Fasting and Post-Calcium Load Serum Calcium, Parathyroid Hormone, Calcitonin, in Male Idiopathic Calcium Urolithiasis - Evidence for a Basic Disturbance in Calcium Metabolism

Abstract

In male healthy controls (n = 12), male renal calcium stone patients with either normocalciuria (NC; n = 12) or idiopathic hypercalciuria (I-HC; n = 12), all ideally matched for age and body weight, the response of variables of mineral metabolism to a calcium-rich oral test meal was evaluated. In all groups the postprandial urinary cyclic AMP is decreased as compared with fasting urine, indicating that the parathyroid glands are suppressible by oral calcium. However, in I-HC serum total calcium was significantly higher than in controls both basally and in the postprandial period; the associated mid-regional (bioinactive) serum parathyroid hormone was also elevated, but serum parathyroid hormone recognizing the amino terminal (bioactive) region of the molecule was significantly decreased. Also in I-HC, serum alkaline phosphatase is elevated, whereas urinary hydroxyproline in both fasting and postprandial urine is unchanged. The NC group holds an intermediate position between I-HC and controls. It can be concluded that I-HC subjects may suffer from a more basic disturbance of calcium metabolism which may help explain the nature of their hypercalciuria.

Evidence that postprandial reduction of renal calcium reabsorption mediates hypercalciuria of patients with calcium nephrolithiasis

“…Differences in filtered load of calcium between IHSF and N and between fasting and fed conditions do not account for the observed changes in urine calcium excretion. Others, using single semisynthetic meal preparations with a large added calcium load (27), found prompt urine calcium increases with modest changes in blood calcium, compatible with our findings. Oral calcium loads without foods and large amounts of high-calcium foods (15,17,27,28) produce only modest increases in blood calcium, but in none of these studies was tubule reabsorption measured.…”

“…Others, using single semisynthetic meal preparations with a large added calcium load (27), found prompt urine calcium increases with modest changes in blood calcium, compatible with our findings. Oral calcium loads without foods and large amounts of high-calcium foods (15,17,27,28) produce only modest increases in blood calcium, but in none of these studies was tubule reabsorption measured. In two studies of fasting IHSF and normal controls, tubule reabsorption of IH patients was slightly lower, as we found here (11,23).…”

“…Fasting calcium reabsorption in IH patients is slightly below that in normal subjects (11,23), suggesting a component of reduced tubule reabsorption. Blood calcium levels rise slightly in IH and normal subjects after oral calcium loads (27), suggesting that a component of increased filtered load may be present.…”

New Insights Into the Pathogenesis of Idiopathic Hypercalciuria

“…Studies have shown that patients with IH have an increased fasting fractional excretion of calcium, and many have fasting hypercalciuria, suggesting a role for decreased tubule calcium reabsorption [26]. Alternatively, the increased absorption of calcium with meals in IH could lead to a post-absorptive rise in blood calcium that increases the filtered load; this has been seen in studies using single high calcium foods or calcium alone [27]. Speculatively, PTH could be suppressed as well, which would decrease tubule calcium reabsorption.…”