Polyuria - various causes. Renal failure polyuria Polyuria pathogenesis

Definition: polyuria - the discharge of more than 3 liters of urine per day. Polyuria is the discharge of urine in a volume of more than 5 liters / day; it must be distinguished from pollakiuria, which consists in the need to urinate many times during the day or night at a normal or reduced daily volume.

Pathogenesis of polyuria

Water homeostasis is regulated by a complex mechanism of balance of water consumption (which itself is also comprehensively regulated), renal perfusion, glomerular filtration and reabsorption of soluble electrolytes in the tubules and water in the collecting system of the kidneys.

When water intake is increased, circulating blood volume increases, which increases renal perfusion and GFR and leads to an increase in urine volume. However, increasing water intake decreases blood osmolality, which decreases the secretion of ADH (also known as arginine vasopressin) from the hypothalamic pituitary system. Since ADH stimulates the reabsorption of water in the collecting tubules of the kidneys, a decrease in ADH increases the volume of urine, which allows the body's water balance to return to normal.

In addition, high concentrations of soluble electrolytes in the renal tubules induce passive osmotic diuresis and thus an increase in urine output. A classic example of such a process is glucose-induced osmotic diuresis in uncompensated diabetes mellitus, when high concentrations of glucose in the urine (more than 250 mg / dl) exceed the reabsorption capacity of the tubules, which leads to a high concentration of glucose in the renal tubules; water enters their lumen passively, causing polyuria and glucosuria.

Therefore, polyuria occurs in any process that includes:

Prolonged increase in the amount of water consumed (polydipsia).
Decreased secretion of ADH (central variant of diabetes insipidus).
Decreased peripheral sensitivity to ADH (renal variant of diabetes insipidus),
Osmotic diuresis.

The causes of polyuria

The duration and severity of polyuria (nocturia, urinary frequency, fluid intake at night).
Family history (diabetes mellitus, polycystic kidney disease, urolithiasis).
Taking medications (diuretics, analgesics, lithium, etc.).
Kidney stones (hypercalcemia).
Weakness (hypocapaemia), depression (hypercalcemia).
The presence of mental disorders.
Endocrine disorders (violation of menstrual function, sexual function, lactation, violation of pubic hair growth).
Other serious illnesses.

Kidney stones: causes

Excessive fluid intake.
Endocrine dysfunction.
Hypokalemia.
Renal diseases (polycystic kidney disease, nephropathy while taking analgesics, polycystic kidney disease, amyloidosis).
Condition after elimination of urinary tract obstruction, for example, after catheterization in a patient with chronic urinary retention. Condition after renal artery angioplasty.
Stimulation of diuresis while taking medications (furosemide, alcohol, lithium preparations, amphotericin B, vinblastine, demeclocycline, cisplatin).

Symptoms and signs of polyuria

Clouding of consciousness (against the background of hyponatremia or dehydration).
Coma.
Proteinuria.
Depression or other mental health problems.

Polyuria: laboratory and instrumental research methods

Urea and electrolytes (kidney disease, hypokalemia).
Blood glucose.
Calcium, phosphates and alkaline phosphatase.
Osmolarity of plasma and urine [the ratio of osmolality of urine and plasma less than 1.0 indicates diabetes insipidus, parenchymal kidney disease (accompanied by hypokalemia) or excessive intake of water against a background of hysteria].
Radiography of the abdominal organs (nephrocalcinosis).
If possible, determine the level of lithium preparations in the blood.
Determination of protein fractions.

Collecting anameses... Collecting an anamnesis of the present disease should include obtaining information on the volume of fluid consumed and excreted in order to differentiate between polyuria and pollakiuria. If polyuria is present, the patient should be asked about the age at which it onset, the rate of onset (i.e., sudden or gradual onset), and any clinically significant recent emerging factors that could cause polyuria (e.g. intravenous infusion, gastric probe, relief of urinary tract obstruction, stroke, head trauma, surgery).

When collecting a medical history, it is necessary to pay attention to the diseases associated with polyuria. It is necessary to find out if there are any cases of polyuria in the family. When collecting a medical history, it should be noted the use of any drugs associated with renal diabetes insipidus, and the use of substances that increase urine output (for example, diuretics, alcohol, drinks with caffeine).

Physical examination... On general examination, signs of obesity and malnutrition or cachexia should be noted, which may indicate an underlying malignant neoplasm or an eating disorder with secret diuretic use.

On examination of the head and neck, it is necessary to note the presence of dry eyes or mucous membranes in the mouth (Sjogren's syndrome). Examination of the skin should look for any hyperpigmented or hypopigmented lesions, ulcers, or subcutaneous nodules that may indicate sarcoidosis. A complete neurologic examination should note the presence of local neurologic deficits, which may indicate a stroke, and assess mental status for signs of a mental disorder.

Warning signs... The following data deserve special attention:

Extra-sudden appearance of polyuria or its appearance during the first years of life.
Night sweats, coughs, and weight loss, especially when there is a long history of smoking.
Mental illness.

Interpreting data... When taking anamnesis, it is often possible to distinguish polyuria from pollakiuria, but in rare cases, daily collection of Sochi may be required.

On clinical examination, a cause can be suspected, but laboratory tests are usually required. Diabetes insipidus is indicated by a history of cancer or chronic granulomatous disease (due to hypercalcemia), the use of certain drugs (lithium, cidofovir, foscarnet, and phosphamide), and more rare diseases (for example, renal amyloidosis, sarcoidosis, Sjogren's syndrome), which often have more bright and early manifestations than polyuria.

The sharp onset of polyuria at a certain time, as well as the patient's tendency to drink cold or ice water, indicate central diabetes insipidus. Symptom onset in the first few years of life is usually associated with hereditary forms of central or renal diabetes insipidus or decompensated type 1 diabetes mellitus. A history of diuretic use or diabetes mellitus indicates polyuria due to diuresis. Psychogenic polydipsia is more common in patients with a history of psychiatric disorders (mainly bipolar disorder or schizophrenia); less often it is one of the symptoms of the onset of the disease.

Laboratory research... If an increase in the amount of excreted urine is confirmed by history or quantitative changes, it is necessary to determine the glucose content in serum or urine to exclude decompensated diabetes mellitus.

If hyperglycemia is absent, the following tests are required:

biochemical analysis of blood and urine;
determination of serum and urine osmolality, sometimes serum ADH levels.

These studies are aimed at detecting hypercalcemia, hypokalemia (due to secret use of diuretics), as well as hyper- and hyponatremia.

Hypernatremia indicates an excessive loss of free water due to central or renal diabetes insipidus.
Hyponatremia (sodium level less than 137 mEq / L) indicates an excess supply of free water due to polydipsia.
Osmolality of urine is usually less than 300 mosm / kg with water diuresis and more than 300 mosm / kg with osmotic diuresis.

If the diagnosis is unclear, serum and urine sodium levels should be measured in response to a water deprivation test and exogenous ADH challenge. Since the study may develop severe dehydration, it should be done only with constant medical supervision, hospitalization is usually required. In addition, patients with suspected psychogenic polydipsia should be observed in order to exclude secret fluid intake.

The test begins in the morning with weighing the patient, taking blood from a vein to determine the concentration of electrolytes in the serum and its osmolality, as well as the osmolality of urine. Every hour the patient urinates and urine osmolality is measured. Dehydration is continued until the appearance of orthostatic hypotension and postural tachycardia, a decrease in the initial body weight by 5% or more, or an increase in urine osmolality of more than 30 mosm / kg in sequentially collected samples. Serum electrolyte levels and osmolality are then determined again, and 5 units of an aqueous solution of s / c vasopressin are injected. The urine for the study of its osmolality is collected for the last time one hour after the injection, and this is the end of the sample.

With a normal response, the maximum urine osmolality is achieved after dehydration (more than 700 mosm / kg) and the osmolality does not increase by more than 5% after vasopressin injection.

