Bone Mineral Content in Idiopathic Renal Stone Disease and in
Primary Hyperparathyroidism

Fuss, Michel; Gillet, C.; Simon, Jonathan; Vandewalle, J.; Schoutens, André; Bergmann, Pierre

doi:10.1159/000474039

Cited by 40 publications

(23 citation statements)

References 8 publications

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“…This finding is in line with the reported predictive value of calciuria on bone loss in stone formers [18]. In line with previous reports [2][3][4]7,8], BMD was diminished in hypercalciuric when compared to normocalciuric patients (Table 4). For most hypercalciuric patients reported in the literature so far, the underlying hypercalciuria-causing mechanism is unknown and the search for monogenic diseases was mostly unsuccessful [19].…”

Section: Discussionsupporting

confidence: 92%

“…The clinical relevance of this association was underlined by large retrospective cohort studies showing an increased risk of vertebral fractures in calcium stone formers [9,10]. Furthermore, the decreased BMD in calcium stone formers was linked to hypercalciuria in most [2][3][4]7,8], but not all [5], studies. Calciuria is a continuous trait and is the final result of numerous regulatory processes, including intestinal calcium absorption, bone resorption and renal reabsorption.…”

Section: Introductionmentioning

confidence: 99%

“…Over the last 30 years, epidemiological evidence associating renal calcium stone disease and decreased bone mineral density (BMD) has accumulated [2][3][4][5][6]. By using single photon absorptiometry [6,7], quantitative computed tomography [2,8], dual photon absorptiometry [3] and dual energy X-ray absorptiometry [4,5], a diminished BMD was found at the lumbar spine [2,3,8], radius [4,6,7] and tibia [5] in calcium stone formers. The clinical relevance of this association was underlined by large retrospective cohort studies showing an increased risk of vertebral fractures in calcium stone formers [9,10].…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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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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“…Taken together, these data suggest that Absorptive and Renal Hypercalciuria should be considered the same rather than two distinct entities, a hypothesis already raised by Coe et al (36) representing a systemic abnormality of calcium homeostasis probably induced by a dysregulation of 1,25(OH) 2 D 3 , leading to alterations in calcium transport in the intestine, kidney and bone (28,37) characterized by increased intestinal calcium absorption and bone resorption, as well as decreased renal tubular calcium reabsorption. Several series in the literature (38)(39)(40)(41)(42)(43)(44)(45)(46), including the one from our group (47), have demonstrated that BMD is reduced in IH patients. Some of them have reported increase of bone resorption markers as well (39,40,42,45,46).…”

Section: Idiopathic Hypercalciuriamentioning

confidence: 61%

Renal stone disease: causes, evaluation and medical treatment

Heilberg

Schor

2006

Arq Bras Endocrinol Metab

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The purpose of the present review is to provide an update about the most common risk factors or medical conditions associated with renal stone formation, the current methods available for metabolic investigation, dietary recommendations and medical treatment. Laboratory investigation of hypercalciuria, hyperuricosuria, hyperoxaluria, cystinuria, hypocitraturia, renal tubular acidosis, urinary tract infection and reduction of urinary volume is based on the results of 24-hr urine collection and a spot urine for urinary sediment, culture and pH. Blood analysis for creatinine, calcium and uric acid must be obtained. Bone mineral density has to be determined mainly among hypercalciurics and primary hyperparathyroidism has to be ruled out. Current knowledge does not support calcium restriction recommendation because it can lead to secondary hyperoxaluria and bone demineralization. Reduction of animal protein and salt intake, higher fluid intake and potassium consumption should be implemented. Medical treatments involve the use of thiazides, allopurinol, potassium citrate or other drugs according to the metabolic disturbances. The correction of those metabolic abnormalities is the basic tool for prevention or reduction of recurrent stone formation. O propósito desta revisão é apresentar uma atualização sobre os fatores de risco ou condições médica comuns associadas com a formação de cálculos renais, os métodos atualmente disponíveis para investigação metabólica, recomendações dietéticas e tratamento médico. A investigação laboratorial para hipercalciúria, hiperuricosuria, hiperoxalúria, cistinúria, hipocitratúria, acidose tubular renal, infecção do trato urinário e redução do volume urinário, é baseada nos resultados das coleções de urina de 24h e amostra isolada para sedimento urinário, cultura e pH. Deve-se obter análises sanguíneas para creatinina, cálcio e ácido úrico. Deve-se determinar a densidade mineral óssea especialmente entre pacientes hipercalciúricos, e o hiperparatiroidismo primário deve ser excluído. O conhecimento atual não endossa as recomendações de restrição de cálcio, já que isto pode levar o hiperaxalúria secundária e desmineralização óssea. Redução da ingesta de proteína animal e de sal deve ser implementada junto com aumento da ingesta de líquidos e do consumo de potássio. Tratamento medicamentoso envolve o uso de tiazídicos, alopurinol, citrato de potássio ou outras drogas, conforme o distúrbio metabólico. A correção dessas anormalidades metabólicas é o instrumento básico para a prevenção ou redução da formação recorrente de cálculos.

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“…II). Bone loss seems to mainly involve those skeletal sites where trabecular bone is more represented, such as vertebral bodies (22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35). However, a reduction in femoral density was reported by several authors (28,29,(31)(32)(33)(34)(35)(36).…”

Section: Ph and Bone Diseasementioning

confidence: 99%

Bone Disease in Primary Hypercalciuria

Giannini

Nobile

Sella

et al. 2005

Critical Reviews in Clinical Laboratory Sciences

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SummaryPrimary Hypercalciuria (PH) is very often accompanied with some degrees of bone demineralization. The most frequent clinical condition in which this association has been observed is calcium nephrolithiasis. In patients affected by this disorder bone density is very frequently low and increased susceptibility to fragility fractures is reported. The very poor definition of this bone disease from a histomorphometric point of view is a crucial aspect. At present, the most common finding seems to be a low bone turnover condition. Many factors are involved in the complex relationships between bone loss and PH. Since bone loss was mainly reported in patients with fasting hypercalciuria, a primary alteration in bone metabolism was proposed as a cause of both hypercalciuria and bone demineralization. This hypothesis was strengthened by the observation that some bone resorbing-cytokines, such as IL-1, IL-6, and TNF-α α are high in hypercalciuric patients. The effect of an excessive response to the acid load induced by dietary protein intake seems an additional factor explaining a primitive alteration of bone. The intestine plays a major role in the clinical course of bone disease in PH. Patients with absorptive hypercalciuria less frequently show bone disease and a reduction in dietary calcium greatly increases the probability of bone loss in PH subjects. It has recently been reported that greater bone loss is associated with a larger increase in intestinal calcium absorption in PH patients. Considering the absence of PTH alterations, it was proposed that this is not a compensatory phenomenon, but probably the marker of disturbed cell calcium transport, involving both intestinal and bone tissues. While renal hypercalciuria is rather uncommon, the kidney still seems to play a role in the pathogenesis of bone loss of PH patients, possibly via the effect of mild to moderate urinary phosphate loss with secondary hypophosphatemia. In conclusion, bone loss is very common in PH patients. Even if most of the factors involved in this process have been identified, many aspects of this intriguing clinical condition remain to be elucidated.

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Bone Mineral Content in Idiopathic Renal Stone Disease and in Primary Hyperparathyroidism

Cited by 40 publications

References 8 publications

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

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

Renal stone disease: causes, evaluation and medical treatment

Bone Disease in Primary Hypercalciuria

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