Recurrent vesical calculi, hypercalciuria and biochemical evidence of increased bone resorption in an adult male with paraplegia due to spinal cord injury: is there a role for intermittent oral disodium etidronate therapy for prevention of calcium phosphate bladder stones?

Vaidyanathan, S; Watson, Ian D.; Jonsson, Olof; Az, Buczyński; Gráses, F.; Heilberg, Ita Pfeferman; Yasui, Takahiro; Wyndaele, Jean Jacques; Tozawa, Keiichi; Kohri, Kenjiro; Schurch, Brigitte; Hughes, Peter L; Singh, G.; Soni, B M; Sett, P; Fraser, WD

doi:10.1038/sj.sc.3101713

Cited by 11 publications

(6 citation statements)

References 16 publications

(11 reference statements)

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“…Similarly, alendronate was able to prevent bone loss and avert hypercalciuria when given in anticipation of 3 weeks of strict bed rest [55], and intravenous pamidronate in the prevention of femoral bone loss and renal stone formation during a 90-day bed rest [56]. A similar approach was taken with the use of bisphosphonate therapy in order to diminish bone resorption and reduce bladder stone formation and hypercalciuria in spinal cord injury paraplegics [57].…”

Section: Role Of Prolonged Immobilizationmentioning

confidence: 94%

Bone disease in idiopathic hypercalciuria

Heilberg

Weisinger

2006

Current Opinion in Nephrology &Amp; Hypertension

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Section: Role Of Prolonged Immobilizationmentioning

confidence: 94%

Bone disease in idiopathic hypercalciuria

Heilberg

Weisinger

2006

Current Opinion in Nephrology &Amp; Hypertension

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“…In general, SCI patients showed negative calcium balance with hypercalciuria after the injury. 2,[86][87][88][89][90][91][92] The increased osteoclastic bone resorption is mainly responsible for hypercalciuria following SCI. In addition, reduced renal function has been observed in acute SCI patients, 92 and the increased urinary elimination of calcium that occurs in response to SCI may be related to diminished renal tubular reabsorption.…”

Section: Calcium Balancementioning

confidence: 99%

“…In general, SCI patients showed negative calcium balance with hypercalciuria after the injury 2,86–92 . The increased osteoclastic bone resorption is mainly responsible for hypercalciuria following SCI.…”

Section: Hormonal Changesmentioning

confidence: 99%

Mechanisms of osteoporosis in spinal cord injury

Jiang

Dai

2006

Clinical Endocrinology

156

109

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SummaryOsteoporosis is a known complication of spinal cord injury (SCI), but its mechanism remains unknown. The pathogenesis of osteoporosis after SCI is generally considered disuse. However, although unloading is an important factor in the pathogenesis of osteoporosis after SCI, neural lesion and hormonal changes also seem to be involved in this process. Innervation and neuropeptides play an important role in normal bone remodelling. SCI results in denervation of the sublesional bones and the neural lesion itself may play a pivotal role in the development of osteoporosis after SCI. Although upper limbs are normally loaded and innervated, bone loss also occurs in the upper extremities in patients with paraplegia, indicating that hormonal changes may be associated with osteoporosis after SCI. SCI-mediated hormonal changes may contribute to osteoporosis after SCI by different mechanisms: (1) increased renal elimination and reduced intestinal absorption of calcium leading to a negative calcium balance; (2) vitamin D deficiency plays a role in the pathogenesis of SCI-induced osteoporosis; (3) SCI antagonizes gonadal function and inhibits the osteoanabolic action of sex steroids; (4) hyperleptinaemia after SCI may contribute to the development of osteoporosis; (5) pituitary suppression of TSH may be another contributory factor to bone loss after SCI; and (6) bone loss after SCI may be caused directly, at least in part, by insulin resistance and IGFs. Thus, oversupply of osteoclasts relative to the requirement for bone resorption and/or undersupply of osteoblasts relative to the requirement for cavity repair results in bone loss after SCI. Mechanisms for the osteoporosis following SCI include a range of systems, and osteoporosis after SCI should not be simply considered as disuse osteoporosis. Unloading, neural lesion and hormonal changes after SCI result in severe bone loss. The aim of this review is to improve understanding with regard to the mechanisms of osteoporosis after SCI. The understanding of the pathogenesis of osteoporosis after SCI can help in the consideration of new treatment strategies. Because bone resorption after SCI is very high, intravenous bisphosphonates and denosumab should be considered for the treatment of osteoporosis after SCI.

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“…Hypercalciuria constitutes an important risk factor of calcium oxalate and calcium phosphate stone development since it increases supersaturation of the compounds [9]. Dilution of urine as observed in our patients with high urinary outputs would decrease the risk of developing hypercalcemia.…”

Section: Discussionmentioning

confidence: 99%

Treatment of immobilization hypercalciuria using weekly alendronate in two quadriplegic patients

Atalay

Turhan

2007

Int Urol Nephrol

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Metabolic and urinary problems encountered in spinal cord injury patients are multifaced. We report two patients with high-level spinal cord injuries who have developed hypercalciuria after admission to the rehabilitation unit. To establish a clean intermittent self-catheterization programme, the hypercalciuria was treated successfully with alendronate. Twenty-four-hour urinary calcium excretion decreased significantly after medical treatment for hypercalciuria. Since high-level quadriplegic patients may not be mobilized in the acute phase of the rehabilitation, use of alendronate for preventing hypercalciuria and maintaining a successful clean intermittent self-catheterization programme can be considered as a supportive/complementary measure.

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Recurrent vesical calculi, hypercalciuria and biochemical evidence of increased bone resorption in an adult male with paraplegia due to spinal cord injury: is there a role for intermittent oral disodium etidronate therapy for prevention of calcium phosphate bladder stones?

Cited by 11 publications

References 16 publications

Bone disease in idiopathic hypercalciuria

Bone disease in idiopathic hypercalciuria

Mechanisms of osteoporosis in spinal cord injury

Treatment of immobilization hypercalciuria using weekly alendronate in two quadriplegic patients

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