Severe reactions to Cuprophan capillary dialyzers.

Five severe reactions occurred in four maintenance hemodialysis patients 1 to 5 minutes after initiating dialysis with Cuprophan capillary dialyzers. All reactions were life-threatening and one resulted in death. Inadequate rinsing of the dialyzers was probably the cause of the reactions. The severe reactions were managed by immediate discontinuation of dialysis and the institution of supportive treatment. Antianaphylactic measures were also attempted, but their therapeutic effectiveness remains to be determined.

Extreme hyperglycemia in dialysis patients.

In 12 diabetic patients who were being treated with maintenance hemodialysis or maintenance peritoneal dialysis, coma and other neurologic deficits did not occur in spite of extremely elevated serum glucose levels. The mean serum values of these patients were: glucose 1,174 +/- 248 (SD) mg/100 ml, sodium 125 +/- 5 mEq/l, calculated total osmolality 342 +/- 13 mOsm/kg water and calculated effective osmolality (without urea) 316 +/- 13 mOsm/kg water. It is suggested that the absence of osmotic diuresis and the lack of substantial osmotic ultrafiltration prevented the development of hypernatremia and marked hyperosmolality. The osmolar effect of glucose alone at these serum concentrations apparently was not sufficient to induce neurologic impairment.

Treatment of refractory hemodialysis ascites with maintenance peritoneal dialysis.

In 5 patients who were receiving maintenance hemodialysis, ascites developed that was refractory to treatment by ultrafiltration during hemodialysis. Use of sequential isolated ultrafiltration and hemodialysis therapy either precipitated side effects or else required prolongation of total treatment time which the patients declined to accept. In 4 of the patients, ascites was believed to be primarily responsible for severe, progressive cachexia. Maintenance peritoneal dialysis was instituted in all patients, and abdominal fluid was removed gradually, over a period of 2 to 3 days. Ascites resolved promptly in each case. Three patients noted a dramatic improvement in appetite after relief of abdominal distension. Follow-up periods ranged from 6 to 4 1/2 years. Our results suggest that maintenance peritoneal dialysis can successfully control hemodialysis ascites.

Hydrostatic ultrafiltration during hemodialysis using decreasing sodium dialysate.

Twelve patients underwent hemodialysis using dialysate containing 130 mEq/L sodium, and, on a separate occasion, dialysis using a dialysate of constantly decreasing sodium concentration (from 150 to 133 mEq/L). Hydrostatic ultra-filtration during dialysis was performed at a constant rate (900 ml/hr) during both treatments, and was continued until a substantial drop in mean arterial pressure (-15%) or symptoms were observed. A double-blind comparison of the two treatment modalities was thus achieved. At the end of ultrafiltration, significantly more fluid had been removed using decreasing sodium dialysate (2.9 +/- 0.3 kg) than when using the low-sodium dialysate (1.9 +/- 0.2 kg, P<0.001). Plasma sodium concentration at the end of ultrafiltration using decreasing sodium dialysate was not significantly different from the predialysis level. Hydrostatic ultrafiltration using a dialysate of decreasing sodium level may prove to be a useful means of removing excess fluid asymptomatically from dialysis patients.

Treatment of metabolic alkalosis with hemofiltration in patients with renal insufficiency.

Hemofiltration using the postdilution technique and a modified saline solution as the replacement fluid succeeded in treating the metabolic alkalosis of two patients with renal failure.