Diabetes insipidus – a disease caused by an absolute or relative deficiency of the hypothalamic hormone vasopressin (ADH-antidiuretic hormone).
The frequency of the disease is unknown; it occurs in 0.5-0.7% of endocrine patients.
Regulation of vasopressin release and its effects
Vasopressin and oxytocin are synthesized in the supraoptic and paraventicular nuclei of the hypothalamus, packaged into granules with the corresponding neurophysins and transported along axons to the posterior lobe of the pituitary gland (neurohypophysis), where they are stored until released. The reserves of vasopressin in the neurohypophysis with chronic stimulation of its secretion, for example, with prolonged abstinence from drinking, are sharply reduced.
Vasopressin secretion is caused by many factors. The most important of them is blood osmotic pressure, i.e. osmolality (or otherwise osmolarity) of plasma. In the anterior hypothalamus, close to, but separate from the supraoptic and paraventicular nuclei, is located osmoreceptor . When plasma osmolality is at a certain normal minimum, or threshold value, the concentration of vasopressin in it is very low. If plasma osmolality exceeds this set threshold, the osmocenter perceives this, and the concentration of vasopressin rises sharply. The osmoregulation system reacts very sensitively and very accurately. Some increase osmoreceptor sensitivity is associated with age.
The osmoreceptor is unequally sensitive to different plasma substances. Sodium(Na +) and its anions are the most powerful stimulators of the osmoreceptor and vasopressin secretion. Na and its anions normally determine 95% of plasma osmolality.
Very effectively stimulate the secretion of vasopressin through the osmoreceptor sucrose and mannitol. Glucose practically does not stimulate the osmoreceptor, just like urea.
The most reliable evaluative factor in stimulating vasopressin secretion is to determineNa + and plasma osmolality.
The secretion of vasopressin is influenced by blood volume and blood pressure level. These influences are exerted through baroreceptors located in the atria and aortic arch. Stimuli from the baroreceptor travel through afferent fibers to the brainstem as part of the vagus and glossopharyngeal nerves. From the brain stem, signals are transmitted to the neurohypophysis. A decrease in blood pressure or a decrease in blood volume (eg, blood loss) significantly stimulates the secretion of vasopressin. But this system is much less sensitive than osmotic stimuli at the osmoreceptor.
One of the effective factors stimulating the release of vasopressin is nausea, spontaneous, or caused by procedures (vomiting, alcohol, nicotine, apomorphine). Even with incoming nausea, without vomiting, the level of vasopressin in plasma increases 100-1000 times!
Less effective than nausea, but an equally constant stimulus for vasopressin secretion is hypoglycemia, especially spicy. A decrease in the level of glucose in the blood by 50% of the initial level increases the content of vasopressin by 2-4 times in humans, and in rats by 10 times!
Increases vasopressin secretion renin-angiotensin system. The level of renin and/or angiotensin required to stimulate vasopressin is not yet known.
It is also believed that nonspecific stress, caused by factors such as pain, emotions, physical activity, increases the secretion of vasopressin. However, it remains unknown how stress stimulates the secretion of vasopressin - in some specific way, or through a decrease in blood pressure and nausea.
Inhibits the secretion of vasopressin vasoactive substances such as norepinephrine, haloperidol, glucocorticoids, opiates, morphine. But it is not yet clear whether all these substances act centrally, or by increasing blood pressure and volume.
Once in the systemic circulation, vasopressin is quickly distributed throughout the extracellular fluid. Equilibrium between the intra- and extravascular space is achieved within 10-15 minutes. Inactivation of vasopressin occurs mainly in the liver and kidneys. A small part is not destroyed and is excreted intact in the urine.
Effects. The most important biological effect of vasopressin is retaining water in the body by reducing urine output. The point of application of its action is the epithelium of the distal and/or collecting tubules of the kidneys. In the absence of vasopressin, the cell membranes lining this part of the nephron form an insurmountable obstacle to the diffusion of water and soluble substances. Under such conditions, the hypotonic filtrate formed in the more proximal parts of the nephron passes unchanged through the distal tubule and collecting ducts. The specific gravity (relative density) of such urine is low.
Vasopressin increases the permeability of the distal and collecting ducts to water. Since water is reabsorbed without osmotic substances, the concentration of osmotic substances in it increases, and its volume, i.e. quantity decreases.
There is evidence that a local tissue hormone, prostaglandin E, inhibits the action of vasopressin in the kidneys. In turn, non-steroidal anti-inflammatory drugs (for example, Indomethacin), which inhibit the synthesis of prostaglandins in the kidneys, increase the effect of vasopressin.
Vasopressin also acts on various extrarenal systems, such as blood vessels, gastrointestinal tract, and central nervous system.
Thirst serves as an indispensable complement to the antidiuretic activity of vasopressin . Thirst is a conscious sensation of the need for water. Thirst is stimulated by many factors that cause the secretion of vasopressin. The most effective of them is hypertensive environment. The absolute level of plasma osmolality at which the feeling of thirst appears is 295 mOsmol/kg. At this osmolality, the blood normally produces urine with maximum concentration. Thirst is a kind of brake, the main function of which is to prevent a degree of dehydration that exceeds the compensatory capabilities of the antidiuretic system.
The feeling of thirst increases rapidly in direct proportion to plasma osmolality and becomes unbearable when the osmolality is only 10-15 mOsmol/kg above the threshold level. Water consumption is proportional to the feeling of thirst. A decrease in blood volume or blood pressure also causes thirst.
Etiology
The development of central forms is not based on diabetes mellitus there is damage to various parts of the hypothalamus or the posterior lobe of the pituitary gland, i.e. neurohypophysis. The following factors may be the reasons:
infections acute or chronic: influenza, meningoencephalitis, scarlet fever, whooping cough, typhus, sepsis, tonsillitis, tuberculosis, syphilis, rheumatism, brucellosis, malaria;
traumatic brain injuries : accidental or surgical; electric shock; birth trauma during childbirth;
mental trauma ;
pregnancy;
hypothermia ;
tumor of the hypothalamus or pituitary gland : metastatic or primary. Breast cancer metastasizes to the pituitary gland more often thyroid glands, bronchi. Infiltration with tumor elements in lymphogranulomatosis, lymphosarcoma, leukemia, generalized xanthomatosis (Hand-Schüller-Crispen disease). Primary tumors: adenoma, glioma, teratoma, craniopharyngioma (especially common), sarcoidosis;
endocrine diseases : Simmonds, Sheehan, Lawrence-Moon-Biedl syndromes, pituitary dwarfism, acromegaly, gigantism, adinosogenital dystrophy;
idiopathic: in 60-70% of patients the cause of the disease remains unclear. Among idiopathic forms, hereditary diabetes mellitus, which lasts for several generations, has a noticeable representation. The type of inheritance is autosomal dominant and recessive;
autoimmune : destruction of the hypothalamic nuclei as a result of an autoimmune process. This form is thought to occur among idiopathic diabetes insipidus, in which autoantibodies to vasopressin-secreting cells appear.
For peripheral in diabetes insipidus, vasopressin production is preserved, but receptor sensitivity is reduced or absent renal tubules to the hormone, or the hormone is intensively destroyed in the liver, kidneys, and placenta.
Nephrogenic diabetes insipidus is more often observed in children, and is caused by anatomical inferiority of the renal tubules (congenital deformities, cystic degenerative processes), or damage to the nephron (amyloidosis, sarcoidosis, lithium poisoning, methoxyfluramine). or decreased sensitivity of renal tubular epithelial receptors to vasopressin.
Diabetes insipidus clinic
Complaints
for thirst from moderate to painful, not letting go of patients day or night. Sometimes patients drink 20-40 liters of water per day. At the same time, there is a desire to drink ice water;
polyuria and frequent urination. The urine produced is light, without urochromes;
physical and mentalweakness;
loss of appetite,weight loss; possible development obesity if diabetes insipidus develops as one of the symptoms of primary hypothalamic disorders.
dyspeptic disorders from the stomach - a feeling of fullness, belching, pain in the epigastrium; intestines - constipation; gallbladder - heaviness, pain in the right hypochondrium;
mental and emotional disorders: headaches, emotional imbalance, insomnia, decreased mental activity, irritability, tearfulness; sometimes psychosis develops.
menstruation disorders, in men - potency.
Anamnesis
The onset of the disease can be acute and sudden; less often - gradual, and symptoms increase as the disease becomes more severe. The cause may be traumatic brain or mental injuries, infections, or surgical interventions on the brain. Most often, the cause cannot be identified. Sometimes a family history of diabetes insipidus is established.
Flow chronic diseases.
Inspection
emotional lability;
the skin is dry, salivation and sweating are reduced;
body weight can be reduced, normal or increased;
the tongue is often dry due to thirst, the borders of the stomach are lowered due to constant fluid overload. With the development of gastritis or biliary dyskinesia, increased sensitivity and pain on palpation of the epigastrium and right hypochondrium is possible;
cardiovascular and respiratory system, the liver is usually not affected;
urinary system: frequent urination, polyuria, nocturia are noted;
signsdehydration of the body, if the fluid lost in the urine is not replenished for some reason - lack of water, conducting a test with “dry eating”, or the sensitivity of the “thirst” center decreases:
sharp general weakness, headaches, nausea, repeated vomiting, aggravating dehydration;
hyperthermia, convulsions, psychomotor agitation;
CVS disorder: tachycardia, hypotension up to collapse and coma;
blood thickening: increase in the number of Hb, red blood cells, Na + (N136-145 mmol/l, or mEq/l) creatinine (N60-132 μmol/l, or 0.7-1.5 mg%);
the specific gravity of urine is low - 1000-1010, polyuria persists.
These phenomena of hyperosmolar dehydration are especially characteristic of congenital nephrogenic diabetes insipidus in children.
