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230 CASE FILES: FAMILY MEDICINE
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COMPREHENSION QUESTIONS
20.1 A 58-year-old man presents to his provider for follow-up of his hypertension and hyperlipidemia. He also reports chest pain and feeling short of
breath after climbing two flights of stairs or walking three to four blocks. The
symptoms resolve after several minutes of rest. Which of the following drugs
would not be indicated as a first-line agent in the treatment of this patient’s
condition?
A. Atorvastatin
B. Nitroglycerin
C. Enalapril
D. Doxazosin
E. Aspirin
20.2 Which one of the following patients presenting with chest pain is at the highest risk for an acute MI?
A. A 40-year-old woman on a proton pump inhibitor for reflux disease
B. A 75-year-old man with parasternal chest pain, lipid abnormalities, and
no past history or cardiac disease
C. A 23-year-old man recently diagnosed with hypertrophic cardiomyopathy
D. A 67-year-old man with a history of a prior angioplasty, with chest pain
radiating to the neck and complaint of diaphoresis
20.3 Which of the following ECG changes makes the determination of acute MI
the most difficult?
A. Q wave
B. ST-segment elevation
C. Left bundle branch block
D. First-degree atrioventricular block
E. T-wave inversion
20.4 A 64-year-old woman with a history of hypertension and angina pectoris
presents with chest pain for the last 3 hours. She describes the pain as “sharp”;
it is worse when she inhales deeply, and it is not relieved by sublingual nitroglycerin. The pain improves if she sits up and leans forward. Her ECG shows
ST elevation in most leads. Cardiac enzymes are negative. Which of the following is the most likely diagnosis in this patient?
A. Unstable angina pectoris
B. Myocardial infarction
C. Aortic dissection
D. Heart failure
E. Pericarditis

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ANSWERS
20.1 D. This patient has a new onset of angina on top of his hypertension and
hyperlipidemia. Aspirin (answer E), statins (answer A), beta-blockers (answer
C), ACE inhibitors, and nitroglycerin (answer B) would all be indicated for
these conditions. Doxazosin (answer D), an alpha-blocker, would not be of
benefit in this situation.
20.2 D. Risk factors for increased likelihood of acute MI are male gender; age older
than 60 years; chest pain radiating to neck, jaw, arm, or shoulder; and a prior
history of angina or acute MI. Proton pump inhibitors (answer A) and hypertrophic cardiomyopathy (answer C) are not risk factors.
20.3 C. The changes of LBBB make the determination of an acute MI by an ECG
extremely difficult. In these patients, it is particularly important to obtain
serum markers of myocardial damage.
20.4 E. This patient likely has pericarditis. The pain is described as sharp in nature
rather than dull, aching, pressure of angina (answer A and B). The pain is
exacerbated by inspiration, and there is global ST-segment elevation noted
on the ECG. The pain of pericarditis tends to decrease when the patient sits
upright and leans forward. Aortic dissection (answer C) would present with
an excruciating and severe “tearing pain” and associated with distress. Heart
failure would present with dyspnea, tachypnea, pedal edema, and jugular
venous distension.
CLINICAL PEARLS
» Angina pectoris is the most frequent symptom of intermittent ischemia.
» Targeted history and physical examinations of patients with angina are
vital to expedite proper diagnosis and treatment of patients. The patient’s
description of their discomfort is key; history must be given attention
because it is the most important diagnostic factor.
» Physical examination may be normal in many patients with angina.
» Aspirin, nitrates, beta-adrenergic antagonists, and statins are the back-
bone in treatment and prevention of myocardial pathology, having
proven benefit for both primary and secondary treatment.
» Time is myocardium. Initial diagnosis and treatment must be done as
soon as possible.
» Be mindful of polypharmacy, as many drugs have side effects that can
exacerbate myocardial damage.
» The most common etiology of chest pain in the primary care setting is
musculoskeletal. However, it is imperative to rule out a cardiac cause of
chest pain before making a musculoskeletal-related diagnosis.