With central diabetes insipidus, patients have an inability to concentrate urine to an osmolality higher than that of plasma, but this ability appears after the administration of vasopressin. The increase in osmolality reaches 50-100% in central diabetes insipidus and 15-45% in subclinical central diabetes insipidus.

In the renal form of diabetes insipidus, patients experience an inability to concentrate urine to an osmolality exceeding that of plasma, and this inability persists with the administration of vasopressin. Sometimes in subclinical renal diabetes insipidus, the increase in urine osmolality can reach 45%, but this increase is much lower than that in subclinical central diabetes insipidus. Four out of five people have had back pain at least once, most often in the lower (lumbar) spine, back, or neck.

Measurement of free ADH is the most direct method for diagnosing central diabetes insipidus. The level at the end of the water deprivation test (before the injection of vasopressin) is reduced in central diabetes insipidus and correspondingly increased in renal diabetes insipidus. However, the ability to determine the level of ADH is not universally present. In addition, the water deprivation test is so accurate that direct measurement of ADH is rarely required.

Polyuria treatment

The state of hydration is assessed (pressure in the jugular vein, blood pressure, changes in blood pressure when changing body position, dynamics of body weight, CVP).

The fluid balance is carefully measured and the patient is weighed daily.

The central vein is catheterized to monitor the CVP.

Determine the content of sodium and potassium in the urine (examination of a separate portion of urine allows at first to suspect excessive loss of these electrolytes in the urine, which is an indication for a more thorough examination with an interval of less than 6 hours).

They compensate for the lack of fluid with saline solutions and glucose solution, maintaining normal homeostasis.

The concentration of potassium, calcium, phosphates and magnesium in the blood is monitored daily, and if necessary twice a day.

They do not pursue the goal of completely replacing the lost fluid. After the patient is adequately rehydrated, it is necessary to stop intravenous fluid administration, allowing the mechanism of physiological homeostasis to independently restore the body's water balance.

If diabetes insipidus is suspected, a fluid restriction test is performed.

Polyuria. Fluid restriction test

All drugs are canceled the day before the test; the patient should not smoke or drink coffee.

The patient is carefully monitored so that he does not secretly drink the liquid.

The patient should empty the bladder after a light breakfast. Then he must not drink.

The patient is weighed at the beginning of the sample, and then after 4, 5, 6, 7, 8 hours (the study is stopped if there is a loss of more than 3% of body weight).

Plasma osmolarity is determined after 30 minutes, 4 hours and then every hour until the end of the study (an increase of more than 290 mOsm / l stimulates the release of antidiuretic hormone).

Collect urine every hour and determine its volume and osmolarity (the volume should decrease, and the osmolarity should increase; stop the study if the osmolarity of urine becomes more than 800 mOsm / l, which excludes diabetes insipidus).

If polyuria continues, desmopressin is administered intranasally at a dose of 20 μg with an interval of 8 hours.

After 8 hours, the patient can be allowed to drink. Continue to determine the osmolarity of urine every hour for the next 4 hours.

Interpretation of the results obtained:

Normal response: urine osmolarity rises to more than 800 mOsm / L and increases slightly after desmopressin is administered.
Diabetes insipidus of central origin: urine osmolarity remains low (<400 мОсм/л) и увеличивается более чем на 50% после назначения десмопрессина.
Diabetes insipidus of nephrogenic origin: urine osmolarity remains low (<400 мОсм/л) и немного (<45%) увеличивается после назначения десмопрессина.
Psychogenic polydipsia: urine osmolarity increases (> 400 mOsm / L) but remains less than normal response.

Polyuria in diabetes mellitus

Polyuria is a disease when urination exceeds 2500-3000 milliliters for a long time. It is usually accompanied by increased thirst (polydipsia).

This is a physiological phenomenon that occurs after drinking a large amount of liquid, but it can also indicate a disease. Kidney disease and hormonal fluctuations such as diabetes can be a common cause of polyuria.

Polyuria may be the first symptom of diabetes mellitus, especially type 1 diabetes, so it should not be neglected, especially in young people. Read more about the treatment of polyuria in diabetes mellitus below in the articles I have collected on this topic.

The clinical picture of diabetes was first described about 2000 years ago by the famous philosopher and physician Celsus. In the 17th century, people learned to separate diabetes with "tasteless" urine (diabetes insipidus) from diabetes, in which the urine of patients is "sweet as honey" (diabetes mellitus).

Diabetes mellitus can begin acutely and imperceptibly. Acute onset is more common in children. Polyuria is often the first symptom that attracts parents' attention. It usually manifests itself as bedwetting.

A child who has learned to wake up on his own to empty his bladder becomes untidy again. Often, the disease debuts in a coma, after which worried parents begin to monitor the child more closely and discover that he has polyuria and polydipsia.

Attention!

Polyuria is often the first sign of diabetes in adults. At the same time, the patient develops dry mouth and increased thirst. Very soon, this is joined by other signs of severe diabetes: polyphagia, paradontosis, increasing weakness.

Most untreated patients lose weight quickly, sometimes up to 15-20 kg within one month. The diagnosis of severe diabetes with absolute insulin deficiency is relatively easy. The pronounced severity of two paired signs - polydipsia with polyuria and polyphagia with emaciation - makes one think about diabetes.

The final diagnosis is established by detecting a reduced level of free insulin in the blood, hyperglycemia, etc. When evaluating the results of laboratory research, it should be borne in mind that the most reliable results are obtained by determining the concentration of immunoreactive insulin in the blood.

Positive results of Fehling's and Venedikt's tests indicate the presence of not only glucose in the urine, but also many other reducing substances. False positive results may be due to the presence of other sugars in the urine: lactose, pentose, galactose.

Pentose and fructose are often found in the urine of healthy children after consuming significant amounts of fruit. These sugars and some amino acids can also appear in the urine as congenital metabolic disorders.

False positive test results may be due to the presence in the urine of significant amounts of uric acid, creatinine, salicylates, terpine hydrate, antipyrine, amidopyrine, camphor, synthetic estrogens, which are often taken to prevent pregnancy or suppress lactation.

Polyuria in diabetes mellitus is osmotic in its genesis. Its value is determined by approximately half glucose and half electrolytes and other dense urine substances: decomposition products of proteins, nucleic acids (ammonia, urea, uric acid, creatinine, amino acids), ketone bodies.

Each gram of glucose with moderate polyuria "carries away" 20-40 ml of urine. The more severe the diabetes, the more pronounced the polyuria and the less urine there is for each gram of glucose. This explains the fact that the severity of glucosuria does not always correspond to the severity of polyuria.

The accumulation of significant amounts of intermediate and final metabolic products of proteins, fats and carbohydrates in the blood is accompanied by tissue dehydration. Drying of the mucous membranes of the mouth and pharynx leads to thirst and polydipsia.

Severe hyperglycemia and glucosuria with polyuria are often part of the clinical picture of acromegaly, Itsenko-Cushing's disease, hemochromatosis, and cranial trauma. The picture of diabetes mellitus becomes quite pronounced only in the late stages of these diseases, when the diagnosis of the main suffering is not difficult.

Source: http://lekmed.ru/info/arhivy/poliyriya-i-polidipsiya_2.html

Polyuria: symptoms and treatment

Polyuria is an increase in the volume of urine excreted per day. The daily rate of urine excretion by the body is a liter or one and a half. With polyuria - two, three liters. The disease is often accompanied by frequent urge to cope with a small need. Polyuria is very often mistaken for frequent urination.

The only difference is that with a real accelerated process, a small part of the contents of the bladder is released each time. With polyuria, every trip to the bathroom is accompanied by a copious flow of urine. This disorder is characterized by a decrease in the specific gravity of urine.

This is especially noted in polyuria concomitant with diabetes mellitus - the specific gravity of urine increases (in comparison with the indicators of the urine of a healthy person). The disease is both a complication after kidney disease and a possible symptom indicating the presence of problems with this organ or the neuroendocrine apparatus.