The diagnosis is made based on classic signs of diabetes insipidus and laboratory and instrumental studies:
polydipsia, polyuria
low specific gravity of urine – 1000-1005
plasma hyperosmolarity, > 290 mOsm/kg (N280-296 mOsm/kg water, or mmol/kg water);
hypoosmolarity of urine,< 100-200 мосм/кг;
hypernatremia, > 155 mEq/L (N136-145 mEq/L, mmol/L).
If necessary, carried out samples :
Test with dry eating. This test is carried out in a hospital setting, its duration is usually 6-8 hours, if well tolerated - 14 hours. No fluid is given. Food should be protein. Urine is collected every hour, and the volume and specific gravity of each hourly portion are measured. Body weight is measured after every 1 liter of urine excreted.
Grade: the absence of significant dynamics in the specific gravity of urine in two subsequent portions with a loss of 2% of body weight indicates a lack of stimulation of endogenous vasopressin.
Test with intravenous administration of 50 ml of 2.5% solutionNaCl within 45 min. In diabetes insipidus, the volume and density of urine do not change significantly. In psychogenic polydipsia, an increase in plasma osmotic concentration quickly stimulates the release of endogenous vasopressin and the amount of urine excreted decreases and its specific gravity increases.
A test with the administration of vasopressin drugs - 5 units IV or IM. With true diabetes insipidus, health improves, polydipsia and polyuria decrease, plasma osmolarity decreases, and urine osmolarity increases.
Differential diagnosis of diabetes insipidus
Based on the main signs of diabetes insipidus - polydipsia and polyuria, this disease is differentiated from a number of diseases that occur with these symptoms: psychogenic polydipsia, diabetes mellitus, compensatory polyuria in chronic renal failure (chronic renal failure).
Nephrogenic vasopressin-resistant diabetes insipidus (congenital or acquired) is differentiated on the basis of polyuria with primary aldosteronism, hyperparathyroidism with nephrocalcinosis, malabsorption syndrome in chronic enterocolitis.
With diabetes
Table 22
With psychogenic polydipsia
Table 23
|
Sign |
Diabetes insipidus |
Psychogenic polydipsia |
|
common reason |
Infections, traumatic brain injuries (including surgical) |
Gradual Psychotrauma, psychogenic stress |
|
Presence of a tumor |
Pituitary tumors, sarcoma, lymphogranulomatosis, etc. |
Absent |
|
Osmolarity: | ||
|
Test with dry eating (no more than 6-8 hours) |
No dynamics |
The amount of urine decreases, specific gravity and osmolality normalize |
|
How you feel during this test |
Worsens, thirst becomes painful |
Condition and well-being are not affected |
|
Test with i.v. injection 50 ml 2.5% NaCl |
The amount of urine and its density without dynamics |
The amount of urine decreases and the specific gravity |
|
Feeling better, polydipsia and polyuria decrease |
Feeling worse (headaches) |
Central (hypothalamic pituitary) with nephrogenic diabetes insipidus
Table 24
|
Sign |
Central diabetes insipidus |
Nephrogenic diabetes insipidus |
|
Traumatic brain injuries, infections, tumors. |
Family; hyperparathyroidism; taking medications - lithium carbonate, demeclocycline, methoxyflurane |
|
|
Test with intravenous administration of 5 units of vasopressin |
The state of health improves, polydipsia and polyuria decrease. Plasma osmolality , and urine osmolality |
No dynamics |
|
Changes are detected in the urine |
None |
Albuminuria, cylindruria |
|
Blood creatine | ||
|
Arterial hypertension |
BP often |
Treatment of diabetes insipidus
Etiological : for tumors of the hypothalamus or pituitary gland - surgery, or radiation therapy, cryodestruction, introduction of radioactive ytrium.
For infectious processes - antibacterial therapy.
For hemoblastoses – cytostatic therapy.
Replacement therapy – drugs that replace vasopressin:
Adiuretin(synthetic analogue of vasopressin) intranasally, 1-4 drops in each nostril 2-3 times a day; Available in bottles of 5 ml, 1 ml - 0.1 mg of active substance;
Adiurecrin(extract of the posterior lobe of the pituitary gland of large cattle). Available in powder form. Inhale 0.03-0.05 2-3 times a day. The duration of action of one inhalation is 6-8 hours. During inflammatory processes in the nasal cavity, the absorption of adiurecrine is disrupted and its effectiveness is sharply reduced;
RP:adiurecrini0.05Dsd№30.S. inhale through the nose, ampoules 1 ml;
Pituitrin. Release form 5 units of activity. Water-soluble extract of the posterior lobe of the pituitary gland of cattle. 5 units (1 ml) are administered 2-3 times a day intramuscularly. Often causes symptoms water intoxication(headaches, abdominal pain, diarrhea, fluid retention) and allergies;
DDAVP(1 deamino-8D-arginine-vasopressin) – a synthetic analogue of vasopressin;
diuretics of the thiazide group(Hypothiazide, etc.). Hypothiazide 100 mg per day reduces glomerular filtration, Na + excretion with a decrease in the amount of urine. The effect of thiazide diuretics is not detected in all patients with diabetes insipidus and weakens over time;
Chlorpropamide(oral glucose-lowering drug) is effective in some patients with diabetes insipidus. Tablets of 0.1 and 0.25. Prescribed in a daily dose of 0.25 in 2-3 doses. The mechanism of antidiuretic action is not fully understood; it is assumed that it potentiates vasopressin, at least with minimal amounts in the body.
To avoid hypoglycemia and hyponatremia, it is necessary to control the level of glucose and Na + in the blood.
Diabetes insipidus is a chronic disease of the hypothalamic-pituitary system that develops due to a deficiency of the hormone vasopressin, or antidiuretic hormone(ADH), the main manifestations of which are the release of large volumes of urine with low density. The prevalence of this pathology is about 3 cases per 100,000 people; both men and women aged 20-40 years suffer from it equally. It also occurs in children.
Despite the fact that the disease is little known in wide circles, knowing the symptoms of the disease is very important, because if diagnosed in time, treatment is greatly simplified.
Vasopressin: effects and basic physiology
Vasopressin causes spasm of small vessels, increases arterial pressure, reduces osmotic pressure and diuresis.Vasopressin, or antidiuretic hormone (ADH), is synthesized by the cells of the hypothalamus, from where it is transported along the supraoptic-pituitary tract to the posterior lobe of the pituitary gland (neurohypophysis), accumulates there and is directly released into the blood. Its secretion increases if the osmotic concentration of blood plasma increases and if for some reason the volume of extracellular fluid becomes less than expected. Inactivation of antidiuretic hormone occurs in the kidneys, liver and mammary glands.
Antidiuretic hormone affects many organs and processes occurring in them:
- (increases the reabsorption of water from the lumen of the distal renal tubules back into the blood; as a result, the concentration of urine increases, its volume becomes smaller, the volume of circulating blood increases, blood osmolarity decreases and hyponatremia is noted);
- cardiovascular system (increases the volume of circulating blood; in large quantities - increases vascular tone, increasing peripheral resistance, and this leads to increased blood pressure; due to spasm of small vessels, increased platelet aggregation (increased tendency to stick them to each other) has a hemostatic effect);
- central nervous system (stimulates the secretion of adrenocorticotropic hormone (ACTH), participates in memory mechanisms and in the regulation of aggressive behavior).
Classification of diabetes insipidus
It is customary to allocate 2 clinical forms of this disease:
- Neurogenic diabetes insipidus (central). Develops as a result of pathological changes in the nervous system, in particular in the hypothalamus or posterior pituitary gland. As a rule, the cause of the disease is in this case are operations for complete or partial removal of the pituitary gland, infiltrative pathology of this area (hemochromatosis, sarcoidosis), trauma or changes of an inflammatory nature. In some cases, neurogenic diabetes insipidus is idiopathic, occurring simultaneously in several members of the same family.
- Nephrogenic diabetes insipidus (peripheral). This form the disease is a consequence of a decrease or complete absence sensitivity of the distal renal tubules to the biological effects of vasopressin. As a rule, this is observed in the case of chronic kidney pathology (with or against the background of polycystic kidney disease), a long-term decrease in the potassium content in the blood and an increase in calcium levels, with insufficient protein intake from food - protein starvation, Sjögren's syndrome, and some birth defects. In some cases, the disease is familial.
Causes and mechanisms of development of diabetes insipidus
Factors predisposing to the development of this pathology are:
- diseases of an infectious nature, especially viral ones;
- brain tumors (meningioma, craniopharyngioma);
- metastases to the hypothalamus of cancer of extracerebral localization (usually bronchogenic - originating from bronchial tissue, and breast cancer);
- skull injuries;
- genetic predisposition.
In case of insufficient synthesis of vasopressin, the reabsorption of water in the distal renal tubules is impaired, which leads to the removal of large volumes of fluid from the body, a significant increase in the osmotic pressure of the blood plasma, irritation of the thirst center located in the hypothalamus, and the development of polydipsia.
Clinical manifestations of diabetes insipidus
The first symptoms of this disease are constant thirst and frequent heavy urination. The disease debuts suddenly, with the appearance and frequent heavy urination (polyuria): the volume of urine excreted per day can reach 20 liters. These two symptoms bother patients both day and night, forcing them to wake up, go to the toilet, and then drink water again and again. The urine excreted by patients is light, transparent, and has a low specific gravity.
Due to constant lack of sleep and decreased fluid content in the body, patients are concerned about general weakness, fast fatiguability, emotional imbalance, irritability, dry skin, decreased sweating.
At the stage of advanced clinical symptoms the following are noted:
- lack of appetite;
- reduction in the patient’s body weight;
- signs of distension and prolapse of the stomach (heaviness in the epigastrium, pain in the stomach);
- signs of biliary dyskinesia (dull or cramping pain in the right hypochondrium, vomiting, heartburn, belching, bitter taste in the mouth, and so on);
- signs (bloating, wandering cramping pain all over the abdomen, unstable stool).
