Diabetes insipidus

Introduction to diabetes insipidus Diabetesinsipindus refers to insufficient secretion of vasopressin (VP) (also known as antidiuretic hormone) (ADH) (also known as central or pituitary diabetes insipidus), or the kidneys pressurize the blood vessels. A group of syndromes caused by defects in the reaction (also known as renal diabetes insipidus), characterized by polyuria, polydipsia, low specific gravity urine and hypotonic urine. Diabetes insipidus is common in young adults, with a male to female ratio of 2:1. Hereditary NDI is more common in children. basic knowledge The proportion of illness: 0.0025% Susceptible people: occur at any age, but more common in young adults, the incidence of men and women is similar. Mode of infection: non-infectious Complications: electrolyte imbalance dehydration

Cause of diabetes insipidus

Primary diabetes insipidus (30%):

About 1/3 to 1/2. Usually in children with onset, very few (<20%) with anterior pituitary dysfunction. This diagnosis can only be determined after careful search for secondary causes that do not exist. When there is anterior pituitary dysfunction or hyperprolactinemia or radiographic examination with evidence of lesions in the sella or on the sella, the cause should be searched as much as possible. The longer the follow-up can not find the primary factor, The diagnosis of primary diabetes insipidus is affirmed. It has been reported that in patients with primary diabetes insipidus, neurons in the supraoptic nucleus and paraventricular nucleus are reduced, and antibodies to the hypothalamic nucleus are present in the circulation.

Secondary diabetes insipidus (20%):

Occurs in hypothalamic or pituitary neoplasms or invasive lesions, including: chromoblastoma, craniopharyngioma, embryonal tumor, pineal tumor, glioma, meningiomas, metastases, leukemia, histiocytosis, Sarcoma, xanthoma, sarcoidosis, and brain infectious diseases (tuberculosis, syphilis, vascular disease).

Hereditary diabetes insipidus (10%):

Hereditary diabetes insipidus is very rare and can be a single hereditary defect or part of the DIDMOAD syndrome (which can be manifested as diabetes insipidus, diabetes, optic atrophy, deafness, also known as Wolfram syndrome).

Physical damage (10%):

It is common in the brain, especially in the pituitary and hypothalamic areas, after isotope treatment, after severe brain injury.

Pathogenesis

1. Physiology of vasopressin

(1) Synthesis and metabolism of AVP

Vasopressin is synthesized in the hypothalamic nucleus and in the paraventricular nucleus. The initial product is preprohormone, which enters the Golgi to form prohormone, which is encapsulated in the neurosecretory vesicle, and the vesicle along the neurohypophysis The axonal flow to the neurohypophysis, through the action of enzymes in the flow of persuasion to produce active nonapeptide, arginine Vasopressin (AVP) and a molecular weight (neurophysin) and a 39 amino acid Glycopeptides, all of which are released into the peripheral blood. AVP is secreted by hypothalamic neurons and descends along the thalamus-neuronal pituitary gland to the distal pit. It is stored in the pituitary gland. In recent years, AVP fibers have also been found in the lateral band of the median ridge. AVP can also be secreted into the pituitary portal system at the bottom of the third ventricle and the brainstem vasculature.

AVP binds to the distal convoluted tubules of the kidney and combines the endothelial cells of the collecting duct to promote the flow of water from the lumen to the interstitial, helping to maintain a constant osmotic pressure and body fluid volume. AVP has a low plasma concentration and no vasoactive effect, but High concentrations of AVP acting on V1 receptors can cause vasoconstriction, and AVPs present in brain axons may be involved in learning and memory processes. AVP fibers in median uplift may be involved in promoting ACTH release.

