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Occurrence of Mixed-Type Hypercalciuria in Stone Formers
Author(s) -
Ariel Sánchez,
Adriana González-Silvera,
Héctor Sarano,
Hugo Palou,
Juan Premoli,
Alejandro Dotta,
María Cristina Vidal,
R. C. Puche
Publication year - 1987
Publication title -
˜the œnephron journals/nephron journals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 72
eISSN - 2235-3186
pISSN - 1660-8151
DOI - 10.1159/000184174
Subject(s) - medicine , hypercalciuria , nephrology , renal stone , kidney stones , urology , calcium , urinary system
Dr. A Sánchez, Urquiza 1358, 2000 Rosario, Santa Fe (Argentina) Dear Sir, We have recently begun to determine ionized serum calcium concentration in stone-forming patients with idiopathic hypercalciuria. We were surprised to find low fasting Ca++ in 5 of 9 patients classified as having absorptive hypercalciuria, according to a clinical protocol that included 24-hour urinary calcium following high-and low-calcium diets, an acute oral calcium load with measurement of the urinary calcium/creatinine ratio before and after the load [1] and serum parathyroid hormone (PTH). Four of those patients plus 4 additional patients with tubular hypercalciuria and 9 control subjects were placed on 400 mg (10 mmol/day) of dietary calcium for 7 days. In the morning of the 8th day, in the fasting state and during mild water-induced diuresis (50–120 ml/h), total [2] and ionized serum calcium (Orion flow-through electrode), phosphate, sodium and creatinine were measured. The same determinations plus cyclic adenosine monophos-phate (cAMP) and citrate were carried out in two 1-hour urine samples. For the calculation of the tubular reabsorption of calcium, ionized serum calcium was employed as an estimate of ultrafilterable calcium. All subjects had normal blood pressure and normal PTH levels, measured with a commercial radioimmu-noassay which recognizes the carboxyl terminus of the molecule. The results obtained are shown in table I. Following dietary calcium restriction and a 12-hour fast, these patients with absorptive hypercalciuria could not maintain their serum calcium levels; the ensuing parathyroid stimulus increased the urinary excretion of cAMP and citrate and decreased the tubular reabsorp-tion of phosphate. Such a stimulus, however, failed to increase calcemia and the tubular reabsorption of calcium. We are not aware of the existence of similar observations in the literature. The information obtained demonstrates that some patients classified as having absorptive hypercalciuria show features (low serum calcium, elevated cAMP) one would expect to find in patients with tubular hypercalciuria. If one admits that stone formation is a multivariate phenomenon and that there may be more than one type of disturbance in the tubular handling of

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