Literature DB >> 2719852

A histomorphometric determination of iliac bone remodeling in patients with recurrent renal stone formation and idiopathic hypercalciuria.

T Steiniche1, L Mosekilde, M S Christensen, F Melsen.   

Abstract

33 normocalcemic patients (22 males and 11 females) aged 20-68 years with recurrent renal stone formation and idiopathic hypercalciuria were compared to 33 approximately sex- and age-matched normal controls. Quantitative histomorphometric analysis of iliac crest biopsies were performed after intravital tetracycline double labeling in the patients and in 30 sex- and age-matched normal controls. No difference was found between patients and controls in albumin adjusted serum calcium levels. Serum phosphorus was significantly reduced (p less than 0.01) in the patient group whereas the urinary phosphorus/creatinine ratio was increased (p less than 0.01). The serum calcium phosphate product (S-CaxS-P) was significantly reduced in the patients (p less than 0.05). As expected, the urinary calcium/creatinine ratio was higher in the patient group than in the controls (p less than 0.001). Serum parathyroid hormone was normal. The histomorphometric analysis revealed signs of a moderate mineralization defect (reduced adjusted appositional rate (p less than 0.05), prolonged mineralization lag time (p less than 0.05) and prolonged formation (p less than 0.05)), and an increased extension of eroded surfaces (P less than 0.05) in the patients. The amount of trabecular bone and the balance between the thickness of bone resorbed and later formed per remodeling cycle and all other histomorphometric parameters were found normal in the patients. The combined histomorphometric and biochemical data are best explained by a primary renal phosphate leak leading to hypophosphataemia and a slight mineralization defect. The hypercalciuria may be explained by an enhanced renal production of 1.25-dihydroxyvitamin D secondary to the reduced serum levels of phosphorus. No signs of secondary or primary hyperparathyroidism were observed.

Entities:  

Mesh:

Substances:

Year:  1989        PMID: 2719852     DOI: 10.1111/j.1699-0463.1989.tb00793.x

Source DB:  PubMed          Journal:  APMIS        ISSN: 0903-4641            Impact factor:   3.205


  12 in total

Review 1.  Bone disease and idiopathic hypercalciuria.

Authors:  Joseph E Zerwekh
Journal:  Semin Nephrol       Date:  2008-03       Impact factor: 5.299

Review 2.  Bone disease in pediatric idiopathic hypercalciuria.

Authors:  Maria Goretti Moreira Guimarães Penido; Marcelo de Sousa Tavares
Journal:  World J Nephrol       Date:  2012-04-06

3.  Expression of fibroblast growth factor 23, vitamin D receptor, and sclerostin in bone tissue from hypercalciuric stone formers.

Authors:  Viviane Barcellos Menon; Rosa Maria Affonso Moysés; Samirah Abreu Gomes; Aluizio Barbosa de Carvalho; Vanda Jorgetti; Ita Pfeferman Heilberg
Journal:  Clin J Am Soc Nephrol       Date:  2014-04-24       Impact factor: 8.237

4.  Evidence for a role of PDZ domain-containing proteins to mediate hypophosphatemia in calcium stone formers.

Authors:  Kristin J Bergsland; Fredric L Coe; Joan H Parks; John R Asplin; Elaine M Worcester
Journal:  Nephrol Dial Transplant       Date:  2018-05-01       Impact factor: 5.992

Review 5.  Nephrolithiasis-associated bone disease: pathogenesis and treatment options.

Authors:  Khashayar Sakhaee; Naim M Maalouf; Rajiv Kumar; Andreas Pasch; Orson W Moe
Journal:  Kidney Int       Date:  2010-12-01       Impact factor: 10.612

6.  Bone disease in primary hypercalciuria.

Authors:  Stefania Sella; Catia Cattelan; Giuseppe Realdi; Sandro Giannini
Journal:  Clin Cases Miner Bone Metab       Date:  2008-05

Review 7.  Bone mineral content in calcium renal stone formers.

Authors:  A Trinchieri
Journal:  Urol Res       Date:  2005-08-03

8.  Pathophysiology of incomplete renal tubular acidosis in recurrent renal stone formers: evidence of disturbed calcium, bone and citrate metabolism.

Authors:  P J Osther; J Bollerslev; A B Hansen; K Engel; P Kildeberg
Journal:  Urol Res       Date:  1993-05

9.  RANKL is a mediator of bone resorption in idiopathic hypercalciuria.

Authors:  Samirah Abreu Gomes; Luciene Machado dos Reis; Irene Lourdes Noronha; Vanda Jorgetti; Ita Pfeferman Heilberg
Journal:  Clin J Am Soc Nephrol       Date:  2008-05-14       Impact factor: 8.237

10.  Intestinal hyperabsorption of calcium and low bone turnover in hypercalciuric postmenopausal osteoporosis.

Authors:  Clarita V Odvina; John R Poindexter; Roy D Peterson; Joseph E Zerwekh; Charles Y C Pak
Journal:  Urol Res       Date:  2008-07-17
View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.