosis and by then succeeded to
hepatocellular carcinoma during the onset of its malignancy. Since the liver is the main
organ in damage, protein synthesis is dysfunctional, thus lowering the total protein and
albumin levels of the patient’s serum under blood chemistry tests. Enzymes, as known to
hasten the synthesis of the proteins intracellularly, due to the patient’s liver disease, leak
outside the bloodstream, thus increasing the levels of enzymes extracellularly.
Name: ______________________________ Date: _________ Score: ____________

1. Increased levels of _________ in the urine may be due to liver disease, such as cirrhosis.

a. bilirubin
b. rbc
c. bacteria

2. The most abundant blood plasma protein and is produced in the liver. Low level of this
protein in blood indicates liver disease.

a. globin
b. albumin
c. fibrinogen

3. Patients with long history of alcoholism may develop ______________.

a. hepatitis
b. cirrhosis
c. jaundice

4. This type of test is requested to detect early stages of liver disease, such as hepatitis.

a. Ictotest
b. AST
c. ALP

5. What test is done to diagnose liver or bone disease?

a. ALT
b. ALP
c. AST

6. The amber color of the urine is due to the presence of ____________in the urine

a. wbc
b. cast
c. bilirubin

7. What causes the appearance of conjugated bilirubin in the urine?

a. disrupted hemoglobin degradation

b. liver damage
c. both

8. An enzyme found in high amounts in heart muscle and liver and skeletal muscle cells.
a. ALT
b. AST
c. ALP

9. This type of jaundice is caused by an interruption to the drainage of bile duct

a. pre hepatic
b. hepatic
 c. post hepatic

10. Its presence helps to determine the cause of clinical jaundice

a. globin
b. albumin
c. conjugated bilirubin
1. A
2. B
3. B
4. A
5. B
6. C
7. C
8. B
9. C
10. C

References:

Strasinger, Susan K. & Di Lorenzo, Marjorie S. Urinalysis and Body Fluids. 5th Edition. F.A.
Davis Company, Thailand. 2005
Calbreath, Donald. Clinical Chemistry
http://www.medicinenet.com/liver_blood_tests/page2.htm
http://www.nlm.nih.gov/medlineplus/ency/article/003470.htm
http://www.abcompany.com/docgolob/bloodchemistry.htm
http://www.labtestsonline.org/understanding/analytes/bilirubin/faq.html
http://digestive.niddk.nih.gov/ddiseases/pubs/cirrhosis/#cause
http://en.wikipedia.org/wiki/Gamma-glutamyl_transpeptidase
http://en.wikipedia.org/wiki/Cirrhosis
http://en.wikipedia.org/wiki/Jaundice#Post-hepatic
http://web2.airmail.net/uthman/lab_test.html

hoAngeles University Foundation

College of Allied Medical Professions

Department of Medical Technology

CASE ANALYSIS
Preliminary term

In partial fulfillment of the requirements in

Clinical Microscopy

Submitted to:
Ms. Crizelda D. Liwanag, RMT, MS

Submitted by:

Guevarra, Sonny
Mungcal, Lilibeth
Sarmiento, Norilie Mae
Tayag, Joseph John S.

Group # 8

Summary of the case

Case #8

A urine specimen is obtained from a 14-year-old boy with a history of a sore throat. Three
weeks ago he was cultured and treated for a streptococcal throat infection with a single
intramuscular dose of penicillin. Two weeks after his initial visit, he showed no abnormal
physical findings; however, his urinalysis revealed microscopic hematuria and he was told to
rest. Currently he has weakness and anorexia. He woke up with a headache and puffy
eyelids and says his urine is dark and there is very little of it.

Urinalysis Results:

Physical Appearance :

color: red (red-brown)

clarity: cloudy

Chemical Screening :

pH 6.0
specific gravity 1.025
protein (strip) 300 mg/dL protein (SSA) 3+
blood large
nitrite negative
leukocyte esterase negative
glucose negative
ketones negative
bilirubin negative
urobilinogen 0.5 EU/dl
Microscopic:

red blood cells 10-25/hpf (dysmorphic forms present)

white blood cells 0-2/hpf
casts 2-5 red blood cell casts/lpf
crystals few amorphous urates

Guide Questions:

1. What urinalysis findings are abnormal or discrepant?

The negative result for leukocyte esterase and the positive result for white blood cells in the
microscopic examination give discrepant information. However, this result may be due to
the sensitivity of the leukocyte esterase test. The test requires at least 5 WBC/hpf in order to
yield a positive result, whereas, the microscopic examination reveals only 0-2 WBC/hpf.

