A study of the prevalence of significant increases in serum creatinine following angiotension-converting enzyme inhibitor administration.

Angiontension-converting enzyme inhibitors (ACEIs) are beneficial in the treatment of diabetic and nondiabetic kidney disease, coronary artery disease and congestive heart failure. One adverse effect of ACEIs use is a rise in serum creatinine and potential renal failure. This paper attempts to quantify this risk and assess the need for pre- and post-ACEI serum creatinine measurements. A computerized search of Kaiser Permanente Northwest's electronic medical record was conducted to find patients over the age of 40 years taking lisinopril between July 1, 2000 and June 30, 2002. Patient demographic information and presence in diabetes and coronary artery disease registries was collected. A subsequent search for pre- and postlisinopril serum creatinine levels within 6 months of initial lisinopril prescription was conducted. Patients with prelisinopril creatinine < or = 1.2 mg/dl and postlisinopril creatinine > 2.5 mg/dl underwent chart review to discern adverse events associated with the rise in serum creatinine. A total of 18,977 patients were prescribed lisinopril between July 1, 2000 and June 30, 2002. In all 13 166 patients had a pre- and postlisinopril creatinine checked. In all, 31 patients had a rise in creatinine from < or = 1.2 mg/dl to > 2.5 mg/dl (0.2%). Possible contributors to rise in creatinine included congestive heart failure, dehydration and infection. No patients developed end-stage renal disease, although three died. In conclusion, end-stage renal disease is an unlikely outcome among patients prescribed lisinopril and is most likely associated with other events.

Treatment of diabetes insipidus with DDAVP.

The treatment of a patient with diabetes insipidus (DI) is described, and the general treatment of the syndrome is reviewed. The patient was a 16-year-old male who had experienced pain, inflammation and tenderness in the left gluteal region owing to an abcess at the site of intramuscular injection of vasopressin tannate in oil (VTO). (He had been diagnosed as having DI at age 8. Since then, he had been maintained on VTO, lypressin and posterior pituitary snuff.) After the abscess healed during hospital treatment, VTO was stopped and the patient's urinary output increased sharply; urine specific gravity and osmolarity decreased correspondingly. Three days after stopping VTO, the investigational drug, 1-deamino-8-D-arginine vasopressin (DDAVP), was begun at 10 microgram every 12 hours. The dose was eventually increased to 20 microgram every 12 hours, and the patient was discharged on this regimen which controlled his urine output, specific gravity and osmolarity. Other treatments reviewed include antidiuretic-hormone-replacement agents (vasopressin, lypressin) and drugs used to potentiate low ADH levels (chlorpropamide, clofibrate and carbamazepine).