Relationship between aortic mineral elements and osteodystrophy in mice with chronic kidney disease.
In chronic kidney disease (CKD), osteodystrophy and arterial calcification often coexist. However, arterial alterations have not been addressed in CKD unaccompanied by evidence of calcification. We investigated the association of phosphate (P) and calcium (Ca) accumulation in calcification-free aortas with CKD-induced osteodystrophy. Aortic accumulation of magnesium (Mg), an inhibitor of calcification, was also examined. Male mice aged 26 weeks with CKD characterized by hyperparathyroidism and hyperphosphatemia (Nx, n = 8) and age-matched healthy male mice (shams, n = 8) were sampled for blood, and thoracic vertebrae and aortas were harvested. Bone structure and chemicals were analyzed by microcomputed tomography and infrared microspectroscopy, respectively, and aortic accumulation of P, Ca, and Mg was evaluated by plasma-atomic emission spectrometry. Volume fractions of cortical and trabecular bones were smaller in Nx than in sham animals (P < 0.05), attributed to cortical thinning and reduction in trabecular number, respectively. Bone chemicals were not different between the groups. No calcification was found in either group, but P, Ca, and Mg contents were higher in Nx than in shams (P < 0.05). The mass ratio of Ca/P was lower in Nx than in shams (P < 0.05), but that of Mg/Ca and Mg/P was not different between the groups. Aortic P and Ca contents were inversely correlated with the volume fraction of cortical bone (P < 0.05). In conclusion, the relationship of osteodystrophy with aortic P and Ca accumulation suggests the existence of a bone-vascular axis, even in calcification-free arteries in CKD. The preservation of ratios of Mg/Ca and Mg/P despite CKD development might contribute to calcification resistance.
Bioengineering Division, Osaka University Graduate School of Engineering Science, 1-3 Machikaneyama-cho, Toyonaka, 560-8531, Japan. matsu@me.es.osaka-u.ac.jp
Takeshi
T
Matsumoto
Shuichiro
S
Fukushima
Takeshi
T
Kanasaki
Shingo
S
Hagino
D000818:Animals; D001013:Aorta, Thoracic / Q000737:chemistry* / Q000378:metabolism / Q000473:pathology; D002118:Calcium / Q000032:analysis* / Q000378:metabolism; D012080:Chronic Kidney Disease-Mineral and Bone Disorder / Q000000981:diagnostic imaging / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D060467:Disease Resistance; D042241:Early Diagnosis; D006962:Hyperparathyroidism, Secondary / Q000209:etiology; D054559:Hyperphosphatemia / Q000209:etiology; D008274:Magnesium / Q000032:analysis / Q000378:metabolism; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D010758:Phosphorus / Q000032:analysis* / Q000378:metabolism; D051436:Renal Insufficiency, Chronic / Q000503:physiopathology*; D012720:Severity of Illness Index; D013054:Spectrophotometry, Atomic; D013055:Spectrophotometry, Infrared; D013904:Thoracic Vertebrae / Q000737:chemistry / Q000000981:diagnostic imaging / Q000473:pathology*; D014057:Tomography, X-Ray Computed; D061205:Vascular Calcification / Q000175:diagnosis / Q000209:etiology* / Q000517:prevention & control
D010758:Phosphorus; D008274:Magnesium; D002118:Calcium