2. What is the significance of dysmorphic red cells in the urine sediment of this patient?

Dysmorphic red blood cells are RBC’s that vary in size, have cellular protrusions and are
fragmented. These abnormal RBC’s are associated primarily with glomerular bleeding.

3. Proteinuria is an important indication of renal disease. Match the following protein tests
(a and b) with the proteins they measure.

a. Reagent strip test for protein?

b. Sulfosalicylic acid test for protein?

_a/b__ albumin
_b___ Tamm-Horsfall glycoprotein
_b__ plasma globulins
 4. What is the significance of red blood cell casts in this patient?

The presence of RBC casts in the urine is more specific. This condition shows bleeding within
the nephron. RBC casts are primarily associated with the damage of the glomerulus that
allows the passage of the cells through the glomerular membrane.

5. Why don't you see bacteria in the microscopic examination of the sediment in this
patient?

Although there is a presence of white blood cells in the microscopic examination, there are
no bacteria seen in the urine. This may be a signal that the renal disease is not of bacterial
etiology.

6. What is the likely diagnosis for this patient?

The physical signs and symptoms and the medical history of the patient, together with the
findings of the urinalysis, constitutes the likely diagnosis for the patient which is acute
glomerulonephritis (specifically acute poststreptococcal glomerulonephritis).

Sample Test Paper

1. What would be the likely cause of the cloudy urine specimen in the case?

a. Red Blood Cells

b. White blood Cells
c. Urinary crystals
d. Squamous Epithelial Cells

1. The following may cause dysmorphic Red Blood Cells except:

a. Strenuous exercise
b. Glomerular bleeding
c. Diabetes mellitus

1. To be considered as UTI, bacteria should be accompanied by:

a. WBC’s
b. RBC’s
c. Bacterial motility
d. Abnormal urinary crystals

1. RBC’s are sometimes confused with WBC’s, yeasts and oil droplets. What reagent
would be likely used to confirm microscopic hematuria and the dysmorphic RBC’s

a. Sternheimer-Malbin
 b. 1% acetic acid
c. Hansel Stain
d. Prussian blue

1. What result in the urinalysis constitutes to glomerulonephritis?

a. Hematuria
b. RBC casts
c. Proteinuria
d. All of the above

1. Red blood cell casts are associated with:

a. Strenuous contact sports

b. Proteinuria
c. Dysmorphic RBC’s
d. Only B and C
e. All of the above

1. Post infection glomerulonephritis is associated by recent infection of:

a. Staphylococcus aureus
b. Streptococcus agalactiae
c. Streptococcus pyogenes
d. B and C
e. All of the above

1. The build up of these substances in the nephron after infection may trigger
glomerulonephritis

a. Immune complexes
b. M protein
c. Streptococcus toxin
d. Penicillin given to the patient

1. In the patient’s urinalysis, why is there presence of white blood cells?

a. To fight bacterial infection

b. The white blood cells attack the substances which inflames the nephron after a
recent infection and are filtered after
c. They pass through the compromised glomerular membrane together with other
particles because
d. The white blood cells are not reabsorbed back into the blood vessels from the
tubules

1. The following produces esterases except

a. Trichomonas
b. Lymphocytes
c. Histiocytes
Answer key
1. A
2. C
3. A
4. B
5. D
6. E
7. C
8. A
9. C
10. B

Pertinent Information

A urinalysis (or "UA") is an array of tests performed on urine and one of the most common
methods of medical diagnosis. Urinalysis has three phases namely; the physical, chemical
and microscopic examination. The physical examination includes the determination of the
urine color and clarity of urine. In the chemical test, the reagent strip is currently used
because it provides simple and rapid means for performing chemical analysis on urine. Tests
include pH, glucose, protein, ketones, blood, bilirubin, leukocyte esterase, urobilinogen and
specific gravity. The last part of urinalysis, microscopic examination, deals with the
determination of urinary sediments. These include RBC’s, WBC’s epithelial cells, casts,
bacteria, parasites, yeasts, crystals mucus, spermatozoa and artifacts.

