Calcium Urolithiasis, Blood Pressure and Salt Intake

Abstract

Objectives: To determine whether stone-formers have higher BP than controls drawn from the general population and matched for age, sex and ethnic origin and to compare the relationship between sodium and calcium excretion in the two groups. Patients and methods: Thirty-six patients [mean (AEstandard deviation, SD) = 49.0 AE 11.7 years; range 27-70 years] with kidney or ureteric stones and 108 controls (mean age of 49.6 AE 6.8 years; range 39-61 years), matched for gender, ethnic origin and age group were studied. Patients and controls underwent physical measurements, a venous blood sample and they were asked to collect a 24-h urine sample for sodium, potassium, calcium and creatinine. Results: Stoneformers were significantly heavier and had higher BP than age-, sex-and ethnic-matched population controls. Whilst the difference in systolic BP was independent of the difference in body mass index [16.8 mmHg (7.2-26.4 mmHg), p = 0.001), the difference in diastolic BP was attenuated after adjustment for body mass [1.8 (À3.4 to 7.1), p = 0.49]. Stone-formers passed less urine than controls [À438 ml/day (95% CI À852 to À25), p = 0.038]. They had higher urinary calcium than controls [3.7 mmol/day (2.8-4.6 mmol/day), p < 0.001], even when expressed as ratio to creatinine [0.20 (0.11-0.29), p < 0.001]. Sodium excretion was positively associated with urinary calcium in both stone-formers and in controls. The slopes were comparable (0.92 vs 0.98 mmol Ca/100 mmol Na) so that for any level of sodium excretion (or salt intake), stone-formers had a higher calcium excretion than controls. Conclusions: In stone-formers, the BP is higher than in controls. Stone-formers excrete more calcium than controls do. In stone-formers and controls, the relationship between urinary sodium and calcium is similar. Since this relationship results from an effect of sodium on calcium, a reduction in salt intake may be a useful method of reducing urinary calcium excretion in stone-formers. However, the "relative" hypercalciuria seen in stone-formers is independent of salt intake and may well reflect an underlying genetic predisposition.

The epithelial sodium/proton exchanger, NHE3, is necessary for renal and intestinal calcium (re)absorption

“…As a control, in parallel, cell lines stably expressing the empty vector pcDNA3.1(ϩ), were generated by the identical procedure. Paracellular 45 Ca 2ϩ flux studies of these cell lines were completed in identical fashion to those of wild-type OK cells as detailed above. For studies performed in the absence of sodium, both the apical and basolateral buffers consisted of 10 mM HEPES, pH 7.4, 140 mM KCl, 1 mM MgCl 2, 1 mM CaCl2, and 10 mM glucose.…”

“…In vivo 45 Ca 2ϩ absorption assay. Intestinal Ca 2ϩ absorption from wild-type and NHE3 Ϫ/Ϫ mice was determined by measuring serum 45 Ca 2ϩ levels at time intervals post-oral gavage of a 45 Ca 2ϩ -containing solution essentially as described previously (2).…”

“…Radioactivity of the samples was measured with a LS6500 Multi-Purpose Scintillation Counter (Beckman Coulter, Brea, CA). Ca 2ϩ flux was then calculated as the rate of 45 Ca 2ϩ appearance in the cold/basolateral side (cpm/min) divided by the specific activity of radioactivity in the hot side (cpm/mol of Ca 2ϩ ). This was then normalized to the surface area of the membrane.…”

“…The volume of buffer in the apical compartment was 250 l and in the basolateral compartment was 1,000 l. First, a 10-l sample was removed from the basolateral compartment for time 0. Next, the apical solution was replaced with an equal volume of radiation buffer that had been supplemented with 25 Ci/ml of 45 Ca 2ϩ (PerkinElmer, Boston, MA). Samples were then collected from the basolateral compartment 4, 6, 8, and 10 min later.…”

Protective effect of magnesium lactate gluconate and Garcinia cambogia fruit extract in experimentally induced renal calculi in rats

“…Therefore, metabolic acidosis induced hypercalciuria and hypocitraturia hastens nucleation and aggregation of CaOx crystals, potentiating the risk of calcium stone formation [29,30]. With respect to phosphate, it has been reported that increased urinary phosphate excretion couple with hyperoxaluria favors CaOx stone formation as CaP crystals act as nuclei for subsequent deposition of CaOx crystals [31].…”