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Low urinary calcium levels and hypomagnesaemia were observed in three subjects with renal tubular abnormalities. The first, with severe hypomagnesaemia due to congenital renal magnesium wasting, had mildly raised serum ionized calcium levels (1.34-1.36 mmol/l). The other two, a brother and sister, had features of Bartter's syndrome with hypokalaemia, mild hypomagnesaemia and hyperreninaemia with normal serum ionized calcium levels. Hypocalciuria was seen in 24-h urine collections and in 2-hourly timed urine collections. Magnesium loading with intramuscular MgSO4 was used to raise serum Mg to within the normal range. Tubular reabsorption of Mg (TMg) rose while TCa fell, with a rise in fractional excretion of ionized Ca and a small drop in serum ionized Ca. Serum parathyroid hormone levels rose or remained constant. This pattern is consistent with a shared Ca/Mg reabsorptive pathway with a rise in TCa when TMg is low, returning to normal when TMg is raised by Mg loading. In one subject, this imbalance was associated with marginal hypercalcaemia. The site for this pathway is likely to be the thick ascending limb of the loop of Henle.

This study reports serum 25-hydroxy vitamin D (25-(OH)D) levels, bone mineral content and bone maturation in 20 adolescent and adult patients with cystic fibrosis, and their response to the internationally recommended dose of supplementary vitamin D (800 iu/day; 20 micrograms/day). Serum 25-(OH)D values were below normal in 75 per cent of patients and serum alkaline phosphatase values, corrected for age, were increased in 60 per cent. Bone mineral content, measured by photon beam absorptiometry, was below the normal range in 45 per cent of patients and bone age retarded in 45 per cent. Following supplementation with vitamin D 40 per cent of patients failed to achieve normal serum 25-(OH)D levels. We concluded that hypovitaminosis D occurs frequently in older patients with cystic fibrosis and is accompanied by osteopenia and retarded bone maturation.

Serum ionized calcium was shown to be significantly elevated in a group of twenty-eight subjects with idiopathic hypercalciuria in whom the mean total serum calcium concentration was within normal limits. Measurement of parathyroid hormone levels confirmed that elevated values are suppressible by infusion of calcium. Ten subjects with simultaneous elevation of serum ionized calcium and parathormone levels above 3 S.D. of normal were referred for neck exploration, and a parathyroid adenoma was found and removed in nine. Significant decreases to normal values of serum ionized calcium and parathormone levels of urine and calcium excretion were documented some weeks following operation. The results conflict with both the alimentary calcium hyperabsorption theory and the renal calcium leak theory of the aetiology of idiopathic hypercalciuria, and support the possibility that idiopathic hypercalciuria in many cases represents an early or mild form of 'normocalcaemic' primary hyperparathyroidism.

A standard oral calcium loading test has been employed in a group of idiopathic hypercalciuria (IH) subjects and in a group of marginally hypercalcaemic subjects with primary hyperparathyroidism (PHPT) in whom the diagnosis was revealed by careful combined measurements of serum ionized calcium and immuno-reactive parathyroid hormone (iPTH). Initial values for serum ionized calcium and creatinine clearance were similar in IH and in a control group of normal subjects, whereas iPTH levels were normal or low. Following oral loading, serum ionized calcium rose to similar levels in both IH and control subjects, with no suggestion of relative hypercalcaemia due to a postulated intestinal hyperabsorption in the IH group. A renal tubular calcium 'leak' was however clearly evident in the IH group, in both the fasting and post-absorptive phase. In the marginally hypercalcaemic PHPT subjects on the other hand, a relative post-absorptive hypercalcaemia was clearly apparent, as well as a gross renal tubular calcium leakage. Thus careful preliminary separation of masked PHPT from IH subjects is an essential step before evaluation of response to oral calcium challenge in stone-forming subjects. When this is done, no evidence of a relative post-absorptive hypercalcaemia can be seen in the residual IH group, and hypercalciuria appears to be 'renal' rather than 'absorptive' in origin.