Download Case Study: The International Student with Renal Disease Nephrotic

Case Study: The International Student with Renal Disease
Nephrotic syndrome
Haddi is a young Nigerian woman studying in the United States. One afternoon in March, she reports to
the university health center complaining that she doesn’t feel well, she has no appetite, and her
stomach hurts. She is told to come back first thing the next morning to give a urine specimen and have a
physical examination. That day, her urine specimen is oddly frothy, and the nurse notes that Haddi’s
eyelids are puffy. A dipstick urinalysis shows a high concentration of protein in the urine. Since this
indicates a possibly serious disorder, the clinic refers Haddi to a urologist.
In taking Haddi’s history, the urologist learns that Haddi often notices that her face is puffy in the
morning, and by afternoon she frequently has swelling in the knees and ankles. She occasionally has
abdominal pains and sometimes difficult breathing. The urologist asks Haddi about her travel history
and history of other illnesses. Haddi says that she goes home to Nigeria during Christmas and summer
breaks, and that she almost always gets malaria when she is there. She last went home in December,
and had a bout of malaria then, as usual, but obtained treatment and her symptoms (chills and fever)
disappeared. The urologist admits Haddi to the hospital for overnight observation and a 24-hour urine
collection. Some of the results of her physical examination and laboratory work are shown below.
Vital sign:
Oral temperature= 98.6 F (37.0 C)
Heart rate; 68 beats/min
Respiratory rate: 24 breaths/min
Blood pressure= 137/73 mmHg
Physical examination:
Edema of lower limbs, mild ascites
Blood:
Hematocrit (Hct)= 34%
RBC count= 3.3 x 10
Total protein= 3.1 g/dL
Albumin=1.6 g/dL
Sodium= 136 mEq/L
Other serum electroyltes=Normal
Blood urea nitrogen (BUN) = 57 mg/dL (mild azotemia)
Lipids: Fat droplets present
Low-density lipoproteins = 220 mg/dL
Triglycerides = 165 mg/dL
Cholesterol = 238 mg/dL
Urine:
pH = 5.5
Specific gravity = 1.052
Protein excretion = 15.5 g/day
Glucose and ketones = Negative
Appearance: Light yellow, frothy.
Urine culture: No pathogenic microorganisms.
Sediment shows fatty casts, RBCs, and WBCs.
Dipstick tests show proteinuria and hematuria.
On the basis of these findings and with Haddi’s consent, the urologist orders a renal biopsy. The
histopathologist observes disruption of the glomerular basement membranes, and a stain for
immunoglobulins in the glomeerulus is positive.
The urologist diagnoses Haddi with nephritic syndrome. He explains to her that nephritic syndrome can
be triggered be certain forms of malaria, and often develops a few months after a malaria attack. He
says that her blood work shows no sign of malarial parasites at the present, and Haddi says she has not
had any of the fever and chills of malaria since returning to school for the semester. The physician
advises her that nephrotic syndrome often clears up when the underlying cause is successfully treated,
as her malaria appears to be. He warns her, however, that repeated bouts of malaria can worsen the
condition and cause potentially fatal renal failure, and furthermore that malaria sometimes does not
yield to drug therapy in people with nephritic syndrome. These facts make it critically important, he
says, that she take extreme measures to avoid malaria-carrying mosquitoes when she goes home and
that she carefully observe malaria prophylaxis-taking drugs in advance of her trips home to prevent
malaria infection even if she is bitten.
In the meantime , the physician advises that Haddi remain in the hospital for treatment. She receives
furosemide, a diuretic to treat her edema; an immunosuppressant to control the immune attack on her
glomeruli; and I.V. albumin. She is placed on a low-fat, low salt diet. From March through May, Haddi’s
serum albumin returns to a normal level of 3.5 g/dL, her urinary protein excretion declines to a low
level, and she is gradually withdrawn from the diuretic and immunosuppressant. Before traveling home
in May, she takes a regimen of chloroquine for protection against malaria.
Questions
1. Nephrotic syndrome is sometimes caused by diabetes mellitus. How do we know this is not the cause
in Haddi’s case?
The characteristic signs of diabetes mellitus are the three polys; polyuria, excessive urine production due
to an inability of the kidneys to reabsorb water; polydipsia, excessive thrist; and polyphagia, excessive
eating, Pg 683. For neprotic syndrome the main indicators are proteinuria, hypoproteinemia and edema.
Also the patient medical history revealed that she has no apppetite and her stomach hurts. The patient
also mentioned that she notices that her face is puffy in the morning and by latest afternoon her knees
and ankles also become swollen.
* Proteinurua: presence of large amounts of protein in the urine, chiefly albumin, in the
urine. It is usually associated with kidney disorder but can result from fever or
other causes.
* Hypoproteinemia: abnormally low level of protein in the blood, usually with
abdominal pain, nause, diarrhea, and edema. It may be caused by inadequate dietary
intake of protein orby intestinal or renal disease.
* Edema: abnormal collection of fluid in spaces between cells, especially under the
skin or in a given cavity, or organ. Many different causes, treatment depends on
cause.
2. In nephritic syndrome, what accounts for the froth in a freshly collected urine specimen?
High concentrations of protein cause the urine to become frothy.
3. Which data obtained from Haddi’s blood and urine are especially consistent with the edema she
experiences?
The low levels of albumin in the blood work are consistent with the edema she is experiencing and
urinalysis revealed proteinuria and hematuria, which indicates she is losing proteins and blood in her
urine.
4. Explain the pathophysiological reasons that Haddi has ascites, azotemia, and hematuria.
Because plasma protein level is a major factor in the osmotic uptake of water from the tissue fluid, this
state of hypoproteinemia typically results in edema and ascites. Hemodynamic changes cause a
decreased glomerular filtration rate this will manifest as azotemia.
