Treatment of primary hypercalciuria

Marangella, Martino and Vitale, Corrado and Bagnis, Cristiana (2004) Treatment of primary hypercalciuria. Clinical cases in mineral and bone metabolism, 1 (1). pp. 47-52. ISSN 1971-3266

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Abstract

diopathic hypercalciuria (HC) occurs in about 50% of patients with nephrolithiasis and is often associated with the fasting HC. While increasing the risk for stone formation HC may in- volve mineral metabolism and bone turnover, as a conse- quence of sustained negative calcium balance, despite in- creased intestinal absorption of calcium. Therapeutic options take account of this. Apart from dietary management, which is treated elsewhere, drugs so far used in HC patients include: thiazides, alkali, bisphosphonates, neutral potassium phos- phate. Issues concerning mechanisms and treatment of some genetic HC are also discussed in this review. Thiazides alone or in association with amiloride, reduce calcium excretion, revert external balance and protect bone from dem- ineralisation. They act by increasing calcium reabsorption at the cortical segment of the distal tubule. Over long-term there is net retention of calcium, which results in a favourable impact on bone, as suggested by a number of epidemiology studies. Thi- azides was also shown to exert direct effects on bone, by acting on osteoblast function. These studies strongly support thi- azides use when negative calcium balance and enhanced bone resorption are suspected. Hypertensive patients with HC are al- so eligible, but no limitation to their extensive use exists. Alkaline potassium citrate has a dual effect on HC: citrate an- ion strongly binds to calcium; alkalinisation expectedly re- duces bone resorption. Thus both ionised and total calcium excretion are decreased by citrate. The same effects are shared by other alkaline compounds, such as potassium bi- carbonate, which improved calcium balance, reduced bone re- sorption and increased bone formation in postmenopausal women. Potassium citrate was shown to induce similar effects in healthy menopausal women over a short-term course. The well known effect of bisphosphonates on bone resorption will theoretically lower calcium excretion. Alendronate, pre- vented HC induced by prolonged bed-rest. Genetic hypercalci- uric rats reduced calcium excretion on alendronate adminis- tration. Alendronate 10 mg/daily reduced both fasting and 24- hr calcium excretion in patients with fasting HC over a two- year follow-up. Renal phosphate leak HC has been treated with neutral potas- sium phosphate. Daily dosages of 40 mmoles decreased urine

Item Type:	Article
Uncontrolled Keywords:	Hypercalciuria, nephrolithiasis, thiazides, potassium citrate, bisphosphonates, potassium phosph
Subjects:	600 Tecnologia - Scienze applicate > 610 Medicina e salute (Classificare qui la tecnologia dei servizi medici) > 616 Malattie (classificare qui la Clinica medica, la medicina basata sull'evidenza, la Medicina interna, la Medicina sperimentale)
Depositing User:	Patrizia Romano
Date Deposited:	19 Mar 2014 16:25
Last Modified:	19 Mar 2014 16:25
URI:	http://eprints.bice.rm.cnr.it/id/eprint/5551

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