When fluid intake is limited, the patient's condition worsens significantly - he is bothered by intense headache, dry mouth, rapid, increased heartbeat. Blood pressure decreases, the blood thickens, which contributes to the development of complications, body temperature rises, mental disorders are noted, that is, dehydration and dehydration syndrome develop.
Symptoms of diabetes insipidus in men are a decrease in libido and potency.
Symptoms of diabetes insipidus in women: up to amenorrhea, associated infertility, and if pregnancy does occur - increased risk spontaneous abortion.
Symptoms of diabetes in children clearly expressed. In newborns and children early age The condition with this disease is usually severe. There is an increase in body temperature, unexplained vomiting occurs, and disorders develop. nervous system. In older children up to adolescence A symptom of diabetes insipidus is bedwetting, or enuresis.
Various other symptoms associated with the underlying disease that caused a deficiency of vasopressin in the body may also be detected, such as:
- severe headaches (with brain tumors);
- pain in chest or in the area of the mammary glands (for cancer of the bronchi and mammary glands, respectively);
- visual impairment (if the tumor presses on the area responsible for visual function);
- increase in body temperature (with inflammatory diseases brain) and so on;
- symptoms of pituitary insufficiency - panhypopituitarism (with organic damage pituitary region).
Diagnosis of diabetes insipidus
The diagnostic criterion is an abundant daily diuresis - from 5 to 20 liters or even more, with a low relative density of urine - 1.000-1.005.
A general blood test shows signs of thickening ( increased content erythrocytes - erythrocytosis, high hematocrit (the ratio of the volume of blood cells to the volume of plasma)). Blood plasma osmolarity is increased (over 285 mmol/l).
When determining the level of antidiuretic hormone in the blood plasma, its decrease is noted - less than 0.6 ng/l.
If, after the studies, the diagnosis of diabetes insipidus still raises doubts among the specialist, the patient may be prescribed a test with abstinence from fluid intake. It should be carried out exclusively under the supervision of a doctor, since, as mentioned above, the patient’s condition worsens significantly when fluid intake is limited - the doctor needs to monitor this condition and provide the patient with medical assistance in a timely manner. The evaluation criteria for this sample are:
- volume of urine excreted;
- its relative density;
- patient's body weight;
- his general health;
- blood pressure level;
- heart rate.
If, during this test, the amount of urine excreted decreases, its specific gravity increases, the patient’s blood pressure, pulse and body weight remain stable, the patient feels satisfactory, without noting the appearance of new unpleasant symptoms for him, the diagnosis of “diabetes insipidus” is rejected.
Differential diagnosis for diabetes insipidus
Main pathological conditions from which neurogenic diabetes insipidus should be distinguished are:
- psychogenic polydipsia;
- chronic renal failure;
- nephrogenic diabetes insipidus.
Common symptoms for diabetes insipidus and psychogenic polydipsia are increased thirst and. However, psychogenic polydipsia does not develop suddenly, but gradually, while the patient’s condition (yes, this disease is specific to women) does not change significantly. With psychogenic polydipsia, there are no signs of blood thickening, and symptoms of dehydration do not develop in the case of a test with fluid restriction: the volume of urine excreted decreases, and its density becomes greater.
Thirst and excessive diuresis may also accompany. However this state is also accompanied by the presence of urinary syndrome (the presence of protein, leukocytes and red blood cells in the urine, not accompanied by any external symptoms) and high diastolic (popularly referred to as “lower”) pressure. In addition, in case of renal failure, an increase in the blood levels of urea and creatinine is determined, which are within normal limits in diabetes insipidus.
In diabetes mellitus, unlike diabetes insipidus, it is determined in the blood high level glucose, in addition, the relative density of urine is increased and glucosuria (excretion of glucose in the urine) is noted.
Nephrogenic diabetes insipidus clinical manifestations is similar to its central form: severe thirst, frequent heavy urination, signs of blood thickening and dehydration, low specific gravity of urine - all this is inherent in both forms of the disease. The difference between the peripheral form is the normal or even increased level of antidiuretic hormone (vasopressin) in the blood. In addition, in this case there is no effect from diuretics, since the cause of the peripheral form is the insensitivity of the receptors of renal tubular cells to ADH.
Treatment of diabetes insipidus
If the cause of diabetes insipidus is a tumor, the main direction of treatment is its removal surgically. Treatment of symptomatic diabetes insipidus begins with eliminating the cause that caused it, for example, with treatment infectious process or brain injury, tumor removal.
Idiopathic diabetes insipidus and its other forms are treated with vasopressin replacement therapy until the cause is eliminated. Synthetic vasopressin - desmopressin today is produced in various dosage forms - in the form of a solution (nasal drops), tablets, spray. The most convenient to use, as well as effective and safe, is the tablet form of the drug, called Minirin. As a result of taking the drug, urine volume decreases, specific gravity increases, and blood plasma osmolarity decreases to normal levels. The frequency of urination and the volume of urine excreted are normalized, and the constant feeling of thirst disappears.
Diabetes . – is a group of metabolic diseases characterized by hyperglycemia that results from defects in insulin secretion, insulin action, or both. (WHO, 1999).
Classification.
- Type 1 diabetes (destruction of pancreas b-cells, leading to absolute insulin deficiency). A) Autoimmune. B) Idiopathic.
- Type 2 diabetes. A) With predominant insulin resistance and relative insulin deficiency. B) With a predominant defect in insulin secretion with and without insulin resistance. In the 21st century, type 2 diabetes began to be recorded in children and adolescents! About 10% of diabetes is “non-type 1 diabetes.”
- Other specific types of diabetes
- Genetic defects in b-cell function. “Mody” - diabetes: 5 subtypes (4 of them are genetic defects that make b-cells “lazy”, and 1 is a defect in glucogenase, which is responsible for the sensitivity of b-cells to the glucose signal)
- Genetic defects in insulin action (type A insulin resistance)
- Diseases of the exocrine pancreas
- Endocrinopathies (thyrotoxicosis, gigantism, etc.)
- Drug- and chemical-induced diabetes
- Infections accompanied by the development of diabetes ( congenital rubella, CMV)
- Unusual shapes immune-mediated diabetes (AT to insulin, AT to insulin)
- Genetic syndromes accompanied by diabetes (Down, Klinefelter, Turner, Huntington's chorea, Bordet-Biedl syndrome, Prader-Willi syndrome).
- Gestational diabetes. Impaired tolerance to gluten during pregnancy.
Diagnostic criteria.
- Fasting capillary blood glucose > 6.7 mmol/l (plasma > 7.0) in at least 2 studies in different days
- 2 hours after a glucose load during a glucose tolerance test, plasma or capillary blood glucose >11.1 mmol/l
- Diabetes symptoms + random blood sample >11.1 mmol/L.
- Impaired glucose tolerance: 2 hours after a glucose load, sugar is more than 7.8 mmol/l, but less than 11.1 mmol/l.
Clinic for overt diabetes mellitus.
75-85% of b-cells are affected by the autoimmune process. Hyperglycemia, glucosuria. “Major” symptoms of diabetes: polyuria, polydipsia, weight loss with good appetite.
Differential diagnosis with diabetes insipidus.
Similarities: polyuria, polydipsia, weight loss
Differences: polyuria with low relative density of urine, aglucosuria, normoglycemia.
Type 1 diabetes mellitus in children. is an autoimmune disease of genetic origin in which absolute or relative insulin deficiency is caused by the progressive destruction of B cells due to an autoimmune disorder associated with certain histocompatibility antigens located on the short arm of chromosome 6, as well as the INS 1 and TNF genes.
Etiology and pathogenesis.
This is a multifactorial disease. Even an individual with a genetic predisposition (1) may not develop the disease. For the disease to occur, so-called provoking events are needed (2): b-cytotropic viruses (Coxsackie, rubella, measles, mumps, CMV, EBV), complicated pregnancy, cow's milk protein (bovine serum albumin peptides can trigger a cross-immune response against b -cells in persons predisposed to autoallergy), food cyanides (almonds, apricot kernels, tapioca), nitrosamines (smoked meats), environmental factors (passive smoking).
- Immunological abnormalities, development of a mixed autoimmune reaction against b-cells (3) à Progressive decrease in insulin secretion, latent diabetes (4) à overt diabetes with residual secretion of C-peptide (5) à terminal diabetes, complete destruction of b-cells. (6)
In brackets are the stages of development of type 1 diabetes.
In approximately 20% of patients with type 1 diabetes, it is a component of 2 multiorgan autoimmune syndromes:
Addison's disease: hypoparathyroidism, vitiligo, hypothyroidism, pernicious anemia, chronic active hepatitis, alopecia, malabsorption syndrome, candidiasis
Graves-Gazedow disease: myasthenia gravis, vitiligo, malabsorption syndrome
Etiology according to Shabalov.
A. Immune-mediated diabetes. Autoimmune processes due to genetic predisposition by HLA genes. Autoimmune inflammation can be spontaneous and induced (viruses).
B. Virus-induced. B-cytotropic viruses.
C. Toxic (dyes, b-adrenergic agonists, thiazides, alpha-IF)
D. Congenital. Congenital hypoplasia/aplasia of b-cells isolated or in combination with pancreas defects (aplasia, hypoplasia, ectopia).
E. Violation exocrine function pancreas (pancreatitis, trauma, cystic fibrosis).
F. Rare forms: “Stiff-man” syndrome, development of antibodies to insulin receptors.
Clinic.
Manifest type 1 diabetes: latent diabetes becomes apparent suddenly, sometimes within 24 hours. The trigger is stress, acute illness or other events that increase the need for insulin.
“Major” symptoms of diabetes: polyuria, polydipsia, weight loss with good appetite.
Polyuria is a consequence of hyperglycemia, glucosuria, and osmotic diuresis.
Weight loss is a consequence of progressive dehydration, increased lipolysis and protein catabolism.
Increased fatigue, increasing weakness, decreased performance.
