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Altered kinetics of an intravenous calcium load in hypertensive patients
Insights
Essential hypertensive patients exhibit abnormal calcium handling, excreting more calcium and showing lower serum ionized calcium levels after an intravenous calcium load compared to controls. This suggests altered body calcium distribution, not just a renal defect.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Calcium Metabolism
Background:
- Essential hypertension (EH) is linked to increased urinary calcium excretion.
- Some studies suggest lower serum ionized calcium in EH patients.
- Calcium's role in vascular tone and blood pressure regulation is under investigation.
Purpose of the Study:
- To investigate calcium load kinetics in essential hypertensive patients.
- To compare intravenous calcium infusion responses between EH patients and normotensive controls.
- To explore potential alterations in calcium distribution and handling in EH.
Main Methods:
- Intravenous infusion of calcium (0.1 mmol Ca2+/kg/h for 2 hours) in 15 EH patients and 12 controls.
- Monitoring of serum ionized calcium and urinary calcium excretion at regular intervals.
- Extended monitoring up to 4 hours post-infusion in subgroups.
Main Results:
- EH patients showed significantly higher urinary calcium excretion rates (P < 0.001).
- Serum ionized calcium levels were significantly lower in EH patients during and after the calcium infusion (P < 0.01 at 60 and 120 min).
- The area under the curve for serum ionized calcium was significantly reduced in EH patients, indicating impaired calcium retention.
Conclusions:
- Essential hypertensive patients demonstrate abnormal handling of an intravenous calcium load.
- The observed abnormality may involve altered calcium distribution among body compartments, beyond a simple renal defect.
- These findings highlight potential dysregulation in calcium homeostasis in essential hypertension.
Abstract:
Essential hypertensive (EH) patients have a higher rate of urinary calcium excretion and, according to some reports, somewhat lower levels of serum ionized calcium. The aim of this study was to investigate the kinetics of an i.v. calcium load in EH patients and in normotensive controls. Fifteen EH patients and twelve sex-and weight-matched controls received a constant ionized rate i.v. calcium infusion (0.1 mmol Ca2+/kg body weight/h) for 2 h. Serum ionized calcium and urinary calcium excretion were determined at regular intervals during the infusion and, in two subgroups of seven hypertensives and seven controls, for up to 4 hours later. EH patients had significantly higher excretion rates (P less than (P less than 0.001) and slightly, but not significantly, lower serum ionized calcium compared to controls. The serum ionized calcium concentration attained at 60 and 120 min of the Ca2+ infusion was significantly lower in EH (P less than 0.01) and it remained appreciably lower for up to 220 min from the beginning of the test. The area under the curve of serum ionized calcium calculated at different time points was significantly reduced in the hypertensives. The mean renal calcium clearance of the patients during the infusion and the elimination phase was somewhat higher, but the difference from controls did not reach statistical significance. These data indicate an abnormal handling of a calcium load by patients with EH and raise the possibility that such abnormality may not be due simply to a renal defect but perhaps to an altered calcium distribution among different compartments in the body.