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The diagnosis of hyperphosphatemia is made through measuring the concentration of phosphate in the blood. A phosphate concentration greater than 1.46 mmol/L (4.5 mg/dL) is indicative of hyperphosphatemia, though further tests may be needed to identify the underlying cause of the elevated phosphate levels. [5]
The plasma total calcium concentration is in the range of 2.2–2.6 mmol/L (9–10.5 mg/dL), and the normal ionized calcium is 1.3–1.5 mmol/L (4.5–5.6 mg/dL). [4] The amount of total calcium in the blood varies with the level of plasma albumin, the most abundant protein in plasma, and therefore the main carrier of protein-bound calcium in the blood.
The cells release the glucose into the bloodstream, increasing blood sugar levels. Hypoglycemia, the state of having low blood sugar, is treated by restoring the blood glucose level to normal by the ingestion or administration of dextrose or carbohydrate foods. It is often self-diagnosed and self-medicated orally by the ingestion of balanced meals.
Phosphate binds to calcium from the circulation, leading to low calcium levels in the blood. [11] Rhabdomyolysis may cause kidney failure by several mechanisms. The most important is the accumulation of myoglobin in the kidney tubules.
Non-calcium-based phosphate binders, including lanthanum carbonate, form insoluble complexes with phosphates in food, thereby reducing the amount of phosphate in the body. [1] Sevelamer carbonate. Sevelamer is an insoluble polymeric amine, which is protonated once in the intestines and this allows it to bind dietary phosphate.
Calcium-binding proteins can be either intracellular and extracellular. Those that are intracellular can contain or lack a structural EF-hand domain. Extracellular calcium-binding proteins are classified into six groups. [2] Since Ca (2+) is an important second messenger, it can act as an activator or inhibitor in gene transcription.