27th February 2025

Chronic kidney disease-mineral and bone disorder (CKD-MBD)

Impaired phosphate excretion and 1-hydroxylation of 25(OH)D (calcifediol) are the primary drivers of mineral bone disease in renal failure. Secondary hyperparathyroidism follows, with subsequent osteopenia, pseudogout, osteitis fibrosa cystica (high-turnover bone disease causing pain and deformity; also called a brown tumour), and calcinosis (soft tissue calcification). Plain film radiographs may demonstrate subperiosteal resorption of the terminal phalanges and soft tissue calcifications, while blood tests show hyperphosphataemia, hypocalcaemia and raised PTH. In addition, calcium phosphate deposition in blood vessels is in part responsible for the increased risk of cardiovascular disease seen in advanced CKD.

Hyperphosphataemia is treated by limiting foods high in phosphate, such as dairy products, egg and protein-rich foods, and prescribing phosphate binders such as sevelamer. Active vitamin D metabolites such as calcitriol are used to treat hypocalcaemia and hyperparathyroidism. Tertiary hyperparathyroidism may develop with subsequent hypercalcaemia, in which case parathyroidectomy or calcimimetics such as cinacalcet are used to reduce PTH.