Dry skin and mucous membranes, the addition of fungal and pustular infections. Thinning of the pancreas, skeletal muscle atrophy, often enlarged liver.
In young children: lack of growth, restlessness, frequent drinking, diaper rash, vulvitis, balanoposthitis, polyuria (stickiness, starchy spots), regurgitation, vomiting, loose stools.
Treatment.
Principles of treatment. Physical exercise, diet therapy, self-control, insulin therapy. Achieving target glycemic values of 5.5-10.0 mmol/l.
Main types of insulins.
- Ultra-short-acting (analogs of human insulin). NovoRapid. Onset of action in 0-15 minutes. Peak action after 1-1.5 hours. Duration of action is 3-5 hours.
- Short action. Actrapid. Starts in 30-45 minutes. Peak in 1-3 hours. Duration 6-8 hours.
- Medium duration. Protafan NM. Starts in 1.5 hours. Peak after 4-12 hours. Duration 24 hours.
- Long-lasting. Lantus. Starts in 1 hour. Peak - no. Duration 24-29 hours.
Doses and regimens.
The dose of insulin is selected individually under glycemic control.
Initial dose in a patient without ketoacidosis: 0.4-0.5 IU/kg/day. The dose of basal insulin can be from 1/3 to 2/3 daily dose depending on the mode of administration.
Insulin therapy from Shabalov.
Short-acting insulin: initial dose 0.25-0.5 IU/kg/day. Take it 30 minutes before meals. 50% before breakfast, 15-20% before lunch, 20-25% before dinner, 5-10% before bed.
Basal insulin - medium or long duration. Its dose is 0.35 units/kg/day. Dose control - based on fasting glucose (optimally 3.5-5.5).
That. basal + ultra-short right before meals (humalog) or short 30 minutes before meals at the rate of 1-1.3 IU per 12.0 g of HC (1 XE).
Modes:
- 2 times a day a mixture of short + medium insulin before breakfast and dinner.
- 3 times/day: a mixture of short + medium before breakfast, short before dinner, medium before bed
- Short insulin before main meals, medium insulin before bed
- Any individual mode
Principles of diet therapy.
- Physiological nutrition by calorie content and composition
- Individual diet for overweight children
- Daily calorie intake = 1000 + (100 x M), where M is age in years
- 50% of the daily calorie content is HC, 20% - B, 30% - F. Enough Vit and minerals
- Exclusion of easily digestible hydrocarbons (sugar, honey, sweets, wheat flour, starch, grapes, bananas). Replacing them with hydrocarbons with a lot of fiber (rye flour, bran, cereals, vegetables, fruits, berries).
- Dependence of meal time and amount of HC on the time of administration and dose of insulin. Those. accounting for XE (12.0 g HC). 1 XE requires 1-1.3 units of insulin. If you have introduced ultra-short, start eating immediately. If it’s short, start eating 30 minutes after the injection.
- Use of sugar substitutes (for children, aspartame 40 mg/kg/day, saccharin 2.0 mg/kg/day).
Indications for prescribing insulin therapy.
We begin insulin therapy from the moment the diagnosis of type 1 diabetes is established (information from Shabalov). In general, type 1 diabetes is absolute reading for insulin therapy. o_o
Compensation criteria .
- Fasting glycemia: ideal 3.6 – 6.1. Optimal 4.0-7.0. Suboptimal >8.0. High risk complications >9.0
- Glycemia after meals: ideal 4.4-7.0. Optimal 5-11.0. Suboptimal 11-14. High risk of complications 11-14.
- Glycemia at night. Ideal 3.6-6.0. Optimal is not lower than 3.6. Suboptimal below 3.6 or above 9.0. High risk of complications less than 3.0 and more than 11.0.
- GlycoHb. Ideal<6,05%. Оптимальный <7,6%. Субоптимальный 7,6-9,0%. Высокий риск осложнений более 9,0%.
Diabetic ketoacidosis . – severe metabolic decompensation of diabetes, developing as a result of absolute insulin deficiency.
Causes.
- Late diagnosed diabetes
- Inadequate insulin therapy for diabetes
- Violation of the insulin therapy regimen (skipping injections, using expired insulin, lack of self-control).
- Severe eating disorders
- A sharp increase in the need for insulin (infections, stress, injuries, concomitant endocrine diseases - thyrotoxicosis, hypercortisolism, pheochromocytoma, use of corticosteroids).
Clinic.
Stages.
- Stage 1 (compensated ketoacidosis, or ketosis): against the background of symptoms of dehydration, nausea, vomiting, and transient abdominal pain appear; Possibly loose stools (toxic gastroenteritis). The mucous membranes are bright, the tongue is dry with a white coating. Smell of acetone from the mouth. pH 7.3 and below, BE = (-10). Glucose 16-20. Ketone bodies 1.7-5.2 mmol/l. K and Na are normal or elevated. Urea – N. Osmolarity 310-320.
- Stage 2 (decompensated ketoacidosis, or precoma): noisy toxic Kussmaul breathing! Abdominal syndrome is pronounced (clinic of “acute abdomen”) - severe pain, tension in the muscles of the anterior abdominal wall, positive symptoms of peritoneal irritation. Repeated vomiting (often “coffee grounds”). The skin and mucous membranes are dry, the tongue is covered with a brown coating. Acrocyanosis. Tachycardia, blood pressure decreased. Sopor. pH = 7.28-7.1. BE to (-20). Glucose 20-30. Ketone bodies 5.2-17.0. Hypokalemia, hyponatremia.
- Stage 3 (diabetic ketoacidotic coma). Lack of consciousness, suppressed reflexes, decreased diuresis up to anuria (“toxic kidney”). Stop vomiting. Increasing hemodynamic disorders. Rare noisy breathing is replaced by frequent shallow breathing. Severe muscle hypotonia. Tachycardia, heart rhythm disturbances. Severe symptoms of dehydration. The tongue is as dry as a brush. pH< 7,1. BE (-25). Глюкоза >25-30, but within 40. Hypokalemia, hyponatremia, increased urea. Ketone bodies 5.2-17.0.
Diagnostics. according to clinical data from stages and laboratory data.
Principles of treatment .
Main goals.
- Administration of insulin to stop catabolic processes and reduce hyperglycemia.
- Rehydration.
- Restoration of CBS, normalization of electrolyte balance
- Elimination of intoxication and treatment of concomitant diseases.
Assessing the degree of dehydration.
Degree 1: weight loss 3%, clinical manifestations are minimal.
Level 2: 5%. Dry mucous membranes, decreased tissue turgor.
Grade 3: 10% Sunken eyeballs, spots on the skin disappear after pressure after 3 seconds or more
Grade 4: >10% Shock, weakness, absence of peripheral pulsations
DKA 1
If the degree of dehydration is less than 5% - rehydration per os and subcutaneous administration of short-acting insulin (Actrapid) after 4-6 hours at the rate of 0.8-1.0 IU/kg/day. Of these, in 1 INJECTION – 0.2-0.3 UNITS/kg (30% of the daily value). In INJECTION 2 – 30%. In the 3rd – 25%. In the 4th - 15%.
Subsequently, he is transferred to one of the insulin therapy regimens: short-acting + long-acting.
DKA 2-3
- Insulin therapy. Continuous intravenous administration of short-acting insulin (Actrapid) in saline solution at a rate of 0.1 U/kg/hour. In small children, 0.05 units/kg/hour.
- Infusion therapy. Conducted by a physicist. From the moment infusion and insulin therapy begins, monitoring of glucose, CBS, and electrolytes begins.
- Calculation of the volume of fluid administered for grade 2-3 DKA.
V infusion on the 1st day = body weight in kg x degree of dehydration + maintenance V
Support volume
- Distribution of V infusion therapy during the day
50% for the first 6 hours
25% for further 6 hours
25% for the remaining 12 hours
- Restoration of electrolyte disturbances.
Potassium deficiency. If before the start of infusion therapy there is evidence of its deficiency, then administer it simultaneously with physiotherapy. More often, it begins to be replenished 1-2 hours after the start of infusion therapy (for every 1 liter of saline - 40 mmol KCl).
- Fighting acidosis. At the beginning of therapy, bicarbonates are not indicated (risk of increased hypokalemia, increased osmolarity, increased hypoxia, increased CNS acidosis). Administer at pH only< 7,0 из расчета 2,5 мл/кг в/в капельно за 1 час с дополнительным введением калия.
- When the CBS is normalized, the child is transferred to subcutaneous administration of short-acting insulin after 4-5 hours (1 unit/kg/day). Actrapid IV infusion is stopped 20 minutes after 1 injection. The next day - on a basal-bolus insulin therapy regimen.
ATTENTION!!
- The decrease in glycemic levels in the first hours should be 4-5 mmol/h
- If this does not happen, increase the insulin dose by 50%, and if glycemia increases - by 50-100%
- When glycemia decreases to 12-15 - replacement infusion solution for glucose to maintain blood sugar 8-12.
- If glycemia increases above 15, the insulin dose is increased by 25%
- If the glucose level drops below 8, change the infusion solution to glucose 10%
- If glycemia remains low despite the injected glucose, it is necessary to reduce the dose of insulin, but not stop its administration! To restore anabolic processes and reduce ketosis, both glucose and insulin are needed!
Vascular complications of diabetes mellitus .
Capillary damage is a pathognomonic symptom of type 1 diabetes (“universal capillaropathy”).
Common to all localizations: aneurysmal changes in capillaries; thickening of the walls of arterioles, capillaries and venules due to the accumulation of glycoproteins and neutral mucopolysaccharides in the basement membrane. Proliferation and desquamation of the endothelium, leading to vascular obliteration.
Pathogenesis.
- Disruption of the exchange of GAGs in the vascular wall and the appearance in it of an excess of products of the glucose metabolic pathway - the sorbitol cycle.
