Tineke De Schutter defended her PhD thesis in september 2012, presenting experimental research into the association between bone pathology and vascular calcification in renal failure.
In contrast to what might be expected, cardiovascular diseases are the most important cause of death in patients with chronic kidney disease. Vascular calcification or the deposition of calcium in the blood vessel wall is the most prominent feature of cardiovascular disease.
The distinctly disturbed mineral metabolism and subsequent secondary hyperparathyroidism in renal failure not only leads to vascular calcification but also significantly affects normal bone health, causing renal osteodystrophy.
This link between disturbed bone metabolism or increased bone loss and vascular calcification is called the ‘calcification paradox’ and is not exclusively related to decreased renal function: the calcification paradox is also observed in postmenopausal women, diabetics and elder persons.
When treatments are started to prevent bone loss such as with bisphosphonates in osteoporosis, or attempts to normalize bone turnover in renal osteodystrophy, the progression of vascular calcification is altered as well. Therefore, a causal link between bone and blood vessels might reasonably be suggested. Mechanisms and triggers of this calcification paradox however, remain unraveled.
The aims of this research were to investigate the effect of:
- increased bone loss on the development of vascular calcification,
- therapeutic interventions to control hyperphosphatemia and normalize bone turnover on the development of vascular calcification,
in rats with experimentally induced renal failure.