However, in other situations, the initial increase in parathyroid hormone and bone remodeling may be slowed excessively by a multitude of factors, including age, ethnic origin, sex, and treatments such as vitamin D, calcium salts, calcimimetics, steroids, and so forth, leading to low bone turnover or adynamic bone disease.Both high and low bone turnover diseases are currently observed equally in CKD patients treated by dialysis, and all types of renal osteodystrophy are associated with an increased risk of skeletal fractures, reduced quality of life, and poor clinical outcomes. Diagnosis
Renal osteodystrophy is usually diagnosed after treatment for end-stage kidney disease begins; however the CKD-MBD starts early in the course of CKD. In advanced stages, blood tests will indicate decreased calcium and calcitriol (vitamin D) and increased phosphate, and parathyroid hormone levels. In earlier stages, serum calcium, phosphate levels are normal at the expense of high parathyroid hormone and fibroblast growth factor-23 levels. X-rays will also show bone features of renal osteodystrophy (subperiostic bone resorption, chondrocalcinosis at the knees and pubic symphysis, osteopenia and bone fractures) but may be difficult to differentiate from other conditions. Since the diagnosis of these bone abnormalities cannot be obtained correctly by current clinical, biochemical, and imaging methods (including measurement of bone-mineral density), bone biopsy has been, and still remains, the gold standard analysis for assessing the exact type of renal osteodystrophy. Differential diagnosis
To confirm the diagnosis, renal osteodystrophy must be characterized by determining bone turnover, mineralization, and volume (TMV system) (bone biopsy).
Signs and symptoms
Renal osteodystrophy may exhibit no symptoms; if it does show symptoms, they include:

Bone pain
Joint pain
Bone deformation
Bone fracture
The broader concept of chronic kidney disease-mineral and bone disorder (CKD-MBD) is not only associated with fractures but also with cardiovascular calcification, poor quality of life and increased morbidity and mortality in CKD patients (the so-called bone-vascular axis). These clinical consequences are acquiring such an importance that scientific working groups (such as the ERA-EDTA CKD-MBD Working Group) or international initiatives are trying to promote research in the field including basic, translational and clinical research. Pathogenesis
Renal osteodystrophy has been classically described to be the result of hyperparathyroidism secondary to hyperphosphatemia combined with hypocalcemia, both of which are due to decreased excretion of phosphate by the damaged kidney.Low activated vitamin D3 levels are a result of the damaged kidneys inability to convert vitamin D3 into its active form, calcitriol, and result in further hypocalcemia. High levels of fibroblast growth factor 23 seem now to be the most important cause of decreased calcitriol levels in CKD patients.In CKD, the excessive production of parathyroid hormone increases the bone resorption rate and leads to histologic bone signs of secondary hyperparathyroidism.