The concentration of AVP in plasma and urine can be determined by immunoassay. In the case of random intake of liquid, the neurohypophysis contains nearly 6 units or 18 mmol (20 g) of AVP, and the peripheral blood AVP concentration is 2.3-7.4 pmol/L (2.5~). 8 ng / L), blood AVP concentration changes with day and night, late at night and early morning, the lowest in the afternoon, in normal water supply, healthy people release AVP 23 ~ 1400pmol (400 ~ 1500ng) from the pituitary gland 24 hours, AVP23 ~ 80pmol from the urine (25-90 ng), after 24 to 48 hours of water ban, the release of AVP increased by 3 to 5 times, blood and urine levels continued to increase, AVP was mainly inactivated in the liver and kidney, and nearly 7% to 10% of AVP was active. The form is discharged from the urine.

(B) the regulation of AVP release

1. Osmotic receptors: The release of AVP is affected by various stimuli. Under normal circumstances, the release of AVP is mainly due to the regulation of osmotic pressure receptors in the hypothalamus. The change of osmotic pressure stimulates the production and release of AVP, changes in plasma osmotic pressure and AVP. The released feedback regulation mechanism maintains the plasma osmotic pressure in a narrow range. After a normal human 20ml/kg water load, the average plasma osmotic pressure is 281.7mOsm/kg·H2O. After injecting hypertonic saline into the water-loaded person, the plasma is injected. The osmotic pressure was 287.3/kg·H 2 O.

2. Volume regulation: The decrease in blood volume stimulates the tension receptors of the left atrium and the pulmonary veins, and stimulates the release of AVP by reducing the tension-suppressing impulse from the baroreceptors to the hypothalamus. In addition, it is shouting, erect, warm environment. The resulting vasodilation can stimulate this mechanism to restore blood volume, and the volume reduction can make the circulating AVP concentration reach 10 times of the AVP concentration caused by high osmotic pressure.

3. Baroreceptors: hypotension stimulates carotid and aortic baroreceptors, stimulates AVP release, and hypotension caused by blood loss is the most effective stimulation. At this time, plasma AVP concentration increases significantly, and at the same time, vasoconstriction can be caused until blood volume is restored. Maintain blood pressure.

4. Neuromodulation: many neurotransmitters and neuropeptides in the hypothalamus have functions to regulate the release of AVP, such as acetylcholine, angiotensin II, histamine, bradykinin, -neuropeptide, etc., which can stimulate the release of AVP. With the increase of age, the reactivity of plasma osmotic pressure increases during AVP, and the plasma AVP concentration increases progressively. These physiological changes may increase the risk of water retention and hyponatremia in the elderly.

5. Drug effects: Drugs that stimulate the release of AVP include nicotine, morphine, vincristine, cyclophosphamide, clofibrate, chlorpropamide and certain tricyclic antidepressants. Ethanol can inhibit neurohypophyseal Function produces diuretic effect, phenytoin, chlorpromazine can inhibit the release of AVP and produce diuretic effect.

(3) AVP's response to water and water load: water ban can increase osmotic pressure to stimulate the release of vasopressin. After ban, the maximum osmotic pressure changes with renal medulla osmotic pressure and other intrarenal factors. After 18-24 hours of water, the plasma osmotic pressure rarely exceeds 292mOsm/kg·H2O, and the plasma AVP concentration increases to 14-23 pmol/L (15-25 ng/L). After influent, AVP release can be inhibited, and normal people drink 20 ml. After a water load of /kg, the plasma osmotic pressure dropped to an average of 281.7 mOsm/kg·H2O.

(4) Relationship between AVP release and craving: Under normal circumstances, the release of AVP and the feeling of thirst are consistent, both caused by a slight increase in osmotic pressure, when the plasma osmotic pressure rises to 292mOsm/kg·H2O Above, the thirst is gradually obvious, until the urine concentration reaches the limit, the water is stimulated. Therefore, under normal circumstances, mild sorghum caused by dehydration can enhance the thirst and increase the fluid intake to restore and Maintain normal plasma osmotic pressure. Conversely, when thirst is lost, fluid loss cannot be corrected in time by drinking water. Although AVP release can maximize urine concentration, hypernatremia can still occur.

