Case Studies

Acute Renal Failure in the Presence of Chronic Renal

Disease in a 31-Year-Old Caucasian Female

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Felix O. Omoruyi, PhD, Anthony O. Okorodudu, PhD, DABCC, Amin A. Mohammad, PhD, DABCC,
John R. Petersen, PhD, DABCC
(Department of Pathology, University of Texas Medical Branch, Galveston, TX)
DOI: 10.1309/PJGY5R1GJKFBY2XG

Case History complained of visual blurring, intermittent chest Current Medications

Patient
31-year-old Caucasian-American female.
Chief Complaint
Headache.
History of Present Illness
The patient was referred to the hospital
because of impaired renal function (stage
V chronic kidney disease) and uncontrolled
hypertension. Her reason for the visit was a
headache that was an 8 on a scale of 10.
She was not taking her medication (Labetalol).
She felt a pulsation in her ear that happens
when her blood pressure goes up. She also
pressure, nonexertional, associated shortness
of breath, and epigastric abdominal pain
associated with some nausea but no vomiting.
Past Medical History
Diabetes mellitus type 1 since 8 years of age
and impaired renal function and hypertension.
She was admitted for hemodialysis initiation as
well as hypertensive urgency and headache.
Family/Social History
She has a family history of diabetes,
hypertension, coronary heart disease, and
cancer. She quit tobacco use 5 months ago.
Labetalol, Lasix, Lantus, Protonix, aspirin, and
Tylenol.
Physical Examination
Temperature (36.7°C), blood pressure (193/98),
pulse (88), and weight (87.5Kg). She was alert and
oriented and in no apparent distress. Pupils equal,
round, reactive to light, extraocular movements
intact, and moist mucous membranes. The
abdomen was soft, nondistended, and normoactive
bowel sounds. She had edema to mid-thigh, no
cyanosis, and no clubbing.
Principal Laboratory Findings
Tables 1, 2, and 3.

Questions
1. What are this patient’s most striking clinical and laboratory
findings?
2. How do you explain these findings?
3. What is this patient’s most likely diagnosis?
4. What is the etiology of this patient’s condition?
5. What is the standard therapy for this patient’s disorder?
6. What is the diagnostic approach of acute renal failure in the
presence of chronic renal disease seen in this patient?
Table 1_Hematology
Test Patient’s Result Reference Interval
Red blood cells 2.88 3.9–5.3 x 103/μL
Hemoglobin 8.1 11.5–15.5 g/dL
Hematocrit 23.2 34–45%
Platelet count 81 150–400 x 103/μL
Hemoglobin (A1c) 6.6 4–6%

failure patients is thought to be caused by protein-energy malnutri-

Possible Answers
1. Headache, uncontrolled hypertension, diabetes (DM1),
impaired renal function (stage V chronic kidney disease), visual
blurring, intermittent chest pressure, nonexertional, associated
shortness of breath, and epigastric abdominal pain associated with
some nausea but no vomiting. In addition, there is evidence of
anemia as demonstrated by the decrease in red blood cells, hemo-
globin level, and hematocrit (Table 1). Serum glucose was slightly
elevated while the serum phosphorus was dramatically increased
and calcium was significantly decreased due to the low albumin
level in the patient (2.6 mg/dL). The corrected calcium (8.0 mg/
dL) is consistent with the low but not critical ionized calcium level
(4.3 mg/dL). The patient’s edema is probably due to a combina-
tion of renal failure and low albumin. The low albumin in renal
tion. This condition has also been reported in nondialyzed patients
with advanced chronic renal failure and in patients with end-stage
renal disease undergoing maintenance hemodialysis.1 The possible
causes of protein-energy malnutrition in patients with chronic
renal failure include the following: reduced energy or protein in-
take; concurrent chronic illnesses with superimposed acute illnesses
and increased inflammatory cytokines; catabolic stimulus due to
hemodialysis; loss of nutrients into the dialysate; and diagnostic or
therapeutic procedures that reduce nutrient intake or engender net
protein breakdown.1,2 Although we do not know the concentra-
tion of cytokines in this patient, she did have an elevated serum
C-reactive protein concentration and hypoalbuminemia similar
to that seen in other chronically ill patients.3 Although the pul-
monary edema resolved after hemodialysis in this patient, the low

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Case Studies

level of albumin may account for the edema observed to mid-thigh.
The blood glucose concentration of 123 mg/dL may be due to the
hemodialysis (the specimen was collected after hemodialysis) and
the variety of insulin administered to the patient. Hemodialysis has
been reported4 to decrease red blood cell (RBC) life span, which
may have affected the value obtained for hemoglobin A1c in this
patient. Fructosamine determination may be more useful under
such conditions. Sodium and total CO2 were both lower than nor-
mal. Acute renal failure in the presence of chronic renal disease is
evidenced by the sharp increase in creatinine and BUN in the pres-
ent visit compared with the levels from the previous visit (Table 2).
Glucose, protein, and blood were present in urine along with in-
creased numbers of white blood cells, red blood cells, and epithelial
Table 3_Urinalysis
Test Patient’s Result Reference Interval
Protein 300 mg/dL negative
Glucose 70 mg/dL negative
Blood 3+ negative
Red blood cells >182 0–3
White blood cells 7 0–5
Bacteria few negative
Epithelial cells 7 0–2

