Daryl Apostol
Pathophysiology Case Study & Integration Concept Map Assignment
Case Study #1
J.H. is a 12-year-old boy diagnosed several months ago with nephrosis following
postinfectious glomerulonephritis secondary to an episode of pneumococcal pneumonia.
He has been coming to the clinic to have his condition monitored and therapies adjusted as
needed. At his latest clinic visit, a decrease in urine output, increasing lethargy,
hyperventilation, and generalized edema are noted. Trace amounts of protein are detected
in J.H.’s urine by dipstick. Blood is drawn for laboratory analysis, and the results are as
follows:
pH = 7.36
PaCO2 = 33 mm Hg 
PaO2 = 100 mm Hg
HCO3 – = 18 mEq/L 
Hct = 30% 
Na+ = 130 mEq/L 
K+ = 5.4 mEq/L 
BUN = 58 mg/dl 
creatinine = 3.9 mg/dl 
albumin = 2.0 g/dl 
Discussion Questions
1. How would a pneumococcal infection lead to glomerulonephritis? How can
glomerulonephritis result in nephrosis? (4 points)
a) The pneumococcal infection initiates an inflammation process that inflames the glomerulus.
b) Glomerulonephritis leads to deposits of mesangial cells that take the place of normal glomerulus
cells that become similar in structure to proliferative lesions. Changes in the glomerular wall 
permeability resulting in larger solvents to pass through into the urine (e.g. protein).
2. Use JH’s laboratory values to determine if he is still experiencing nephrosis or is
his condition progressing to renal failure. (4 points)
Based on the abnormal lab values: PaCO2, HCO3-, Hct 30%, Na+ 130 mEq/L, K+ 5.4 mEq/L, BUN 58
mg.dl, creatinine 3.9 mg/dl, albumin 2.0 g/dl & traces of protein in urine suggests that pt is
experiencing renal failure.
3.
What additional physical or laboratory findings would be helpful in determining
JH’s degree of renal impairment? (4 points)
Lab findings: BUN 58 mg/dl & creatinine 3.9 mg/dl. Physical assessment of decreased urine output
leads to patient experiencing edema, increased lethargy due to decreased Hct percentage and
hyperventilation (respiratory compensation) from low HCO3- (metabolic acidosis).
4. Draw a concept map depicting how glomerulonephritis can result in nephrotic
syndrome. (25 points)
Case Study # 2
D.K., a 42-year-old female, is being seen in the clinic for complaints of urinary frequency,
urgency, and burning. She reports that her urine appears cloudy and smells abnormal. A
urine dipstick reveals leukocyte esterase and is positive for nitrites. D.K. is given a
prescription for antibiotics.
Discussion Questions
1. What is the most likely cause of D.K.’s signs and symptoms? (4 points)
Signs & symptoms of polyuria, urgency & burning, cloudy, + leukocyte esterase & nitrate is +
for bacterial infection.
2. What organism is the most common cause of this disorder? (4 points)
E. coli is the most common cause of bacterial cystitis.
3. What factors may have predisposed D.K. to the development of this disorder?
(4 points)
The factors that predisposed patient to cystitis may have been from being female, age,
possible poor hygiene, & possible family Hx of UTIs.
Case Study #3
P.W. is 23 years old. He was involved in an MVA and has had quite a bit of blood loss due
to his injuries. He is brought to the emergency department by ambulance. It is estimated
that P.W. has had a blood loss of about 2500 ml. A urinary catheter is inserted to monitor
urine output, and fluid resuscitation is initiated while his wounds are cleaned and sutured.
The urine output is averaging 15 ml/hr, with a high urine osmolality and low urine sodium.
Discussion Questions
1. What type of renal failure is P.W. likely developing? What data support this
conclusion? (4 points)
a) Patient is experiencing prerenal kidney failure.
b) Supporting data is a decrease in circulating volume in the body due to blood loss
(hemorrhage) of half his blood volume that decreases renal perfusion urine output of 15
mL.
2. Without adequate therapy, what may develop? Why? What is the best therapy for
preventing this from occurring? (4 points)
a) Without adequate therapy, hypoxic renal cells will turn into acute tubular necrosis (ATN).
b) ATN may develop due to hemorrhaging. In hemorrhage, there is a large amount of blood
loss, in this case about half of total body blood volume is lost, therefore causing
hypovolemia which causes hypotensio. There is less perfusion within the kidney causing
oliguria and ischemia that result in tubular cell death in the kidneys.
c) The best therapy for preventing ATN from occurring is address etiology. In this case,
stop site of hemorrhage, start blood transfusion and IV fluids to increase perfusion. If pt
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is taking NSAIDS, ACE inhibitors, or AII blockers, discontinue them. Provide nutrition
and monitor for the development of infection.
3. In addition to urine output, what laboratory data should be monitored to assess
changes in P.W.’s renal function? (4 points)
In addition to urine output, GFR, BUN, creatinine, CBCs (for infection and RBC count), F &
E, and urinalysis should be monitored for changes in renal function.
4. If P.W.’s renal function does not return to normal, but continues to be diminished,
what are the subsequent stages of his renal disorder and what clinical problems do
they present? (4 points)
If P.W.’s renal function does not improve it could turn into acute tubular necrosis (ATN). In ATN
the pt will encounter 3 phases. The first phase, Prodromal phase, the pt will experience normal
or declining urine output and  BUN & creatinine levels. The next phase is the oliguric phase; pt
will develop oliguria or be nonoliguric. Depending on the severity of the injury, pt may become
anuric. Urine output continues to drop, F&E imbalance occurs that result in hypertension &
edema & other hypervolemia S&Sx. Protein, casts, WBCs, & RBCs are found in the urine, and
eventually uremia. Pt can develop hyperkalemia (fatal) & metabolic acidosis (at the same time).
What also may be seen in this phase are anorexia, N/V, weakness, seizures, acidosis,
confusion, & coma. The last phase, the postoliguric phase, begins when oliguria has stopped. In
this phase of AKI 5% of pts do not recover & is irreversible. Pt will experience polyuria & sodium
wasting, & lost of electrolytes in the urine.
If no renal function recovery is made after more than 3 months, renal disorder will become
chronic and can result in ESRD, the last stage of CKD.
Case Study #4
Terry is a 54 y.o. male who was in the other vehicle involved in the MVA with JH. He has
also lost a large volume of blood. Upon admission he is lethargic and these are his
parameters.