(5) The role of glucocorticoids: Adrenal cortex hormones and AVP have anti-inflammatory effects on water excretion. Cortisone can increase the osmotic pressure threshold of AVP release caused by normal infusion of hypertonic saline. Glucocorticoid can prevent water intoxication. And when the adrenal insufficiency declines, the body responds abnormally to water load. When the adrenal function declines, the decrease of urine release capacity may be partly due to excessive AVP in the circulation, but glucocorticoid can directly act on AVP deficiency. The renal tubules reduce the permeability of water and increase the excretion of free water in the absence of AVP.

(VI) The cytological mechanism of AVP action The mechanism of AVP effect on small renal tubules:

1AVP binds to the V2 receptor on the tubular membrane of the renal tubule opposite the lumen.

2 The hormone-receptor complex activates adenylate cyclase by a guanylate-binding stimulating protein.

The production of 3-cyclic adenosine monophosphate (cAMP) is increased.

4c-AMP is transferred to the cell membrane of the luminal surface to activate the protein kinase on the membrane.

5 protein kinases lead to membrane protein phosphorylation.

The 6-cavity mask increases the permeability of water, which increases the reabsorption of water. Many ions and drugs can affect the action of AVP. Calcium and lithium inhibit the reaction of adenylate cyclase to AVP, and also inhibit cAMP-dependent protein kinase. In contrast, chlorpropamide enhances AVP-induced adenylate cyclase activation.

2, dysfunction in any part of AVP production and release leads to disease

By comparing normal drinking water, water load, and changes in plasma and urine osmotic pressure under water-free conditions, central diabetes insipidus can be classified into four types:

Type 1: When the blood osmotic pressure is significantly increased when the water is forbidden, the urine osmotic pressure is rarely increased, and there is no release of AVP when the hypertonic saline is injected. This type does have AVP deficiency.

Type 2: Urine osmotic pressure suddenly increases when water is absent, but there is no osmotic pressure threshold when injecting saline. These patients lack the osmotic pressure sensation mechanism and can stimulate AVP release only when severe dehydration leads to low school capacity.

Type 3: As plasma osmotic pressure increases, urine osmolality increases slightly, AVP release threshold increases, and these patients have a slow AVP release mechanism, or osmotic receptor sensitivity is reduced.

Type 4: Both the blood and urine osmotic pressure curves are shifted to the normal right side. This patient begins to release AVP when the plasma osmotic pressure is normal, but the release is lower than normal. Patients with type 2~4 have nausea, nicotine, and acetylcholine. , chlorpropamide, clofibrate has a good anti-diuretic effect, suggesting that the synthesis and storage of AVP is present, released under appropriate stimulation, in rare cases, patients with type 2 to 4 can be asymptomatic Hypernatremia and diabetes insipidus are very mild, and even lack the basis of diabetes insipidus.

Diabetes insipidus prevention

prevention

1, to avoid long-term mental stimulation, long-term mental stimulation (such as intimidation, sadness, anxiety or refreshment, etc.) can cause cerebral cortical dysfunction, which in turn causes endocrine disorders, so that the secretion of antidiuretic hormone is more sufficient, more urine, so that The disease is more serious.

2, avoid eating high-protein, high-fat spicy and salty foods and tobacco and alcohol, because these can increase the plasma osmotic pressure, thereby exciting the brain thirst center, and easy to help the heat, dry and yin, Aggravate the symptoms such as polydipsia.

3, avoid drinking tea and coffee, tea and coffee contain theophylline and caffeine, can excite the central nervous system, enhance myocardial contractility, expand the kidney and surrounding blood vessels, and diuretic effect, so that the amount of urine increased, the condition worsened.

Diabetes insipidus complications Complications, electrolyte imbalance, dehydration

There are complications such as renal ureteral hydrops and bladder dilatation.

