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Diagnosis is generally based on a blood phosphate level exceeding 1.46 mmol/L (4.5 mg/dL). [1] Levels may appear falsely elevated with high blood lipid levels, high blood protein levels, or high blood bilirubin levels. [1] Treatment may include a phosphate low diet and antacids like calcium carbonate that bind phosphate. [1]
Hyperphosphatemia causes acute kidney injury in tumor lysis syndrome, because of deposition of calcium phosphate crystals in the kidney parenchyma. [2] Hypocalcemia. Because of the hyperphosphatemia, calcium is precipitated to form calcium phosphate, leading to hypocalcemia. [2] Symptoms of hypocalcemia include (but are not limited to): [9] tetany
In dystrophic calcification, basophilic calcium salt deposits aggregate, first in the mitochondria, then progressively throughout the cell. [citation needed] These calcifications are an indication of previous microscopic cell injury, occurring in areas of cell necrosis when activated phosphatases bind calcium ions to phospholipids in the membrane.
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.
PTHrP acts similarly to parathyroid hormone in that it binds to the parathyroid hormone 1 receptors on the kidneys and bones and causes an increased tubular reabsorption of calcium and activation of osteoclast activity, respectively. [22] Osteoclasts are a type of bone cell which cause bone resorption, releasing calcium into the bloodstream.
Disorders of calcium metabolism occur when the body has too little or too much calcium. The serum level of calcium is closely regulated within a fairly limited range in the human body. In a healthy physiology, extracellular calcium levels are maintained within a tight range through the actions of parathyroid hormone , vitamin D and the calcium ...
One of the principal causes of arterial stiffening with age is vascular calcification. Vascular calcification is the deposition of mineral in the form of calcium phosphate salts in the smooth muscle-rich medial layer of large arteries including the aorta. DNA damage, especially oxidative DNA damage, causes accelerated vascular calcification. [11]