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REFERENCES
McConaghy JR, Oza RS. Outpatient diagnosis of acute chest pain in adults. Am Fam Physician.
2013;87(3):177-182.
Mehta LS, Beckie TM, DeVon HA, et al. Acute myocardial infarction in women: a scientific statement
from the American Heart Association. Circulation. 2016;133(9):916-947.
O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of
ST-elevation myocardial infarction: a report of the ACCF/AMA Task Force on Practice Guidelines
[published correction appears in Circulation. 2013;128(25):e481]. Circulation. 2013;127(4):
e362-e425.
Smith JN, Negrelli JM, Manek MB, et al. Diagnosis and management of acute coronary syndrome: an
evidence-based update. J Am Board Fam Med. 2015;28(2):283-293.
Switaj TL, Christensen SR, Brewer DM. Acute coronary syndrome: current treatment. Am Fam Physician.
2017;95(4):232-240.

CASE 21
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A 46-year-old woman presents to the clinic for the first time, complaining of
decreased urinary output with a foamy appearance for 5 months. She also
complains of swelling in both legs and nonbloody, nonbilious emesis a few times
a week. She was diagnosed with type 2 diabetes 10 years ago and has been taking
insulin for 2 years. She does not check her sugar levels at home. When asked about
her diet, she states that she eats the best she can for what she can afford but often
has very little appetite and vomits sometimes. The patient last saw her health care
provider 8 months ago, and insulin is her only medication.
On examination, the patient is an obese woman. Her temperature is 99°F
(37.2°C), heart rate is 108 beats/min, blood pressure is 198/105 mm Hg, respirations
are 19 breaths/min, and oxygen saturation is 94% on room air. She has periorbital
edema. Her skin is hyperpigmented on both lower extremities. Her heart is
tachycardic with an S4 gallop auscultated and without murmurs or rubs. When
palpating the heart’s point of maximal impulse (PMI), it is lateral to the left
midclavicular line. There are vesicular breath sounds throughout both lungs.
Her neck reveals no jugular venous distension (JVD), and there are no carotid
bruits. The lower extremities reveal pitting pretibial edema with a pit recovery
time less than 40 seconds. Laboratory studies in your office include a urinalysis
showing hyaline casts, 3+ proteinuria, and glucose, but negative for ketones. Her
hemoglobin is 10.9 g/dL, and her hematocrit is 32% with a mean corpuscular
volume (MCV) of 82.3 fL.
▶ What is the most likely diagnosis?
▶ What is your next diagnostic step?
▶ What is the next step in therapy?

234 CASE FILES: FAMILY MEDICINE
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ANSWERS TO CASE 21:
Chronic Kidney Disease
Summary: A 46-year-old woman presents with
A history of uncontrolled diabetes and currently-uncontrolled hypertension
Periorbital edema and long-standing lower extremity edema
An S
Central obesity
Urinalysis showing hyaline casts, 3+ proteinuria and glucose, and negative ketones
Hemoglobin 10.9 g/dL with an MCV of 82.3 fL
Most likely diagnosis: Acute worsening of chronic kidney disease (CKD).
Next diagnostic step: Measurement of serum electrolytes, blood urea nitrogen
(BUN), and creatinine (Cr); imaging of the kidneys.
Next step in therapy: Further history to identify and remove any offending agents
(eg, nonsteroidal anti-inflammatory drugs [NSAIDs]) and implement measures to
control blood pressure and diabetes; she may require dialysis if she develops complications such as pulmonary edema, severe hyperkalemia, or anuria.
heart sound and displaced PMI, indicating left ventricular hypertrophy (LVH)
4
with diastolic dysfunction
ANALYSIS
Objectives
1. Be able to list the common risk factors for developing CKD. (EPA 1, 12)
2. Be able to name common tests used to evaluate CKD. (EPA 3)
3. Be able to report outpatient management strategies and medications for
patients with CKD. (EPA 4)
4. Be able to report common complications associated with CKD. (EPA 1, 2, 10)
Considerations
This 46-year-old patient presents with a concerning symptom of a decrease in urination with a change in the appearance of the urine. The most immediate concern is how
often she is urinating and to what degree is she urinating less. A significant reduction
requires immediate evaluation of renal function (serum creatinine) and volume status.
Volume status is assessed clinically by skin turgor, mucous membranes, specific gravity in
the urinalysis, and orthostatic blood pressure. A low-volume status with an elevated Cr
requires that the patient be given intravenous fluids to see if there can be any recovery
of kidney function. The patient’s uncontrolled diabetes and hypertension predispose
her to kidney damage. Another common offender in a patient with this history is the
use of NSAIDs. This will increase the patient’s already high risk of damage.
With CKD, patients are often able to compensate for the metabolic imbalances
that occur, such as hyper- or hyponatremia, hyperkalemia, elevated uric acid levels,