1, diabetes insipidus combined with hypopituitarism:

Surgery, tumor and inflammation in the hypothalamus or pituitary can cause diabetes insipidus and pituitary dysfunction, vascular lesions of postpartum pituitary necrosis, and can also damage the supra-nucleus pituitary system and cause diabetes insipidus and mat Han syndrome, diabetes insipidus and pituitary dysfunction, polyuria symptoms, urine osmolality is higher; because glucocorticoids and vasopressin antagonism, so when glucocorticoid deficiency, vasopressin deficiency The condition will be alleviated. In addition, when glucocorticoids and thyroxine are reduced, the excretion of urinary solute is reduced, and the symptoms of polyuria can be alleviated.

2, diabetes insipidus with thirst sensation syndrome:

This syndrome is a deficiency of vasopressin, and the feeling of thirst also decreases or disappears. The patient's kidney can not regulate the excretion of water normally. The patient does not have the thirst, and cannot increase the amount of drinking water at any time for the needs of the human body. Drink more, have severe dehydration and high blood sodium, body fluids are hypertonic, accompanied by hyperosmotic signs, headache, myalgia, tachycardia, personality changes, irritability, confusion, paralysis and even coma, with vasopressin The dosage is not easy to adjust during treatment, and it is easy to overdose and cause water retention. It is hypotonic or water poisoning. It can be treated with chlorpropamide, 250mg/d, the urine volume can be reduced, and the function of thirsty center can be improved.

3, diabetes insipidus combined with pregnancy:

Diabetes in patients with diabetes insipidus with pregnancy, the condition of diabetes insipidus can be aggravated, because the secretion of adrenal cortex hormone in pregnant women increases, it can antagonize the antidiuretic effect of vasopressin, or inhibit the secretion of vasopressin, in addition, pregnancy Adrenal cortex hormones and thyroid hormones increase, urinary solute excretion increases, so that the amount of urine increases, throughout the pregnancy, especially in the middle, the patient's need for vasopressin increased, often also make the condition of diabetes insipidus worse. Diabetes insipidus is relieved after childbirth.

Symptoms of diabetes insipidus Common symptoms Urinary collapse Kidney urinary collapse Polyuria Dry skin Drinking often thirst Insomnia Thirst Adrenal cortical hormone deficiency High fever

1, hypotonic polyuria

Polyuria is the most significant symptom in patients with DI, and CDI patients generally have a more urgent and clear date. The amount of urine exceeds 2500ml/d or 50ml/(kg.d)], accompanied by polydipsia and polydipsia. There is a significant increase in nocturia. The urine volume is generally above 4L/d, and very few can exceed 10L/d, but it has also been reported to reach 40L/d. The urine specific gravity is 1.0001 to 1.0005, and the urine osmotic pressure is 50 to 200 mOsm/L, which is significantly lower than the plasma osmotic pressure. Long-term polyuria can lead to an increase in bladder capacity, so the number of urination is reduced. Patients with partial diabetes insipidus have milder symptoms and the urine volume is 2.4-5L/d. If the water intake leads to severe dehydration, the urine specific gravity can reach 1.010~1.016, and the urine osmotic pressure can exceed the plasma osmotic pressure by 290-600mOsm/ L. If the patient's thirst is not involved in the center and the drinking water is not restricted, it usually only affects sleep, and the physical strength is weak and not life-threatening. If the patient's hunger declines or disappears, and fails to replenish water in time, it can cause severe water loss, plasma osmotic pressure and serum sodium levels, and extreme weakness, fever, mental symptoms, and even death. Once diabetes insipidus is associated with hypopituitarism, diabetes insipidus can be alleviated and symptoms can be reappeared or aggravated after glucocorticoid replacement therapy.