- Non-enzymatic glycosylation of blood proteins, incl. and Hb in conditions of chronic hyperglycemia
- The role of platelets: in diabetes, they have an increased tendency to aggregation, increased production of thromboxanes and prostaglandins, and decreased production of prostocyclin by the endothelium.
Diabetic nephropathy.
Stages of development.
- Hyperfunction of the kidneys. Increased GFR (>140/ml/min). PC increase. Kidney hypertrophy. Normoalbuminuria (<30 мг/сут). Развивается в дебюте СД.
- Stage of initial structural changes. Thickening of basement membranes. Expansion of the mesangium. High GFR and normoalbuminuria remain. 2-5 years from the onset of diabetes.
- Beginning nephropathy. Microalbuminuria (from 30 mg/day). GFR is high or normal. Unstable increase in blood pressure. 5-15 years from the onset of diabetes.
- Severe nephropathy. Proteinuria (>500 mg/day). GFR is normal or moderately reduced. Arterial hypertension. 10-25 years from the onset of diabetes.
- Uremia. Decrease in GFR<10 мл/мин. Интоксикация. АГ. Более 20 лет от начала СД или через 5-7 лет от появления протеинурии.
Clinic.
Treatment.
- With normal urinary albumin excretion.
Careful correction of hydrocarbon metabolism, strive to maintain glycoHb no more than 7.8%
- In the presence of microalbuminuria
- Careful correction of hydrocarbon metabolism. Insulin therapy regimen, diabetes compensation.
- Blood pressure correction. ACE inhibitors: captopril, Renitec.
- Correction of intrarenal hemodynamics: ACE inhibitors even with normal blood pressure.
- In the presence of proteinuria
- Correction of hydrocarbon exchange
- Blood pressure correction: ACE inhibitors (captopril, Renitec).
- Low-protein diet: it is advisable to replace animal B with vegetable, limiting animal to 0.6 g/kg/day. Expanding the HC diet to cover energy costs.
- Correction of lipid metabolism. Lipid-lowering diet; for cholesterol levels > 6.5, prescribing fibrates, nicotinic acid, and hydroxymethylglutaryl-coenzyme A reductase inhibitors (mevacor).
- At the stage of chronic renal failure:
- Reducing the dose of insulin (renal insulinase, which inactivates insulin, is inhibited).
- Treatment of patients together with nephrologists.
- If creatinine increases > 150 µmol/l, decide on preparation for dialysis or peritoneal dialysis.
Diabetic retinopathy
- Non-proliferative retinopathy. The presence of microaneurysms, isolated hemorrhages, retinal edema, and exudative foci in the retina. Dilation and tortuosity of the venules in the fundus.
- Preproliferative. The presence of venous anomalies (tortuosity, loops, duplication and pronounced changes vessel caliber). A large amount of hard and “cotton” exudates. Intraretinal microvascular abnormalities. Multiple large retinal hemorrhages.
- Proliferative. Neovascularization of the optic disc and other parts of the retina. Hemorrhages in vitreous. Education fibrous tissue in the area of preretinal hemorrhages. Newly formed vessels of the iris (rubeosis) cause secondary glaucoma.
Treatment
Stage 1: compensation of diabetes. Angioprotectors (sulodexide).
Stages 2 and 3: laser photocoagulation (focal, barrier, panretinal).
Diabetes insipidus or diabetes insipidus- a disease in which, due to a lack of vasopressin (antidiuretic hormone), severe thirst appears, and the kidneys excrete a large amount of low-concentrated urine.
This rare disease occurs equally often in women, men and children. However, young people aged 18 to 25 are most prone to it.
Anatomy and physiology of the kidneys
Bud- a paired bean-shaped organ, which is located behind the abdominal cavity in the lumbar region on both sides of the spine at the level of the twelfth thoracic and first and second lumbar vertebrae. The weight of one kidney is about 150 grams.Kidney structure
The kidney is covered with membranes - a fibrous and fatty capsule, as well as renal fascia.In the kidney, a distinction is made between the renal tissue itself and the pyelocaliceal system.
Kidney tissue responsible for filtering blood to form urine, and pyelocalyceal system- for the accumulation and excretion of formed urine.
Kidney tissue has two substances (layers): cortical (located closer to the surface of the kidney) and medulla (located inward from the cortex). They contain a large number of closely interconnected tiny blood vessels and urinary tubules. These are the structural functional units of the kidney - nephrons(there are about one million of them in each kidney).
Each nephron begins from the renal corpuscle(Malpighi-Shumlyansky), which is a vascular glomerulus (an intertwined cluster of tiny capillaries), surrounded by a spherical hollow structure (Shumlyansky-Bowman capsule).
The structure of the glomerulus
The glomerular vessels originate from the renal artery. Initially, upon reaching the kidney tissue, it decreases in diameter and branches, forming bringing vessel(afferent arteriole). Next, the afferent vessel flows into the capsule and branches into the smallest vessels (the glomerulus itself), from which the efferent vessel(efferent arteriole).
It is noteworthy that the walls of the glomerular vessels are semi-permeable (have “windows”). This ensures the filtration of water and some solutes in the blood (toxins, bilirubin, glucose and others).
In addition, in the walls of the afferent and efferent vessels there is juxtaglomerular apparatus of the kidney, in which renin is produced.
The structure of the Shumlyansky-Bowman capsule
It consists of two leaves (outer and inner). Between them there is a slit-like space (cavity), into which the liquid part of the blood from the glomerulus penetrates, along with some substances dissolved in it.
In addition, a system of convoluted tubes originates from the capsule. First, the urinary tubules of the nephron are formed from the inner layer of the capsule, then they flow into the collecting tubules, which connect with each other and open into the renal calyces.
This is the structure of the nephron in which urine is formed.
Physiology of the kidney
Basic functions of the kidney- removal from the body of excess water and metabolic end products of certain substances (creatinine, urea, bilirubin, uric acid), as well as allergens, toxins, medications and others.In addition, the kidney is involved in the exchange of potassium and sodium ions, the synthesis of red blood cells and blood clotting, regulation of blood pressure and acid-base balance, metabolism of fats, proteins and carbohydrates.
However, in order to understand how all these processes are carried out, it is necessary to “arm yourself” with some knowledge about the functioning of the kidney and the formation of urine.
The process of urine formation consists of three stages:
- Glomerular filtration(ultrafiltration) occurs in the glomeruli of the renal corpuscles: through the “windows” in their wall, the liquid part of the blood (plasma) with some substances dissolved in it is filtered. Then it enters the lumen of the Shumlyansky-Bowman capsule
- Reverse suction(resorption) occurs in the urinary tubules of the nephron. During this process, water is reabsorbed and useful material, which should not be excreted from the body. While substances to be excreted, on the contrary, accumulate.
- Secretion. Some substances that must be excreted from the body enter the urine already in the renal tubules.
How does urine formation occur?
This process begins with the fact that arterial blood enters the vascular glomerulus, in which its flow slows down somewhat. This is due to high pressure in the renal artery and an increase in the capacity of the vascular bed, as well as a difference in the diameter of the vessels: the afferent vessel is slightly wider (20-30%) than the efferent vessel.
Thanks to this, the liquid part of the blood, together with the substances dissolved in it, begins to exit through the “windows” into the lumen of the capsule. At the same time, normally the walls of the glomerular capillaries retain formed elements and some blood proteins, as well as large molecules whose size is more than 65 kDa. However, toxins, glucose, amino acids and some other substances, including useful ones, pass through. This is how primary urine is formed.
Next, primary urine enters the urinary canaliculi, where water and useful substances are reabsorbed from it: amino acids, glucose, fats, vitamins, electrolytes and others. In this case, substances to be excreted (creatinine, uric acid, medications, potassium and hydrogen ions), on the contrary, accumulate. Thus, primary urine turns into secondary urine, which enters the collecting ducts, then into the collecting system of the kidney, then into the ureter and bladder.
It is noteworthy that about 150-180 liters of primary urine are formed within 24 hours, while secondary urine is from 0.5 to 2.0 liters.
How is kidney function regulated?
This is a rather complex process in which vasopressin (antidiuretic hormone), as well as the renin-angiotensin system (RAS), take the most active part.
Renin-angiotensin system
Main functions
- regulation of vascular tone and blood pressure
- increased sodium reabsorption
- stimulation of vasopressin production
- increased blood flow to the kidneys
In response to the stimulating effect of the nervous system, a decrease in blood supply to the renal tissue, or a decrease in the level of sodium in the blood, renin begins to be produced in the juxtaglomerular apparatus of the kidney. In turn, renin promotes the conversion of one of the blood plasma proteins into angiotensin II. And, in fact, angiotensin II determines all the functions of the renin-angiotensin system.
Vasopressin
This is a hormone that is synthesized (produced) in the hypothalamus (located in front of the cerebral peduncles), then enters the pituitary gland (located at the bottom of the sella turcica), from where it is released into the blood.
The synthesis of vasopressin is mainly regulated by sodium: when its concentration in the blood increases, the production of the hormone increases, and when it decreases, it decreases.
Hormone synthesis also increases when stressful situations, a decrease in fluid in the body or the entry of nicotine into it.
In addition, the production of vasopressin decreases with increased blood pressure, inhibition of the renin-angiotensin system, decreased body temperature, intake of alcohol and certain medications (for example, clonidine, haloperidol, glucocorticoids).
How does vasopressin affect kidney function?
The main task of vasopressin- promote the reabsorption of water (resorption) in the kidneys, reducing the amount of urine formation.
Mechanism of action
With the blood flow, the hormone reaches the renal tubules, where it attaches to special areas (receptors), leading to an increase in their permeability (the appearance of “windows”) for water molecules. Thanks to this, water is absorbed back and urine is concentrated.
In addition to urine resorption, vasopressin regulates several other processes occurring in the body.
Functions of vasopressin:
- Helps reduce capillaries circulatory system , including glomerular capillaries.
- Supports blood pressure.