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and metabolic acidosis. Patients may also experience secondary hyperparathyroidism. Significantly elevated potassium levels require treatment with sodium polystyrene sulfonate (Kayexalate), insulin with glucose, and retention enemas, depending
on the degree of elevation. When the patient is no longer compensating, there are
symptoms of pulmonary edema, which include shortness of breath, lower extremity edema, JVD, and abnormal lung sounds (rales).
This patient was compensating and mostly demonstrated the result of a hypoalbuminemic state from the loss of protein in the urine. She had lower extremity
edema with a long pit time that reflected her low albumin state. Her occasional
emesis reflected high levels of urea and other toxins. Persistent emesis mandates
treatment. Her normocytic anemia was the result of reduced erythropoietin from
the kidneys. In this setting, treatment with exogenous erythropoietin improves
prognosis for cardiovascular mortality. The hyaline casts reflected the long-standing damage to the kidneys.
Increasing the patient’s chance of improved kidney function requires glucose
and blood pressure control, removing offenders such as NSAIDs and diuretics
(if allowable), maintaining normal volume status (which is difficult with a low albumin state), and adding agents that both treat blood pressure and improve kidney
and cardiovascular function, such as angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs). CKD itself is a cardiovascular risk
factor. Patients are more likely to die from cardiovascular disease than to develop
end-stage renal disease (ESRD) requiring dialysis. The patient’s gross proteinuria
of 3+ reflects her high risk for cardiovascular disease.
DEFINITIONS
CHRONIC KIDNEY DISEASE: A spectrum of processes associated with abnormal kidney function and progressive decline in glomerular filtration rate (GFR)
that are present for > 3 months.
ENDSTAGE RENAL DISEASE: The irreversible loss of kidney function such
that the patient is permanently dependent on renal replacement therapy (dialysis
or transplantation). Also defined as a GFR of less than 15 mL/min.
CLINICAL APPROACH
Epidemiology
Chronic kidney disease is becoming more common in the United States. The most
common etiologies are diabetes, hypertension, and glomerulonephritis. Diabetic
kidney disease occurs in 30% to 40% of type I diabetics, in 25% of type 2 diabetics,
and in 24% of hypertensive patients. Within the diabetic patient population, 20%
to 60% have hypertension. Many patients develop ESRD after years of poor control
APPROACH TO:
Chronic Kidney Disease

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Table 21–1 • STAGES OF CHRONIC KIDNEY DISEASE
Stage 1 GFR more than 90 mL/min in the presence of signs of kidney disease,
such as proteinuria, hematuria, or abnormal renal structure
Stage 2 GFR of 60-89 mL/min
Stage 3a
Stage 3b
Stage 4 GFR of 15-29 mL/min
Stage 5 GFR less than 15 mL/min or dialysis
GFR of 45-59 mL/min
GFR of 30-44 mL/min
of their hypertension and diabetes, which is why good control of these medical
conditions has such a priority with new insurance payment mechanisms, such as
Medicare’s Merit Incentive Payment System (MIPS). Underlying causes may be
ascertained through clinical presentation, symptomatology, and past medical and
family history.
Pathophysiology
The Kidney Disease Outcomes Quality Initiative (KDOQI) from the National
Kidney Foundation (NKF) recommends both a serum Cr to estimate GFR and a
random urinalysis for albuminuria in those groups at risk for CKD. The stage of
CKD is based on the GFR, which is normally between 90 and 120 mL/min (see
Table 21–1). The GFR can be estimated with a random Cr level calculated with one
of two commonly used equations:
Modification of diet in renal disease (MDRD) equation:
GFR (mL/min/1.73 m2) = 175 × (SCr)
–1.154
× (age)
× (0.742, if female) × (1.210, if black)
–0.203
Cockcroft-Gault equation:
CCr (mL/min) = {(140 − age) × weight [kg]}/(72 × SCr) × (0.85, if female)
(SCr = serum creatinine concentration; CCr = creatinine clearance).
The Cockcroft-Gault equation is preferred for older patients and in renal dosing
of medications. It is important to note that these equations do not give an accurate
calculation of GFR in the setting of an acute change in renal function, such as acute
kidney injury. Serial measurements of renal function are recommended for newly
diagnosed cases to determine the pace of renal deterioration and whether the disease is truly chronic, as opposed to acute or subacute. A 24-hour urine collection is
recommended for persons with extremes of age and weight, malnutrition, skeletal
muscle disease, paraplegia or quadriplegia, or a strict vegetarian diet.
Imaging. The evaluation in all patients with CKD includes renal imaging (typically with renal ultrasound). Treatment may be more successful in patients with
normal-size kidneys. Small kidneys are a sign of irreversible disease. Asymmetry
suggests renovascular disease.
Urine Evaluation. Evidence of proteinuria or microalbuminuria should be evaluated in all patients with CKD. If the urine dipstick does not reveal gross proteinuria,