Many people who have this disease accept it as the norm, and do not even try to fight it in any way. This condition is usually caused by kidney disease. But these are not the only etiological factors that can provoke the progression of the disease.

Diseases that cause polyuria include:

chronic renal failure;
pyelonephritis;
sarcoidosis;
various disorders of the nervous system;
cancerous tumors, in particular in the pelvic region;
heart failure;
diseases of the prostate;
diabetes;
stones in the kidneys.

In addition, pregnancy is another cause of increased urine output. During this period of a woman's life, the increased amount of urine produced is due to hormonal disorders, as well as the fact that the fetus exerts strong pressure on the bladder.

But not only internal processes can cause the formation of a manifestation of such a process. An increase in the volume of emitted urine is provoked by the intake of a person: diuretics; a large amount of liquid.

All of the above reasons become prerequisites for the appearance of nocturnal polyuria, which in medicine is called nocturia. In five percent of cases of detection of the disease, the cause of its formation was a genetic predisposition.

Varieties of polyuria

According to the degree of the course of polyuria, it can be:

temporary - provoked by infectious processes in the body or pregnancy;
constant - arising against the background of pathological disorders of the kidneys.

According to the factors of origin, the disease is:

pathological - as a complication after illness. This type includes nocturnal polyuria. Confirmation of the presence of this particular disease is going to the toilet at night (twice or more times). Polyuria in diabetes mellitus is considered pathological;
physiological - associated with the use of drugs that increase urine production.

The only symptom of polyuria is an increase in the amount of urine produced by the body per day. The volume of urine excreted in the presence of polyuria can exceed two liters, with a complicated course or pregnancy - three. In the case when the disease appears due to diabetes mellitus, the number of liters of urine emitted per day can reach ten.

The secondary symptoms of polyuria that a person feels are actually signs of painful or infectious processes occurring in his body (against which polyuria arose). Depending on what disease caused the increase in daily urine volumes, additional symptoms characteristic of this particular pathological process will also appear.

Diagnosis of polyuria

A person who is not related to medicine will not be able to independently diagnose polyuria. Because it is quite difficult to distinguish the signs of this disease from the usual frequent urges for little need. It is also worth noting that polyuria is not always characterized only by frequent trips to the toilet.

The main diagnostic method is the collection of the entire amount of excreted urine per day, and its further study in a clinical setting. This study aims to measure: discharge volume; specific gravity. Next, you need to identify the true cause of the onset of the disease.

For this, the patient is subjected to forced dehydration of the body, which lasts from four to eighteen hours. The patient is then given an injection that contains an antidiuretic hormone. Several urine tests are then taken again.

Then there is a comparison of the obtained fluids - before and after the administration of the drug. In this case, the water balance of the blood plasma is assessed. After comparing urine and plasma analyzes, the main cause of polyuria is determined.

Polyuria treatment

First of all, treatment is aimed at eliminating the disease that provoked the appearance of polyuria. During the treatment of a concomitant disease, losses by the body can be detected:

potassium;
calcium;
sodium;
chlorides.

To restore the normal concentration of these substances in the human body, they resort to drawing up an individual diet plan, and also calculate the rate of fluid consumed. With a severe course of the disease or a high level of fluid loss by the body, they resort to infusion therapy - the introduction of sterile solutions into a vein.

To speed up the treatment, special exercises are also prescribed to strengthen the muscles of the pelvis and bladder - Kegel exercises.

Prevention of polyuria

Preventive measures for polyuria include: normalization of the diet; the use of small quantities of foods that can increase the body's production of urine - seasonings; control over daily fluid intake.

The rate should be one and a half or two liters; complete rejection of alcoholic beverages; timely diagnosis and treatment of diseases that can cause polyuria; undergoing a full medical examination twice a year.

Source: http://simptomer.ru/bolezni/zheludochno-kishechnyj-trakt/1517-poliuriya-simptomy

Polyuria - diabetes mellitus

Polyuria in diabetes mellitus is caused by glucosuria, which leads to an increase in osmotic pressure in the lumen of the tubules and a decrease in water reabsorption. On average, the patient secretes 3-5 liters of fluid per day. Type I diabetes mellitus is also characterized by: polydipsia, increased appetite, weight loss.

Attention!

In patients with type II diabetes mellitus, polyuria is lower, such signs as recurrent furunculosis, pyoderma, itching of the perineum and genitals are characteristic. The decisive methods for diagnosing diabetes mellitus are the study of blood sugar, in some situations, a glucose tolerance test.

The undoubted signs of diabetes mellitus are the fasting blood sugar content of more than 6.7 mmol / l and more than 11.1 mol / l 2 hours after glucose load.

Source: http://www.diabet-inet.narod.ru/cache/vvedenie/symptomy_k_r.html

Polyuria: what is it, causes, treatment, symptoms, signs

Pathogenesis of polyuria

Since ADH stimulates the reabsorption of water in the collecting tubules of the kidneys, a decrease in ADH increases the volume of urine, which allows the body's water balance to return to normal. In addition, high concentrations of soluble electrolytes in the renal tubules induce passive osmotic diuresis and thus an increase in urine output.

A classic example of such a process is glucose-induced osmotic diuresis in uncompensated diabetes mellitus, when high concentrations of glucose in the urine (more than 250 mg / dl) exceed the reabsorption capacity of the tubules, which leads to a high concentration of glucose in the renal tubules; water enters their lumen passively, causing polyuria and glucosuria.

That's why polyuria occurs in any process that includes:

The causes of polyuria:

The duration and severity of polyuria (nocturia, urinary frequency, fluid intake at night).
Family history (diabetes mellitus, polycystic kidney disease, urolithiasis).
Taking medications (diuretics, analgesics, lithium, etc.).
Kidney stones (hypercalcemia).
Weakness (hypocapaemia), depression (hypercalcemia).
The presence of mental disorders.
Endocrine disorders (violation of menstrual function, sexual function, lactation, violation of pubic hair growth).
Other serious illnesses.

Kidney stones: causes:

Excessive fluid intake.
Endocrine dysfunction.
Hypokalemia.
Renal diseases (polycystic kidney disease, nephropathy while taking analgesics, polycystic kidney disease, amyloidosis).
Condition after elimination of urinary tract obstruction, for example, after catheterization in a patient with chronic urinary retention.
Condition after renal artery angioplasty.
Stimulation of diuresis while taking medications (furosemide, lithium preparations, amphotericin B, vinblastine, demeclocycline, cisplatin).

Symptoms and signs of polyuria

Polyuria: laboratory and instrumental research methods

Urea and electrolytes (kidney disease, hypokalemia).
Blood glucose.
Calcium, phosphates and alkaline phosphatase.
Osmolarity of plasma and urine [the ratio of osmolality of urine and plasma less than 1.0 indicates diabetes insipidus, parenchymal kidney disease (accompanied by hypokalemia) or excessive intake of water against a background of hysteria].
Radiography of the abdominal organs (nephrocalcinosis).
If possible, determine the level of lithium preparations in the blood.
Determination of protein fractions.

Collecting anameses

Collecting an anamnesis of the present disease should include obtaining information on the volume of fluid consumed and excreted in order to differentiate between polyuria and pollakiuria. If polyuria is present, the patient should be asked about:

the age at which she appeared,
rate of appearance (i.e. sudden or gradual appearance),
all clinically significant factors that have recently appeared and can cause polyuria (for example, intravenous infusion, gastric tube feeding, relief of urinary tract obstruction, head trauma, surgery).

Examination of organs and systems should look for symptoms that indicate a possible causative disorder, including dryness of the conjunctiva and oral mucosa (Sjogren's syndrome), weight loss, and night sweats (cancer). When collecting a medical history, it is necessary to pay attention to the diseases associated with polyuria.

It is necessary to find out if there are any cases of polyuria in the family. When collecting a medical history, it should be noted the use of any drugs associated with renal diabetes insipidus, and the use of substances that increase urine output (for example, diuretics, alcohol, drinks with caffeine).

