Renal osteodystrophy

Renal osteodystrophy bone disease is currently defined as an alteration of bone morphology in patients with chronic kidney disease (CKD). It is one measure of the skeletal component of the systemic disorder of chronic kidney disease-mineral and bone disorder (CKD-MBD).The term "renal osteodystrophy" was coined in 1943, 60 years after an association was identified between bone disease and kidney failure.

The traditional types of renal osteodystrophy have been defined on the basis of turnover and mineralization as follows: mild, slight increase in turnover and normal mineralization; osteitis  fibrosa, increased turnover and abnormal mineralization; osteomalacia, decreased turnover and abnormal mineralization; adynamic, decreased turnover and acellularity; and, mixed, increased turnover with abnormal mineralization.A Kidney Disease: Improving Global Outcomes report has suggested that bone biopsies in patients with CKD should be characterized by determining bone turnover, mineralization, and volume (TMV system).

On the other hand, CKD-MBD is defined as a systemic disorder of mineral and bone metabolism due to CKD manifested by either one or a combination of the following: abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism;  abnormalities in bone turnover, mineralization, volume, linear growth, or strength (renal osteodystrophy); and  vascular or other soft-tissue calcification.

Signs and symptoms:-

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 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 hypophosphatemia combined with hypocalcaemia, both of which are due to decreased excretion of phosphate by the damaged kidney.

In CKD, the excessive production of parathyroid hormone increases the bone resorption rate and leads to histologic bone signs of secondary hyperparathyroidism. However, in other situations, the initial increase in parathyroid hormone and bone remodelling 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.

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 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.

Recovery from renal osteodystrophy has been observed following kidney transplantation. Renal osteodystrophy is a chronic condition with a conventional haemodialysis schedule. Nevertheless, it is important to consider that the broader concept of CKD-MBD, which includes renal osteodystrophy, is not only associated with bone disease and increased risk of fractures but also with cardiovascular calcification, poor quality of life and increased morbidity .

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With Regards,

David Paul

Editorial Assistant

Journal of Clinical Nephrology and Research