Why do loop diuretics cause hypocalcemia

Hypocalcemia is particularly a problem for people who are hospitalized. If your calcium is only a little low, you might not notice any symptoms from hypocalcemia. You are also less likely to experience symptoms if your calcium has been gradually lowered over time. Hypocalcemia may cause symptoms such as the following:. However, not everyone will experience all these symptoms. Sometimes these symptoms are relatively mild, but in other situations they may cause life-threatening problems.

Most people know that calcium is a component of your bones. In fact, calcium is involved in many important biological processes. For example, it plays roles in blood clotting and in helping certain enzymes to function. It is also critical for proper signaling in your nerves and muscles, including your heart muscle. Because of this, your body works to tightly regulate the amount of calcium present in your blood.

For example, if your calcium levels are too low, your parathyroid glands will normally release parathyroid hormone PTH. This hormone works to increase your calcium in different ways, like reducing the amount of calcium released in your urine. Normally, the action of PTH brings the calcium back into a normal range.

Hypocalcemia can have many different potential underlying causes. Because of the key role of PTH, it is not surprising that a low level of this hormone called hypoparathyroidism is one of the main causes of low calcium. Some of the reasons for this include injury to the parathyroid gland from surgery or radiation treatment, autoimmune disease, or a genetic disease leading to low PTH.

Low vitamin D is also another important cause of hypocalcemia. People can have low vitamin D from a number of different problems, such as:. Problems with certain blood electrolytes can also sometimes lead to hypocalcemia. For example, abnormal levels of the electrolytes magnesium and phosphate might indirectly cause hypocalcemia. Some other less common causes of hypocalcemia include pancreatitis and cancer which has spread to the bones.

A number of drugs sometimes cause hypocalcemia as a side effect. Some of these include the following:. For a variety of reasons, people who are critically ill have a higher risk of hypocalcemia. This can be due to underlying medical problems, sepsis, electrolyte problems, certain kinds of blood transfusions that affect calcium, or other factors.

Various signs and symptoms might make a clinician suspect hypocalcemia. Your healthcare provider will take a full medical history and ask you about your recent symptoms. Things like muscle cramps or pain and tingling in the fingers might make the clinician think of hypocalcemia. A complete exam is also an important part of diagnosis. Your healthcare provider might tap you lightly at a certain place on your cheek.

People with hypocalcemia may involuntarily contract their facial muscles in response. Definitive diagnosis of hypocalcemia requires a blood test for calcium. Calcium is a common blood test often performed with other tests as part of a basic metabolic panel BMP or a complete metabolic panel CMP.

Calcium is usually first assessed through a total calcium blood test. This measures the calcium that is free in the blood as well as the calcium that is bound to a common protein in the blood called albumin. If this test is low, you might need a test of your albumin. This can help your clinician get a more accurate idea about whether your calcium level really is a problem.

Hypocalcemia is usually defined as having a corrected total serum calcium of less than 2. The PCT, which lies within the cortex , is the site of sodium, water and bicarbonate transport from the filtrate urine , across the tubule wall, and into the interstitium of the cortex. This sodium is reabsorbed isosmotically, meaning that every molecule of sodium that is reabsorbed is accompanied by a molecule of water.

As the tubule dives into the medulla, or middle zone of the kidney, the tubule becomes narrower and forms a loop Loop of Henle that reenters the cortex as the thick ascending limb TAL that travels back to near the glomerulus.

Because the interstitium of the medulla is very hyperosmotic and the Loop of Henle is permeable to water, water is reabsorbed from the Loop of Henle and into the medullary interstitium.

This loss of water concentrates the urine within the Loop of Henle. The TAL, which is impermeable to water, has a cotransport system that reabsorbs sodium, potassium and chloride at a ratio of Finally, the tubule dives back into the medulla as the collecting duct and then into the renal pelvis where it joins with other collecting ducts to exit the kidney as the ureter.