*Ascitees, build up of fluid in the abdomen. In mild cases the additional fluid build up
is not observable, in more severe cases the additional fluid causes the stomach to
Protrude.
*Azotemia is the presence of urea or other nitrogen-containing substances in the
blood .
*Hematuria is the presence of blood in the urine.
*Hemodynamics: the physical principles of blood flow, based mainly on pressure and
resistance.The greater the pressure difference,between two points the greater the flow.
The greater the resistance, the less flow there is .
5. Why is Haddi given intravenous albumin? Which of her symptoms would be relieved by this
treatment?
She is given albumin because it helps remove extra fluid from tissues. Her edema should be relieved.
6. Aside from malaria prophylaxis, what are some other protective measures Haddi could take on her
trips home in order to reduce her risk of kidney failure?
The most common treatments include dietary restrictions, low salt and low fat, protein supplements to
restore the plasma albumin level, anti-inflammatory drugs (most often steroids), and diuretics to control
edema or hypertension. Also, people with nephritic syndrome should avoid dehydration, limit caffeine,
and take precaution to avoid any type of infection, especially kidney infections.
*Glomerulopathies are diseases that affect mainly the function of the glomureelus. These disorders may
be the primary disease, or they may result secondarily from some other systemic disease. All cases are
distinguished by damage to the glomeration with changes in capillary permeability. The two most
common are glomeruopathies are glomerulonephritis and nephritic syndrome.
Internet sources:
www.scribd.com/doc/13050603/Nephrotic-Syndrome
www.pathologystudent.com/%3Fp%3D888
The case study was taken from Clinical Applications for Anatomy and Physiology
Case Study # 23
Author Collen J Nolan and Kenneth S. Saladin
Questions:
1. The energy derived from hydrolysis of ATP is used to “pump” a substance across a membrane.
a. Secondary Active Transport
b. Primary Active Transport
c. Transport Maximum
d. Obligatory Water Reabsorption
e. Symporters
2. A substance passes from the fluid in the tubular lumen through the apical membrane of a tubule cell,
across the cytosol, and out into interstitial fluid through the basolateral membrane.
a. Apical Membrane
b. Basolateral Membrane
c. Primary Active Transport
d. Transcellular Reabsorption
e. Paracellular Reabsorption
3. The loop of Henle thus sets the stage for independently regulation of both the ___________ and
_________ of body fluids.
a. blood; osmolarity
b. volume; osmolarity
c. volume; interstitial flui1.
d. osmolarity’ interstitial fluid
e. blood; volume
4. The organ which helps rid the body of several waste materials such as heat, water, salts, and some
solids is_____________. (Pg.1053)
A. Liver
B. Lungs
C. Gastrointestinal Tract
D. Body Buffers
5. The kidneys shrink in size and filters less blood during aging. These changes lead to the following
problems of the urinary system except for: (Pg. 1053)
A. Hematuria
B. Urinary Tract Infection
C. Renal Calculi
D. Urinary Retention
6. _______________refers to a progressive and usually irreversible decline in glomerular filtration rate
(GFR). Pg. 1056
A. Nephrotic Syndrome
B. Acute Renal Failure
C. Glomerulonephritis
D. Chronic Renal Failure
7. Swelling of the kidney due to dilation of the renal pelvis and calyces as a result of an obstruction to
the flow of urine is known as: (Pg. 1057)
A. Metanephros
B. Hydronephrosis
C. Mesonephros
D. Pronephros
8. This hormone stimulates reabsorption of more water into the blood, subsequently producing a more
concentrated urine.
(a) Atrial natriuretic peptide
(b) Antidiuretic hormone pg. 1042
(c) Parathyroid hormone
(d) Corticol
(e) Angiotensis II
9. The intercalated cells of the distal convoluted tubule secrete which of the following ?
(a) potassium
(b) Hydrogen pg. 1039
(c) Sodium
(d) Urea
(e) Bicarbonate ions
10. How does Angiogenesis II affect renal physiology?
(a) It increases glomerular filtration rate by causing vasodilation of the afferent arterioles
(b) It stimulates the adrenal cortex to release insulin
(c) Itdecreases glomerular filtration by causing vasoconstriction of the afferent arterioles pg. 1040
(d) It inhibits reabsorption of Na+, Cl-, and water in the proximal convoluted tubule
(e) It has no effect on renal physiology
11. Glomerular filtrate has the same ratio of water and solute particles as blood.
(a) True pg. 1042
(b) False
12. Atrial natriuretic peptide suppresses the secretion of aldosterone and antidiuretic hormones.
(a) True pg. 1041
(b) False
13. Which hormone acts as both a neurotransmitter when its released by the sympathetic system and a
hormone when its released by the adrenal medullae?
(a) Parathyroid hormone
(b) Oxytocin
(c) Insulin
(d) norepinephrine pg. 643
(e) Cortisol
14. Parathyroid hormone is a major regulator of ?
(a) Prolactin
(b) Aldersterone
(c) Human growth hormone (hGH)
(d) Thyroid stimulating hormone (TSH)
(e) Calcium pg. 662
15. What is the principal action of glucagon ?
(a) Has no effect on blood glucose
(b) Increase blood glucose pg. 671
(c) Decrease blood glucose
(d) Increase insulin
(e) Decrease insulin
16. What is the most common abnormality associated with the posterior pituitary?
(a) Cushing’s syndrome
(b) Diabetes mellitus
(c) Grave’s disease
(d) goiter
(e) Diabetes insipidus pg. 682
17. Thyroid-stimulating hormone stimulates the synthesis and secretion of
(a) Insulin
(b) Glucagon
(c) Throxine pg. 654
(d) Human growth hormone
(e) Luteinizing
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