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Phosphate-binding medications include sevelamer, lanthanum carbonate, calcium carbonate, and calcium acetate. [7] Previously aluminum hydroxide was the medication of choice, but its use has been largely abandoned due to the increased risk of aluminum toxicity .
Hypophosphatemia is an electrolyte disorder in which there is a low level of phosphate in the blood. [1] Symptoms may include weakness, trouble breathing, and loss of appetite. [1]
The disorder is inherited in an X-linked dominant manner. [ 1 ] [ 2 ] This means the defective gene responsible for the disorder (PHEX) is located on the X chromosome, and only one copy of the defective gene is sufficient to cause the disorder when inherited from a parent who has the disorder.
The levels of chloride in the blood can help determine if there are underlying metabolic disorders. [20] Generally, chloride has an inverse relationship with bicarbonate, an electrolyte that indicates acid-base status. [20] Overall, treatment of chloride imbalances involve addressing the underlying cause rather than supplementing or avoiding ...
Delayed growth and development are common symptoms of phosphate diabetes in children, resulting in stunted growth and a shorter stature compared to their peers. This symptom is typically one of the earliest indicators of the disorder and may require treatment with growth hormone therapy to promote normal growth and development. [citation needed]
When kidney function is impaired, phosphate excretion declines. Without specific treatment, hyperphosphataemia occurs almost universally, despite dietary phosphate restriction and conventional dialysis treatment. [12] [13] In patients on dialysis, hyperphosphataemia is an independent risk factor for fractures, cardiovascular disease and mortality.
It is an X-linked recessive disorder that results in defective glucose-6-phosphate dehydrogenase enzyme. [1] Glucose-6-phosphate dehydrogenase is an enzyme which protects red blood cells, which carry oxygen from the lungs to tissues throughout the body. A defect of the enzyme results in the premature breakdown of red blood cells.
It represents a systemic disorder of mineral and bone metabolism due to CKD manifested by either one or a combination of the following: [1] [2] Abnormalities of calcium, phosphorus , parathyroid hormone, or vitamin D metabolism; Abnormalities in bone turnover, mineralization, volume, linear growth, or strength