Physical examination. On general examination, signs of obesity and malnutrition or cachexia should be noted, which may indicate an underlying malignant neoplasm or an eating disorder with secret diuretic use.

A complete neurologic examination should note the presence of local neurologic deficits, which may indicate a stroke, and assess mental status for signs of a mental disorder.

Warning signs of polyuria

The following data deserve special attention:

Interpretation of data. Anamnesis can often distinguish polyuria from pollakiuria, but in rare cases, daily urine collection may be required. On clinical examination, a cause can be suspected, but laboratory tests are usually required.

Diabetes insipidus is indicated by a history of cancer or chronic granulomatous disease (due to hypercalcemia), the use of certain drugs (lithium, cidofovir, foscarnet, and phosphamide), and more rare diseases (for example, renal amyloidosis, sarcoidosis, Sjogren's syndrome), which often have more bright and early manifestations than polyuria.

A history of diuretic use or diabetes mellitus indicates polyuria due to diuresis. Psychogenic polydipsia is more common in patients with a history of psychiatric disorders (mainly bipolar disorder or schizophrenia); less often it is one of the symptoms of the onset of the disease.

Laboratory research. If an increase in the amount of excreted urine is confirmed by history or quantitative changes, it is necessary to determine the glucose content in serum or urine to exclude decompensated diabetes mellitus.

If hyperglycemia is absent, the following tests are required:

biochemical and blood;
determination of serum and urine osmolality, sometimes serum ADH levels.

These studies are aimed at identifying:

hypercalcemia,
hypokalemia (due to secret intake of diuretics),
hyper- and hyponatremia.

Hypernatremia indicates an excessive loss of free water due to central or renal diabetes insipidus. Hyponatremia (sodium level less than 137 mEq / L) indicates an excess supply of free water due to polydipsia. Osmolality of urine is usually less than 300 mosm / kg with water diuresis and more than 300 mosm / kg with osmotic diuresis.

If the diagnosis is unclear, serum and urine sodium levels should be measured in response to a water deprivation test and exogenous ADH challenge. As a result of the study, severe dehydration may develop.

It should be done only under the condition of constant medical supervision, hospitalization is usually required. In addition, patients with suspected psychogenic polydipsia should be observed in order to exclude secret fluid intake. The test begins in the morning.

Carry out: weighing the patient, taking blood from a vein to determine the concentration of electrolytes in the serum and its osmolality, as well as the osmolality of urine. Every hour the patient urinates and urine osmolality is measured. Dehydration is continued until the appearance of orthostatic hypotension and postural tachycardia, a decrease in the initial body weight by 5% or more, or an increase in urine osmolality of more than 30 mosm / kg in sequentially collected samples.

Serum electrolyte levels and osmolality are then determined again, and 5 units of an aqueous solution of s / c vasopressin are injected. The urine for the study of its osmolality is collected for the last time one hour after the injection, and this is the end of the sample.

With a normal response, the maximum urine osmolality is achieved after dehydration (more than 700 mosm / kg) and the osmolality does not increase by more than 5% after vasopressin injection. With central diabetes insipidus, patients have an inability to concentrate urine to an osmolality higher than that of plasma, but this ability appears after the administration of vasopressin.

The increase in osmolality reaches 50-100% in central diabetes insipidus and 15-45% in subclinical central diabetes insipidus. In the renal form of diabetes insipidus, patients experience an inability to concentrate urine to an osmolality exceeding that of plasma, and this inability persists with the administration of vasopressin.

Sometimes in subclinical renal diabetes insipidus, the increase in urine osmolality can reach 45%, but this increase is much lower than that in subclinical central diabetes insipidus. Four out of five people have had back pain at least once, most often in the lower (lumbar) spine, back, or neck.

In psychogenic polydipsia, urine osmolality is less than 100 mosm / kg. A decrease in water load leads to a decrease in urine excretion, an increase in plasma osmolality and serum sodium concentration. Measurement of free ADH is the most direct method for diagnosing central diabetes insipidus.

The level at the end of the water deprivation test (before the injection of vasopressin) is reduced in central diabetes insipidus and correspondingly increased in renal diabetes insipidus. However, the ability to determine the level of ADH is not universally present. In addition, the water deprivation test is so accurate that direct measurement of ADH is rarely required.

Polyuria treatment

The state of hydration is assessed (pressure in the jugular vein, blood pressure, changes in blood pressure when changing body position, dynamics of body weight, CVP). The fluid balance is carefully measured and the patient is weighed daily. The central vein is catheterized to monitor the CVP.

They compensate for the lack of fluid with saline solutions and glucose solution, maintaining normal homeostasis. The concentration of potassium, calcium, phosphates and magnesium in the blood is monitored daily, and if necessary twice a day. They do not pursue the goal of completely replacing the lost fluid.

After the patient is adequately rehydrated, it is necessary to stop intravenous fluid administration, allowing the mechanism of physiological homeostasis to independently restore the body's water balance. If diabetes insipidus is suspected, a fluid restriction test is performed.

Polyuria. Fluid restriction test

All drugs are canceled the day before the test; the patient should not smoke or drink coffee. The patient is carefully monitored so that he does not secretly drink the liquid. The patient should empty the bladder after a light breakfast. Then he must not drink.

The patient is weighed at the beginning of the sample, and then after 4, 5, 6, 7, 8 hours (the study is stopped if there is a loss of more than 3% of body weight). Plasma osmolarity is determined after 30 minutes, 4 hours and then every hour until the end of the study (an increase of more than 290 mOsm / l stimulates the release of antidiuretic hormone).

Attention!

If polyuria continues, desmopressin is administered intranasally at a dose of 20 mcg with an interval of 8 hours. After 8 hours, the patient can be allowed to drink. Continue to determine the osmolarity of urine every hour for the next 4 hours.

Interpretation of the results obtained:

Normal response: urine osmolarity rises to more than 800 mOsm / L and increases slightly after desmopressin is administered.
Diabetes insipidus of central origin: urine osmolarity remains low (<400 мОсм/л) и увеличивается более чем на 50% после назначения десмопрессина.
Diabetes insipidus of nephrogenic origin: urine osmolarity remains low (<400 мОсм/л) и немного (<45%) увеличивается после назначения десмопрессина.
Psychogenic polydipsia: urine osmolarity increases (> 400 mOsm / L) but remains less than normal response.

A pathological condition in which the volume of urine excreted by the urinary system per day increases significantly is called polyuria. Polyuria does not belong to an isolated disease, but is included in the totality of signs of trouble in the urinary system or the neuroendocrine apparatus. The disease causes a lot of discomfort due to the frequent urge to urinate with the release of copious amounts of urine. In women, polyuria develops more often, especially during pregnancy.

In healthy people, the optimal volume of urine excreted per day is 1500 ml. This is an average indicator of the norm, indicating that the urinary system is working optimally, without failures, and the kidneys are coping with the load. In polyuria, diuresis (daily volume of excreted urine) reaches 2000-3000 ml, in some forms of renal failure or diabetes mellitus - up to 10 liters.

The mechanism of occurrence of the pathology is associated with a violation of the process of reabsorption of water during the passage of primary urine through the renal tubule system. Normally, only toxins and harmful substances are filtered from the primary urine, which subsequently enter the bladder, while the necessary components and water remain in the body. With polyuria, this process is disrupted - the body loses fluid in increased volumes.

Classification

In urology, polyuria syndrome is classified according to the characteristics of the course and provoking factors. According to the degrees of the course of polyuria, it happens:

temporary - arising as a response of the body to inflammatory or bacterial processes, or the gestation period in women;
constant - developed as a result of pathological renal dysfunction.

