Renal osteodystrophy - Disorders of the kidney

Renal osteodystrophy

Definition

This term refers to the various bone diseases that develop due to chronic renal failure.

Pathophysiology

The main mechanism is that of secondary hyperparathyroidism:

1.     Chronic renal failure causes reduced hydroxylation of 25(OH)D2 to the active vitamin D metabolite, 1,25(OH)2D3. This leads to reduced absorption of calcium from the diet and therefore lowers serum calcium levels. In addition, phosphate levels rise, due to reduced renal excretion. This binds calcium, further lowering serum calcium levels and also causes calcium deposits in tissues.

2.     In response to the low serum calcium, the parathyroid glands in the neck are stimulated to produce increased amounts of parathyroid hormone (i.e. secondary hyperparathyroidism).

3.     Hyperparathyroidism leads to increased osteoclastic activity (to mobilise calcium from bone, and partially restore serum calcium levels to normal. Hyperparathyroidism also releases PO4, which cannot be excreted and so contributes further to hyperphosphataemia.

Other mechanisms include:

·        Metabolic acidosis also promotes demineralisation of bone.

·        On long-term renal dialysis aluminium is retained, which deposits in bone, blocking calcification of the osteoid.

Clinical features

See Osteomalacia, Osteoporosis, Secondary and Tertiary Hyperparathyroidism for the clinical features and X-ray findings.

Osteosclerosis may also occur, where there are alternate stripes of sclerotic and osteoporotic bone. This affects the trabecular bone of the spine, to produce a ‘ruggerjersey spine’ appearance on X-ray.

Investigations

·        Serum Ca2+ may be normal or low, PO42− is high and often alkaline phosphatase is raised.

·        Raised parathyroid hormone.

·        25(OH)D2 (Vitamin D2) is normal but 1,25(OH)2D3 (Vitamin D3) is low.

Management

Serum PO42− must be lowered by restricting dietary intake and taking phosphate binders such as calcium carbonate with meals. Vitamin D supplements (active analogues, e.g. alfacalcidol which do not require renal activation) are used in addition to ensuring an adequate calcium intake. The aim of treatment is to suppress the PTH to slightly higher than normal levels, control the parameters, avoid ectopic calcification and bone disease.