Hereditary NDI often begins in infants and young children, and most have a family history. Mostly transmitted by women, males are ill. After birth, there are both polyuria and polydipsia. If not found in time, it is often caused by severe water shortage, hypernatremia and high permeability coma. If you can survive, you may have slow growth and reduce or disappear symptoms after adulthood. Repeated dehydration and hyperosmolarity in infancy can lead to mental retardation and impaired vascular endothelium, and diffuse calcification in the brain and blood vessels.

2, the clinical manifestations of the primary disease

Patients with secondary diabetes insipidus also have symptoms and signs of primary disease. Patients with traumatic CDI may present with transient diabetes insipidus and three-dimensional diabetes insipidus. Three-phase diabetes insipidus can be divided into acute phase, intermediate phase and duration. The acute phase manifests as polyuria, which occurs after injury and generally lasts for 4-5 days, mainly because of the shock caused by neuronal shock, the inability to release AVP or the release of biologically inactive precursor substances. The intermediate period is characterized by an increase in oliguria and urinary osmotic pressure, which is caused by AVP overflowing from degenerated neurons, resulting in a sudden increase in AVP in the circulation. The duration was persistent polyuria, and the time was variable. The large cell neurons in the supraoptic nucleus and paraventricular nucleus disappeared >90% or the irreversible damage of the pituitary stalk was >85%.

Diabetes insipidus (GDI) during pregnancy: refers to a group of syndromes that appear mainly in the third trimester of pregnancy with polyuria, low specific gravity urine, polydipsia, polydipsia, and electrolyte imbalance, mostly transient. Among the various factors that cause GDI, the role of vasopressin secreted by the placenta is the most important, which increases the degradation of AVP, and the balance between the degradation of AVP in the human body and the increased secretion of pituitary compensatory AVP is hit. Indiscriminate, the remaining AVP levels do not maintain sufficient antidiuretic activity, causing diabetes insipidus. The level of this enzyme decreased rapidly after delivery, and its activity was not detected in plasma after 4 weeks.

Examination of diabetes insipidus

1. Valuation of the relationship between plasma osmotic pressure and urine osmotic pressure

The normal relationship between blood scholarship and osmolality. If a patient with multiple urine tests several times and the osmotic pressure of both blood and urine falls on the right side of the shadow, the patient has central diabetes insipidus or renal diabetes insipidus. If the response to vasopressin is lower than normal (see the water-free test below) or the blood or urine AVP concentration increases, it is diagnosed as renal diabetes insipidus. The relationship between blood and urine osmotic pressure is very useful, especially in After neurosurgery or head trauma, the relationship between the two can be used to quickly identify the diabetes insipidus and extra-gastrointestinal fluid supply. For these patients, intravenous infusion can be temporarily slowed down, repeated measurement of hematuria osmotic pressure, urine osmotic pressure It is 50-200 mOsm/kg H2O, which is significantly lower than plasma osmotic pressure, and the plasma osmotic pressure can be higher than 300 mmol/L (normal reference value is 280-295 mmol/L).

2, water test

Comparing the osmotic pressure after deflation with vasopressin is a simple and feasible method for determining diabetes insipidus and identifying vasopressin deficiency and other causes of polyuria. Due to urine osmotic pressure, it is often used in combination with osmotic pressure 15-21.

Principle: The normal person's blood osmotic pressure is increased after the water is banned, and the circulating blood volume is reduced. Both of them stimulate the release of AVP, so that the urine volume is reduced, the urine specific gravity is increased, the urine penetration is increased, and the blood osmotic pressure is not changed much.

Method: The water is banned for 6 to 16 hours (usually 8 hours of water ban), depending on the severity of the disease. Before the test, the body weight, blood pressure, plasma osmotic pressure and urine specific gravity, urine volume per hour, urine specific gravity and Urinary osmotic pressure, when the urine volume changed little twice, the urine osmotic pressure changes <30mOsm/kg·H2O, it shows that the endogenous AVP secretion has reached the maximum value (mean), at this time the plasma osmotic pressure is measured, and then immediately subcutaneous The injection of vasopressin 5u, and then urine was taken to determine the urine volume and urine osmotic pressure 1 to 2 times.