Urinary findings in the case

Color and Clarity
The color of urine may range from colorless to black. These may indicate normal conditions,
physical activity, metabolic functions or pathologic conditions.
Urine color Possible Clinical Significance
Colorless Recent fluid consumption
Pale yellow Polyuria or Diabetes
Dark Yellow Concentrated Urine
Yellow green Bilirubin oxidized to biliverdin
Green Pseudomonas infection
Pink/Red Hematuria (RBC’s, hemoglobin and
myoglobin)
Brown/Black Methemoglobin, Alkaptonuria, Melanin

Color and clarity are routinely determined at the same time. Clarity refers to the
transparency of the urine specimen. Freshly voided normal urine is usually clear.
Clarity Term
Clear No visible particulates, transparent
Hazy Few particulates
Cloudy Many particulates
Turbid Print cannot be seen through urine
Milky May precipitate or clotted

*Clinical Significance of the physical examination

The urine specimen is said to be red and cloudy. This may indicate hematuria with
many particulates.

Protein
The presence of proteinuria is often associated with renal disease. Normal urine contains
very little protein (<10mg/dL or 100mg per 24hours) is excreted. These proteins are
primarily low-molecular-weight serum proteins that have been filtered by the glomerulus
and proteins produced from the genitourinary tract. Albumin is the major protein found in
normal urine. Normal albumin content is low because majority is not filtered by the
glomerulus and the filtered albumin is reabsorbed back into the tubules. Other proteins may
include microglobulins, Tamm-horsfall protein and proteins from prostatic, seminal and
vaginal secretions. Demonstration of proteinuria does not always signify renal disease.
Clinical proteinuria is indicated at >30mg/dL.

*Clinical Significance of the protein test in the case

The result of the test reveals a large amount of protein present in the blood. This
condition may be associated to a renal disease, giving the disability of the glomerulus and
tubules to properly filter and reabsorb the proteins

Blood
Macroscopically, blood may be seen in the urine by means of hematuria (cloudy red
urine) or hemoglobinuria (clear red urine). Any amount of blood greater than 5 cells per
microliter of urine is significant. In the chemical examination, the test for hemoglobin is the
most reliable means for determining blood.
Hematuria is closely associated with the renal and genitorurinary disorders in which
bleeding is the result of trauma or damage to the organs of these systems. Common causes
may include renal calculi, glomerular diseases, tumors and pyelonephritis. On the other
hand, hemoglobinuria results from the lysis of the red blood cell in which hemoglobin is
released. It may also be a result of intravascular hemolysis and the subsequent filtering of
hemoglobin through the glomerulus. Intravascular hemolysis is evident in urine without red
blood cells.
Another type of protein which may produce a red pigment is myoglobin. Its presence
in the urine, myoglobinuria, is indicative of muscular destruction. Myoglobin is a heme
containing protein found in the muscle that may react positively with the reagent strip for
blood. The diagnosis of myoglobinuria is also based on the patient’s medical history and
serum levels of certain enzymes.
 *Clinical Significance of the blood test in the case
The test is required to confirm if the red pigment in blood is caused by blood itself.
Other substances such as beets may produce red urine similar to hematuria. Blood gave a
large result in the chemical test signifying “true hematuria”.

Leukocyte Esterase
The Leukocyte esterase test is a urine test for the presence of white blood cells and
other abnormalities associated with infection. White blood cells in the urine, accompanied by
bacteria, usually indicate a urinary tract infection. The leukocyte esterase (LE) test detects
esterase, an enzyme released by white blood cells specifically granulocytes and monocytes.
Positive test results are clinically significant. The LE test is also used to screen for gonorrhea
and for amniotic fluid infections. The combination of the LE test with the urinary nitrite test
provides an excellent screen for establishing the presence of a urinary tract infection (UTI).
Urine sample that tests positive for both nitrite and leukocyte esterase should be cultured
for pathogenic bacteria.
Normal values for leukocyte esterase are based on the microscopic examination of 0-
5 per hpf. Women tend to have a higher number than men because of vaginal
contamination.

