Renal actions of endothelin

An 83-year-old male was evaluated by the Renal Service because of an increase in serum creatinine from 1.7 mg/dl to 3.5 mg/dl over a 48-hour period after cardiac catheterization. He had hypertension for more than 30 years and non-insulin-dependent diabetes mellitus for approximately 25 years. One year ago, he sustained an inferior wall myocardial infarction and subsequently underwent two percutaneous transluminal coronary angioplasty procedures. Since that time he had been free of chest pain and had had minimal evidence of congestive cardiac failure. The current admission was prompted by progressive shortness of breath over several days; on presentation to the emergency room he was found to have atrial fibrillation and severe pulmonary edema. He was intubated and admitted to the coronary care unit. A non-Q-wave myocardial infarction was diagnosed and, after a prolonged course marked by recurrent episodes of supraventricular tachyarrythmias, he became hemodynamically stable. Blood urea nitrogen and creatinine were 24 mg/dl and 1.9 mg/dl, respectively, at the time of admission and 23 mg/dl and 1.7 mg/dl, respectively, when he was discharged from the coronary care unit. Cardiac catheterization was performed to evaluate his coronary circulation; normal saline was administered intravenously prior to the procedure (50 mllhr) and mannitol, 25 g, was administered intravenously immediately after the procedure. Intravenous normal saline was continued at a rate of 100 mI/hr for 8 hours post catheterization but, despite positive fluid balance, the serum creatinine increased to 2.3 mg/dl. Over the subsequent 24 hours, his urine output decreased to 900 ml124 hr and the serum creatinine increased further to 3.5 mg/dl. His blood pressure remained normal, and he had no signs of hemodynamic instability over the 48-hr post-catheterization period. Medications included digoxin, a beta-blocker, subcutaneous heparin, and enteric-coated aspirin; no known nephrotoxic agents had been administered, other than the contrast agent (50 ml Omnipaque, a low osmolar agent) used during the cardiac catheterization procedure. On physical examination, the patient was alert, cooperative, and in no obvious distress. His blood pressure was 140/80mm Hg in the supine position; the pulse rate was 90 beats/mm and regular; and he was afebrile. Cardiac examination disclosed an S4 gallop with no murmurs, and his lungs were clear to auscultation. Abdominal examination was unremarkable and peripheral edema was absent. Laboratory studies revealed: serum sodium, 133 mEq/liter; potassium, 4.2 mEq/liter; chloride, 101 mEq/Iiter; total carbon dioxide, 26 mM/liter; blood urea nitrogen, 37 mg/dl; serum creatinine, 3.5 mg/dl; calcium, 8.0 mg/dl; phosphorus, 4.4 mg/dl; and albumin, 2.6 g/dl. The hemoglobin was 10.9 g/dl; hematocrit, 32.7%; white blood cell count, 8300 mm3; and platelet count, 315,000 mm3. Urinalysis revealed: pH, 5.0; protein, 30 mg/dl; occasional red blood cells/high-power field, and occasional granular casts. Over the subsequent 72 hours, his fluid intake was adjusted to match his urine output. The serum creatinine increased to 4.2 mg/dl, and his urine output gradually increased to 1400 ml/24 hr without additional therapy. The following day he experienced another acute myocardial infarction, became markedly hypotensive, and required intubation. Intravenous furosemide, 40 mg/hr over 10 hrs, was given on each of 5 successive days; the urine output increased to 2000 ml/24 hr. The serum creatinine peaked at 5.6 mg/dl but fell during the following week to the admission value of 1.7 mg/dl. He subsequently underwent successful triple-vessel coronary bypass surgery without additional renal insult. He was discharged home 12 days postoperatively with stable renal function.