Calcium and phosphate metabolism are upset in moderate to severe CKD, and marked disturbances in either should usually lead to referral for detailed assessment, or enquiries for advice. Severe disturbances are usually restricted to stages 4 and 5 CKD.
The aim in Stage 3+ CKD is to keep [Ca] normal, serum phosphate at or below 1.8 mmol/l, and PTH below twice (to three times) the upper limit of normal.
Calcium is commonly low-normal or low in renal failure. High PTH is a physiological response to low calcium, and to the phosphate retention that occurs in renal failure. Often dietary advice and phosphate binders taken with food are needed to keep phosphate within acceptable limits. Vitamin D derivatives (alfacalcidol, calcitriol) are used to correct hypocalcaemia resulting from reduced renal activation of vitamin D, and also have a direct suppressive effect on PTH secretion. Initiation of these agents is usually a matter for specialist advice.
High calcium causes renal impairment. If it is a presenting feature in a patient with kidney disease, 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 management of renal bone disease is subject to variable local protocols, and these are additionally complicated by the introduction of several new agents recently.
Information for patients
Calcium, phosphate and bone are upset in a complicated way in kidney disease. This page covers what can be done in general practices, but even this is complex. The following webpages provide useful information about renal bone disease (renal osteodystrophy) and how it can be prevented: