Increased phosphate intake, phosphate migration out of cells, and decreased phosphate excretion all contribute to hyperphosphatemia, which is defined by an elevated amount of phosphate in the blood. Those with chronic kidney disease, diabetic ketoacidosis, uncontrolled diabetes, and low parathyroid hormone levels usually have hyperphosphatemia. The excessive amounts of phosphate in the blood are controlled by Hyperphosphatemia Drugs, which frequently contain phosphate binders. Furthermore, phosphorus absorption through the digestive system is decreased by Hyperphosphatemia Drugs. They create an excreted compound by exchanging an anion phosphate with an active cation like carbonate, acetate, oxyhydroxide, or citrate. Many basic and animal-based clinical research have been prompted by the need to treat hyperphosphatemia in patients with kidney disease.