Types of polyuria, based on pathogenetic factors:

pathological - develops as a complication of the transferred diseases; pathological polyuria is often accompanied by polydipsia - excessive thirst that disappears after taking large portions of fluid; the combination of symptoms is polyetiological, and is called polyuria-polydipsia syndrome;
physiological - occurs in healthy people when taking drugs that increase diuresis.

Noteworthy is the classification of pathology according to the types of increased diuresis and its specificity:

increased water diuresis with the excretion of urine in a reduced concentration can occur in healthy people when drinking large volumes of liquid or when switching from a regime of increased physical activity to a regime with low physical activity; polyuria with hypo-resinous urine is typical for people with hypertension, various forms of diabetes, chronic alcoholism, renal failure;
increased osmotic diuresis is associated with the release of large volumes of urine with a simultaneous loss of endo- and exogenous active substances (glucose, sugar, salt); polyuria with osmotic diuresis accompanies the course of diseases associated with metabolic disorders - sarcoidosis, neoplasms in the adrenal cortex, Itsenko-Cushing's syndrome;
renal (renal) increased urine output is caused by a disorder of the adequate functioning of the kidneys due to congenital and acquired changes, acute and chronic forms of renal failure;
extrarenal (extrarenal) - occurs as a result of a slowdown in general blood flow, failures in neuroendocrine regulation and problems with the genitourinary organs.

A special place in the classification of polyuria is occupied by nocturia - frequent and profuse urination at night. People with renal or heart failure are more likely to suffer from nocturia. This is due to the fact that at night the total volume of plasma circulating in the body increases and the bulk of the fluid is actively filtered by the kidneys. In pregnant women, periodic nocturia is included in the concept of the norm and does not require treatment. However, in the presence of concomitant endocrine pathologies, it is necessary to monitor the day and night volume of urine excreted by the kidneys.

Causes

The causes of polyuria are physiological and pathological in nature. Physiological ones are not associated with the presence of diseases in the body - taking an increased amount of water and other liquids, medicines with a diuretic effect, foods with a high glucose content naturally increases the volume of excreted urine. Mild hypothermia is one of the physiological causes of polyuria - sweating decreases in the cold, respectively, excess fluid is excreted from the body in the urine. The cause of polyuria in men can be hard work with intense physical activity in hot conditions.

Pathological causes of polyuria include:

calculi in the kidneys;
inflammatory diseases - cystitis, pyelonephritis;
inflammation of the prostate in men;
diverticula in the bladder;
malignant neoplasms in the kidneys and bladder;
multiple cysts in the kidneys;
hydronephrosis;
Barter's syndrome;
disorders of the nervous system.

Clinical manifestations

Polyuria is characterized by clinical symptoms:

frequent urination, urine is excreted in abundant quantities;
drop in blood pressure;
a feeling of dryness in the mouth, a feeling of thirst;
a general weakened state with dizziness and darkening of the eyes;
violation of heart rhythm.

Long-term polyuria combined with kidney disease causes dehydration, even if a person consumes a lot of water. Together with urine, electrolytes are excreted, as a result, signs of dehydration appear: the skin becomes dry, pale, the eyes sink. Deep cracks may appear on the skin and mucous membranes.

If polyuria accompanies the course of diseases of the urinary system, simultaneously with increased diuresis, characteristic signs develop:

pain syndrome with varying intensity (from aching pains to acute in the form of attacks) and localization in the lumbar zone, sides, lower abdomen;
discomfort during urination - from a slight burning sensation to intense cuts;
an increase in temperature in case of infection;
urinary incontinence;
morning swelling under the eyes and on the legs;
general malaise - drowsiness, fatigue, muscle pain;
diarrhea;
attacks of nausea, vomiting.

In the presence of pathologies of the endocrine system, along with polyuria, specific symptoms develop:

polyphagia - a constant feeling of hunger that does not go away after eating, gluttony;
obesity;
imbalance in body proportions;
excess hair growth in women in unusual places - face, chest, back.

The course of pathology in children

Polyuria in children is rarely confirmed. A baby's kidneys are initially unable to filter large volumes of fluid. Therefore, children are hypersensitive to dehydration and excess water intake. For each age stage, an optimal indicator of daily urine output is characteristic. So, for infants, diuresis in a volume of 600 to 700 ml is considered the norm, for younger preschoolers (4-6 years old) - 900 ml, for adolescents - 1400 ml. By the age of 18, the daily diuresis reaches stable indicators - 1500 ml, depending on the adequacy of the drinking regime and lifestyle.

It is important to differentiate the symptoms of polyuria in children with the habit of attracting the attention of adults by visiting the toilet and drinking uncontrolled liquids (water, juices, milk). With polyuria of a persistent nature, the child must be examined at a nephrological center.

Common causes of childhood polyuria include:

latent (including congenital) kidney disease;
latent decompensation for heart defects;
Connes syndrome (a tumor in the adrenal glands);
mental disorders;
diabetes;
Fanconi's disease is a severe hereditary pathology associated with abnormalities in the structure of the tubular epithelium of the kidneys.

Diagnostics

Self-diagnosis of "polyuria" without a comprehensive examination is impossible. It is difficult for a person without medical education to distinguish true polyuria from the banal frequent urination. If you suspect an increased urine output of a pathological nature, you should contact a nephrologist or urologist.

The leading method for detecting polyuria is the Zimnitsky test - collection of urine excreted per day, with the determination of the volume of each portion and subsequent study in laboratory conditions. The volume of the excreted urine and its specific gravity are subject to research. If the daily volume slightly exceeds the norm, then the patient has a banal frequent urination.

A special test with fluid deprivation allows you to reliably identify the underlying disease that caused the polyuria. The essence of the method is the deliberate introduction of the body into a state of dehydration for a period of 4 to 18 hours. During this time, the patient's osmolality is monitored - a special indicator that characterizes the concentration ability of the kidneys. At the same time, the balance of fluid in the blood plasma is assessed.

Less informative, but useful in confirming the diagnosis and differentiating it are the following procedures:

urine analysis with microscopic examination of the sediment;
blood biochemistry to detect the concentration of free protein C, alkaline phosphatase, nitrogenous components, ions;
coagulogram - a coagulation test;
cytoscopy;
sonography of the kidneys and peritoneal organs;
excretory urography of the kidneys;
CT and MRI.

If you suspect endocrine diseases, they are prescribed:

blood test for sugar and hormones;
sonography of the thyroid gland;
bone x-rays;
glucose tolerance test;
pneumorenal examination of the adrenal glands by means of a series of x-rays;
radiograph of the sella turcica to exclude an increase in the pituitary gland.

Treatment methods

Treatment of polyuria is aimed at eliminating the underlying pathology. To speed up the healing process and establish the full activity of the kidneys, the patient must adhere to a diet that restricts table salt and spices, fatty foods and foods with additives, canned foods containing vinegar, coffee, and confectionery. In the presence of diabetes mellitus, animal fat and sugar in all forms should be excluded from the diet. Reduce the intake of carbohydrate foods - pasta and bakery products, potatoes.

The main groups of medicines used in the treatment of polyuria:

electrolyte infusion solutions (calcium chloride, magnesium sulfate) - for the prevention and elimination of dehydration, the effects of intoxication, creating an equilibrium in the acid-base balance of the blood;
cardiac glycosides (Digoxin, Verapamil) and thiazide diuretics (Chlortizide, Indapamed) - to restore normal functioning of the cardiovascular system and treat heart disease burdened by excessive diuresis;
hormonal therapy is indicated for endocrine pathologies.

