The Effect of Prostaglandin Inhibition on the Clinical Course of Chronic Hemodialysis

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Abstract
We studied the hypothesis that dialysis hypotension may be triggered by dialysis-induced release of prostaglandin/prostacyclin. Indomethacin (50 mg 5 .times. in 30 h) was given before dialysis to 10 stable, chronic hemodialysis patients, comparing it to placebo in a double-blind, crossover manner. Mean arterial blood pressure (MAP) before dialysis was 106.6 .+-. 17.7 and 99.7 .+-. 10.4 (SD) mm Hg for indomethacin and placebo, respectively. MAP after dialysis was 95.4 .+-. 13.9 and 85.2 .+-. 11.0 mm Hg for indomethacin and placebo, respectively. Ultrafiltration, expressed as a weight loss, was 1.82 .+-. 1.1 kg for indomethacin and 1.38 .+-. 1.29 kg for placebo dialysis. The amount of saline given during dialysis was 339 .+-. 139 ml for indomethacin and 388 .+-. 83 ml for placebo. Although indomethacin treatment resulted in more ultrafiltrate, less saline infusion, and higher MAP before and after dialysis, none of these differences were statistically significant. This preliminary trial indicates that prostaglandin/prostacyclin inhibition by indomethacin does not alter the clinical course of hemodialysis of chronic stable patients.