- Affects the secretion of adrenocorticotropic hormone(synthesized in the pituitary gland), which regulates the production of hormones from the adrenal cortex.
- Enhances the release of thyroid-stimulating hormone(synthesized in the pituitary gland), which stimulates the production of thyroxine thyroid gland.
- Improves blood clotting due to the fact that it causes aggregation (sticking together) of platelets and increases the release of certain blood clotting factors.
- Reduces the volume of intracellular and intravascular fluid.
- Regulates the osmolarity of body fluids(total concentration of dissolved particles in 1 l): blood, urine.
- Stimulates the renin-angiotensin system.
Types of diabetes insipidus
Considering the mechanisms of development of diabetes insipidus, it can be divided into two main types:- Central diabetes insipidus. It is formed when there is insufficient production of vasopressin in the hypothalamus or a violation of its release from the pituitary gland into the blood.
- Renal (nephrogenic) diabetes insipidus. In this form, vasopressin levels are normal, but the kidney tissue does not respond to it.
In addition, sometimes the so-called psychogenic polydipsia(increased thirst) in response to stress.
Also diabetes insipidus can develop during pregnancy. The reason is the destruction of vasopressin by placental enzymes. As a rule, symptoms of the disease appear in the third trimester of pregnancy, but disappear on their own after childbirth.
Causes of diabetes insipidus
Depending on the development of what type of diabetes insipidus they can lead to, they are divided into two groups.Causes of central diabetes insipidus
Brain lesions:
- tumors of the pituitary gland or hypothalamus
- complications after brain surgery
- sometimes develops after previous infections: ARVI, influenza and others
- encephalitis (inflammation of the brain)
- skull and brain injuries
- disruption of the blood supply to the hypothalamus or pituitary gland
- metastases of malignant neoplasms in the brain that affect the functioning of the pituitary gland or hypothalamus
- the disease may be congenital
- the disease may be congenital(most common reason)
- the disease is sometimes caused by certain conditions or diseases, in which the medulla of the kidney or the urinary tubules of the nephron are damaged.
- rare form of anemia(sickle cell)
- polycystic disease(multiple cysts) or amyloidosis (deposition of amyloid in the tissue) of the kidneys
- chronic renal failure
- increased potassium or decreased calcium in the blood
- taking medications that have a toxic effect on kidney tissue (for example, Lithium, Amphotericin B, Demeclocillin)
- sometimes occurs in debilitated patients or in old age
However, in 30% of cases the cause of diabetes insipidus remains unclear. Since all the studies conducted do not reveal any disease or factor that could lead to the development of this disease.
Symptoms of diabetes insipidus
Despite various reasons, which lead to the development of diabetes insipidus, the signs of the disease are almost the same for all variants of its course.However, the severity of the manifestations of the disease depends on two points:
- How resistant are nephron tubule receptors to vasopressin?
- degree of antidiuretic hormone deficiency or absence
The most first signs of illness- severe, painful thirst (polydipsia) and frequent excessive urination (polyuria), which bother patients even at night.
From 3 to 15 liters of urine can be released per day, and sometimes its amount reaches up to 20 liters per day. Therefore, the patient is tormented by severe thirst.
Later, as the disease progresses, the following symptoms appear:
- Signs of dehydration (lack of water in the body) appear: dry skin and mucous membranes (dry mouth), decreased body weight.
- Due to the consumption of large amounts of liquid, the stomach stretches and sometimes even drops.
- Due to lack of water in the body, the production of digestive enzymes in the stomach and intestines is disrupted. Therefore, the patient’s appetite decreases, gastritis or colitis develops, and there is a tendency to constipation.
- Due to the release of urine in large volumes, the bladder is stretched.
- Since there is not enough water in the body, sweating decreases.
- Blood pressure often drops and increases heartbeat.
- Sometimes there is unexplained nausea and vomiting.
- The patient gets tired quickly.
- Body temperature may increase.
- Sometimes bedwetting (enuresis) occurs.
- insomnia and headaches
- emotional lability (sometimes even psychosis develops) and irritability
- demotion mental activity
Symptoms of diabetes insipidus in men
The above described signs will be accompanied by a decrease in libido (desire for opposite sex) and potency (male impotence).Symptoms of diabetes insipidus in women
The disease occurs with normal symptoms. However, in women, the menstrual cycle is sometimes disrupted, infertility develops, and pregnancy ends in spontaneous miscarriage.Diabetes insipidus in children
In adolescents and children over three years of age, the symptoms of the disease are practically no different from those in adults.However, sometimes the signs of the disease are not clearly expressed: the child eats poorly and gains weight, suffers from frequent vomiting when eating, has constipation and bedwetting, and complains of pain in the joints. In this case, the diagnosis is made late, when the child is already lagging behind in physical and mental development.
Whereas in newborns and infants (especially with the renal type), the manifestations of the disease are striking and differ from those in adults.
Symptoms of diabetes insipidus in children under one year of age:
- The baby prefers water to mother's milk, but sometimes there is no thirst
- baby urinates frequently and in large quantities
- anxiety appears
- body weight is quickly lost (the child literally loses weight before our eyes)
- tissue turgor decreases (if the skin is folded and released, it slowly returns to its normal position)
- no or few tears
- frequent vomiting occurs
- heart rate increases
- Body temperature can either rise or fall quickly
Diagnosis of diabetes insipidus
First, the doctor clarifies several points:- What is the amount of fluid drunk and urine excreted by patients? If its volume is more than 3 liters, this indicates diabetes insipidus.
- Is there bedwetting and frequent excessive urination at night (nocturia), and does the patient drink water at night? If yes, then the volume of liquid drunk and urine excreted must be specified.
- Isn’t increased thirst also associated with a psychological reason? If it is absent when the patient is doing what he loves, walking or visiting, then most likely he has psychogenic polydipsia.
- Are there any diseases?(tumors, endocrine disorders and others), which can give impetus to the development of diabetes insipidus.
- the osmolarity and relative density of urine are determined (characterizes the filtering function of the kidneys), as well as the osmolarity of blood serum
- computed tomography or nuclear magnetic resonance of the brain
- radiography of the sella turcica and skull
- echoencephalography
- excretory urography
- Kidney ultrasound
- the level of sodium, calcium, potassium, nitrogen, urea, glucose (sugar) is determined in the blood serum
- Zimnitsky's test
Based on laboratory data diagnostic criteria diabetes insipidus are the following indicators:
- increased blood sodium (more than 155 mEq/L)
- increase in blood plasma osmolarity (more than 290 mOsm/kg)
- decreased urine osmolarity (less than 100-200 mOsm/kg)
- low relative density of urine (less than 1010)
It is noteworthy that this test allows not only to make a diagnosis, but also to determine the type of diabetes insipidus.
Test procedure with liquid restriction
After a night's sleep, the patient is weighed on an empty stomach, and blood pressure and pulse are measured. In addition, the level of sodium in the blood and the osmolarity of the blood plasma, as well as the osmolarity and relative density of urine (specific gravity) are determined.The patient then stops taking liquids (water, juices, tea) for as long as possible.
The test is stopped if the patient:
- weight loss is 3-5%
- there is an unbearable thirst
- the general condition sharply worsens (nausea, vomiting, headache appears, heart rate increases)
- blood sodium and osmolarity levels are higher than normal
An increase in blood osmolarity and sodium in the blood, as well as a decrease in body weight by 3-5% indicates in favor of central diabetes insipidus.
While a decrease in the amount of urine excreted and the absence of weight loss, as well as normal serum sodium levels, indicate renal diabetes insipidus.
If this test confirms diabetes insipidus, a minirhin test is performed for further diagnosis.
Methodology for conducting the minirin test
The patient is prescribed Minirin tablets and urine is collected according to Zimnitsky before and while taking it.What do the test results say?
With central diabetes insipidus, the amount of urine excreted decreases, and its relative density increases. Whereas in renal diabetes insipidus these indicators practically do not change.
It is noteworthy that to diagnose the disease, the level of vasopressin in the blood is not determined, since the technique is too expensive and difficult to perform.
Diabetes insipidus: differential diagnosis
Most often it is necessary to distinguish diabetes insipidus from diabetes mellitus and psychogenic polydipsia.| Sign | Diabetes insipidus | Diabetes | Psychogenic polydipsia |
| Thirst | strongly expressed | expressed | strongly expressed |
| Amount of urine excreted per day | from 3 to 15 liters | up to two or three liters | from 3 to 15 liters |
| Onset of the disease | usually spicy | gradual | usually spicy |
| Bed-wetting | sometimes present | absent | sometimes present |
| Increased blood glucose | No | Yes | No |
| Presence of glucose in urine | No | Yes | No |
| Relative density of urine | downgraded | increased | downgraded |
| General state when conducting a test with dry eating | getting worse | does not change | does not change |
| Volume of urine excreted during dry eating test | does not change or decreases slightly | does not change | decreases to normal numbers, while its density increases |
| Level uric acid in blood | more than 5 mmol/l | increases in severe disease | less than 5 mmol/l |
Treatment of diabetes insipidus
First, if possible, the cause of the disease is eliminated. Then they are appointed medications depending on the type of diabetes insipidus.Treatment of central diabetes insipidus
It is carried out taking into account how much fluid the patient loses in the urine:- If your urine volume is less than four liters per day, no medications are prescribed. It is only recommended to replenish lost fluid and follow a diet.
- When the amount of urine is more than four liters per day, substances are prescribed that act like vasopressin (replacement therapy) or stimulate its production (if hormone synthesis is partially preserved).
For more than 30 years, intranasal Desmopressin (Adiuretin) (injection of medication into the nasal passages) has been used as replacement therapy. However, its production has now been discontinued.
Therefore, currently the only drug that is prescribed as a replacement for vasopressin - Minirin(tablet form of Desmopressin). 
