Synopsis
Recognise defective adult bone mineralisation, distinguish nutritional vitamin-D deficiency from renal or phosphate-wasting causes, interpret the calcium-phosphate-parathyroid pattern, and replace missing substrate safely while treating the underlying disorder.
- Osteomalacia is failure to mineralise newly formed adult osteoid; suspect it with diffuse bone tenderness, proximal weakness, waddling gait, insufficiency fractures or Looser pseudofractures.
- The common nutritional pattern is low 25-hydroxyvitamin D, raised ALP, raised PTH and low phosphate; adjusted calcium may be low or preserved by secondary hyperparathyroidism.
- Request adjusted calcium, phosphate, ALP, PTH, vitamin D, magnesium, renal and liver profiles first, then distinguish substrate deficiency, CKD and phosphate wasting.
- If phosphate remains low, paired fasting blood and urine measurements with fractional excretion or TmP/GFR determine whether the kidney is inappropriately wasting phosphate.
- Treat nutritional deficiency with a total colecalciferol loading dose near 300,000 units over six to ten weeks, then 800–2,000 units daily maintenance, ensuring adequate calcium intake.
- Check adjusted calcium about one month after loading or earlier when high risk; investigate rather than repeatedly loading if vitamin D, ALP, phosphate or symptoms fail to improve.
- Do not give routine calcitriol for ordinary nutritional deficiency; CKD, hypoparathyroidism and phosphate-wasting disorders need specialist cause-specific plans.
- Correct osteomalacia before potent antiresorption because denosumab or intravenous bisphosphonate can precipitate serious hypocalcaemia when mineral substrate is inadequate.
Key red flags
Perioral tingling, carpopedal spasm, seizure, laryngospasm or arrhythmia with low calcium requires monitored emergency replacement rather than an outpatient vitamin-D course.
Sudden focal pain, deformity or inability to bear weight may indicate an insufficiency fracture through poorly mineralised bone and needs urgent imaging and protection.
Severe persistent hypophosphataemia with weakness, respiratory compromise, haemolysis or rhabdomyolysis needs acute correction and cause-directed inpatient assessment.
Weight loss, anaemia, gastrointestinal symptoms, renal tubular abnormalities or a focal tumour syndrome suggests malabsorption, Fanconi syndrome or oncogenic phosphate wasting.
Investigation priorities
Identify the biochemical mineralisation pattern and kidney, liver or magnesium contributions before replacement.
Management branches
Diffuse pain, proximal weakness, low-trauma fracture or unexpectedly low density raises a mineralisation concern.
- Obtain mineral, renal, liver, magnesium, PTH and vitamin-D tests before high-dose replacement when clinical stability permits.
- Identify urgent hypocalcaemia, critical phosphate depletion or fracture, then separate common vitamin-D deficiency from CKD and isolated renal phosphate wasting.
- Use targeted coeliac, endocrine, medicine, tubular and malignant investigations rather than assuming every low vitamin-D result explains the phenotype.
- Image focal or weight-bearing pain and protect a suspected insufficiency fracture while advanced imaging or orthopaedic review is arranged.