Approaches to the management of renal bone disease

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Summary: The major, although not the exclusive, factors in the pathogenesis of renal bone disease are: (i) inappropriate renal production of calcitriol; (ii) variable resistance to the action of calcitriol, both abnormalities eliciting; (iii) secondary hyperparathyroidism with increased hormonal secretion and in the long‐term parathyroid hyperplasia: first polyclonal and then monoclonal; and (iv) variable resistance to parathyroid hormone (PTH) on the receptor and also the post receptor level altering the relationship between PTH concentration and bone turnover. Unresolved in pathogenesis issues concern the role of phosphate (direct or indirect stimulatory action on the parathyroid and the quantitative contribution to parathyroid stimulation of changes in calcaemia (altered Ca sensor‐mediated signal to the parathyroid?). Unresolved practical problems concern: (i) optimal time of administration of calcitriol (prophylactic vs therapeutic); (ii) the dose of calcitriol (recent evidence showing that very low levels are both safe with respect to hypercalcaemia and efficaceous); (iii) the mode of administration (continuous vs intermittent; intravenous [i.v.] vs per oral; [p.o.]); and (iv) the choice of dialysate Ca concentration (low concentration permitting higher CaCO3 and calcitriol dosage, but exposing to the risk of negative Ca balance). Recent controlled studies have shed some light on these issues. Very low doses of calcitriol (0.125 μg/day) prevent a further rise of 1,84 PTH without causing hypercalcaemia, hypercalciuria or hyperphosphataemia. A controlled head‐on comparison failed to show a significant difference between i.v. and p.o. calcitriol with respect to PTH response or side effects. Because of the high prevalence of monoclonal growth in advanced nodular parathyroid hyperplasia there is an increasing tendency to advocate early parathy‐roidectomy or alternative procedures (injection of alcohol in the parathyroids).