Dehydration?
Trying to figure out this sodium/water situation. My sodium level was relatively high (143, which is at the highest end of normal) when I saw my nephrologist last week, and yet she told me to not only drink a lot of water but also eat salty foods and drink Gatorade for a few days until the next blood draw (which was yesterday).
This instruction to eat salty food when my sodium level was already on the high side has confused me. I've been trying to figure it out by searching online, but have had a lot of trouble.
Hypernatremia
From Wikipedia:
Hypernatremia or hypernatraemia (see American and British English spelling differences) is an electrolyte disturbance that is defined by an elevated sodium level in the blood.[1] Hypernatremia is generally not caused by an excess of sodium, but rather by a relative deficit of free water in the body. For this reason, hypernatremia is often synonymous with the less precise term, dehydration.
From later in the same Wikipedia article re: causes of hypernatremia:
Hypovolemic:
- Inadequate intake of free water associated with total body sodium depletion. Typically in elderly or otherwise disabled patients who are unable to take in water as their thirst dictates and also are sodium depleted. This is the most common cause of hypernatremia.
- Excessive losses of water from the urinary tract, which may be caused by glycosuria, or other osmotic diuretics - leads to a combination of sodium and free water losses.
...
Euvolemic:
- Excessive excretion of water from the kidneys caused by diabetes insipidus, which involves either inadequate production of the hormone vasopressin, from the pituitary gland or impaired responsiveness of the kidneys to vasopressin.
Diabetes Insipidus
The Wikipedia page on diabetes insipidus also notes:
Excessive urination and extreme thirst (especially for cold water and sometimes ice or ice water) are typical for DI.[2] The symptoms of excessive urination and extreme thirst are similar to what is seen in untreated diabetes mellitus, with the distinction that the urine does not contain glucose. Blurred vision is a rarity. Signs of dehydration may also appear in some individuals, since the body cannot conserve much (if any) of the water it takes in.
The extreme urination continues throughout the day and the night. In children, DI can interfere with appetite, eating, weight gain, and growth, as well. They may present with fever, vomiting, or diarrhea. Adults with untreated DI may remain healthy for decades as long as enough water is consumed to offset the urinary losses. However, there is a continuous risk of dehydration and loss of potassium.
Also, later in the same article:
To distinguish DI from other causes of excess urination, blood glucose levels, bicarbonate levels, and calcium levels need to be tested. Measurement of blood electrolytes can reveal a high sodium level (hypernatremia as dehydration develops).
Also:
Electrolyte and volume homeostasis is a complex mechanism that balances the body's requirements for blood pressure and the main electrolytes sodium and potassium. In general, electrolyte regulation precedes volume regulation. When the volume is severely depleted, however, the body will retain water at the expense of deranging electrolyte levels.
The regulation of urine production occurs in the hypothalamus, which produces ADH in the supraoptic and paraventricular nuclei. After synthesis, the hormone is transported in neurosecretory granules down the axon of the hypothalamic neuron to the posterior lobe of the pituitary gland, where it is stored for later release. In addition, the hypothalamus regulates the sensation of thirst in the ventromedial nucleus by sensing increases in serum osmolarity and relaying this information to the cortex.
Neurogenic/central DI results from a lack of ADH; occasionally it can present with decreased thirst as regulation of thirst and ADH production occur in close proximity in the hypothalamus. It is encountered as a result of hypoxic encephalopathy, neurosurgery, autoimmunity or cancer, or sometimes without an underlying cause (idiopathic).
The main effector organ for fluid homeostasis is the kidney. ADH acts by increasing water permeability in the collecting ducts and distal convoluted tubules; specifically, it acts on proteins called aquaporins and more specifically aquaporin 2 in the following cascade; ADH (argenine vasopressin-AVP) produced in the hypothalamus and stored in the posterior pituitary. When released, ADH binds to V2 G-protein coupled receptors within the distal convoluted tubules, increasing cyclic AMP, which couples with protein kinase A, stimulating translocation of the aquaporin 2 channel stored in the cytoplasm of the distal convoluted tubules and collecting ducts into the apical membrane. These transcribed channels allow water into the collecting duct cells. The increase in permeability allows for reabsorption of water into the bloodstream, thus concentrating the urine.
Vasopression
This article also points to a separate Wikipedia article on vasopressin:
Arginine vasopressin (AVP), also known as vasopressin, argipressin or antidiuretic hormone (ADH), is a neurohypophysial hormone found in most mammals. Its two primary functions are to retain water in the body and to constrict blood vessels. Vasopressin regulates the body's retention of water by acting to increase water absorption in the collecting ducts of the kidney nephron.[1][2] Vasopressin is a peptide hormone that increases water permeability of the kidney's collecting duct and distal convoluted tubule by inducing translocation of aquaporin-CD water channels in the kidney nephron collecting duct plasma membrane.[3] It also increases peripheral vascular resistance, which in turn increases arterial blood pressure. It plays a key role in homeostasis, by the regulation of water, glucose, and salts in the blood.
In the same article:
Lack of AVP
Decreased AVP release or decreased renal sensitivity to AVP leads to diabetes insipidus, a condition featuring hypernatremia (increased blood sodium concentration), polyuria (excess urine production), and polydipsia (thirst).
I'm not sure what all I learned, except that -- as the nephrologist mentioned when I last saw her -- diabetes insipidus may still be a problem for me. I'm not thirsty or peeing as much as I was when I was on lithium, but it's still much more extreme than the average person.
