Hyperphosphataemia

Hyperphosphataemia is an elevated serum phosphate, and because phosphate is renally excreted, chronic kidney disease is by far the commonest cause. It is a central component of chronic kidney disease-mineral and bone disorder, driving secondary hyperparathyroidism, vascular calcification and increased cardiovascular mortality.

Other causes fall into three groups: reduced excretion (acute kidney injury, hypoparathyroidism), massive cellular release (tumour lysis syndrome, rhabdomyolysis, haemolysis, severe catabolic states), and increased intake or absorption (phosphate-containing enemas and laxatives, excessive vitamin D, intravenous phosphate).

Acutely, the main hazard is not phosphate itself but the hypocalcaemia it produces through calcium-phosphate precipitation, and the acute kidney injury that follows deposition in renal tissue.

• Serum phosphate, interpreted alongside calcium, PTH, magnesium and renal function, since phosphate in isolation says little
• The calcium-phosphate product is a useful indicator of precipitation risk, with a markedly raised product carrying a risk of metastatic calcification
• Renal function to identify acute or chronic kidney disease as the underlying driver
• Where phosphate is high and renal function is normal, consider hypoparathyroidism (low calcium, low PTH), tumour lysis syndrome or rhabdomyolysis (check LDH, urate, potassium, creatine kinase), and exogenous phosphate load, phosphate-containing bowel preparations and enemas are a recognised and preventable cause of severe hyperphosphataemia, particularly in older patients and those with renal impairment
• Pseudohyperphosphataemia can occur with haemolysed samples, paraproteinaemia or hyperbilirubinaemia
• In chronic kidney disease, phosphate is monitored serially as part of routine bone mineral management rather than investigated afresh each time

Acute severe hyperphosphataemia:

• Treat the underlying cause, which is usually the definitive action
• Intravenous saline promotes phosphaturia where renal function permits
• Haemodialysis for severe hyperphosphataemia with renal failure, symptomatic hypocalcaemia, or tumour lysis syndrome
• Manage the associated hypocalcaemia cautiously: giving calcium while phosphate is very high risks precipitating calcium-phosphate in tissues, so calcium is generally reserved for symptomatic hypocalcaemia rather than given to normalise the number

Chronic kidney disease:

• Dietary phosphate restriction, with dietitian input, focusing particularly on processed foods containing inorganic phosphate additives, which are far more readily absorbed than the organic phosphate in natural foods and are frequently the largest modifiable contributor
• Phosphate binders, taken with meals so they bind dietary phosphate in the gut rather than being given between meals, which is a common and consequential administration error:
• Calcium-based binders (calcium carbonate, calcium acetate), effective but contribute to calcium load and vascular calcification
• Non-calcium binders (sevelamer, lanthanum), preferred where calcium load or vascular calcification is a concern
• Iron-based binders (sucroferric oxyhydroxide, ferric citrate), which also provide iron
• Manage secondary hyperparathyroidism alongside, with activated vitamin D analogues and calcimimetics as indicated
• Adequate dialysis in dialysis-dependent patients

Prevention: avoid phosphate-containing bowel preparations and enemas in renal impairment and in older patients.

Referral: nephrology for chronic kidney disease-mineral and bone disorder management and for dialysis decisions.