Analysis of results: normal people's weight, blood pressure, blood osmotic pressure after drinking water is not much <295mOsm / kg · H2O, osmotic pressure can be greater than 800mOsm / kg · H2O, after injection of vasopressin, urine osmotic pressure is not increased More than 9%, mental polydipsia is close to or similar to normal people. Patients with central diabetes insipidus have a rest loss of >3% after water inhibition. In severe cases, blood pressure may drop. Symptoms such as irritability may be divided into partial parts according to the severity of the disease. Diabetes insipidus and complete diabetes insipidus, the former plasma osmotic flattening top value is not higher than 300mOsm / kg · H2O, urine osmotic pressure can slightly exceed the plasma osmotic pressure, urine osmotic pressure can continue to rise after the injection of vasopressin, The osmotic flattening value of complete diabetes insipidus is more than 300mOsm/kg·H2O, the urine osmotic pressure is lower than the blood osmotic pressure, and the urine osmotic pressure is increased by more than 9% after the injection of vasopressin, even doubled. Urine insipidus can not concentrate and concentrate after the water is banned, and there is still no reaction after the injection of vasopressin.

Test characteristics: This method is simple and reliable, and has been widely used. The side effect is that vasopressin raises blood pressure, induces angina pectoris, abdominal pain, and uterine contraction.

3. Hypertonic saline test

This test is rarely used in the diagnosis of diabetes insipidus. It is necessary to demonstrate that the osmotic pressure threshold for AVP release can be used in this test and is of value in the analysis of certain low sodium and hypernatremia properties.

4, plasma AVP determination

Partial diabetes insipidus and psychiatric polydipsia due to long-term polyuria, renal medullary due to elution (washout) caused by decreased osmotic gradient, affecting the kidney's response to endogenous AVP, it is not easy to with partial renal diabetes insipidus Identification, at this time do the water test to determine plasma AVP, plasma and urine osmotic pressure to help differential diagnosis.

5. The cause diagnosis of central diabetes insipidus

Once the diagnosis of central diabetes insipidus is established, it is necessary to further clarify the cause of the diagnosis. It is necessary to measure vision, visual field, sphenoidal film, sella CT, MRI, etc. to determine the cause.

6, plasma antidiuretic hormone value

Decreased (normal basal value is about 1 ~ 1.5pg / ml), especially when the water is forbidden and instilled with hypertonic saline, it can not increase, suggesting that the pituitary vasopressin reserve capacity is reduced.

(1). X-ray examination of patients with diabetes insipidus can sometimes find enlargement of the sella, space-occupying lesions on the saddle, calcification, and increased intracranial pressure.

(2). Gas-brain examination (now eliminated) and head CT can also be seen similar abnormalities. Because the bone structure of the saddle area is more complicated, ordinary X-ray films can not provide valuable information for the diagnosis of diabetes insipidus. The vertebral structure of the socket and occipital slopes limits the display of CT on the saddle area, especially the subtle lesions.

(3). Magnetic resonance imaging: High-resolution MRI can find the following lesions related to central diabetes insipidus: 1 pituitary volume is small. 2 The pituitary stalk is thickened. 3 The pituitary stalk is interrupted. 4 pituitary full upper edge light convex. 5 The high signal of the pituitary gland disappeared, in which the high signal of the pituitary gland disappeared and the function of the pituitary gland was low, and the AVP secretion of the posterior lobe was decreased. It was the MRI feature of central diabetes insipidus. The secondary central diabetes insipidus MRI showed pituitary stalk. Thickening is presumed to be caused by infiltration of tumor or systemic disease.

(4). The gene probe for the renal diabetes insipidus gene on the X chromosome can be used for prenatal diagnosis of postpartum pregnancy in hereditary renal diabetes insipidus, with 96% reliability.