My nephrologist says she can talk to me on the phone tomorrow morning, so I can ask her questions then. I've been anxious and confused, so it will be good to get some answers. Also, maybe she'll have my new lab results by then.
This instruction to eat salty food when my sodium level was already on the high side has confused me. I've been trying to figure it out by searching online, but have had a lot of trouble.
Hypernatremia
From Wikipedia:
Hypernatremia or hypernatraemia (see American and British English spelling differences) is an electrolyte disturbance that is defined by an elevated sodium level in the blood.[1] Hypernatremia is generally not caused by an excess of sodium, but rather by a relative deficit of free water in the body. For this reason, hypernatremia is often synonymous with the less precise term, dehydration.
From later in the same Wikipedia article re: causes of hypernatremia:
Hypovolemic:
- Inadequate intake of free water associated with total body sodium depletion. Typically in elderly or otherwise disabled patients who are unable to take in water as their thirst dictates and also are sodium depleted. This is the most common cause of hypernatremia.
- Excessive losses of water from the urinary tract, which may be caused by glycosuria, or other osmotic diuretics - leads to a combination of sodium and free water losses.
...
Euvolemic:
- Excessive excretion of water from the kidneys caused by diabetes insipidus, which involves either inadequate production of the hormone vasopressin, from the pituitary gland or impaired responsiveness of the kidneys to vasopressin.
Diabetes Insipidus
The Wikipedia page on diabetes insipidus also notes:
Excessive urination and extreme thirst (especially for cold water and sometimes ice or ice water) are typical for DI.[2] The symptoms of excessive urination and extreme thirst are similar to what is seen in untreated diabetes mellitus, with the distinction that the urine does not contain glucose. Blurred vision is a rarity. Signs of dehydration may also appear in some individuals, since the body cannot conserve much (if any) of the water it takes in.
The extreme urination continues throughout the day and the night. In children, DI can interfere with appetite, eating, weight gain, and growth, as well. They may present with fever, vomiting, or diarrhea. Adults with untreated DI may remain healthy for decades as long as enough water is consumed to offset the urinary losses. However, there is a continuous risk of dehydration and loss of potassium.
Also, later in the same article:
To distinguish DI from other causes of excess urination, blood glucose levels, bicarbonate levels, and calcium levels need to be tested. Measurement of blood electrolytes can reveal a high sodium level (hypernatremia as dehydration develops).
Also:
Electrolyte and volume homeostasis is a complex mechanism that balances the body's requirements for blood pressure and the main electrolytes sodium and potassium. In general, electrolyte regulation precedes volume regulation. When the volume is severely depleted, however, the body will retain water at the expense of deranging electrolyte levels.
The regulation of urine production occurs in the hypothalamus, which produces ADH in the supraoptic and paraventricular nuclei. After synthesis, the hormone is transported in neurosecretory granules down the axon of the hypothalamic neuron to the posterior lobe of the pituitary gland, where it is stored for later release. In addition, the hypothalamus regulates the sensation of thirst in the ventromedial nucleus by sensing increases in serum osmolarity and relaying this information to the cortex.
Neurogenic/central DI results from a lack of ADH; occasionally it can present with decreased thirst as regulation of thirst and ADH production occur in close proximity in the hypothalamus. It is encountered as a result of hypoxic encephalopathy, neurosurgery, autoimmunity or cancer, or sometimes without an underlying cause (idiopathic).
The main effector organ for fluid homeostasis is the kidney. ADH acts by increasing water permeability in the collecting ducts and distal convoluted tubules; specifically, it acts on proteins called aquaporins and more specifically aquaporin 2 in the following cascade; ADH (argenine vasopressin-AVP) produced in the hypothalamus and stored in the posterior pituitary. When released, ADH binds to V2 G-protein coupled receptors within the distal convoluted tubules, increasing cyclic AMP, which couples with protein kinase A, stimulating translocation of the aquaporin 2 channel stored in the cytoplasm of the distal convoluted tubules and collecting ducts into the apical membrane. These transcribed channels allow water into the collecting duct cells. The increase in permeability allows for reabsorption of water into the bloodstream, thus concentrating the urine.
Vasopression
This article also points to a separate Wikipedia article on vasopressin:
Arginine vasopressin (AVP), also known as vasopressin, argipressin or antidiuretic hormone (ADH), is a neurohypophysial hormone found in most mammals. Its two primary functions are to retain water in the body and to constrict blood vessels. Vasopressin regulates the body's retention of water by acting to increase water absorption in the collecting ducts of the kidney nephron.[1][2] Vasopressin is a peptide hormone that increases water permeability of the kidney's collecting duct and distal convoluted tubule by inducing translocation of aquaporin-CD water channels in the kidney nephron collecting duct plasma membrane.[3] It also increases peripheral vascular resistance, which in turn increases arterial blood pressure. It plays a key role in homeostasis, by the regulation of water, glucose, and salts in the blood.
In the same article:
Lack of AVP
Decreased AVP release or decreased renal sensitivity to AVP leads to diabetes insipidus, a condition featuring hypernatremia (increased blood sodium concentration), polyuria (excess urine production), and polydipsia (thirst).
I'm not sure what all I learned, except that -- as the nephrologist mentioned when I last saw her -- diabetes insipidus may still be a problem for me. I'm not thirsty or peeing as much as I was when I was on lithium, but it's still much more extreme than the average person.
My nephrologist says she can talk to me on the phone tomorrow morning, so I can ask her questions then. I've been anxious and confused, so it will be good to get some answers. Also, maybe she'll have my new lab results by then.