Strontium causes osteomalacia in chronic renal failure rats

• Published in: Kidney international Vol. 54; no. 2; pp. 448 - 456
• Main Authors: Schrooten, Iris, Cabrera, Walter, Goodman, William G., Dauwe, Simonne, Lamberts, Ludwig V., Marynissen, Rita, Dorriné, Walter, De Broe, Marc E., D’Haese, Patrick C.
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.08.1998; Nature Publishing
• Subjects: adynamic bone disease; aluminum; Aluminum - metabolism; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animals; Biological and medical sciences; bone; bone mineralization; Calcium - metabolism; dialysis; Emergency and intensive care: renal failure. Dialysis management; Female; hyperparathyroidism; hypomineralization; Intensive care medicine; Kidney Failure, Chronic - complications; Medical sciences; osteodystrophy; Osteomalacia - chemically induced; Osteomalacia - metabolism; Osteomalacia - pathology; Parathyroid Hormone - blood; Rats; Rats, Wistar; Renal Dialysis - adverse effects; Strontium - pharmacokinetics; Strontium - toxicity; dialysis; hypomineralization; bone; aluminum; hyperparathyroidism; adynamic bone disease; osteodystrophy; bone mineralization; Rat; Diseases of the osteoarticular system; Bone disease; Peritoneal dialysis; Strontium; Extrarenal dialysis; Histopathology; Biological effect; Localization; Osteomalacia; Nutritional status; Kidney disease; Charge storage; Urinary system disease; Rodentia; Nutrition disorder; Dialysis fluid; Vitamin deficiency; Vertebrata; Chronic; Experimental disease; Mammalia; Treatment; Animal; Renal failure; Bone
• ISSN: 0085-2538; 1523-1755
• DOI: 10.1046/j.1523-1755.1998.00035.x

Strontium causes osteomalacia in chronic renal failure rats. We recently reported an association between increased bone strontium (Sr) levels and osteomalacia in dialysis patients. To delineate whether or not Sr acts as a causal factor in the development of osteomalacia, we devised the following study: four groups of chronic renal failure (CRF) rats were given Sr, aluminum (Al), both of these compounds or none of the elements (controls). Administration of Sr and/or Al resulted in increased bone levels of the respective elements. Histological examination revealed impairment of mineralization in the Sr group and to a lesser extent in the Al group as compared to the control group. There was also a significant increase in osteoid area in the Sr group, but not in the Al group. No differences in bone surface or erodic perimeter were noted between the various study groups. Histochemically, Sr could be localized in calcified bone, mainly in new bone close to the osteoid/calcification front, a critical site of bone mineralization. Histochemical findings were confirmed by electron probe X-ray microanalysis. These findings indicate that Sr accumulation in chronic renal failure rats resulted in the development of osteomalacic lesions, in contrast to the Al group where adynamic bone disease was induced in the present set-up. Further studies are required to define the mechanism by which way Sr causes osteomalacia in chronic renal failure rats.