Microscopic Red Blood Cells and Red Blood Cell Casts

Red blood cells in the urine sediments appear as smooth, non-nucleated and bi-
concave disks and are reported as the average number seen per 10 hpfs. RBC’s shrink and
may appear crenated in concentrated urine, due to the loss of water. In dilute solutions,
RBC’s may rupture releasing the hemoglobin.
Dysmorphic RBC’s have cellular protrusions and are fragmented. They are primarily
associated with glomerular bleeding. The number and appearance of dysmorphic RBC’s
must also be considered because abnormal urine concentration affects RBC appearance.
Dysmorphic cells are also associated with strenuous exercise. The presence of RBC’s in the
urine is associated with glomerular membrane or vascular injury within the genitourinary
tract.
The presence of RBC casts in the urine specifically indicates bleeding within the
nephron. RBC casts are associated with glomerulonephritis that allow the passage the
passage of cells through the glomerular membrane. RBC casts associated with glomerular
damage are usually accompanied by proteinuria and dysmorphic RBC’s. Like dysmorphic
cells, RBC cast formation may be triggered by strenuous activities. RBC casts should be
accompanied by free standing RBC to prevent inaccurate reporting or misidentification of
the casts.

White Blood Cells

WBC’s are slightly larger than RBC’s. The predominant WBC found in urine sediment
is the neutrophil. Neutrophils exposed to hypotonic urine absorb water and swell. Brownian
movement of the granules within these cells produces a sparkling appearance known as
glitter cells. Presence of eosinophils upon staining indicates drug induced interstitial
nephritis, UTI and renal transplant rejection.
Pyuria (increase in urinary WBC indicates the presence of inflammation in the genitourinary
system. Examples of bacterial infections are pyelonephritis, cystitis, and prostatitis. Pyuria
may also be present in nonbacterial disorders such as glomerulonephritis, lupus
erythemathosus and tumors.

Amorphous Urates
Amorphous urates are microspically yellow brown granules and are normal crystals
seen in acidic urine. They occur in clumps that may resemble casts.

Acute Glomerulonephritis
Acute glomerulonephritis is characterized by the sudden appearance of hematuria,
proteinuria and red blood cell casts in the urine, edema (most noticeable around the eyes),
fatigue and hypertension with or without oliguria. It can follow streptococcal infections. This
illness was first recognized as a complication of the convalescence period of scarlet fever in
the 18th century. A link between hemolytic streptococci (group A and contains the M protein
in the cell wall) and acute glomerulonephritis was recognized in the 20th century.

Pathophysiology
Poststreptococcal glomerulonephritis follows infection with only certain strains of
streptococci, designated as nephritogenic. The offending organisms are virtually always
group A streptococci. Acute poststreptococcal glomerulonephritis (APSGN) follows
pyodermatitis with streptococci M types 47, 49, 55, 2, 60, and 57 and throat infection with
streptococci M types 1, 2, 4, 3, 25, 49, and 12.
APSGN is believed to be an immune-mediated disease, in which an immune complex
containing a streptococcal antigen is deposited in the affected glomeruli. The size of
glomerular basement membrane (GBM) pores and the molecular size of the streptococcus-Ig
complex are also important determinants. The molecular size of the streptococcus-Ig
complex is about 15 nm (10 nm for streptococcus group A and 5 nm for immunoglobulin).
The GBM pore sizes in children and adults are 2-3 nm and 4-4.5 nm, respectively. Therefore,
the immune complex molecule can be more easily rodded into the glomerulus in children
than in adults and, thus, may explain the increased frequency of APSGN in children
compared to that in adults.
Successful management of the secondary complications, until the immune
complexes have been cleared from the blood will result in no permanent kidney damage.

References:
S. K. Strasinger and M.S. Di Lorenzo, Urinalysis and Body Fluids, 4th ed., 2001
http://emedicine.medscape.com/article/777272-overview
http://emedicine.medscape.com/article/240337-overview
http://en.wikipedia.org/wiki/Glomerulonephritis
http://library.med.utah.edu/WebPath/TUTORIAL/URINE/URINE.html
http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=cm&part=A5435
http://medres.med.ucla.edu/Education/Lectures_and_Conferences/IMS_2007_pdf/CCJM
%20Proteinuria%202003.pdf