Surgical intervention is used when malignant neoplasms and large multiple cysts in the kidneys are detected. As an alternative option in the complex treatment of polyuria, therapeutic exercises are used, the purpose of which is to strengthen the pelvic muscles and the muscles of the bladder. Kegel exercises have worked well, especially for polyuria in women.

ethnoscience

In folk medicine, there are recipes that can improve the condition of a patient with polyuria. But pathology should be treated with the help of herbal medicine carefully, taking into account the individual characteristics of the organism, and before using folk methods, a consultation with a nephrologist is necessary. Two recipes are very popular in the treatment of high urine output and other kidney problems:

anise infusion - with regular use, it helps to relieve inflammation and improve the process of urination; for cooking, take 5 g of anise fruit, steam 200 ml of boiling water, let it brew for half an hour; drink 50 ml 4 times a day every day, the course - at least a month or until a steady improvement in the condition;
plantain leaf infusion - helps to cure inflammatory kidney diseases and normalizes the genitourinary system; to prepare 10 g of crushed leaves, pour 200 ml of boiling water, leave for 2-3 hours, filter; take 100 ml twice a day for 2 weeks.

Preventive measures

Preventive measures against polyuria are simple, but when taken regularly can minimize the risk of health problems, including the urinary system:

optimization of nutrition with the exclusion of semi-finished products, food with dyes and preservatives;
the use of limited amounts of food that can increase the production of urine - strong tea and coffee, chocolate, spices, salt;
control over daily fluid intake, the optimal volume for an adult is no more than 2 liters of water per day;
refusal to drink alcohol;
timely diagnosis when warning signs appear (frequent urination, not previously typical; discomfort and pain in the abdomen and lower back, discoloration and transparency of urine) and timely treatment of diseases that can provoke polyuria;
passing preventive medical examinations at least once a year.

Meningoencephalitis is a severe inflammatory disease of an infectious nature that affects the central nervous system (the lining of the brain, its substance, in other cases, the spinal cord). The disease is, as it were, a combination of two pathological conditions: meningitis, in which the pia mater is affected, and encephalitis, which occurs with damage to the medulla.

The disease can be caused by various microorganisms: bacteria, viruses, protozoa and even free-living amoeba in fresh water. Many of them are carried by ixodid ticks, so the peak incidence is observed during periods of active life of the insect. In addition, the disease can be independent or become a complication of other infectious processes in the body (flu, pneumonia, tuberculosis, measles, mumps, and many others).

Meningoencephalitis, as an independent disease, is more often diagnosed in children (meningococcal infection), although it is possible in adults, it is often fatal, often leaves consequences in the form of more or less gross changes in the structures of the brain, less often it passes completely without a trace.

Meningoencephalitis treatment is always difficult, since to start it, it is necessary to identify the pathogen (therapy of viral and treatment of bacterial infections have nothing to do with each other).

Causes of the inflammatory process in the central nervous system

Meningoencephalitis is distinguished by a special polyetiology, because a variety of circumstances can contribute to the development of the pathological process. Along with infectious pathogens, infectious-allergic and toxic factors can play a negative role. All the causes of meningitis and encephalitis are simultaneously prerequisites for the formation of a combined disease (inflammation of the brain and pia mater). From this, the severity of an isolated disease and its prognosis, of course, are aggravated.

Yet the most common cause of dangerous inflammation localized in the central nervous system is infections:

The predisposing factor for this pathology is age - in children, due to the insufficient development of the immune system and the failure of the blood-brain barrier, meningoencephalitis is diagnosed much more often than in adults. True, in this case, elderly people can be equated with children - their immunity is low, the body can no longer fully resist infections. The risk group for this inflammatory process is also made up of patients with acute or chronic pathology of ENT organs - sinusitis, sinusitis, mastoiditis, etc. In such patients, as a rule, purulent meningoencephalitis develops as a complication.

How does the pathogen manage to enter the brain from the external environment?

How the infectious agent enters the body depends on the type of pathogen, for example:

Infection with the causative agent of the membranes of the brain occurs predominantly by the hematogenous route, in second place is the lymphogenous route of spread, however direct contact with bacterial flora during the breakthrough of purulent cavities or open craniocerebral injuries is also not excluded.

How is this inflammatory process classified?

The patient may not be interested in how doctors call this process, however, they distinguish between the following forms of the disease:

Primary meningoencephalitis, which develops as a result of infection with an arbovirus (with a tick bite), herpes virus, rabies, typhoid pathogen, as a result of the penetration of treponema pallidum into the central nervous system (neurosyphilis);
Secondary process - it, as a rule, acts as a complication of another pathology of an infectious nature (chickenpox, measles, tuberculosis, purulent diseases of the ENT organs caused by the bacterial flora).

The nature of the course of the inflammatory process in the central nervous system can also include several forms:

Fulminant option - the disease develops rapidly, the patient's condition deteriorates sharply in a matter of hours, often death occurs in a similar situation;
Spicy meningoencephalitis - the clinical picture unfolds rather quickly, but not as rapidly as in the case of fulminant form, so doctors have more time to provide assistance;
Subacute course - there is a slow development of erased symptoms;
Chronic inflammatory process - a sluggish development of events, signs of inflammation in the brain are poorly expressed, the disease proceeds with remissions and exacerbations.

In addition, meningoencephalitis differs in the nature of the inflammatory reaction, which determines the quality of the cerebrospinal fluid:

Serous- the cerebrospinal fluid is transparent, a small amount of protein, the number of lymphocytes is sharply increased;
Purulent- against the background of cloudy (purulent) cerebrospinal fluid, a huge number of leukocytes;
Hemorrhagic- The cerebrospinal fluid due to the admixture of blood becomes reddish, in the cerebrospinal fluid, in addition to white blood cells, a large number of erythrocytes.

The cause of purulent meningoencephalitis in most cases is bacterial infection(pyogenic coccal flora, Pseudomonas aeruginosa, etc.), the development of serous and hemorrhagic forms is mainly due to the impact viruses.

Common Symptoms

The difficulty in diagnosing meningoencephalitis lies in the fact that the causative agent in the first hours of the disease "does not say anything" about itself, and each form may have its own specific signs, which, however, may resemble a wide range of pathological conditions. However, it is useful to know the general symptoms characteristic, in general, for the entire group of diseases called "meningoencephalitis", these are:

Of course, the patient himself or his relatives can hardly understand all the meningeal signs, but some of them can be easily mastered by many people on their own. For example, try tilting the patient's head so that the chin touches the sternum: in the absence of meningeal symptoms, this is easy, the patient will react to even the slightest downward movement.

If you suspect a dangerous ailment, you can ask a person with suspected meningoencephalitis to passively bend the leg (lying on the back) at an angle of 90 degrees (hip and knee joints), and then force him to straighten the limb. With irritation of the meninges, this will not work, therefore this condition should be regarded as a meningeal sign (Kernig's symptom).

Separate forms

The described pathological condition is also classified by the nature of the pathogen, and if it is reliably established, the disease is presented in a more accurate version, indicating its culprit. For example, herpetic meningoencephalitis (it is, of course, also viral), tuberculous, implying a bacterial nature, the name amoebic already indicates that protozoa have become the culprit of the disease.

Viral meningoencephalitis (for example, herpetic)

Herpetic meningoencephalitis, the main cause of which is the DNA-containing herpes simplex virus of both the first and second types, can occur as an independent form (in adults against the background of a drop in immunity) or act as a component of a generalized viral infection (in newborns and early children age). It is known that HSV is found in adults in more than 90% of cases. Due to the wide distribution of the pathogen, only a few manage to avoid meeting with HSV, but the highest probability of "catching" it is present when an infected woman passes through the birth canal and in early childhood (airborne transmission). The most dangerous is intrauterine infection of the fetus, which leads to serious consequences.(up to 2/3 of newborns die in infancy, the rest await the fate of children with disabilities).

It is impossible to predict in advance what to expect from herpetic meningoencephalitis, its course is quite variable:

Acute meningoencephalitis;
Chronic process;
The development of the disease under the guise of other pathological conditions of the central nervous system (neoplasms, epilepsy, strokes, dementia);
Almost asymptomatic.

The first signs of this disease:

Intense headache, localized in most cases in the frontal and parietal region;
High body temperature;
Impairment of consciousness, change in behavioral functions, up to complete inadequacy;
General cerebral symptoms, against the background of which focal manifestations can often be observed.

