The action of hormones such as atrial natriuretic peptide and vasopressin along with signals such as blood volume and reduced blood pressure are what stimulates the kidneys to release sodium and water.
When your blood volume increases, your kidneys respond by filtering more fluid and excreting more sodium and water through a process called pressure natriuresis.
And Atrial Natriuretic Peptide is released by your heart in response to high blood volume and atrial natriuretic peptide inhibits sodium and water reabsorption in your kidneys and promotes their excretion.
And ADH, also called antidiuretic hormone is released in response to low blood pressure or high blood osmolarity and promotes water reabsorption in your kidneys and conserves water.
The RAAS is also a complex system which regulates your blood pressure and your fluid volume.
And when your blood pressure drops, your kidneys release renin, which triggers the production of angiotensin II which in turn stimulates the release of aldosterone.
Aldosterone is what promotes sodium reabsorption in your kidneys and leads to water retention and also increased blood volume.
Low levels of antidiuretic hormone decreases water reabsorption in the kidneys which decrease the permeability of the cells of the collecting duct so that large quantities of dilute urine are excreted.
And an antidiuretic hormome arginine vasopressin is secreted from your posterior pituitary gland, under the influence of the hypothalamus.
To increase water retention in the kidneys vasopressin also known as ADH or antidiuretic hormone is released.
The antidiuretic hormone signals the kidneys to reabsorb more water and decreases urine output and also increasing the water levels in your body.
ADH or antidiuretic hormones are produced in the hypothalamus and is stored in the posterior pituitary gland and acts primarily on your kidneys to increase water reabsorption.
The ADH triggers the insertion of water channels called aquaporins into the collecting duct cells of your kidneys and allows water to move out of your urine and back into your bloodstream.
Other hormones are also involved which include the renin-angiotensin, aldosterone system, which plays a role in water and sodium balance, with aldosterone, which is another hormone, promoting sodium retention, which leads to water retention indirectly.
The release of ADH is triggered by factors such as increased blood osmolarity, concentrations of solutes in the blood, low blood pressure and decreased blood volume.
And in some cases your body may produce too much ADH which leads to excessive water retention and hyponatremia which is low sodium levels in your blood and is a condition called SIADH.
The urine sodium level in SIADH is often greater than 40 mEq/L or 40 mmol/L as a result of the body retaining water and diluting the sodium levels in your blood.
Normal urine sodium levels are often between 40 to 220 mEq/day or 40 to 220 mmol/day.
In SIADH the kidneys inappropriately retain water which leads to dilution of the sodium levels in your blood which is called hyponatremia and also causes a decrease in urine output.
And in some cases of SIADH, the increase in water in your body signals the kidneys to release an increased amount of salt in your urine.
The organ that SIADH affects is the kidneys which causes the kidneys to retain excess water and causes hyponatremia which is low sodium levels in your blood.
The way you fix sodium in SIADH is through fluid restriction and in some cases medications which increase water excretion or block the effects of vasopressin.
A salt solution given through an IV in the hospital is sometimes used for fixing sodium levels in SIADH.
With SIADH you don't restrict sodium but instead you restrict fluid and in some cases a high sodium diet may be considered in chronic situations to help manage the hyponatremia in SIADH.
Fluid restriction is the first line treatment for SIADH, which aims to prevent further dilution of sodium levels.
And the specific amount of fluid restriction will also vary depending on the individuals urine output, symptoms and severity of hyponatremia.
A common starting point when restricting fluid intake for SIADH is less than the urine output or a target of 800-1200 mL per 24 hours.
Restricting fluid intake is the most common treatment for SIADH as the condition of SIADH involves your body retaining too much water.
Medications such as loop diuretics are also sometimes used to help the kidneys excrete excess water and sodium although they are also often used in conjunction with fluid restriction.
And vasopressin receptor antagonists such as vaptans are medications which block the action of ADH or antidiuretic hormone and allows your kidneys to excrete more water.
And an antibiotic called demeclocycline can also be used to reduce the effects of ADH.
A hypertonic saline may also be used in severe cases of hyponatremia when associated with SIADH and is given through an IV which is a concentrated salt solution that can be used to rapidly raise your sodium levels but it has to be done under close medical solution.
And Urea which is a solute that must be excreted by your kidneys can be used to increase your osmotic load and increase urine volume which can help with free water excretion.
The drug of choice for SIADH is vasopressin receptor antagonists or vaptans such as conivaptan and tolvaptan, which are used along with fluid restriction and in severe enough cases hypertonic saline.
The reason why you should not give normal saline in SIADH is because it can worsen hyponatremia which is low sodium levels by causing water retention and diluting of the blood as the persons kidneys are already retaining water as a result of excessive ADH.
In SIADH, your body retains water as a result of the inappropriate release of antidiuretic hormone ADH which leads to hyponatremia.
Giving normal saline in SIADH will lower the serum sodium even more.
The most serious complication of SIADH is hyponatremia which causes your body to retain too much water and leads to a dilution of sodium in your blood.
Other serious complications that can occur from SIADH are brain swelling and brain damage that can lead to seizures, confusions, hallucinations, coma and even death if your sodium levels drop too rapidly.
And other complications such as respiratory failure and brain herniation can occur with SIADH although they are less common.
The 4 patterns of SIADH are types A, B, C and D and each are characterized by a distinct pattern of arginine vasopressin secretion across a range of plasma osmolalities.
Type A SIADH is characterized by secretion of AVP that is unregulated, independent of plasma osmolality, leading to severe hyponatremia.
Type B SIADH involves elevated basal secretion of AVP despite normal regulation by osmolality, with AVP secretion occurring at lower plasma osmolalities than normal.
Type C SIADH is failure to suppress AVP at plasma osmolalities below the osmotic threshold, resulting in inappropriately high AVP levels even at low plasma osmolalities.
Type D SIADH is when you have low or undetectable AVP levels and potentially due to a gain of function mutation of the V2 receptor, which may be more appropriately termed syndrome of inappropriate antidiuresis.
SIADH is also known as syndrome of inappropriate antidiuretic hormone secretion.