The Hypercalciurias CAUSES, PARATHYROID FUNCTIONS, AND DIAGNOSTIC CRITERIA

Abstract

A B S T R A C T The causes for the hypercalciuria and diagnostic criteria for the various forms of hypercalciuria were sought in 56 patients with hypercalcemia or nephrolithiasis (Ca stones), by a careful assessment of parathyroid function and calcium metabolism. A study protocol for the evaluation of hypercalciuria, based on a constant liquid synthetic diet, was developed. In 26 cases of primary hyperparathyroidism, characteristic features were: hypercalcemia, high urinary cyclic AMP (cAMP, 8.58+3.63 SD gmol/g creatinine; normal, 4.02±0.70 umol/g creatinine), high immunoreactive serum parathyroid hormone (PTH), hypercalciuria, the urinary Ca exceeding absorbed Ca from intestinal tract (CaA), high fasting urinary Ca (0.2 mg/mg creatinine or greater), and low bone density by 'I photon absorption. The results suggest that hypercalciuria is partly secondary to an excessive skeletal resorption (resorptive hypercalciuria). The 22 cases with renal stones had normocalcemia, hypercalciuria, intestinal hyperabsorption of calcium, normal or low serum PTH and urinary cAMP, normal fasting urinary Ca, and normal bone density. Since their CaA exceeded urinary Ca, the hypercalciuria probably resulted from an intestinal hyperabsorption of Ca (absorptive hypercalciuria). The primacy of intestinal Ca hyperabsorption was confirmed by responses to Ca load and deprivation under a metabolic dietary regimen. During a Ca load of 1,700 mg/day, there was an exaggerated increase in the renal excretion.of Ca and a suppression of cAMP excretion. The urinary Ca of 453±+154 SD mg/day was significantly higher than the control group's 211+42 mg/ day. The urinary cAMP of 2.26±0.56 umol/g creatinine was significantly lower than in the control group. In contrast, when the intestinal absorption of calcium was limited by cellulose phosphate, the hvpercalciuria was kc'ceiz(l for plblicatifn 9 July 1073 and in rezxsed form 11 September 1973. corrected and the suppressed renal excretion of cAMP returned towards normal. Two cases with renal stones had normocalcemia, hypercalciuria, and high urinary cAMP or serum PTH. Since CaA was less than urinary Ca, the hypercalciuria may have been secondary to an impaired renal tubular reabsorption of Ca (renal hypercalciuria). Six cases with renal stones had normal values of serum Ca, urinary Ca, urinary cAMP, and serum PTH (normocalciuric nephrolithiasis). Their CaA exceeded urinal Ca, and fasting urinary Ca and bone density were normal. The results support the proposed mechanisms for the hypercalciuria and provide reliable diagnostic criteria for the various forms of hypercalciuria.

DASH-Style Diet and 24-Hour Urine Composition

“…Although the shape of the calcium intake/urinary calcium curve at typical levels of calcium intake remains incompletely defined, the existence of a "plateau effect" for intestinal calcium absorption is well established (22)(23)(24). For example, in a study of 13 In constructing the DASH score, higher intakes of these components received lower scores.…”

Intestinal Calcium Absorption among Hypercalciuric Patients with or without Calcium Kidney Stones

“…This test is practical, feasible, and because of its duration, estimates calcium absorption in duodenum and jejunum (14). Previous findings showed higher strontium excretion and absorption in HSFs than in normocalciuric stone formers (14,15), consistent with the known alteration of calcium metabolism in these patients (5,10). In addition, strontium absorption was negatively correlated with lumbar BMD values in hypercalciuric stone-forming women (11).…”

“…It has been mainly studied in patients producing kidney stones but was also found in 20% of osteoporotic women and 10% of the general population (2)(3)(4). Patients with idiopathic hypercalciuria are characterized by high intestinal absorption and low tubular reabsorption of calcium and may have decreased bone mass (3)(4)(5). A primary increase of enteral calcium absorption was hypothesized to cause hypercalciuria in a large portion of patients (6).…”

Hyperoxaluria or hypercalciuria in nephrolithiasis: the importance of renal tubular functions

“…The fasting urinary excretion ofcalcium is therefore used to classify the type of hypercalciuria. When more detailed classifications of IHC were first proposed [39,40], it was believcd that a high fasting urinary calcium mainly reflected a high bone resorption, so-called resorptive hypercalciuria, presumably caused by an excess of PTH [40]. It was also recognized that in some instances a high fasting urinary calcium could be due to primary renal calcium wasting, the so-called 'renal leak' of calcium.…”