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.