Hyperphosphatemia E83.38

Serum phosphate concentration > 4.5 mg/dl (> 1.46 mmol/l).

The most common cause of hyperphosphatemia is decreased renal phosphate excretion due to reduced glomerular filtration and/or increased tubular reabsorption. Causes include acute or chronic renal insufficiency (GFR < 30 ml/min).

Disturbances in renal excretion of phosphate without existing renal insufficiency may occur in:

• Pseudohypoparathyroidism
• Hypoparathyroidism
• parathyroid suppression (such as hyperkalemia due to vitamin A or D excretion).

Massive phosphate overload due to transcellular shift of phosphate into extracellular space so extensive that renal excretory capacity is exceeded:

• Diabetic ketoacidosis (most pat. with diabetic ketoacidosis are hyperphosphatemic prior to initiation of therapy).
• Crush injuries
• Non-traumatic rhabdomyolysis
• Overwhelming systemic infections
• Tumor lysis syndrome

Hyperphosphatemia also occurs with excessive oral phosphate administration and, in isolated cases, with excessive use of phosphate-containing enemas.

False-high levels of phosphate may occur with hyperproteinemia (e.g., multiple myeloma or macroglobulinemia), dyslipidemia, hemolysis, or hyperbilirubinemia.

Most patients with hyperphosphatemia are asymptomatic. Possibly symptoms of hypocalcemia up to tetany (concomitant hypocalcemia). Soft tissue calcifications(cutaneous nodules detectable=calcinosis cutis) often occur in patients with chronic kidney disease. Imaging can often detect vascular calcifications along the major arteries.Hyperphosphatemia is diagnosed by phosphate concentration. If the etiology is not obvious (e.g., rhabdomyolysis, tumor lysis syndrome, renal failure, abuse of phosphate-containing laxatives), further investigation is needed to rule out hypoparathyroidism or pseudohypoparathyroidism, which is due to end-organ resistance to parathyroid hormone (PTH). False-high values for serum phosphate should be identified by measuring the concentrations of serum proteins, lipids and bilirubin.

Determination of serum phosphate concentration (phosphate concentration > 4.5 mg/dl (> 1.46 mmol/l)

Therapy consists of limiting phosphate intake and administration of phosphate-binding antacids such as calcium carbonate, phosphate-binding resins without calcium (e.g., sevelamer). Another phosphate binder is lanthanum carbonate (doses of 500-1000 mg p.o. 3 times daily with meals).

In severe cases, use of hemodialysis.

Note: Although very effective, aluminium-containing antacids should not be used as phosphate binders in patients with end-stage renal disease because of the risk of aluminium-related dementia (see Aluminium below) and osteomalacia.

Hyperphosphatemia can lead to calcium precipitation in soft tissues, especially when the serum calcium × phosphate product in patients with chronic kidney disease is consistently > 55. Soft tissue calcification in the skin is a cause of excessive pruritus in patients with ESRD undergoing chronic dialysis.

Vascular calcification also occurs in dialysis patients with chronically elevated calcium x phosphate product; vascular calcification is an important risk factor for cardiovascular morbidity including stroke, myocardial infarction, and intermittent claudication.