It is important to note two things about this transporter. First, its activity is dependent on the tubular concentration of sodium, so that when sodium is high, more sodium is reabsorbed and more potassium and hydrogen ion are excreted. Second, this transporter is regulated by aldosterone, which is a mineralocorticoid hormone secreted by the adrenal cortex. Increased aldosterone stimulates the reabsorption of sodium, which also increases the loss of potassium and hydrogen ion to the urine.

Finally, water is reabsorbed in the collected duct through special pores that are regulated by antidiuretic hormone , which is released by the posterior pituitary. ADH increases the permeability of the collecting duct to water, which leads to increased water reabsorption, a more concentrated urine and reduced urine outflow antidiuresis.

Diuretic drugs increase urine output by the kidney i. This is accomplished by altering how the kidney handles sodium. If the kidney excretes more sodium, then water excretion will also increase. Most diuretics produce diuresis by inhibiting the reabsorption of sodium at different segments of the renal tubular system. Sometimes a combination of two diuretics is given because this can be significantly more effective than either compound alone synergistic effect.

The reason for this is that one nephron segment can compensate for altered sodium reabsorption at another nephron segment; therefore, blocking multiple nephron sites significantly enhances efficacy. Loop diuretics inhibit the sodium-potassium-chloride cotransporter in the thick ascending limb see above figure. This altered handling of sodium and water leads to both diuresis increased water loss and natriuresis increased sodium loss.

By acting on the thick ascending limb, which handles a significant fraction of sodium reabsorption, loop diuretics are very powerful diuretics. These drugs also induce renal synthesis of prostaglandins, which contributes to their renal action including the increase in renal blood flow and redistribution of renal cortical blood flow.

Thiazide diuretics , which are the most commonly used diuretic, inhibit the sodium-chloride transporter in the distal tubule. Nevertheless, they are sufficiently powerful to satisfy many therapeutic needs requiring a diuretic.

Their mechanism depends on renal prostaglandin production. Because loop and thiazide diuretics increase sodium delivery to the distal segment of the distal tubule, this increases potassium loss potentially causing hypokalemia because the increase in distal tubular sodium concentration stimulates the aldosterone-sensitive sodium pump to increase sodium reabsorption in exchange for potassium and hydrogen ion, which are lost to the urine.

The increased hydrogen ion loss can lead to metabolic alkalosis. Does Hypernatremia cause water retention? In hypernatremia, high blood sodium levels draw water out of the brain cells, causing dehydration and shrinkage. Water excretion by the kidneys is mainly regulated by vasopressin, a hypothalamic hormone that causes the kidneys to retain water in response to low blood volume or high plasma osmolality. How does Hypernatremia affect the heart?

Hypernatremia can cause brain shrinkage, resulting in vascular rupture and intracranial bleeding. The actual pathophysiology of hypernatremia on cardiac dysfunction is unknown.

Why is there Hypernatremia in diabetes insipidus? The main symptom of all cases of diabetes insipidus is frequently needing to pass high volumes of diluted urine. Extreme dehydration can lead to hypernatremia, a condition in which the sodium concentration of the serum in the blood becomes very high due to low water retention.

The cells of the body also lose water. What causes elevated sodium? Certain conditions may cause an excess of sodium in the blood. Specific causes of hypernatremia include: Dehydration or a loss of body fluids from prolonged vomiting, diarrhea, sweating or high fevers.

Drugs such as steroids, licorice, and certain blood pressure lowering medicines. Which is the initial treatment for Hypernatremia? Does Lasix increase serum sodium? A loop diuretic, for example, furosemide, may be added to this treatment, as it may cause hypotonic urine. Do potassium sparing diuretics cause hyponatremia?

This carries out sodium, water, and potassium. Potassium sparing diuretics work in the cortical collecting duct to prevent sodium reabsorption, thereby preventing potassium secretion. Thiazide diuretics can cause hypercalcemia while loop diuretics increase the excretion of calcium which can lead to hypocalcemia.