Acute decreases in serum potassium augment blood pressure

Abstract

Potassium depletion is a risk factor for cardiovascular diseases, including hypertension, and frequently is encountered in patients with end-stage renal disease. Since the treatment of end-stage renal disease might result in K + depletion and postdialysis hypokalemia, we investigated the relationship between acute K + removal by hemodialysis and changes in blood pressure at the completion of treatment compared with predialysis and 1-hour postdialysis blood pressure. The effects of three different dialysate potassium concentrations ([K −] d; 1.0, 2.0, and 3.0 mmol/L) were investigated in 11 patients. Hemodialysis-induced K + removal, serum [K +], total body K +, and blood pressure were measured. The use of 1.0, 2.0, or 3.0 mmol/L [K +] d resulted in the removal of 77.0 ± 6.5, 54.5 ± 7.9, and 42.5 ± 9.9 mmol of K + per treatment, respectively ( P < 0.05, [K +] d 1.0 v [K +] d 3.0). Predialysis and postdialysis serum [K +] were 4.9 ± 0.2 and 3.6 ± 0.1 mEq/L for 1.0 mmol/L [K +] d, 5.1 ± 0.3 and 3.9 ± 0.1 mEq/L for 2.0 mmol/L [K +] d, and 5.3 ± 0.3 and 4.2 ± 0.2 mEq/L for 3.0 mmol/L [K +] d, respectively ( P < 0.001 for each [K +] d). The baseline total body K + corrected for gender, age, and race was 92% of predicted normal level and did not change significantly with the use of different [K +] d. Blood pressure decreased during hemodialysis as excess fluid was removed, regardless of [K +] d. Significant increases in blood pressure did occur 1 hour postdialysis compared with levels measured at the completion of treatment (“rebound hypertension”) when hemodialysis was performed with 1.0 and 2.0 mmol/L, but not with 3.0 mmol/L [K +] d. Mean blood pressure increased from 93.4 ± 4.6 mm Hg and 92.3 ± 3.1 mm Hg for 1.0 and 2.0 mmol/L [K +] d to 106.9 ± 5.7 mm Hg ( P < 0.05) and 102.1 ± 4.6 mm Hg ( P < 0.05), respectively. In contrast, mean blood pressure was 94.6 ± 5.0 mm Hg and 94.3 ± 7.4 mm Hg at completion and 1 hour postdialysis with 3.0 mmol/L [K +] d. The results of this study demonstrate that an acute decrease in serum potassium due to hemodialysis produces “rebound hypertension” that is likely mediated, at least in part, by constriction of arterioles in the systemic circulation.