PTH, vitamin D, calcium and phosphate in CKD

Assessment of PTH in Stage 3+ CKD

PTH can be estimated from EDTA samples in many labs, in which it is relatively stable permitting estimation from samples taken out of hospital. The UK CKD guidelines suggest this as a 'one-off' test in patients newly found to have stable stage 3 CKD. It is monitored regularly but infrequently in higher stages. Interpret as follows:

PTH<70ng/l no further check required unless patient reaches Stage 4 CKD.

PTH>70ng/l check serum 25-hydroxyvitamin D:

If 25-OH D is low (<80nmol/l, 30 micrograms/l), prescribe ergocalciferol or colecalciferol 800u/day in a preparation that contains calcium lactate or carbonate (not phosphate). Colecalciferol 10,000u by IM injection once monthly is an alternative. Recheck PTH in 3 months. If now <70, continue; if still high, refer

If 25-OH D is normal with high PTH, refer.

Alternatively seek advice if PTH is >70ng/l. This is an area where local protocols may vary.

In some areas it may be difficult to measure PTH outside a secondary care setting because of requirement for rapid transport and freezing of samples.

Abnormalities of calcium and phosphate

Significant disturbance of calcium or phosphate in CKD should usually lead to nephrological referral or advice. The aim in Stage3+ CKD is to keep [Ca] normal, serum phosphate =/<1.8 mmol/l, and PTH below twice the upper limit of normal.

Calcium is commonly low-normal or low in renal failure. High PTH is a physiological response to low calcium. Phosphate is retained in renal failure and high phosphate is a physiological stimulus to PTH release. Often dietary advice and phosphate binders taken with food are needed to keep phosphate within acceptable limits.

High calcium causes renal impairment. If it is a presenting feature, the hypercalcaemia or the cause of hypercalcaemia must be suspected to be the cause of the renal problem. In treated CKD it may be caused by oral calcium and vitamin D treatment, or by tertiary hyperaparathyroidism.

Further information

Further management of renal bone disease is subject to variable local protocols, and these are additionally complicated by the introduction of several new agents recently.