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

APMIS - Tập 97 Số 1-6 - Trang 309-316 - 1989
Torben Steiniche1, Leif Mosekilde1, Merete Sanvig Christensen1, F. Melsen1
1University institute of Pathology and Medical Department III, Aarhus amtssygehus, DK 8000 Aarhus C, Denmark

Tóm tắt

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<0.01) in the patient group whereas the urinary phosphorus/creatinine ratio was increased (p<0.01). The serum calcium phosphate product (S‐CaxS‐P) was significantly reduced in the patients (p<0.05). As expected, the urinary calcium/creatinine ratio was higher in the patient group than in the controls (p<0.001). Serum parathyroid hormone was normal. The histomorphometric analysis revealed signs of a moderate mineralization defect (reduced adjusted appositional rate (p <0.05), prolonged mineralization lag time (p<0.05) and prolonged formation period (p<0.05)), and an increased extension of eroded surfaces (P<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.

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