The dose of Minirin, which suppresses the symptoms of the disease, is not affected by the patient’s age or weight. Since everything depends on the degree of deficiency of antidiuretic hormone or its complete absence. Therefore, the dosage of Minirin is always selected individually during the first three to four days of taking it. Treatment begins with minimal doses, which are increased if necessary. The drug is taken three times a day.
To medicinal substances that stimulate the production of vasopressin, include Chlorpropamide (especially effective in the combination of diabetes mellitus and diabetes insipidus), Carbamazepine and Miscleron.
Treatment of renal diabetes insipidus.
First of all, a sufficient supply of fluid to the body is ensured, then, if necessary, medications are prescribed.Treatment with medications
Appointment is practiced medicinal substances, which, paradoxically, reduce the amount of urine - thiazide diuretics (diuretics): Hydrochlorothiazide, Indapamide, Triampur. Their use is based on the fact that they prevent the reabsorption of chlorine in the urinary tubules of the nephron. As a result, the sodium content in the blood decreases slightly, and the reabsorption of water increases.
Anti-inflammatory drugs (Ibuprofen, Indomethacin and Aspirin) are sometimes prescribed as an adjunct to treatment. Their use is based on the fact that they reduce the flow of certain substances into the urinary tubules of the nephron, thereby reducing the volume of urine and increasing its osmolality.
However, successful treatment of diabetes insipidus is impossible without following certain nutritional rules.
Diabetes insipidus: diet
Nutrition for diabetes insipidus has goals - reducing urine output in large volumes and thirst, as well as replenishing nutrients which are lost in urine.Therefore, first of all salt intake is limited(no more than 5-6 grams per day), and it is handed out, and food is prepared without adding it.
Useful dried fruits, since they contain potassium, which enhances the production of endogenous (internal) vasopressin.
Besides, you need to give up sweets, so as not to increase thirst. It is also recommended to refrain from drinking alcoholic beverages.
The power is included sufficient quantity fresh vegetables, berries and fruits, milk and lactic acid products. In addition, juices, compotes, and fruit drinks are useful.
It is very important that phosphorus enters the body(it is necessary for normal operation brain), therefore it is recommended to use low-fat varieties fish, seafood and fish oil.
Besides, lean meats and eggs are healthy(yolk). However, it must be remembered that in case of diabetes insipidus you should still limit proteins, so as not to increase the load on the kidneys. While fats (for example, butter and vegetable oil), as well as carbohydrates (potatoes, pasta and others) must be present in the diet in sufficient quantities.
It is advisable to eat meals in fractions: 5-6 times a day.
Diabetes insipidus: treatment with folk remedies
To improve the condition of patients with this disease, Mother Nature has prepared several wonderful recipes.To reduce thirst:
- Take 60 grams of crushed burdock root, place it in a thermos and pour one liter of boiling water. Leave it overnight and express in the morning. Take two-thirds of a glass three times a day.
- Take 20 grams of elderberry flowers, pour a glass of boiling water and leave for an hour. Then strain and add honey to taste. Take one glass three times a day.
- Take 5 grams (one teaspoon) of crushed young walnut leaves and pour a glass of boiling water. Let it brew and take it like tea.
Consume one teaspoon of pea flour per day, which is rich in glutamic acid.
To improve sleep and reduce irritability sedative fees apply:
- Take equal parts of crushed valerian roots, hop cones, motherwort herbs, rose hips, mint leaves and mix everything thoroughly. From the resulting mixture, take one tablespoon of raw material and pour a glass of boiling water. Let it sit for an hour and then express. Take 1/3 glass at night for insomnia or increased nervous agitation.
- Take equal parts of crushed valerian roots, fennel and caraway fruits, motherwort herbs and mix everything thoroughly. Then, from the resulting mixture, take two tablespoons of the raw material and pour 400 ml of boiling water, let it brew until cool and decant. Take half a glass if you feel irritable or nervous.
RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2013
Diabetes insipidus (E23.2)
Endocrinology
general information
Short description
Approved
minutes of the meeting of the Expert Commission
on health development issues of the Ministry of Health of the Republic of Kazakhstan
Diabetes insipidus(ND) (lat. diabetes insipidus) is a disease caused by a violation of the synthesis, secretion or action of vasopressin, manifested by the excretion of large amounts of urine with low relative density (hypotonic polyuria), dehydration and thirst.
Epidemiology .
The prevalence of ND in different populations varies from 0.004% to 0.01%. There is a worldwide trend toward an increase in the prevalence of ND, in particular, due to its central form, which is associated with an increase in the number of surgical interventions performed on the brain, as well as the number of traumatic brain injuries, in which cases of ND development account for about 30%. It is believed that ND affects both women and men equally often. The peak incidence occurs at the age of 20-30 years.
Protocol name:Diabetes insipidus
ICD-10 code(s):
E23.2 - Diabetes insipidus
Date of development of the protocol: April 2013.
Abbreviations used in the protocol:
ND - diabetes insipidus
PP - primary polydipsia
MRI - magnetic resonance imaging
BP - blood pressure
DM - diabetes mellitus
Ultrasound - ultrasound examination
Gastrointestinal tract - gastrointestinal tract
NSAIDs - non-steroidal anti-inflammatory drugs
CMV - cytomegalovirus
Patient category: men and women aged 20 to 30 years, a history of trauma, neurosurgical interventions, tumors (craniopharynoma, germinoma, glioma, etc.), infections (congenital CMV infection, toxoplasmosis, encephalitis, meningitis).
Protocol users: local therapist, endocrinologist at a clinic or hospital, neurosurgeon at a hospital, traumatologist at a hospital, local pediatrician.
Classification
Clinical classification:
The most common are:
1. Central (hypothalamic, pituitary), caused by a violation of the synthesis and secretion of vasopressin.
2. Nephrogenic (renal, vasopressin-resistant), characterized by kidney resistance to the action of vasopressin.
3. Primary polydipsia: a disorder in which pathological thirst (dipsogenic polydipsia) or compulsive desire to drink (psychogenic polydipsia) and associated excess water consumption suppress the physiological secretion of vasopressin, ultimately leading to the characteristic symptoms of diabetes insipidus, while the synthesis of vasopressin occurs when the body is dehydrated is being restored.
There are also other rare types of diabetes insipidus:
1. Progestational, associated with increased activity placental enzyme - arginine aminopeptidase, which destroys vasopressin. After childbirth the situation returns to normal.
2. Functional: occurs in children of the first year of life and is caused by the immaturity of the renal concentration mechanism and increased activity of phosphodiesterase type 5, which leads to rapid deactivation of the vasopressin receptor and a short duration of action of vasopressin.
3. Iatrogenic: use of diuretics.
Classification of ND by severity:
1. light form- urine output up to 6-8 l/day without treatment;
2. average - urine output up to 8-14 l/day without treatment;
3. severe - urine output more than 14 l/day without treatment.
Classification of ND by degree of compensation:
1. compensation - during treatment, thirst and polyuria do not bother;
2. subcompensation - during treatment there are episodes of thirst and polyuria during the day;
3. decompensation - thirst and polyuria persist.
Diagnostics
List of basic and additional diagnostic measures:
Diagnostic measures before planned hospitalization:
- general urine analysis;
- biochemical blood test (potassium, sodium, total calcium, ionized calcium, glucose, total protein, urea, creatinine, blood osmolality);
- assessment of diuresis (>40 ml/kg/day, >2l/m2/day, urine osmolality, relative density).
Basic diagnostic measures:
- Test with dry food (dehydration test);
- Test with desmopressin;
- MRI of the hypothalamic-pituitary zone
Additional diagnostic measures:
- Ultrasound of the kidneys;
- Dynamic tests of kidney function status
Diagnostic criteria:
Complaints and anamnesis:
The main manifestations of ND are severe polyuria (urine output more than 2 l/m2 per day or 40 ml/kg per day in older children and adults), polydipsia (3-18 l/day) and associated sleep disorders. A preference for plain cold/ice water is typical. There may be dry skin and mucous membranes, decreased salivation and sweating. Appetite is usually reduced. The severity of symptoms depends on the degree of neurosecretory insufficiency. With partial vasopressin deficiency, clinical symptoms may not be so clear and may manifest themselves in conditions of drinking deprivation or excessive fluid loss. When collecting anamnesis, it is necessary to clarify the duration and persistence of symptoms in patients, the presence of symptoms of polydipsia, polyuria, diabetes in relatives, a history of trauma, neurosurgical interventions, tumors (craniopharyngioma, germinoma, glioma, etc.), infections (congenital CMV infection , toxoplasmosis, encephalitis, meningitis).
In newborns and infants clinical picture The disease is significantly different from that in adults, since they cannot express their desire for increased fluid intake, which makes timely diagnosis difficult and can lead to the development of irreversible brain damage. These patients may experience weight loss, dryness and pale skin, lack of tears and sweating, increased body temperature. They may prefer breast milk water, and sometimes the disease becomes symptomatic only after the baby is weaned. Urine osmolality is low and rarely exceeds 150-200 mOsmol/kg, but polyuria appears only if the child’s fluid intake is increased. In children of such an early age, hypernatremia and hyperosmolality of the blood with convulsions and coma very often and quickly develop.
In older children, priority is given to clinical symptoms Thirst and polyuria may occur, and if fluid intake is inadequate, episodes of hypernatremia occur, which can progress to coma and convulsions. Children grow poorly and gain weight; they often vomit when eating, lack appetite, experience hypotension, constipation, and delayed mental development. Overt hypertensive dehydration occurs only in cases of lack of access to fluid.
Physical examination:
Upon examination, symptoms of dehydration may be detected: dry skin and mucous membranes. Systolic blood pressure is normal or slightly decreased, diastolic blood pressure is increased.
Laboratory research:
According to general analysis urine - it is discolored, does not contain any pathological elements, with a low relative density (1.000-1.005).
To determine the concentration ability of the kidneys, a Zimnitsky test is performed. If in any portion the specific gravity of urine is higher than 1.010, then the diagnosis of ND can be excluded, but it should be remembered that the presence of sugar and protein in the urine increases the specific gravity of urine.
