What are the symptoms of hyperphosphatemia?
Acute hyperphosphatemia is usually asymptomatic, but when there are symptoms, they are typically consistent with the concurrent hypocalcemia seen with hyperphosphatemia. Hypocalcemia primarily causes cardiac and CNS toxicity. The primary ECG changes are QTc prolongation and it can also cause myocardial depression leading to hemodynamic instability. The neurologic effects include perioral numbness, Chvostek and Trousseau signs, lethargy, laryngospasm, seizure, and coma.
Chronic hyperphosphatemia is generally asymptomatic; however, there are a few complications that are significant. Increased phosphorus is associated with poor patient outcomes. In a study of inpatients, those with hyperphosphatemia had a longer length of stay (6 compared to 3 days) and higher mortality. The CARE study was a randomized, controlled trial of pravastatin in patients with a previous myocardial infarction and hypercholesterolemia. The average GFR was 70 mL/min. The investigators found a 27% increase in the risk of death for every 1 mg/dL (0.32 mmol/L) increase in phosphorus. In patients on dialysis, multiple studies from all over the world have found an association with high phosphorus and mortality.
Another complication of hyperphosphatemia is calcific uremic arteriolopathy (formerly known as calciphylaxis). This disease is usually seen in dialysis patients and affects the arterioles. Histologically, it is characterized by apoptosis, differentiation of smooth muscle cells into bone forming osteoblast-like cells, and increased inflammation. Patients develop painful, deep soft-tissue plaques that progress to black eschars and necrotic ulcers. Sodium thiosulfate administered with dialysis has emerged as a promising treatment strategy.