Renal osteodystrophy



Chronic kidney disease (CLD) and skeletal disorders are highly coprevalent.

Kidney osteodystrophy is present in nearly all patients with end stage kidney disease, and a significant fraction of patients with earlier CKD.

Caused by secondary hyperparathyroidism and deficiency of 1a,25-dihydroxycholecalciferol.

Encompasses a variety of bone disorders caused by chronic renal disease.

Osteoporosis defined as a T score of -2.5 or lower is two times more common in patients with CKD compared with those without renal disease.

The most commonly encountered renal Osteodystrophy is osteitis fibrosa cystica with extensive bone marrow fibrosis and increased osteoclastic bone resorption attributed to uncontrolled secondary hyperparathyroidism.

The increased osteoclastic activity results in bone resorption, affecting skeletal sites such as subperiosteal, subligamentous, intracortical, endosteal, trabecular, subchondral, and subtendinous areas.

In patients with ESRD and chronic hemodialysis, maintenance of serum PTH levels between 150 and 300 pg/mL is considered adequate.

A 4-8 fold increase in PTH levels is predictive of high turnover bone disease, and correlates with osteitis fibrosa cystica.

In severe cases, bone deformities and fragility fractures can occur.

Fractures are associated with prolonged rehabilitation, prolonged pain, increased healthcare costs, and risk of dying.

Resorption of the terminal phalanges may cause acro-osteolysis.

Thoracic vertebral fractures increase the anterior posterior diameter of the thorax.

Treatments include: parathyroidectomy, suppression of parathyroid hormone secretion by vitamin D analogs, calcimetic agents and inhibition of gastrointestinal absorption of phosphates by binders.

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