Bone disease (Osteodystrophy)

Renal bone disease (osteodystrophy) is a mixture of changes seen in blood and bones of patients who have had kidney failure for a long time. It continues to be a problem in patients on long term dialysis. It is quite complicated and something of a specialist topic. Read the top couple of sections – beyond that is getting quite deep.

Features of renal osteodystrophy

Patients who have had kidney disease for (usually) many decades may develop a characteristic and severe bone disease. We’re better at preventing and treating it now, so it rarely gets as severe as the old photos shown. The problems are:

  • Thin bones that fracture easily
  • Brown tumours form bone cysts. These are a consequence of severe hyperparathyroidism, now rarely seen.
  • Rickets (vitamin D deficiency), so that bones don’t calcify properly. Growing bones will bend, and show delayed ossification. Now largely preventable.
  • Weak muscles – proximal myopathy is a prominent feature of rickets.
  • Calcium deposits in artery walls. Remains very common.
  • Calcium deposits in other inappropriate places – in muscles and around joints.

The major players in renal osteodystrophy are:

Increased phosphate levels in the blood – this causes the parathyroid glands to produce more Parathyroid Hormone, PTH. Healthy kidneys respond to PTH by putting out more phosphate in urine.

Treatment: Phosphate comes from what you eat, so cutting down on foods that are high in phosphate and taking “phosphate binders” with food help. If you are on dialysis, more dialysis is likely to help – especially long or frequent dialysis treatments (phosphate is removed slowly by conventional dialysis).

Low calcium levels in the blood – caused by failure of the kidneys to process Vitamin D normally. Low calcium levels make the parathyroid glands produce more PTH.

Treatment: Active vitamin D is available for renal patients (Alfacalcidol, Calcitriol and some others).

Vitamin D deficiency (osteomalacia)

Kidneys process vitamin D that you eat into an ‘active’ form that does the work. Active Vitamin D causes the gut to take in more calcium from food. Vitamin D is also necessary for normal bone formulation – without it you get rickets. In rickets bones don’t calcify properly. They may break or bend in growing children, to cause bow legs and other abnormalities.
Caused by failure of the 1α-hydroxylation of vitamin D to form 1,25 dihydroxycholecalciferol, a step that usually occurs in renal tubular cells. Prevented by administration 1α-hydroxylated derivatives of vitamin D, (alfacalcidol or calcitriol). This raises serum calcium and also directly suppresses PTH secretion.


Increased secretion of parathyroid hormone (PTH) is driven by hypocalcaemia (in part due to effective vitamin D deficiency) and high serum phosphate (as renal excretion is reduced). After some years, responsiveness of PTH to lowered phosphate and raised calcium levels is lost (tertiary hyperparathyroidism). Prevention is through control of calcium and phosphate levels. PTH has been suspected of causing various other elements of ‘uraemic syndrome’, but its role in most of them is speculative.

High parathyroid hormone causes two things:

  • Healthy kidneys respond by putting out more phosphate.
  • Calcium is released from the bones, eventually thinning them to a dangerous degree. After a long period it gets out of control and becomes less responsive to calcium levels, even causing high blood calcium, (‘Tertiary hyperthyroidism).

Treatment: removing the parathyroid gland (parathyroidectomy) is commonly needed at some point in the lives of people with longstanding dialysis/transplantation.

As a temporary fix, drugs that increase the sensitivity of parathyroid cells to calcium can lower PTH levels. They work by affecting the calcium monitoring system – to make the PTH cells ‘think’ the calcium is even higher. This reduces PTH production.

Adynamic bone disease

Recognised more recently. Thought to be at least partially due to over-suppression of PTH by excessive use of vitamin D therapy. In the past aluminium toxicity (from dialysis and use of aluminium hydroxide as a phosphate binder) may have contributed to this.

Other issues

Phosphatonins (e.g. FGF23) like PTH, phosphatonins make the kidneys put out more phosphate. So as kidneys fail, the levels of these in the blood rise. It isn’t proven that these cause any particular problems, but they should respond to the same treatment you’d use to lower phosphate.

Gut – The amount of calcium and phosphate that the body takes from food in your gut can be varied by vitamin D (increases it) and phosphate binders (reduce phosphate absorption).

Is bone density testing useful in Renal Osteodystrophy?

This unusual combination of features makes standard methods for assessing bone density of very uncertain value in patients with chronic kidney failure.

Further info