The viral nature of the disease (especially in the case of acute meningoencephalitis) does not bode well for the patient: often DIC syndrome is added to the destructive changes in the brain, aggravating the patient's already serious condition.

The therapeutic effect is mainly due to the antiviral drug - acyclovir (virolex), which significantly increases the chances of life, but, unfortunately, does not protect against serious consequences.

Video: lecture on herpetic encephalitis in children

Bacterial meningoencephalitis (tuberculous, etc.)

The culprits of tuberculosis of the central nervous system and meninges, which in 70% of cases leads to tuberculous meningoencephalitis, are mycobacteria (Mycobacterium tuberculosis). Being the most severe form of tuberculous brain damage, this form of the disease gives a rather vivid clinical picture:

Severe headache, not subject to analgesics;
Progressive malaise and general weakness, loss of appetite;
Nausea, vomiting, photophobia;
Decreased concentration of attention;
Vegetative disorders;
Pronounced cerebral symptoms;
Presence of meningeal signs;
Symptoms of focal lesions (impaired motor functions, lesion of FMN), which indicates the involvement of the meninges and brain matter;
The development of hydrocephalus.

The course of the disease under more or less favorable circumstances (mortality rate is approximately 30%) is long and painful, leaving serious consequences.

The main treatment for meningoencephalitis of a bacterial nature is antibiotics.

Video: lecture on tuberculous meningoencephalitis

Amebic meningoencephalitis

Amebic meningoencephalitis is the result of entry into the body (usually through the upper respiratory tract) of small, free-living protozoa called amoebas.

In addition to fresh water bodies, it is possible to find amoeba in tap water, in hot mineral springs or in those discharged by power plants, as well as in the soil, on vegetables and mushrooms. In rare cases, the amoeba can inhabit the nasal passages of children without causing them much harm.

Amebic meningoencephalitis is most commonly diagnosed in children and young adults. A pathological condition can manifest itself in two forms:

Treatment of acute meningoencephalitis of a similar origin, since it often ends tragically, can sometimes be successful, but only with very early diagnosis. Patients are prescribed monotherapy with amphotericin B or a combination of drugs:

Amphotericin B + rifampicin + chloramphenicol;

Amphotericin B + rifampicin + ketoconisole.

As for the granulomatous form, to date, no reliable control methods have been found. Combinations of sulfadiazine + fluconazole, pentamidine + ketonazole (cream) + chlorhexidine (topical) are used. Imidazole derivatives sometimes help. In this case, hormones are excluded - they will further aggravate the course of the process and lead to the rapid progression of the disease.

Consequences of meningoencephalitis

People who have undergone such a dangerous condition can expect various "surprises" from this disease in the future. There are not so many cases when meningoencephalitis (of any origin) was cured like a runny nose. Usually, even small, barely noticeable or completely invisible to strangers, the consequences remain. It depends on many factors: when a person has comprehended an ailment, what pathogen "tried", how the process proceeded, what state of immunity, etc. nervous system (CNS).

The most pronounced consequences await in case of intrauterine infection with the virus. If the baby did not die in the womb, then later she will have to deal with epilepsy, mental disorders. Although such children grow poorly, their mental development lags behind even further. In addition, given the damage to the central nervous system in the early stages of its formation, paresis and paralysis are considered a natural phenomenon.

Meningoencephalitis is especially dangerous for children, after all, in the event of a favorable completion of the process, the membranes and matter of the brain still turn out to be not as healthy as before the disease. Often, the further development of the central nervous system is inhibited, intelligence suffers, and although some children continue to do well in school (who are lucky), exact sciences begin to be given to them with difficulty. In addition, there is always the danger of developing convulsive syndrome and.

Adults also have problems, the least of which are hearing and vision loss. And yet, it would seem, intellectual abilities have been formed, therefore, no troubles are expected from this side. But no, various types of dementia, mental disorders against the background of epileptic seizures, paresis and paralysis can lie in wait for any person, even if he is a yesterday's scientist or a simple hard worker.

However, some are really lucky, except for the dispensary registration with a neurologist and periodic examinations, nothing reminds them of the suffering they have experienced.

Nocturia - Frequent nocturnal urge to urinate associated with the predominance of nocturnal urine output over daytime. Frequent urination at night can be a symptom of a serious medical condition.

Whether a person will sleep all night without voluntary urination depends on the diuretic rhythm, according to which the volume of urine generated during a night's sleep should not exceed the capacity of the bladder. Disorders can occur due to decreased osmotic concentration in the kidney, increased urinary sodium excretion, soluresis, or decreased bladder capacity. All polyuretic conditions can lead to the development of nocturia.

In most cases, kidney disease is associated with a decrease in their concentrating ability, and often this occurs at an early stage of the disease. Even if there is no profuse polyuria, the volume of urine produced at night often exceeds the capacity of the bladder.

Nocturia also occurs in clinical conditions for which edema is typical. With congestive heart failure, nephrotic syndrome, and cirrhosis with ascites, fluid builds up in certain parts of the body throughout the day. At night, when a person takes a horizontal position, the forces of action of tissue capillaries change, which contributes to the mobilization of some of the edematous fluid. There is an effect of intravenous saline solution. Venous insufficiency, accompanied by edema of the legs during the day and mobilization of edematous fluid at night, can also cause nocturia. Nocturia also results from decreased bladder capacity.

An infection, lump, or stone can cause inflammation and irritation of the mucous membrane. Chronic partial obstruction of the pathway of urine exit from the bladder, caused by hypertrophy of the prostate gland, the structure of the urethra, a benign or malignant tumor, a stone, causes frequent urge to urinate, and in addition, thickening of the muscular wall of the bladder, reducing its compliance (extensibility). Based on the frequent urination of small portions, it can be assumed that nocturia is associated with a process in the lower urinary tract. However, in the early stage of chronic obstruction at night, there may be a single urination, which is moderate in volume.

Polyuria - pathological excess of the normal daily volume of urine excreted. A characteristic sign of polyuria is considered to be the volume of excreted urine more than 3 l / day. However, when diagnosing polyuria, the tendency of the person to consume large amounts of fluids and, therefore, to excrete more urine should be excluded. The patients themselves, usually, cannot distinguish polyuria from increased frequency of urination, i.e. frequent urination in small portions. Since it is difficult for a patient to obtain clear information about the volume of urine excreted, before identifying the cause of the disease, the fact of polyuria is established by daily collection of urine.

The causes of polyuria

Polyuria may be due to inadequate secretion of vasopressin, loss of the ability of the renal tubules to respond to it, diuresis of solutes (soluresis), or natriuresis. It can serve as a mechanism of physiological adaptation in order to remove fluid.

The main causes of polyuria are as follows:

I. Insufficiency of the concentrating function of the kidneys:

1.Diabetes insipidus

a) Diabetes of central origin

Posthypophysectomy syndrome; the consequences of injury, removal of the pituitary gland; idiopathic; tumors or cysts located above and inside the Turkish saddle; histiocytosis or granuloma; compression by aneurysm; Sheikhen's syndrome; meningoencephalitis; Guillain-Barré syndrome; fat embolism; "Empty" turkish saddle

b) Nephrogenic diabetes

Acquired tubulointerstitial kidney disease (pyelonephritis, analgesic nephropathy, multiple myeloma, amyloidosis, obstructive uropathy, sarcoidosis, hypercalcemic and hypokalemic nephropathy, Sjogren's syndrome, sickle cell anemia, kidney transplant)
The action of medicinal or toxic substances (lithium, demeclocycline, methoxyflurane, ethanol, diphenylhydantoin, propoxyphene, amphotericin)
Congenital diseases (hereditary diabetes insipidus of a nephrogenic nature, polycystic or cystic disease of the medulla of the kidney)

2.Solurez (glucosuria, feeding the patient through a gastric tube with food rich in proteins, intravenous administration of urea or mannitol, administration of a radiographic contrast agent into the blood, chronic renal failure)