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a sample should be sent to evaluate for microalbumin. A test is positive if there is
more than 30 mg of microalbumin per gram Cr. In the case of less than 200 mg of
protein per gram Cr, it is recommended that the test be repeated yearly. Any patient
with more than 200 mg of protein per gram Cr will need diagnostic evaluation and
treatment. The protein-to-Cr ratio in an early morning random urine sample may
be used instead of a 24-hour urine protein excretion.
Laboratory Values. Some common laboratory studies include ANA (antinuclear
antibody), antiphospholipid antibodies, C3, C4, ESR (erythrocyte sedimentation
rate) and/or CRP (C-reactive protein) (looking for lupus nephritis); hepatitis
panel and HIV test (looking for infectious etiologies); serum and urine protein
electrophoresis (looking for multiple myeloma) for those patients older than age 35;
hemoglobin A1c; fasting blood sugar; and analysis of urine sediment.
Biopsy. Renal biopsy, if not contraindicated by comorbidities, is indicated in
patients with unknown etiology after history and laboratory evaluation, if parenchymal disease is suspected, or if treatment or prognosis will be based on the
biopsy. However, biopsy is contraindicated if bilateral small kidneys are seen on
imaging, as there is a low likelihood of improving outcome due to the presence of
late-stage disease. Patients should be tested for common conditions associated with
CKD, such as anemia and hyperphosphatemia.
Treatment
Treating Reversible Causes. Managing CKD includes treatment of reversible causes.
Hypovolemia, hypotension, infection leading to sepsis, and drugs that lower the
GFR all reduce renal perfusion. History and physical examination allow for this
diagnosis, and a trial of fluids may improve kidney function. Drugs such as NSAIDs,
ACE inhibitors, ARBs, aminoglycosides at full strength, and radiographic contrast
material can affect kidney function. Urinary tract obstruction, commonly caused by
prostate enlargement in elderly men, is a potentially reversible cause.
Controlling Blood Pressure. Nonproteinuric renal disease requires strict blood
pressure control. The Eighth Joint National Committee (JNC 8) guidelines
recommend a blood pressure goal of less than 140/90 mm Hg in all patients
age18years or older with CKD. Multiple guidelines recommend a blood pressure
goal of less than 130/80 mm Hg, especially if there is diabetes or proteinuria.
Another goal is the reduction of protein excretion to less than 500 to 1000 mg/d
(or at least 60% of the baseline value). JNC 8 guidelines recommend starting with
an ACE inhibitor or an ARB for blood pressure control in patients with CKD,
followed by a thiazide diuretic or calcium channel blocker if the blood pressure
goal is not achieved. When using ACE inhibitors or ARBs, be aware that a Cr
increase of less than 30% is considered acceptable, as this lowers the pressure in
the glomerulus. Beta-blockers may also be considered as a second- or third-line
treatment for blood pressure control. Combining an ACE inhibitor with an ARB
is not recommended.
Phosphate Binders. When the GFR is below 25 to 30 mL/min, oral phosphate
binders are usually required. Caution is used when treating hyperphosphatemia in
stages 3 to 5 of CKD. It is suggested that calcium intake not exceed 2000 mg/d, as
this may contribute to cardiovascular disease.

