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Effects of acetylsalicylic acid on renal function in patients with chronic heart failure

Article Abstract:

Congestive heart failure is the inability of the heart to pump blood, leading to accumulation of fluid in the lungs. It is characterized by decreased blood volume and reduced blood flow within the kidneys. Consequently, circulation within the kidney is regulated more by other nervous or hormonal systems and factors, including prostaglandins (which cause blood vessel dilation) and the renin system (which leads to blood vessel constriction). One study showed that patients with congestive heart failure had increased levels of prostaglandins and elevated renin activity. The drug indomethacin interferes with prostaglandin production, and has adverse effects on the kidney and heart in patients with congestive heart failure. Prostaglandins have been shown to be important in maintaining kidney function in heart failure. Acetylsalicylic acid (aspirin) also interferes with prostaglandin synthesis and may have adverse effects on kidney function in patients with congestive heart failure. The effects of aspirin on the kidney function of 40 patients with congestive heart failure with and without increased activity of the renin system were assessed. The patients were divided into four groups and were given (1) a low-sodium diet; (2) a low-sodium diet and aspirin; (3) a normal diet; and (4) a normal diet and aspirin. The low sodium diet increased blood levels of renin and aldosterone and the kidney excretion of prostaglandin E2 and potassium, but decreased kidney sodium excretion. Depletion of sodium was associated with a decreased glomerular filtration rate, or speed at which blood is filtered through the kidney. Aspirin decreased elevated prostaglandin E2 excretion, but had no effect on sodium excretion in patients placed on a low-sodium diet. Aspirin decreased kidney sodium excretion by 29 percent in patients with a normal sodium intake. These findings show the adverse effects of sodium depletion on kidney function in congestive heart failure patients. In addition, doses of aspirin that decrease prostaglandin synthesis reduce kidney sodium excretion. (Consumer Summary produced by Reliance Medical Information, Inc.)

Author: Riegger, Gunter A.J., Kahles, Heinz W., Elsner, Dietmar, Kromer, Eckhard P., Kochsiek, Kurt
Publisher: Elsevier B.V.
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
Physiological aspects, Congestive heart failure, Aspirin, Renal manifestations of general diseases, Renal manifestations

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Procainamide-induced pleural fibrosis

Article Abstract:

Systemic lupus erythematosus (SLE) is an autoimmune disease which commonly features antinuclear antibodies (ANAs), antibodies inappropriately produced against structures in the cell nucleus. In an SLE-like syndrome, drug-induced lupus erythematosus (DIL), involvement of the pleura (membrane surrounding the lungs) and lungs is common and can include pleurisy (pleural inflammation), pleural effusion (escape of fluid into the pleural cavity), and pulmonary infiltrates (infiltration of lung by cells from blood). Significant pleural thickening usually is accompanied by effusion. Procainamide, a drug used in treatment of heart arrhythmias, is well recognized to cause DIL, and up to half of patients who take this drug over six months may develop the disorder. Almost all patients develop joint pain, and half have lung or systemic effects. An unusual case is described of a 65-year-old man who had a complex heart arrhythmia that had been treated for five years with five drugs, including procainamide, for five years. He was hospitalized after having joint pain and increasing pleurisy-like chest pain over a three-week period. ANAs were present in blood. Pleural effusion was not present. Lung function was reduced, and biopsy and computed tomography showed fibrous changes and thickening of the pleura. The patient was medicated for pain, and another drug was substituted for procainamide. After one year, restrictive lung problems had resolved, and the pleura was no longer thickened. The case is unusual in that pleural fibrosis was present without effusion, showing a different manifestation of procainamide-induced DIL. (Consumer Summary produced by Reliance Medical Information, Inc.)

Author: Sheikh, Shabbir, Seggev, Joram S.
Publisher: Elsevier B.V.
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
Case studies, Pleural diseases, Procainamide

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Subjects list: Complications and side effects
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