Mr. K.G. is a thin 60-year-old man admitted to the hospital for cardiac catheterization for recurrent angina. Past medical history includes hypertension, type 2 diabetes mellitus, and a previous myocardial infarction 2 years ago. Current medications are metformin (Glucophage), glipizide (Glucotrol), entericcoated aspirin (Ecotrin), and lisinopril (Zestril). Laboratory tests on admission revealed the following: normal electrolyte levels; blood urea nitrogen (BUN), 40 mg/dL; and serum creatinine, 2.0 mg/dL. A complete blood cell count and urinalysis were unremarkable. Mr. K.G. receives intravenous fluids at 20 mL/hr on the morning of the procedure. He successfully undergoes the catheterization and returns to the telemetry unit. The day after the procedure, Mr. K.G.’s urine output decreases to less than 10 mL/hr. Mr. K.G. is given a fluid bolus of normal saline without any increase in urine output. Furosemide is administered intravenously, with a slight increase in urine output to 15 mL/hr for several hours. Laboratory studies reveal the following: potassium, 5.9 mEq/L; BUN, 70 mg/dL; serum creatinine, 7.1 mg/dL, and carbon dioxide total content, 16 mEq/L. The next day Mr. K.G. has 2+ edema and basilar crackles, and he complains of feeling short of breath. A preliminary diagnosis of AKI is made.
Questions
1. What are possible factors predisposing Mr. K.G. for AKI?
2. What laboratory studies assist in the diagnosis of AKI? Describe expected results for a patient with acute tubular necrosis.
3. What medical interventions do you anticipate for Mr. K.G.?
4. What interventions could have been taken before Mr. K.G.’s cardiac catheterization to possibly prevent his AKI?
5. Discuss the advantages and disadvantages of using diuretic therapy in patients with AKI.
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