3.Natriuretic syndromes (nephritis accompanied by loss of salt; diuretic phase of acute renal tubular necrosis; diuretics)

II. Primary polydipsia

1. Psychogenic polydipsia
2. Disease of the hypothalamus
3. Taking medicines(thioridazine, chlorpromazine (chlorpromazine), anticholinergics)

Diabetes insipidus

The term diabetes insipidus applies to those clinical conditions in which inadequate concentrating kidney function leads to polyuria and secondary thirst. The cause of the pathology is either insufficient secretion of vasopressin (diabetes insipidus of central origin), or renal insensitivity to it (nephrogenic diabetes insipidus). In both cases, the reabsorption of water is reduced throughout the distal section of the nephron, since the passive transition of water from the lumen of the tubules to the hypertensive interstitium of the outer and inner medulla of the kidney occurs slowly. However, even though the rate of passage of water from the collecting ducts is not high (for a given osmotic difference between the lumen of the tubule and the interstitial fluid), the fluid entering the collecting ducts of the kidney is so diluted and its volume is so great that its substance is supplied more than in a normal state. This promotes the "flushing" of solutes from the medulla of the kidney into the straight vessels. This process is not complete enough, and therefore the administration of vasopressin can lead to the formation of osmotically concentrated urine. However, the maximum osmosis of urine that will be achieved with this drug will remain below normal.

Diabetes insipidus of central origin it happens primary(idiopathic) iln secondary due to reasons such as hypophysectomy, trauma, swelling, inflammation, infection, vascular disease.

ANDdiopathic diabetes insipidus can be inherited in a dominant autosomal manner, but most often it is sporadic and develops in childhood. In any form of central diabetes insipidus, neurons that produce the antidiuretic hormone vasopressin are selectively damaged in the supraoptic nucleus of the hypothalamus.

Nephrogenic diabetes insipidus rarely hereditary. It is usually associated with kidney disease. Its important and opposite reasons include hypercalcemia and hypokalemic nephropathy. Exposure to lithium carbonate, the narcotic drug methoxyfuran (1,1-difluoro-2,2-dichloroethyl methyl ether) and demeclocycline (a tetracycline derivative) can also lead to the development of this type of diabetes.

Solurez

Excessive filtration of hard-to-absorb solutes, such as glucose, mannitol, or urea, inhibits the reabsorption of water and sodium chloride in the proximal tubule, leading to their loss in the urine and the development of polyuria. Since the concentration of sodium ions in urine is lower than in blood, more water is excreted from the body, rather than salt, as a result of which the serum can become hypertonic. Glucosuria in diabetes mellitus - the most common case of solurez. Intravenous administration of mannitol, an angiographic radiopaque contrast agent, as well as feeding the patient through a gastric tube with drugs with a high protein content cause excessive excretion of urea and can lead to the development of iatrogenic soluresis. Solures of any degree can cause polyuria; therefore, the study of the concentrating ability of the kidneys should be postponed until the solures is corrected.

Natriuretic syndromes

Chronic excessive urinary sodium loss is possible with tubulointerstitial or cystic kidney disease. Polyuria and polydipsia are associated with unusually high daily sodium requirements. Examples of such a phenomenon, when the excretion of water and sodium from the body is very high, include cystosis of the medullary layer of the kidneys, Barter's syndrome and the diuretic phase of acute tubular necrosis.

Primary polydipsia

Psychogenic polydipsia. Some people, either because of their habit, addiction, mental disorders, specific brain damage, or because of taking medications, consume so much water during the day that they develop polyuria. In chronic polydipsia, the body and kidneys are very rarely affected, but it can be mistaken for diabetes insipidus due to the very similarity of their symptoms. With deliberate polydipsia, the volume of extracellular fluid remains within the normal range or increased, and the secretion of vasopressin is reduced to the basal level, since serum osmosis tends to the lower limit of the norm.

Since the reabsorption of water from the lumen of the distal end of the convoluted tubules and collecting ducts is weakened, all excess water is excreted in the urine. Due to the washout process, which occurs in diabetes insipidus, in the inner layer of the medulla of the kidney, the gradients of urea and sodium chloride decrease. However, the washout process is more intense than in diabetes.

The fact is that in primary polydipsia there is a tendency to an increase in the volume of extracellular fluid, while in diabetes insipidus, the loss of primary urine in the kidneys leads to the opposite effect. An increase in the volume of extracellular fluid increases the total amount of sodium chloride and water delivered to the enlarged section of the ascending knee of the nephron loop (Henle), and therefore to the inner layer of the medulla of the kidney, and all processes are equal. Renal blood flow also increases. An increase in blood flow through the vasa recta reduces their ability to retain solutes in the medulla of the kidney.

Examination of a patient with polyuria

Soluresis (osmotic diuresis) and natriuretic syndromes are usually detected during questioning of the patient, physical examination, urinalysis (glucosuria), according to clinical symptoms, leukocyte count, blood glucose, serum creatinine or urea nitrogen in the blood. Difficulties in diagnosis are mainly associated with stable chronic polyuria and polydipsia of unknown origin. In such cases, an attempt should be made to differentiate central diabetes insipidus from nephrogenic and primary polydipsia. For this, a well-established method, the essence of which is to study the dynamics of the osmotic concentration of urine upon cessation of water consumption and the appointment of vasopressin.

The patient is allowed free water intake for 3 days against the background of a normal diet, which provides the body with sodium chloride in an amount of about 100 mmol / day. Then complete fasting is prescribed, during which the patient's pulse rate and blood pressure are measured every 30 minutes, every hour he is weighed on an accurate balance. After a decrease in the patient's body weight by 3% or after. 14 h fasting measure the osmosis of serum and urine. In a healthy person, the volume of excreted urine will decrease and will be less than 0.5 ml / min, and its osmotic concentration will reach approximately 700 mOsmol / kg (water).

With complete diabetes insipidus (central or nephrogenic), urine osmosis remains below 200 mOsmol / kg, and its excretion is above 0.5 ml / min. However, with incomplete diabetes, there will be a slight increase in urine osmosis and a decrease in its volume. If by the end of fasting the osmotic concentration is less than 700 mOsmol / kg, then intravenous (drip) administration of an aqueous solution of vasopressin at a dose of 5 IU / min is prescribed. In patients with complete or partial diabetes insipidus of central origin, the osmosis of urine will increase by more than 9%. With complete nephrogenic diabetes insipidus, there is no reaction to vasopressin. Still, some reaction in incomplete nephrogenic diabetes sometimes occurs. To determine violations of the osmoregulatory function of the kidneys, it is advisable to prescribe intravenous hypertonic saline solution.

The reaction of patients with primary polydipsia is somewhat different. With the cessation of fluid intake, the secretion of vasopressin increases. By the time the test is completed, the urine excretion rate and osmosis will reflect a certain physiological level of vasopressin, which acts on the intact renal tubules that penetrate the interstitium of the medulla, the very interstitium in which the concentration of urea and sodium chloride was low due to their chronic washout. In other words, the washout process determines the upper limit of the osmotic value of urine. Consequently, in patients with primary polydipsia, renal concentrating capacity will be submaximal, despite normal vasopressin secretion.

Exogenous vasopressin is able to increase the osmotic concentration of urine, but by a little, only less than 9%. The main reason for the limitation of osmosis lies precisely in the process of washing out solutes from the medulla of the kidney, and not in the absence of sufficient secretion of vasopressin or insensitivity of the renal tubules to it. Usually, by the end of the liquid deprivation test, the osmosis of urine excreted exceeds 400 mOsmol / kg. In contrast, in patients with diabetes insipidus, the values of this indicator are lower (about 200 mOsmol / kg). In some cases, using only one test with deprivation of fluid intake, it is impossible to distinguish incomplete diabetes insipidus from primary polydipsia. However, it is possible to improve the diagnosis using a radioimmunoassay of the concentration of antidiuretic hormone in serum.