Evidence for a prostaglandin-mediated bone resorptive mechanism in subjects with fasting hypercalciuria

Filipponi, P; Mannarelli, C.; Pacifici, Roberto; Grossi, Enzo; Moretti, I; Tini, S.; Carloni, C; Blass, Andrea; Morucci, P; Hruska, Keith A.; Avioli, Louis V.

doi:10.1007/bf02555148

Cited by 40 publications

(12 citation statements)

References 24 publications

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“…Moreover, PGE 2 could induce hypercalciuria by stimulating renal 1 ␣ -hydroxylase activity and consequently serum 1,25-(OH) 2 vitamin D concentrations, which play a central role in calcium metabolism at the intestinal, renal, and bone levels. A disorder in vitamin D's pathway is the most attractive hypothesis to explaining the different forms of hypercalciuria [17][18][19]. The possibility that PGE 2 could increase 1,25-(OH) 2 vitamin D synthesis was supported by the fi ndings of our group [13] and those of Hasanoglu et al [20] of a positive correlation between 1,25-(OH) 2 vitamin D and PGE 2 in adults and children with idiopathic hypercalciuria.…”

Section: Best-fit Modelsupporting

confidence: 74%

Fatty Acids and Idiopathic Calcium Nephrolithiasis

Baggio¹,

Budakovic²

2005

Urol Int

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Clinical and experimental investigations seem to underline the important role of fatty acids in the pathogenesis of hypercalciuria, a well-known risk factor for lithogenesis. To evaluate the relationships between the previously reported increase in plasma phospholipid arachidonic acid level and the factors responsible for calcium metabolism in idiopathic calcium nephrolithiasis, a best-fit model was constructed. This new statistical application shows a causal relationship between plasma phospholipid arachidonic acid content, intestinal calcium absorption, biochemical markers of bone turnover, urinary calcium excretion and bone mineral density at the lumbar spine. This model suggests that a defect in the phospholipid fatty acid composition could represent the primary event responsible for the mosaic of metabolic and clinical alterations that are distinctive features of renal stone formers, such as kidney, intestine, and bone calcium metabolism, and several forms of idiopathic hypercalciuria.

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Section: Best-fit Modelsupporting

confidence: 74%

Fatty Acids and Idiopathic Calcium Nephrolithiasis

Baggio¹,

Budakovic²

2005

Urol Int

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“…The origin of such a decrease has been investigated over the past few years. The pathogenesis of bone mass loss has been related to increased monocyte interleukin-1 activity [3], to increased prostaglandin E2 (PGE2) production [4], to decreased dietary calcium intake [5,6], to an increase in animal protein intake [7] and, recently, to increased interleukin-6 activity [8].…”

Section: Introductionmentioning

confidence: 99%

Bone mineral density in pediatric patients with idiopathic hypercalciuria

García‐Nieto

Ferrández

Monge

et al. 1997

Pediatric Nephrology

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It is well known that some patients with renal lithiasis due to idiopathic hypercalciuria (IH) may exhibit decreased bone mineral density (BMD). We have studied a large group of children with IH and related their BMD values to several renal function parameters and calcium and bone metabolism markers. Children with IH had higher osteocalcin and calcitriol levels and higher urinary excretion of magnesium and prostaglandin E2, as well as lower tubular reabsorption of phosphate, urinary excretion of ammonium, maximum urinary PCO2, and BMD compared with control group of children. In children with IH we observed a negative correlation between BMD and age. We found osteopenia in 22 of 73 children with IH (30.1%); these children showed lower citraturia levels and higher fractional excretion of uric acid than children with normal BMD. In osteopenic children there was a negative correlation between BMD and calcitriol levels. Several possible pathogenetic factors have been proposed for the bone mass loss. Our results demonstrate that, at least in some cases, it may be related to high levels of calcitriol, which has a wellknown resorption ability. Whether a certain degree of intracellular acidosis or a higher production of prostaglandin E2 could play a role in some cases is still an open question. In children with normal BMD we observed a direct correlation between osteocalcin and tartrate-resistant acid phosphatase levels; this correlation did not hold for children with osteopenia.

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“…In previous studies investigating the relationship between calcium stone formers and reduced BMD, patients were classified according to the amount of urinary calcium excretion, followed by an analysis of the corresponding BMD [2][3][4][5]17]. The focus of our investigation was different.…”

Section: Discussionmentioning

confidence: 99%

PTH and 1.25 vitamin D response to a low-calcium diet is associated with bone mineral density in renal stone formers

Frey

Eisenberger

Mohaupt

et al. 2008

Nephrology Dialysis Transplantation

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Background. Renal calcium stones and hypercalciuria are associated with a reduced bone mineral density (BMD). Therefore, the effect of changes in calcium homeostasis is of interest for both stones and bones. We hypothesized that the response of calciuria, parathyroid hormone (PTH) and 1.25 vitamin D to changes in dietary calcium might be related to BMD. Methods. A single-centre prospective interventional study of 94 hyper-and non-hypercalciuric calcium stone formers consecutively retrieved from our stone clinic. The patients were investigated on a free-choice diet, a low-calcium diet, while fasting and after an oral calcium load. Patient groups were defined according to lumbar BMD (z-score) obtained by dual X-ray absorptiometry (group 1: z-score <−0.5, n = 30; group 2: z-score −0.5-0.5, n = 36; group 3: z-score >0.5, n = 28). The effect of the dietary interventions on calciuria, 1.25 vitamin D and PTH in relation to BMD was measured.Results. An inverse relationship between BMD and calciuria was observed on all four calcium intakes (P = 0.009). On a free-choice diet, 1.25 vitamin D and PTH levels were identical in the three patient groups. However, the relative responses of 1.25 vitamin D and PTH to the low-calcium diet were opposite in the three groups with the highest increase of 1.25 vitamin D in group 1 and the lowest in group 3, whereas PTH increase was most pronounced in group 3 and least in group 1. Conclusion. Calcium stone formers with a low lumbar BMD exhibit a blunted response of PTH release and an apparently overshooting production of 1.25 vitamin D following a low-calcium diet.

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Evidence for a prostaglandin-mediated bone resorptive mechanism in subjects with fasting hypercalciuria

Cited by 40 publications

References 24 publications

Fatty Acids and Idiopathic Calcium Nephrolithiasis

Fatty Acids and Idiopathic Calcium Nephrolithiasis

Bone mineral density in pediatric patients with idiopathic hypercalciuria

PTH and 1.25 vitamin D response to a low-calcium diet is associated with bone mineral density in renal stone formers

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