B/P 90/50

MAP 63

HR 124

UOP a0-a5 cc/hr

BUN 40

Cr. 0.8
1. Based on the information presented what is accounting for Terry’s low UOP?
(2 points)
a. Urinary obstruction
b. Acute glomerulonephritis
c. Decreased renal perfusion secondary to hypovolemia
d. Acute tubular necrosis (ATN)
2. What does his BUN and Creatinine tell you about his renal function?
(2 points)
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a.
b.
c.
d.
He has chronic renal failure
He has prerenal acute renal failure
He has intrarenal acute renal failure
He has postrenal acute renal failure
Terry is given a fluid challenge of 500cc NS and 2 units of PRBC’s over the next 3 hours.
His B/P is now 118/80; HR 96; and UOP 100cc/hr.
3. What does this response indicate about his renal function?
(2 points)
a. Intravascular volume was decreased
b. Kidney function is normal and able to respond to increased perfusion by
increasing UOP
c. Post obstructive diuresis
d. This is an excessive response because UOP should be 40cc/hr
24 hours later Terry is taken to surgery for internal bleeding. It was determined that he
suffered an intraoperative anterior MI. These are his postoperative parameters:






Auscultation revealed crackles
Irregular and labored respirations
B/P 76/48
HR 102
BUN 64
Cr. 6.2
4. What type of renal failure is this? ______________________________
(2 points)
5. The most likely cause of the above type of renal failure in this patient is?
(2 points)
a. Nephrotoxicity from furosemide
b. Renal constriction from norepinephrine
c. Diminished cardiac output (remember the most common cause of acute
intrarenal failure is untreated acute prerenal failure)
d. Toxins from death of myocardial cells
6.
Draw a concept map depicting the development of acute prerenal failure in this
case. (25 points)
See next page
Prerenal Kidney Injury
Risk Factors/Etiology:
Hemorrhage
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 Absolute  in circulating volume
 Hemorrhage
 Dehydration
 Burns
 Relative  in circulating volume
 Distributive shock
Hypovolemia


Third-spacing & edema
  cardiac output
 Cardiogenic shock
 Dysrhythmias
 Cardiac temponade
 Heart failure
 Myocardial infarction
 Primary renal hemodynamic abnormalities


Occlusion/stenosis of renal
artery
Drug-induced impairment
of renal autoregulation in
susceptible persons
Diagnostic tests:







GFR
BUN
Creatinine
Urinalysis
CBCs
Chemistry panel, comprehensive
Creatinine clearance
Na+
reabsorption
Low urine
Na+
 renal perfusion
Aldosterone
secretion
GFR
renal hypoxia
Renal ischemia
(more than few
hours)
oliguria
Acute tubular
necrosis (ATN)
Treatment:
 Identify etiology and treat it (e.g. blood transfusion)
 IV diuretics to address oliguria
 Diet restrictions (e.g. Na+ intake)
 Dialysis (if waste products start to build up in body fluid)
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