The patient has significant symptoms during recurrent epi-sodes of atrial fibrillation. She has multiple risk factors for thromboembolism (age, female gender, and hypertension). Therefore, she is a candidate for lifelong anticoagulation. Warfarin was the standard drug. The factor Xa (eg, apixa-ban, rivaroxiban) and the direct thrombin (eg, dabigatran) inhibitors are newer classes of anticoagulants that offer more patient-acceptable alternatives but at a higher cost. The peak heart rate in this patient’s atrial fibrillation is not particularly high. Maintenance of sinus rhythm appears to be important in this patient. The echocardiogram demon-strates impairment of left ventricular function. Selection of a drug that is tolerated in heart failure and has documented ability to convert or prevent atrial fibrillation, eg, dofetilide or amiodarone, would be appropriate. The use of catheter ablation for treatment of the initial episode of atrial fibril-lation is not the standard of care but is undergoing clinical trials.
Ramin Sam, MD, Harlan E. Ives, MD, PhD, & David Pearce, MD
A 65-year-old man has a history of diabetes and chronic kidney disease with baseline creatinine of 2.2 mg/dL. Despite five different antihypertensive drugs, his clinic blood pres-sure is 176/92 mm Hg; he has mild dyspnea on exertion and 2–3+ edema on exam. He has been taking furosemide 80 mg twice a day for 1 year now. At the clinic visit, hydrochlorothi-azide 25 mg daily is added for better blood pressure control and also to treat symptoms and signs of fluid overload. Two weeks later, the patient presents to the emergency depart-ment with symptoms of weakness, anorexia, and generalized malaise. His blood pressure is now 91/58 mm Hg, and he has lost 15 kg in 2 weeks. His laboratory tests are signifi-cant for a serum creatinine of 10.8 mg/dL. What has led to the acute kidney injury? What is the reason for the weight loss? What precautions could have been taken to avoid this hospitalization?
Abnormalities in fluid volume and electrolyte composition are common and important clinical disorders. Drugs that block specific transport functions of the renal tubules are valuable clinical tools in the treatment of these disorders. Although various agents that increase urine volume (diuretics) have been described since antiquity, it was not until 1937 that carbonic anhydrase inhibitors were first described and not until 1957 that a much more useful and powerful diuretic agent (chlorothiazide) became available.
Technically, a “diuretic” is an agent that increases urine volume, whereas a “natriuretic” causes an increase in renal sodium excretion and an “aquaretic” increases excretion of solute-free water. Because natriuretics almost always also increase water excretion, they are usually called diuretics. Osmotic diuretics and antidiuretic hormone antagonists (see Agents That Alter Water Excretion) are aquaretics and are not directly natriuretic. Most recently, an entirely new class of agents has been developed that block urea transport. These agents result in increased urine output and increased urea excretion but not increased excretion of electrolytes. Even though they are technically aquaretics, they have also been referred to as urearetics. These agents are not yet available for therapy but are in early investigational stages.