The causes of hypocalcaemia in chronic renal failure.

1. Serum calcium and phosphate, calcium absorption and calcium excretion were measured in twenty-seven cases of chronic renal failure. 2. Hypocalcaemia was present in thirteen cases and tended to be more severe in patients with the most severe degree of renal failure. 3. The hypocalcaemia could not be attributed to hyperphosphataemia since many of the patients with hypocalcaemia had normal serum phosphate concentrations. 4. Malabsorption of calcium was observed in all but three patients, and was significantly related to the degree of renal failure, but there was only a weak correlation between absorption and the serum calcium concentration. The 24 h calcium excretion was not significantly related to creatinine clearance or to calcium absorption. 5. The relation between serum calcium concentration and fasting urine calcium excretion, expressed in mg per 100 ml of glomerular filtrate, was grossly abnormal. Instead of the positive correlation previously established in normal subjects, plasma calcium and urine calcium expressed in this way were inversely related, signifying a severe reduction in the tubular reabsorption of calcium. 6. Calcium and sodium excretion (each expressed in units per 100 ml of glomerular filtrate) were significantly related, but calcium excretion and serum bicarbonate were not. However, examination of the urine calcium/sodium relationship at urine sodium excretion rates below 1.5 mEq per 100 ml of glomerular filtrate indicated that, within this range, urine calcium excretion was inversely related to serum bicarbonate concentration and positively related to urine sodium excretion. 7. We conclude that there is reduced tubular reabsorption of calcium in renal failure, and this is attributable both to metabolic acidosis and to the increased rate of sodium excretion per nephron, and that it could be a significant contributory factor in the hypocalcaemia which may be observed in renal failure without hyperphosphataemia.