MICROARCHITECTURAL AND MORPHOMETRIC CHANGES IN FEMORAL BONE TISSUE UNDER CKD–MBD: A LITERATURE REVIEW
Keywords:
Chronic kidney disease changes the skeleton long before the patient necessarily develops a clinically evident fracture. The term CKD–MBD describes the systemic disturbance of mineral and bone metabolism associated with CKD, whereas renal osteodystrophy is reserved for the morphological bone abnormalities that can be characterized histologically and histomorphometrically [1]. The distinction is important because a patient may have abnormal serum phosphate, parathyroid hormone or vitamin D concentrations without having a single uniform histological form of renal osteodystrophy. The skeletal phenotype is determined by the interaction of bone turnover, mineralization and bone volume, traditionally summarized by the turnover–mineralization–volume (TMV) concept [2].Abstract
Chronic kidney disease–mineral and bone disorder (CKD–MBD) is
accompanied by profound disturbances in bone remodeling, mineralization, and
skeletal microarchitecture. These changes may affect both cortical and trabecular
compartments of the femur and contribute to reduced bone strength and an increased
risk of fragility fractures. This literature review summarizes current evidence on
microarchitectural and morphometric alterations of femoral bone tissue associated
with CKD–MBD. Particular attention is given to changes in cortical thickness, cortical
porosity, trabecular number, trabecular thickness, trabecular separation, bone volume
fraction, and volumetric bone mineral density. Evidence from bone histomorphometry,
quantitative computed tomography, high-resolution peripheral quantitative computed
tomography, micro-computed tomography, and magnetic resonance imaging is
considered. Available studies indicate that CKD progression and abnormalities in
parathyroid hormone and bone turnover are associated with cortical thinning, increased
cortical porosity, deterioration of trabecular structure, and reductions in bone density
and mechanical competence. At the same time, the degree and pattern of these
alterations vary according to CKD stage, turnover status, mineralization abnormalities,
and other clinical factors.
References
1.
Kidney Disease: Improving Global Outcomes (KDIGO) CKD
MBD Work Group. (2017). KDIGO 2017 clinical practice guideline update for
the diagnosis, evaluation, prevention, and treatment of chronic kidney disease
mineral and bone disorder (CKD–MBD). Kidney International Supplements,
7(1), 1–59. https://doi.org/10.1016/j.kisu.2017.04.001
2.
Moe, S., Drüeke, T., Cunningham, J., Goodman, W., Martin, K.,
Olgaard, K., Ott, S., Sprague, S., Lameire, N., & Eknoyan, G. (2006).
Definition, evaluation, and classification of renal osteodystrophy: A position
statement from KDIGO. Kidney International, 69(11), 1945–1953.
https://doi.org/10.1038/sj.ki.5000414
3.
Evenepoel, P., Cunningham, J., Ferrari, S., Haarhaus, M., & others.
(2021). Diagnosis and management of osteoporosis in chronic kidney disease
stages 4 to 5D: A call for a shift from nihilism to pragmatism. Osteoporosis
International, 32, 2391–2405.
4.
Wehrli, F. W., Leonard, M. B., Saha, P. K., & Gomberg, B. R.
(2004). Quantitative high-resolution magnetic resonance imaging reveals
structural implications of renal osteodystrophy on trabecular and cortical bone.
Journal
of
Magnetic
Resonance
https://doi.org/10.1002/jmri.20085
5.
Imaging,
20(1),
83–89.
Sharma, A. K., Toussaint, N. D., Masterson, R., Holt, S. G.,
Rajapakse, C. S., Ebeling, P. R., Mohanty, S. T., Baldock, P., & Elder, G. J.
