Dietary Calcium Restriction may be Good for Patients’ Stones — but not for Their Bones

Velentzas, C.; Dg, Oreopoulos; Meema, S; Meema, H. E.; Nutsuga, T.; Alison, E; Katirtzoglou, A; Crassweller, P.O.

doi:10.1007/978-1-4684-8977-4_136

Cited by 6 publications

(3 citation statements)

References 12 publications

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“…Although early studies relied on the less sensitive singlephoton absorptiometry technique and did not discriminate stone-forming patients by their underlying mechanisms for stones, the studies, in general, disclosed lower BMD in stone formers as compared to age-and gender-matched controls [17][18][19][20][21]. The majority (6/10) of studies in normocalciuric stone formers demonstrated normal BMD at both the spine and cortical-rich sites such as proximal radius and femur [17,[20][21][22][23]. Even when the nature of the stone-forming patients' hypercalciuria was delineated as to absorptive, fasting, or renal leak hypercalciuria, there is a rather consistent decrease in BMD observed for the stone formers versus the age-and gender-matched control BMD values.…”

Section: Clinical Studiesmentioning

confidence: 94%

“…Taylor and Curhan [13] cited the limited effectiveness against stone formation of a lowcalcium diet [34] and fear of bone loss from the dietary calcium restriction. In addition, the epidemiological and clinical studies discussed above [12,17,44] suggest that reduced calcium intake in stone formers may actually serve to perturb the bone loss. Our approach has been to employ calcium restriction only in hypercalciuric patients [87] in combination with a hypocalciuric agent and potassium citrate [88].…”

Section: Calciummentioning

confidence: 94%

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Bone Disease and Idiopathic Hypercalciuria

Zerwekh

2008

Clinic Rev Bone Miner Metab

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There is sufficient epidemiological and clinical data demonstrating an association between reduced bone mineral density and idiopathic hypercalciuria (IH). There have been relatively few studies that have addressed the underlying defect in bone remodeling. The limited studies to date suggest that increased bone turnover occurs in some forms of IH such as fasting hypercalciuria or renal calcium leak and explains the bone loss observed in these forms of IH. On the other hand, defective bone formation is the major defect observed in patients with IH resulting from intestinal hyperabsorption of calcium. These alterations in bone remodeling have been ascribed to genetic, metabolic, and nutritional causes. Although there are several therapeutic options available for treating such patients and preventing stone recurrence, prevention of future bone loss should also be considered to prevent the increased risk of osteoporotic fracture in patients with IH.

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Section: Clinical Studiesmentioning

confidence: 94%

Section: Calciummentioning

confidence: 94%

Bone Disease and Idiopathic Hypercalciuria

Zerwekh

2008

Clinic Rev Bone Miner Metab

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“…Several studies have also examined BMD in normocalciuric stone-formers. Again, the findings were mixed with about half of the studies reporting no significant differences in BMD or BMC as compared to age-and gender-matched normal subjects (4,(6)(7)(8)(9). On the other hand, studies that utilized methods for measuring BMD considered to be more sensitive, found significant reductions of BMD in normocalciuric calcium stone-formers (5,(10)(11)(12)(13).…”

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confidence: 99%

Bone Disease and Idiopathic Hypercalciuria

Zerwekh

2008

Seminars in Nephrology

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Observational and epidemiologic studies alike have shown that idiopathic hypercalciuric (IH) stone-forming patients typically show bone mineral density scores that are significantly lower than those observed for age- and sex-matched normal subjects or those for nonhypercalciuric stone-forming patients. Most of these studies have relied on changes in bone mineral density and have not explored the mechanism(s) involved. There have been a small number of studies that have relied on dynamic bone histomorphometry to ascertain the nature of the bone defect in IH patients. When performed, these studies clearly have shown increased bone resorption and high bone turnover in patients with fasting hypercalciuria whereas suppressed bone formation indices are the most consistent finding in patients with the absorptive variant of IH. The causes of this apparent difference in bone remodeling between the 2 variants of IH still is uncertain. Available evidence suggests that potential mechanisms may be dependent in large part to genetic, metabolic, and nutritional causes of hypercalciuria and bone loss in patients with IH.

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