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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]
Symptoms of hyperparathyroidism are caused by inappropriately normal or elevated blood calcium excreted from the bones and flowing into the blood stream in response to increased production of parathyroid hormone. [1] In healthy people, when blood calcium levels are high, parathyroid hormone levels should be low.
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.
High potassium levels may lead to potentially fatal disruptions in heart rhythm. 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.
Familial hypocalciuric hypercalcemia (FHH) is an inherited condition that can cause hypercalcemia, a serum calcium level typically above 10.2 mg/dL; although uncommon. [1] It is also known as familial benign hypocalciuric hypercalcemia (FBHH) where there is usually a family history of hypercalcemia which is mild, a urine calcium to creatinine ratio <0.01, and urine calcium <200 mg/day ...
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.
[7] [8] In 1926 the Japanese physician Tetsushiro Shinosaki, from Fukuoka, observed the high rate of thyroid disease in Japanese people with periodic paralysis. [9] [10] The first English-language report, in 1931, originated from Dunlap and Kepler, physicians at the Mayo Clinic; they described the condition in a patient with features of Graves ...
If the sodium level is <120 mEq/L, the person can be treated with hypertonic saline as extremely low levels are associated with severe neurological symptoms. [14] In non-emergent situations, it is important to correct the sodium slowly to minimize risk of osmotic demyelination syndrome.