Milk-alkali syndrome, which might happen if you take too many calcium antacids like calcium carbonate (TUMS) Medications, such as lithium, thiazide diuretics, and tamoxifen There are other causes of hypercalcemia, though they are less common. Certain kinds of cancer are more likely to lead to high calcium, such as: It can also release proteins that work just like parathyroid hormone. CancerĬancer can increase calcium in the blood by spreading to bone and breaking it down. When there’s too much of it in the body, calcium levels start to rise. It releases parathyroid hormone, which plays a critical role in bone metabolism and the control of calcium levels. The parathyroid gland sits right behind the thyroid gland in the neck. Hyperparathyroidism occurs when the parathyroid gland makes too much hormone. More than 90% of all cases of hypercalcemia are the result of two conditions - hyperparathyroidism and cancer. We’ll cover the different causes of hypercalcemia, associated symptoms, medical complications, and treatment. And in severe cases, this condition can be life-threatening. People with mild cases might feel normal, but moderate or high levels of calcium can often cause symptoms. Certain conditions and circumstances can disrupt these processes, leading to high calcium levels. The body controls calcium levels by changing the way it takes it from bone or filters it through the kidneys. Hypercalcemia is the medical term for too much calcium in the blood.
Although severe cases are rare, they can be life-threatening and require emergency care to lower the calcium level quickly. Hydration is the main treatment for hypercalcemia. It can even lead to a dangerously low heart rate or high blood pressure. One caveat to this may be patients who have developed an interstitial nephritis (secondary to calcium deposition in the medulla ) from prolonged hypercalcaemia.Symptoms of hypercalcemia include weakness and fatigue, loss of appetite, mood changes such as depression, and constipation. Thankfully, the polyuria and concentrating defects associated with hypercalcaemia tend to regress with correction of the calcium levels.
Activation of these, in the setting of increased distal calcium delivery, down-regulates AQP2 expression, again resulting in an inability to concentrate the urine.įinally, there may be hypercalcaemia-induced PGE2 production in the thick ascending limb, which can further inhibit sodium chloride reabsorption. This in turn inhibits potassium recycling and thereby shuts off the NKCC2 cotransporter, leading to decreased reabsorption of sodium, potassium and chloride in this segment.įollowing on from this, the medullary concentration gradient is diminished, leading to an inablility to concentrate urine and subsequent polyuria.ĬaSR are also found on the luminal surface of cells in the inner medullary collecting duct. Binding of calcium, with subsequent receptor activation, appears to induce a downstream message to close off the luminal K channel. I wanted to share what I have learned in relation to the mechanisms of this phenomenon.Ĭalcium-sensing receptors (CaSR) are found on the basolateral membrane of the cells of the thick ascending limb of the loop of Henle. So Leo’s post got me thinking about the pathophysiology of hypercalcaemia-induced polyuria.
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