THE CAUSE OF MAINTAINED HYPERCALCIURIA AFTER THE SURGICAL CURE OF PRIMARY HYPERPARATHYROIDISM IS A DEFECT IN RENAL CALCIUM REABSORPTION

The hypercalciuria that eventually remains after the successful remova l of a solitary parathyroid adenoma may originate from excessive intes tinal calcium absorption, bone resorption or deficient renal reabsorpt ion, In order to clarify this question, ten patients surgically cured from primary hyperparathyroidism (PH Pr), ten age-matched normal subje cts and five nephrolithiasic patients with renal hypercalciuria (RH) w ere studied after five days on a low calcium diet, either during fasti ng or after oral calcium load, Fasting serum calcium, amino-terminal a nd intact PTH levels and also urinary cAMP excretion were normal in ev ery individual patient. Serum ionized calcium and inulin clearance (GF R) were used for calculations of the filtered load (FL Ca) and the fra ctional excretion of calcium (FE Ca). Six PHPx patients displayed fast ing calciuria above the upper limit calculated for control subjects, d espite having the lowest GFR and FL Ca (p<0.05 vs control). These pati ents (h-PHPx) had a small calciuric response to oral calcium load, Ser um 1,25-(OH)(2)D-3 and 250HD(3) did not correlate with calciuria, Our findings exclude intestinal hyperabsorption and excessive bone resorpt ion in h-PHPx patients, and strongly suggest a renal tubular defect in calcium reabsorption as the cause of their hypercalciuria, This defec t could be primary, as in RH, but only three hPHPx patients had recurr ent kidney stones before surgery, On the other hand, as a negative cor relation between GFR and FE Ca was only found in PHPx patients, it see ms probable that the disturbances in glomerular and tubular functions were secondary to the long standing hypercalcemic hyperparathyroidism.