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Treating Anemia. Guidelines suggest evaluation of anemia with a hemoglobin
less than 12 g/dL in women and 13.5 g/dL in men. This should include evaluation
for nonrenal causes of anemia. In patients with CKD whose hemoglobin is less
than 10 g/dL, treatment with erythropoietin is helpful, with a goal of 12 mg/dL
in low-risk patients and 13 mg/dL in those at risk for stroke and cardiovascular
events. This may reduce symptoms of anemia, show cardiovascular improvement,
and possibly decrease mortality.
Other Treatments. Other treatments may be beneficial in CKD. Dietary protein restrictions of 0.8 to 1.0 mg/kg/d may be beneficial. Statins are recommended for treatment of hyperlipidemia in most CKD patients not on dialysis.
The volume overload associated with CKD responds well to sodium restriction
and loop diuretics. Hyperkalemia may be prevented by a low-potassium diet,
avoiding drugs such as NSAIDs, and adding diuretics to the regimen of patients
on ACE inhibitor/ARB therapy. Metabolic acidosis may be treated with sodium
bicarbonate, with a goal of maintaining a concentration of 22 mEq/L. Dietary
phosphate restriction may limit the development of secondary hyperparathyroidism in these patients. There is evidence for vitamin D supplementation reducing
all-cause mortality. Patients should also have influenza and pneumococcal vaccinations. Those with a high risk of progression should also receive hepatitis B
vaccination.
Renal Replacement Therapy. Ultimately, the patient who is proceeding toward
ESRD must be identified and adequately prepared for renal replacement therapy. It
is recommended that patients with a GFR < 30 mL/min, difficult-to-control
comorbidities, or significant proteinuria or sudden worsening of renal function be
referred to a nephrologist for evaluation and preparation for possible dialysis.
Patients with ESRD have high rates of medical complications and therefore are
ideal patients for interprofessional care management.
CASE CORRELATION
See also Case 30 (Hypertension) and Case 51 (Diabetes Mellitus).
COMPREHENSION QUESTIONS
21.1 A 56-year-old man with known CKD presents to the emergency center with
a 3-day history of shortness of breath and rapid weight gain. On examination
of the heart, you are able to auscultate an S3 heart sound and hear crackles at
the lung bases. You also see moderate JVD. The oxygen saturation is 90% on
room air. Which of the following is your next step in evaluation?
A. Order an echocardiogram.
B. Order a chest x-ray.
C. Measure a Cr to calculate GFR.
D. Order a computed tomographic (CT) angiograph of the chest.

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21.2 A 39-year-old woman with hypertension and type 2 diabetes has been noted
to have progressively worsening renal insufficiency. Which of the following
measures is most important in the prevention of ESRD?
A. Tobacco cessation
B. Triglyceride control
C. Glycemic control
D. Weight control
E. Dietary sodium restriction
21.3 A 72-year-old man with a long history of hypertension presents to the
emergency department complaining of not being able to urinate for the last
36hours. He also has a 1-day history of nausea, vomiting, and abdominal
pain. He states that his urinary stream has been decreasing over the past
2years. On examination, the abdomen is firm and tender, and the prostate is
enlarged. His serum Cr level is 3.4 mg/dL. Which of the following is the best
next step?
A. Give intravenous fluids and see if he begins to make urine.
B. Perform a renal ultrasound in the emergency department.
C. Maintain tight control of his blood pressure.
D. Place an indwelling Foley catheter.
21.4 A 45-year-old woman with type 2 diabetes presents to the clinic for followup. She states that over the past year, she has decreased vision in the left eye.
She also has had some occasional chest pain for the past 2 months. On examination, the blood pressure is 145/92 mm Hg. The cardiac and lung examinations are normal. Laboratory tests show the urinalysis reveals 1+ proteinuria.
Serum laboratory tests reveal a baseline Cr of 1.6 mg/dL, a low-density lipoprotein (LDL) cholesterol level of 135 mg/dL. Which of the following is the
best medication to start the patient on at this time?
A. ACE inhibitor
B. Hydralazine
C. Oral nitrate
D. Thiazide diuretic
ANSWERS
21.1 B. This patient has CKD with volume overload, as evidenced by symptoms of
shortness of breath, weight gain, the presence of an S3, crackles, and moderate JVD. Because oxygenation is the most important first priority, respiratory
status should be addressed first. A quick and simple first step is to do a chest
x-ray to confirm what you already suspect—pulmonary edema. After initiating furosemide (Lasix), the chest x-ray may be repeated to see to what degree
the diuresis has improved the overload. Echocardiography (answer A) may be
indicated but would not be the first test performed. Answer C (measure Cr to
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