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cells (Table 3). A few bacteria were also present in urine.
2. Her headache may be due to the uncontrolled hyperten-
sion resulting from not taking her prescribed medication. The
visual blurring is associated with the increased blood pressure.
Decreased erythropoietin production is the principal factor re-
sponsible for the anemia of chronic renal failure,5 which could
account for the evidence of anemia in this patient. Apart from
the noncompliance of this patient to her prescribed medication,
uncontrolled hypertension is also an important manifestation of
chronic renal disease and increases in prevalence as renal function
declines.6 The observed hyponatremia is due to impaired renal
capacity to excrete solute-free water, resulting in a disproportion-
ate retention of water relative to the amount of sodium retained.7
The decrease in CO2 total is a result of the failure of the kidney
to excrete acid as NH4+ and to reabsorb bicarbonate. The hyper-
phosphatemia is due to phosphate retention by her failing kidney.
The observed hypocalcemia could be attributable to the inability
of the impaired kidney to produce calcitriol and also because hy-
perphosphatemia causes calcium-phosphate precipitation in the
tissues. The sharp increase in creatinine and BUN is due to a rapid
decrease in renal function, leading to the accumulation of these
nitrogenous products in the blood.8
3. Most likely diagnosis: Uncontrolled hypertension due to
noncompliance and acute renal failure in the presence of chronic renal
failure versus progressive chronic renal failure.
4. Acute renal failure in the presence of chronic renal dis-
ease involves acute renal failure in the background of preexisting
chronic kidney disease. Preexisting chronic kidney disease is a
strong risk factor for the development of acute renal failure9;
however, the most frequent causes of acute renal failure in patients
with preexisting chronic renal failure are acute tubular necrosis
and prerenal failure.10 Nasr and colleagues11 had reported that
superimposed acute renal failure on chronic renal failure could be
explained by either acute interstitial nephritis (AIN) with focal
granulomatous features or renal atheroembolic disease. A biopsy
of this patient’s kidney is not available; however, the renal biopsy
of a patient with a similar disease condition showed acute tubular
necrosis, acute interstitial nephritis, atheroembolic disease, and
pauci-immune rapidly progressive glomerulonephritis (RPGN).11
The etiology of AIN in that patient was attributed to treatment
with Protonix similar to the treatment of this patient. Their con-
clusion was supported by the excellent clinical outcome following
discontinuation of pantoprazole and the institution of immuno-
suppressive therapy. Also, nonsteroidal anti-inflammatory drugs
(NSAIDs) may induce acute renal failure in patients with chronic
renal disease. Giovanni and Giovanni12 demonstrated that selec-
tive COX-2 inhibitors such as NSAIDs can be the causative agent
of acute renal failure in patients with chronic renal disease and
recommended their cautious use or complete avoidance in these
patients. The use of aspirin by this patient could also have con-
tributed to the observed development of acute renal failure in the
presence of chronic renal disease.

Table 2_Chemistry

Test Patient’s Result Reference Interval

Sodium 134 135–145 mmol/L

CO2 total 18 23–31 mmol/L
Glucose 123 70–110 mg/dL
Calcium 6.9 8.6–10.6 mg/dL
Phosphorus 10.9 2.5–5 mg/dL
C-reactive protein 28.5 0–0.8 mg/dL

Previous admission (average) Current admission

Before Withdrawal After Withdrawal

of Offending Drugs of Offending Drugs

Average (± SD) Day 1 Day 3 Day 1 Day 3 Normal Ranges

BUN 45.11 ± 4.11* 103 113 52 48 7–23 mg/dL
Creatinine 5.05 ± 0.45* 12 14.4 8.8 7.7 0.7–1.7 mg/dL
*n=7

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5. The acute renal failure in the presence of chronic renal dis-
ease in this patient is drug induced; the offending drugs, Protonix
and aspirin, were withdrawn. Pulmonary edema was also evident
in this patient, and this resolved following hemodialysis, support-
ing the supposition that the edema was partly due to renal failure.
6. The diagnostic approach should include obtaining a thor-
ough medical history and a complete physical examination. Diag-
nosis is usually based on laboratory tests of renal function, including
serum creatinine. Occasionally, renal biopsy is necessary to establish
the diagnosis, determine the prognosis, or guide therapy.13 Although
this patient had previous baseline serum creatinine levels indica-
tive of chronic renal disease, there was a sudden increase from the
baseline serum creatinine level of approximately 138% (Table 2)
that usually suggests acute renal failure. Other diagnostic approaches
reported by Madala8 include ultrasound, which usually shows
shrunken kidneys with the exception of diabetic nephropathy,
HIV-associated nephropathy, amyloidosis, and autosomal dominant
polycystic renal disease where the size of the kidney is preserved.
However, of note in this patient is the non-return of the BUN and
creatinine to the previous admission levels even after the withdrawal
of the offending drugs. This is suggestive of incomplete recovery.14
Patient Follow Up
Medications (Labetolol, Protonix, and aspirin) prior to the patient’s
admission were discontinued, and for better control of the patient’s
blood pressure she was given a prescription for hydralazine. LM
Keywords: acute renal failure, chronic renal disease, creatinine,
hemodialysis, hypertension.
labmedicine.com September 2008 j Volume 39 Number 9 j LABMEDICINE 535
Case Studies
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