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

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

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


Possible Answers tion. This condition has also been reported in nondialyzed patients
1. Headache, uncontrolled hypertension, diabetes (DM1), with advanced chronic renal failure and in patients with end-stage
impaired renal function (stage V chronic kidney disease), visual renal disease undergoing maintenance hemodialysis.1 The possible
blurring, intermittent chest pressure, nonexertional, associated causes of protein-energy malnutrition in patients with chronic
shortness of breath, and epigastric abdominal pain associated with renal failure include the following: reduced energy or protein in-
some nausea but no vomiting. In addition, there is evidence of take; concurrent chronic illnesses with superimposed acute illnesses
anemia as demonstrated by the decrease in red blood cells, hemo- and increased inflammatory cytokines; catabolic stimulus due to
globin level, and hematocrit (Table 1). Serum glucose was slightly hemodialysis; loss of nutrients into the dialysate; and diagnostic or
elevated while the serum phosphorus was dramatically increased therapeutic procedures that reduce nutrient intake or engender net
and calcium was significantly decreased due to the low albumin protein breakdown.1,2 Although we do not know the concentra-
level in the patient (2.6 mg/dL). The corrected calcium (8.0 mg/ tion of cytokines in this patient, she did have an elevated serum
dL) is consistent with the low but not critical ionized calcium level C-reactive protein concentration and hypoalbuminemia similar
(4.3 mg/dL). The patient’s edema is probably due to a combina- to that seen in other chronically ill patients.3 Although the pul-
tion of renal failure and low albumin. The low albumin in renal 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. Table 3_Urinalysis
The blood glucose concentration of 123 mg/dL may be due to the
hemodialysis (the specimen was collected after hemodialysis) and Test Patient’s Result Reference Interval
the variety of insulin administered to the patient. Hemodialysis has
Protein 300 mg/dL negative
been reported4 to decrease red blood cell (RBC) life span, which Glucose 70 mg/dL negative
may have affected the value obtained for hemoglobin A1c in this Blood 3+ negative
patient. Fructosamine determination may be more useful under Red blood cells >182 0–3
such conditions. Sodium and total CO2 were both lower than nor- White blood cells 7 0–5
Bacteria few negative
mal. Acute renal failure in the presence of chronic renal disease is Epithelial cells 7 0–2
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

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

534 LABMEDICINE j Volume 39 Number 9 j September 2008 labmedicine.com


Case Studies

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ease in this patient is drug induced; the offending drugs, Protonix J Nutr. 1999;129:S247–251.
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serum creatinine. Occasionally, renal biopsy is necessary to establish
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this patient had previous baseline serum creatinine levels indica- Little Brown; 1997: 1333–1365.
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baseline serum creatinine level of approximately 138% (Table 2) pathogenesis to treatment. Hepatology. 1998;28:851–864.
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2007;25:395–398.
HIV-associated nephropathy, amyloidosis, and autosomal dominant
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Keywords: acute renal failure, chronic renal disease, creatinine,
2006;11:381–385.
hemodialysis, hypertension.

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