DUTCH ELDERLY CARE PHYSICIAN: A NEW GENERATION OF NURSING HOME PHYSICIAN SPECIALISTS

transaminase of 256 U/L (normal range 7–40 U/L), albumin of 3.6 g/dL (normal range 3.5–5.5 g/dL), international normalized ratio of 1.0 (normal range 0.8–1.2), carbohydrate antigen 19–9 of 438,075 U/mL (normal rangeo40 U/mL), and carcinoembryonic antigen of greater than 200 ng/mL (normal rangeo5.0 ng/mL). Her renal function was normal, with serum creatinine of 0.8 mg/dL (normal range 0.6–1.2 mg/dL), blood urea nitrogen of 20 mg/dL (normal range 7–18 mg/dL), and a calculated creatinine clearance of greater than 60 mL/min per 1.73 m (normal range). An ultrasound of her abdomen and kidneys was unremarkable. A noncontrast computed tomography scan and noncontrast magnetic resonance imaging showed a soft tissue mass in the porta hepatis associated with intrahepatic biliary dilatation. Over the next 7 days, her total bilirubin continued to rise as high as 15. An endoscopic retrograde cholangiopancreatography was attempted, but the procedure had to be aborted because of a stricture of the biliary duct secondary to the soft tissue mass. A percutaneous transhepatic biliary stent was placed, and the patient underwent a cholangiogram to confirm the location of the biliary stent. Approximately 24 hours after the procedure, the patient developed dyspnea with bibasilar crackles on examination. Her serum creatinine had increased from 0.8 to 3.1 mg/dL, and continued to rise to as high as 3.4 mg/dL, with a calculated creatinine clearance of less than 20 mL/ min per 1.73 m. Her blood urea nitrogen rose from 20 to 55 mg/dL, and her urine output dropped to 20 to 30 mL/h. A thorough chart review confirmed that no intravenous contrast was used during any of the procedures and that she had not received any nephrotoxic drugs. A renal and bladder ultrasound showed normal kidney architecture and minimal postvoid residual urine of 50 mL (normal range 50–100 mL). Urine analysis showed more than 15 granular casts, urine sodium of 96 mEq/L (normal rangeo40 mEq/ L), and a fractional excretion of sodium greater than 3% (normal range 1–3%). Stains for eosinophils were negative, and cultures showed no growth after 48 hours. This confirmed the diagnosis of acute tubular necrosis after the use of contrast in the biliary tree. This case demonstrates an example of acute tubular necrosis causing acute renal failure in patients undergoing a cholangiographic study. We could find only one retrospective study, published close to 25 years ago, that reported this phenomenon. Of the 72 patients with a mean age of 63, three (aged 70, 75, and 61) had a rise in serum creatinine of greater than 2 mg/dL within 24 hours of the procedure. Two of these patients had retention of contrast medium in the kidney demonstrated on abdominal roentgenogram. The patient’s renal failure was unprovoked by any other etiology. We hypothesize that the mechanism by which a cholangiogram can cause acute renal failure involves contrast entering the vascular system during the procedure. This might be due to direct entry secondary to local trauma or systemic absorption in the biliary circulation. Geriatricians and other physicians and health professionals who care for elderly patients should be aware of the risk of renal failure after cholangiography. Although this appears to be an infrequent phenomenon, it has the potential to acute volume overload, as it did in this patient, as well as permanent renal dysfunction.