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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] It is considered significant when levels are greater than 1.6 mmol/L (5 mg/dL). [2]
If this is successful, PTH levels return to normal levels, unless PTH secretion has become autonomous (tertiary hyperparathyroidism). [50] Hyperphosphatemia may be treated by decreasing dietary intake of phosphate. If phosphate remains persistently elevated above 5.5 mg/dL with dietary restriction, then phosphate binders may be used. [55]
The effects of excess thyroid hormone typically respond to the administration of a non-selective beta blocker, such as propranolol (as most of the symptoms are driven by increased levels of adrenaline and its effect on the β-adrenergic receptors). Subsequent attacks may be prevented by avoiding known precipitants, such as high salt or ...
Renal management of phosphate is impaired in secondary hyperparathyroidism which results in hyperphosphatemia. [4] [6] Primary hyperplasia of the parathyroid gland, results from both hypocalcaemia and increased phosphate levels by decreasing expression of calcium sensing receptors and vitamin D receptors at the parathyroid gland.
Calcium levels initially tend to be low, but as the situation improves calcium is released from where it has precipitated with phosphate, and vitamin D production resumes, leading to hypercalcemia (abnormally high calcium levels). This "overshoot" occurs in 20–30% of those people who have developed kidney failure.
Elevated alkaline phosphatase occurs when levels of alkaline phosphatase (ALP) exceed the reference range. This group of enzymes has a low substrate specificity and catalyzes the hydrolysis of phosphate esters in a basic environment. The major function of alkaline phosphatase is transporting chemicals across cell membranes. [1]
If the underlying cause of the hypocalcemia can be addressed, the hyperparathyroidism will resolve. In people with chronic kidney failure, treatment consists of dietary restriction of phosphorus; supplements containing an active form of vitamin D, such as calcitriol, doxercalciferol, paricalcitol; and phosphate binders, which are either calcium-based and non-calcium based.
High turnover of tumor cells leads to spill of potassium into the blood. Symptoms usually do not manifest until levels are high (> 6.5 mmol/L) [normal 3.5–5.0 mmol/L] and they include [8] palpitations, cardiac conduction abnormalities, and arrhythmias (can be fatal) muscle weakness or paralysis; Hyperphosphatemia.