Idiopathic Hypercalcuria

Henneman, Philip H.; Benedict, Patricia H.; Forbes, Alexander; Dudley, H. Robert

doi:10.1056/nejm195810232591702

Cited by 204 publications

(55 citation statements)

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“…We have administered hydrochlorothiazide, in a dosage of 50 mg. twice daily, to 29 patients with idiopathic hypercalciuria and in 7 of these, complete metabolic balance studies were performed. All balance studies were done on the Farquharson Investigation Unit and biochemical determinations were done in a research laboratory.…”

Section: Methodsmentioning

confidence: 99%

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The Effects of Thiazides in Idiopathic Hypercalciuria

Er¹,

Rj²,

Cohanim³

1966

The American Journal of the Medical Sciences

111

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Section: Methodsmentioning

confidence: 99%

“…Absorption from the intestine appears to be increased. 7 In a few cases this overabsorption of calcium has been considered to be the primary cause of the disease8 but in the majority it is felt to be secondary to a primary renal loss of calcium.9' 10 …”

mentioning

confidence: 99%

The Effects of Thiazides in Idiopathic Hypercalciuria

Er¹,

Rj²,

Cohanim³

1966

The American Journal of the Medical Sciences

111

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“…In most cases, the elevated urine calcium excretion was accompanied by normal serum calcium, normal or slightly low serum phosphorus, and no overt evidence of bone disease; known causes of hypercalciuria such as primary hyperparathyroidism, sarcoidosis, Cushing's syndrome, cancer, excess vitamin D intake, hyperthyroidism, glucocorticoid use, Paget's disease, or renal tubular acidosis were absent. The term idiopathic hypercalciuria (IH) was coined to describe this constellation of findings [4]. IH is the most common metabolic abnormality found in adult calcium stone formers, present in 30-60% of such patients; it is common among pediatric calcium stone formers, as well [5].…”

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confidence: 99%

New Insights Into the Pathogenesis of Idiopathic Hypercalciuria

Worcester

Coe

2008

Seminars in Nephrology

146

125

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Idiopathic hypercalciuria (IH) is the commonest metabolic abnormality in patients with calcium kidney stones. It is characterized by normocalcemia, absence of diseases that cause increased urine calcium, and calcium excretion that is above 250 mg/day in women and 300 mg/day in men. Subjects with IH have a generalized increase in calcium turnover, which includes increased gut calcium absorption, decreased renal calcium reabsorption, and a tendency to lose calcium from bone. Despite the increase in intestinal calcium absorption, negative calcium balance is commonly seen in balance studies, especially on a low calcium diet. The mediator of decreased renal calcium reabsorption is not clear; it is not associated with either an increase in filtered load of calcium or altered PTH levels. There is an increased incidence of hypercalciuria in first-degree relatives of those with IH, but IH appears to be a complex polygenic trait with a large contribution from diet to expression of increased calcium excretion. Increased tissue vitamin D response may be responsible for the manifestations of IH in at least some patients. Definition of HypercalciuriaCalcium, the most abundant cation in human beings, is an important participant in many physiologic processes, including hormonal secretion, cardiac contraction, blood clotting, and neurotransmission. In addition, growth and repair of our skeleton demands an adequate supply of calcium, and careful maintenance of extracellular calcium concentrations. For this reason, prevailing levels of intracellular and extracellular calcium are tightly regulated, by a complex system of control mechanisms. These mechanisms control calcium absorption by gut and renal tubular epithelia, as well as fluxes of calcium on and off bone, during varying dietary calcium intakes. In healthy, non-pregnant adults, whose skeleton is no longer growing, net intestinal calcium absorption is matched by renal excretion, and provides sufficient calcium for skeletal maintenance; however, under pathologic conditions, some urine calcium may derive from bone loss.Abnormalities of calcium homeostasis could result in a number of undesired consequences, including abnormally high or low serum calcium levels, or inadequate maintenance of bone mineral. Hypercalciuria might be defined as any level of urine calcium that exceeds net intestinal absorption, leading to net loss of calcium. However, in practice net intestinal absorption is seldom measured, and under the assumption that urine calcium is primarily derived from intestinal absorption, the working definition of hypercalciuria is urine calcium excretion that exceeds that found in the majority of healthy adults eating their usual diets. In practice, this is usually defined as a daily calcium excretion over 250 mg/day in women or 300Mailing address: Elaine Worcester, M.D., Nephrology Section, Suite 511 / MC 5100, University of Chicago, 5841 S. Maryland Avenue, Chicago, Illinois 60637, Phone: 773-702-7459, Fax: 773-702-5818. Publisher's Disclaimer: This is a PDF file ...

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“…Two cases with renal stones had normocalcemia, hypercalciuria, and high urinary cAMP or serum PTH. Since CaA was less than urinaryINTRODUCTION Hypercalciuria is frequently encountered in primary hyperparathyroidism and is the hallmark of idiopathic hypercalciuria (1,2). The term resorptive hypercalciuria has been used to describe the hypercalciuria of primary hyperparathyroidism because of the frequent association of excessive skeletal resorption (3).…”

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confidence: 99%

The Hypercalciurias CAUSES, PARATHYROID FUNCTIONS, AND DIAGNOSTIC CRITERIA

Pak¹,

Oata²,

Lawrence³

et al. 1974

J. Clin. Invest.

496

137

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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.

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Idiopathic Hypercalcuria

Cited by 204 publications

References 5 publications

The Effects of Thiazides in Idiopathic Hypercalciuria

The Effects of Thiazides in Idiopathic Hypercalciuria

New Insights Into the Pathogenesis of Idiopathic Hypercalciuria

The Hypercalciurias CAUSES, PARATHYROID FUNCTIONS, AND DIAGNOSTIC CRITERIA

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