Dietary chloride and urinary calcium in stone disease.

We studied six patients with renal stone disease, hypercalciuria, cystinuria and/or hyperuricosuria, during variations in dietary Na and Cl intake. Switching between equimolar NaCl and NaHCO3 intakes reduced urinary Ca (UCa) during the NaHCO3 phase, despite steady-state urinary Na. Switching between equimolar NaCl and KCl did not change UCa, despite a sharp fall in UNa. The results suggest a predominant role for Cl rather than Na ions during sodium-chloride-induced changes in UCa. In stone disease of mixed aetiology, where alkalinization of the urine as well as reduction in UCa may be desirable, treatment with NaHCO3 loading is not accompanied by a rise in UCa, provided that dietary Cl is maintained moderately low at 80-100 mmol/day. The mechanism whereby Cl intake influences UCa remains undefined. Plasma PTH and calcitriol levels showed no significant alteration, and atrial natriuretic peptide levels in one patient remained unchanged.

Reversible hypocalciuria with marginal hypercalcaemia in renal magnesium wasting.

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.

Hypercalciuria in parathyroid disorders: effect of dietary sodium control.

Moderate dietary Na restriction (80 mmol/d for 7 days) during constant Ca intake can reduce high urinary Ca excretion to normal levels in idiopathic hypercalciuria (IH). A similar protocol was used to test its effect in primary hyperparathyroidism (PHPT) and also in hypoparathyroid subjects (HOPT) during treatment with dihydrotachysterol (DHT). Nine subjects with PHPT, 10 with HOPT, and one with pseudo-HOPT were evaluated after Na-restricted (80 mmol/d) and Na-supplemented (200 mmol/d) diets for 7 days each with dietary Ca constant. Na restriction resulted in a decrease in mean urinary 24-hour Ca excretion in PHPT subjects (10.6 v 7.6 mmol/d [424 v 304 mg], P less than 0.0001) and in one pseudo-HOPT subject, similar to the pattern seen previously in IH subjects. In contrast, Na restriction was not accompanied by significant change in Ca excretion in HOPT. There was no change in serum immunoreactive PTH (iPTH) or 1,25(OH)2 vitamin D levels in either group when Na intake was altered. Thus, the presence of parathyroid hormone (PTH) is necessary for sodium-related alterations in urinary Ca to occur. The effect of PTH appears to be "permissive" rather than "active." Dietary Na restriction may have a role in the management of hypercalciuria in mild PHPT cases when parathyroidectomy is contraindicated.

Determination of ionised calcium by ion selective electrode is not independent of albumin concentration.

The relationship of ionised calcium measurement to changes in serum total protein and albumin were studied both in vivo and in vitro. During venostasis serum ionised calcium was determined in 10 control subjects using an Orion SS20 analyser. A slight but significant increase in ionised calcium occurred only after prolonged venostasis (15 min), when gross changes in total protein and albumin were seen. The effect of albumin concentration on serum ionised calcium was studied in vitro by the dialysis technique of Payne. The increase in ionised calcium in 40 sera was 0.0198 mmol/l per 10 g albumin change. We conclude that albumin-related variation in serum ionised calcium determination required such gross changes that correction is rarely necessary in clinical practice. When gross albumin alteration occurs, the appropriate correction for the analyser used should be determined and applied.

Hypovitaminosis D and response to supplementation in older patients with cystic fibrosis.

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.

Hypovitaminosis D and elevated serum alkaline phosphatase in elderly Irish people.

The vitamin D status of 181 elderly Irish community-dwelling and institutionalized subjects was studied during Winter-Spring. The mean serum 25-hydroxyvitamin D level was 10 nmol/L (95% range less than 5.0-59 nmol/L); values were below 25 nmol/L in 79 percent of subjects. A significant seasonal variation of serum 25-hydroxyvitamin D levels was noted in elderly community-dwelling subjects. The previously documented age-related increase in serum alkaline phosphatase activity was significantly less in vitamin D replete subjects than in vitamin D deplete subjects in this study (P less than 0.005). The higher serum alkaline phosphatase values found in the vitamin D deplete subjects may represent mild secondary hyperparathyroidism or osteomalacia. The relationship of vitamin D status to both dietary intake and effective sunlight (latitude) is examined.

Osteomalacia and osteoporosis: evaluation of a diagnostic index.

Data from a retrospective study in 41 patients is used to suggest an index of bone disease. This is designed as a means of collating available results, clarifying the significance of each in diagnosing either osteomalacia or osteoporosis, and reducing the significance of a single abnormal finding--for example, a raised alkaline phosphatase activity or low serum 25 hydroxy vitamin D, when the overall index score is low. Index scores above 35% would be diagnostic of osteomalacia; scores below 15% if associated with collapsed vertebrae suggest osteoporosis. Scores between 15% and 35% would indicate the need for a bone biopsy to discriminate between osteoporosis and osteomalacia.

Importance of dietary sodium in the hypercalciuria syndrome.

Daily urinary calcium excretion in renal stone-forming subjects is shown to vary directly with moderate changes in dietary sodium intake. The changes produced are sufficient to alter the basic diagnostic classification from 'hypercalciuric' to 'normocalciuric' because dietary sodium is reduced from 200 to 80 mM/day. Similar changes were observed in fasting morning 'spot' urine samples, resulting in alteration of diagnostic subclassification between so-called 'absorptive' and 'renal' categories, in the absence of demonstrable change in parathyroid function. Diagnostic and therapeutic studies in stone-forming subjects require control of both dietary calcium and dietary sodium if misinterpretations are to be avoided. Habitual high sodium intake may be an etiological factor in the generation of excessive excretion of calcium, sodium, and phosphate--the hypercalciuria syndrome.