Plasma hyperosmolality is more than 300 mOsmol/kg. Normal plasma osmolality is 280-290 mOsmol/kg.
Urine hypoosmolality (less than 300 mOsmol/kg).
Hypernatremia (more than 155 mEq/L).
At central shape ND there is a decrease in the level of vasopressin in the blood serum, and in the nephrogenic form it is normal or slightly increased.
Dehydration test(test with dry food). G.I. Dehydration Test Protocol Robertson (2001).
Dehydration phase:
- take blood for osmolality and sodium (1)
- collect urine to determine volume and osmolality (2)
- measure the patient’s weight (3)
- blood pressure and pulse control (4)
In the future, at regular intervals, depending on the patient’s condition, repeat steps 1-4 after 1 or 2 hours.
The patient is not allowed to drink; it is also advisable to restrict food, according to at least, during the first 8 hours of the test; When feeding, food should not contain a lot of water and easily digestible carbohydrates; preferred boiled eggs, grain bread, lean meats, fish.
The test stops when:
- loss of more than 5% of body weight
- unbearable thirst
- objectively serious condition of the patient
- an increase in sodium and blood osmolality above normal limits.
Desmopressin test. The test is carried out immediately after the end of the dehydration test, when the maximum possibility of secretion/action of endogenous vasopressin has been reached. The patient is given 0.1 mg of tableted desmopressin under the tongue until completely absorbed or 10 mcg intranasally as a spray. Urine osmolality is measured before taking desmopressin and 2 and 4 hours after. During the test, the patient is allowed to drink, but not more than 1.5 times the volume of urine excreted during the dehydration test.
Interpretation of the results of the test with desmopressin: Normally or with primary polydipsia, urine concentration occurs above 600-700 mOsmol/kg, blood osmolality and sodium remain within normal values, well-being does not change significantly. Desmopressin practically does not increase urine osmolality, since the maximum level of its concentration has already been reached.
With central ND, urine osmolality during dehydration does not exceed blood osmolality and remains at a level of less than 300 mOsmol/kg, blood osmolality and sodium increase, severe thirst, dry mucous membranes, increased or decreased blood pressure, and tachycardia are noted. When desmopressin is administered, urine osmolality increases by more than 50%. With nephrogenic ND, blood osmolality and sodium increase, urine osmolality is less than 300 mOsmol/kg, as with central ND, but after using desmopressin, urine osmolality practically does not increase (up to 50% increase).
The interpretation of the sample results is summarized in Table. .
Instrumental studies:
Central ND is considered a marker of pathology of the hypothalamic-pituitary region. MRI of the brain is the method of choice for diagnosing diseases of the hypothalamic-pituitary region. For central ND, this method has several advantages over CT and other imaging modalities.
MRI of the brain is prescribed to identify the causes of central ND (tumors, infiltrative diseases, granulomatous diseases of the hypothalamus and pituitary gland, etc. For nephrogenic diabetes insipidus: dynamic tests of renal function and renal ultrasound. In the absence of pathological changes according to MRI, this study is recommended in dynamics, since there are often cases when central ND appears several years before the detection of a tumor
Indications for consultation with specialists:
If pathological changes in the hypothalamic-pituitary region are suspected, consultations with a neurosurgeon and ophthalmologist are indicated. When pathology is detected urinary system- a urologist, and if the psychogenic variant of polydipsia is confirmed, a referral to a consultation with a psychiatrist or neuropsychiatrist is necessary.
Differential diagnosis
It is carried out between three main conditions accompanied by hypotonic polyuria: central ND, nephrogenic ND and primary polydipsia. Differential diagnosis is based on 3 main stages. 
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Treatment
Treatment goals:
Reducing the severity of thirst and polyuria to such an extent that would allow the patient to lead a normal lifestyle.
Treatment tactics:
Central ND.
Most preferred drug desmopressin remains. Most patients can be treated with desmopressin tablets (0.1 and 0.2 mg), although many patients continue to be treated successfully with desmopressin intranasal spray. Due to individual pharmacokinetic characteristics, it is extremely important to determine the duration of action of a single dose of the drug individually for each patient.
Therapy with desmopressin in tablet form is prescribed at an initial dose of 0.1 mg 2-3 times a day orally 30-40 minutes before meals or 2 hours after meals. Average doses of the drug vary from 0.1 mg to 1.6 mg per day. Concomitant food intake can reduce the degree of absorption from the gastrointestinal tract by 40%. For intranasal use, the initial dose is 10 mcg. When injected, the spray is distributed over the anterior surface of the nasal mucosa, which ensures a longer concentration of the drug in the blood. The need for the drug varies from 10 to 40 mcg per day.
The main goal of treatment with desmopressin is to select the minimum effective dose of the drug to relieve thirst and polyuria. A mandatory increase in the relative density of urine should not be considered as a goal of therapy, especially in each of the Zimnitsky urine test samples, since not all patients with central ND against the background of clinical compensation of the disease achieve normal indicators of concentrated renal function in these tests (physiological variability of urine concentration during the day, concomitant kidney pathology, etc.).
Diabetes insipidus with inadequate thirst.
When the functional state of the thirst center changes towards a decrease in the sensitivity threshold, hyperdipsia, patients are predisposed to the development of such a complication of desmopressin therapy as water intoxication, which is a potentially life-threatening condition. Such patients are advised to periodically skip doses of the drug to release retained excess fluid or a fixed fluid intake.
The state of adipsia in central ND can manifest itself as alternating episodes of hypo- and hypernatremia. Management of such patients is carried out with a fixed daily volume of fluid intake or with recommendations for fluid intake according to the volume of urine excreted + 200-300 ml of additional fluid. Patients with impaired thirst sensation require special dynamic monitoring of their condition with monthly, and in some cases more often, determination of blood osmolality and sodium.
Central ND after surgery on the hypothalamus or pituitary gland and after head trauma.
The disease in 75% of cases has a transient course, and in 3-5% - a three-phase course (phase I (5-7 days) - central ND, phase II (7-10 days) - syndrome of inadequate secretion of vasopresiin, phase III - permanent central ND ). Desmopresiin is prescribed in the presence of symptoms of diabetes insipidus (polydipsia, polyuria, hypernatremia, blood hyperosmolality) at a dose of 0.05-0.1 mg 2-3 times a day. Every 1-3 days, the need to take the drug is assessed: the next dose is skipped, and the resumption of symptoms of diabetes insipidus is monitored.
Nephrogenic ND.
Thiazide diuretics and a low-sodium diet are prescribed to reduce symptomatic polyuria. The antidiuretic effect in this case is due to a reduction in the volume of extracellular fluid, a decrease in the glomerular filtration rate, increased reabsorption of water and sodium from primary urine in the proximal tubules of the nephrons and a decrease in the amount of fluid entering the collecting ducts. However, studies demonstrate that thiazide diuretics can increase the number of aquaporin-2 molecules on the membranes of nephron tubular epithelial cells independently of vasopressin. While taking thiazide diuretics, it is advisable to compensate for potassium losses by increasing its intake or prescribing potassium-sparing diuretics.
When indomethacin is prescribed, additional very beneficial effects develop, however, NSAIDs can provoke the development of duodenal ulcers and gastrointestinal bleeding.
Non-drug treatment:
In case of central ND with normal function of the thirst center - free drinking regime, normal diet. In the presence of dysfunction of the thirst center: - fixed fluid intake. For nephrogenic ND - limit salt, eat foods rich in potassium.
Drug treatment:
Minirin, tablets 100, 200 mcg
Minirin, oral lyophilisate 60, 120, 240 mcg
Presaynex, spray for nasal use dosed 10 mcg/dose
Triampur-compositum, tablets 25/12.5 mg
Indomethacin - enteric-coated tablets 25 mg
Other types of treatment: -
Surgical intervention: for neoplasms of the hypothalamic-pituitary region.
Preventive actions: unknown
Further management: outpatient observation
Indicators of treatment effectiveness and safety of diagnostic and treatment methods described in the protocol: reduction of thirst and polyuria.
- List of used literature: 1. Guidelines edited by Dedova I.I., Melnichenko G.A. “Central diabetes insipidus: differential diagnosis and treatment”, Moscow, 2010, 36 p. 2. Melnichenko G.A., V.S. Pronin, Romantsova T.I. and others - “Clinic and diagnosis of hypothalamic-pituitary diseases”, Moscow, 2005, 104 p. 3. Endocrinology: national guide, ed. Dedova I.I., Melnichenko G.A., Moscow, GEOTAR-Media, 2008, 1072 pp. 4. Pigarova E.A. - Diabetes insipidus: epidemiology, clinical symptoms, treatment approaches, - “Doctor.ru”, No. 6, part II, 2009. 5. Practical endocrinology / ed. Melnichenko G.A.-Moscow, “Practical Medicine”, 2009, 352 pp. 6. Neuroendocrinology / Henry M. Kronenberg, Shlomo Melmed, Kenneth S. Polonsky, P. Ried Larsen, translation from English. Ed. Dedova I.I., Melnichenko G.A., Moscow, ReadAlsiver, 2010, 472 pp.
Information
List of developers:
1. Danyarova L.B. - candidate medical sciences, Head of the Endocrinology Department of the Research Institute of Cardiology and Internal Medicine, endocrinologist of the highest category.
2. Shiman Zh.Zh. - Junior Researcher, Department of Endocrinology, Research Institute of Cardiology and Internal Medicine, endocrinologist.
Disclosure of no conflict of interest: absent.
Reviewers: Erdesova K.E. - Candidate of Medical Sciences, Professor, Internship Department of KazNMU.
Indication of the conditions for reviewing the protocol: The protocol is revised at least once every 5 years, or upon receipt of new data on the diagnosis and treatment of the corresponding disease, condition or syndrome.
Attached files
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