Prevention of hypercalcaemic nephropathy and tissue calcification by glucagon during phosphate infusion

Abstract 

Patients with serum calcium above 4.5 mmol/litre risk sudden death. Rehydration and frusemide may decrease calcium levels by 0.5–1 mmol/litre but result in a high renal filtered load of calcium which, if above 3.7 mmol/litre, causes calcium phosphate protein complexes to form giving rise to hypercalcaemic nephropathy. Current drugs namely clodronate, calcitonin and plicamycin take days to lower serum calcium and have disadvantages.

Intravenous phosphate rapidly lowers serum calcium but when the calcium phosphate product rises above 4.6 mmol/litre the saturation point for the precipitation of calcium hydrogen phosphate is reached and tissue calcification occurs.

Intravenous glucagon results in a steep reduction in serum phosphate within minutes and also lowers serum calcium, resulting in a marked fall in the calcium phosphate product to well below the critical level of 4.6 mmol/litre. If, in addition to glucagon, intravenous phosphate is now given, it should have a further calcium-lowering effect by inhibiting bone osteoclasts.

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