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Bicarbonate dialysate is claimed to be superior to acetate for both chronic and acute hemodialysis. We compared acetate and bicarbonate dialysates in 30 acute renal failure patients during 120 dialyses. 4 patients were diabetic and 2 had liver failure. Patients were dialyzed alternating acetate and bicarbonate dialysate in a double-blind cross-over manner; each patient was his own control. BUN, creatinine, Na+, K+, osmolality, Δ osmolality, % ultra-filtration, arterial blood gases, pre, post and lowest dialysis mean arterial blood pressure, dialysis with hypotensive episodes and symptoms of hypotension were recorded. The measurements obtained for each patient during dialyses with acetate and bicarbonate were compared. There was no difference in predialysis chemistries, osmolality or osmolality fall, no change in mean arterial blood pressure or hypotensive episodes and symptoms and ultrafiltration. PCO₂ and pH were slightly lower for the acetate group at the 2nd h but not at the end of dialysis. 4 patients had serum acetate determinations, all metabolized acetate normally. These findings contradict recent suggestions that severely ill patients should not be dialyzed against acetate. Since acetate is technically much easier to use and has no clinical drawbacks, it does not need to be replaced with bicarbonate in acute patients. Other factors must be more important than acetate in generating hypotension during acute dialysis.

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We studied the hypothesis that dialysis hypotension may be triggered by dialysis-induced release of prostaglandin/prostacyclin. Indomethacin (50 mg 5 × 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.

No abstract