Plasma Calcium Concentration Modifies the Blood Sodium During Hemodialysis: Lessons from Hard Water Syndrome

Abstract

Abstract Introduction. Extracellular sodium (Na+) concentration is maintained within a tight physiological range due to hormonal control, that mainly modulates thirst, Na+ and water renal excretion. Extra-renal regulation of Na+ and water homeostasis is only partially understood. Recently it has been debated whether the osmotically inactive Na+ storage is fixed or variable. Methods. In the present study, fourteen End-Stage Renal Disease (ESRD) patients treated by chronic hemodialysis underwent by accident to a sharp increase in plasmatic calcium (Ca+2) levels due to the failure of the water control system, leading to the so-called hard water syndrome. The levels of plasmatic Ca+2 after 1 hr of hemodialysis were correlated with urea, Na+, potassium (K+) and creatinine levels. Eleven ESRD patients treated with hemodialysis under similar conditions were used as controls. Results. The hard water syndrome resulted in hypercalcemia, while mean plasma levels of Na+, K+ and urea were not different compared to controls. Plasma creatinine levels were slightly but significantly higher that control. A correlation analysis on the measured variables has showed a positive correlation between plasma Ca+2 and Na+ levels (Pearson=0.428, p=0.032), and the absence of any correlation with K+, creatinine and urea concentration. Conclusions. Our study suggests that acute changes in plasmatic Ca+2 levels may affect Na+ concentration in the absence of renal function; it is possible that hypercalcemia may trigger Na+ release from the osmotically inactive storage. These data further support previous observations on the interplay of sodium and calcium at extrarenal sites.