Strict volume control normalizes hypertension in peritoneal dialysis patients

The aim of this study is to investigate whether normal blood pressure (BP) can be achieved in patients with hypertension on continuous ambulatory peritoneal dialysis (CAPD) therapy by strict volume control without the use of antihypertensive drugs. Of the 78 patients in our center, 47 persons had hypertension and/or were on antihypertensive drug therapy. After discontinuing these drugs, a strong dietary salt restriction was imposed by repeatedly explaining the need for it to patients and families. If this approach did not result in sufficient BP decrease, ultrafiltration (UF) was added by increased use of hypertonic (3.86% glucose) peritoneal dialysis solution. Cardiothoracic index (CTI) on the chest radiograph was also used as a measure of volume control. With salt restriction alone or combined with UF, body weight decreased by a mean of 2.8 +/- 0.5 kg, and BP decreased from a mean of 158.2 +/- 17.0/95.7 +/- 10.3 to 119.7 +/- 16.0/77.9 +/- 9.7 mm Hg in 37 patients, accompanied by a decrease in CTI from 48.0% +/- 5.6% to 42.9% +/- 4.5%. In 19 patients who had residual renal function, 24-hour urine volume decreased to 28% of the pretreatment volume, accompanied by a mean decrease in Kt/V urea from 2.06 +/- 0.5 to 1.85 +/- 0.4. In 7 of the remaining patients who did not respond to the applied treatment, BP decreased from 158.8 +/- 23.2/111.6 +/- 9.8 to 113.5 +/- 14.3/76.4 +/- 6.2 mm Hg after administration of an angiotensin-converting enzyme (ACE) inhibitor. Their CTI was 41.2% +/- 1.3%, indicating the absence of hypervolemia, in 3 patients, the desired results could not be reached because of noncompliance. Our findings show that normal BP can be achieved by severe salt restriction combined with increased UF in the majority of CAPD patients. This is accompanied by a decrease in CTI from upper limits into the normal range, but also by a decrease in residual renal function and Kt/V index. In most of the remaining patients, normal BP can be reached by the use of ACE inhibitors. (C) 2001 by the National Kidney Foundation, Inc.