(5). Fundus examination can find abnormalities, such as visual field defects, hemianopia, optic disc edema or fundus arteriosclerosis.

Diagnosis and identification of diabetes insipidus

diagnosis

The diagnosis of typical diabetes insipidus is not difficult. Anyone who has polydipsia, polydipsia, polyuria and low specific gravity should consider this disease. If necessary, the test can be performed with vasopressin and blood and urine osmotic pressure. diagnosis.

Differential diagnosis

Diabetes insipidus must be differentiated from other types of polyuria, some can be identified by medical history (such as the recent use of lithium or mannitol, surgery under methoxyflurane anesthesia or recent kidney transplantation), in other patients, through physical examination or A simple laboratory examination will prompt a diagnosis (eg diabetes, kidney disease, sickle cell anemia, hypercalcemia, hypokalemia, primary aldosteronism).

Congenital renal diabetes insipidus is a rare polyuria. Due to the lack of response to AVP, women are milder than men. Concentrated urine can be concentrated when water is banned. It is effective with a large amount of desmopressin. In the family suffering from this disease, there is an abnormal gene on the short arm of the X-ray chromosome. Most patients have abnormal V2 receptors, some patients have defects in the receptor, and all patients have normal V1 receptor function, when renal diabetes insipidus When the central diabetes insipidus cannot be identified by osmotic pressure measurement, the blood or urine AVP concentration associated with plasma osmotic pressure is increased, and the diagnosis of renal diabetes insipidus can be confirmed.

Primary polydipsia or polydipsia may sometimes be difficult to distinguish from diabetes insipidus, or both forms may exist at the same time. Excessive long-term water intake may cause hypotonic polyuria to be confused with diabetes insipidus. Intermittent large amounts of drinking water Even if the ability to dilute urine is normal, it can lead to water intoxication and dilute hyponatremia. This phenomenon is rare, but the tendency of these patients to have low sodium is often unstable. Often no nighttime polyuria, which is different from the long-term polydipsia of diabetes insipidus from urine, combined with low plasma osmotic pressure and low osmotic pressure, can confirm the diagnosis of primary polydipsia, normal or often normal, water-free test When the osmolality is stable, the osmolality does not increase or increase after injection of vasopressin. The long-term large amount of water intake inhibits the release of AVP and long-term polyuria, resulting in loss of renal medullary osmotic pressure gradient, urine osmotic pressure. Compared with blood osmotic pressure, it can be lower than normal. Therefore, it is sometimes difficult to identify primary polydipsia and incomplete central diabetes insipidus, and some patients may have both cases.

1, the diagnosis of diabetes insipidation is established, should be further identified as its central or renal nature, to guide treatment, and must be identified with mental polydipsia.

2. After the diagnosis of diabetes insipidus is established, partial diabetes insipidus and complete diabetes insipidus can be distinguished according to clinical manifestations and examination results.

3, central diabetes insipidus can also be associated with thirsty sensation syndrome.

4. The central diabetes insipidus caused by craniocerebral surgery may be temporary or persistent. The former occurs more than 1 to 4 days after surgery. After several days, the symptoms disappear and the urine volume returns to normal. The release of AVP is temporarily inhibited for surgical trauma, and its synthesis is not affected. This can also occur after encephalitis, which destroys the access of the suprachiasmatic nucleus to the paraventricular nucleus to the neurohypophyseal bundle. The pituitary stalk is severed, the ability to synthesize and release AVP is lost, and permanent diabetes insipidus is formed. AVP long-term replacement therapy is required.

5, diabetes insipidus should be differentiated from other common medical diseases caused by polyuria, such as diabetes, hypercalciuria, hyperkalemia, hyperosmotic polyuria and hypotonic polyuria.

(1) Diabetes: often have more drink, more urine, more food, weight loss symptoms, elevated blood sugar, urine sugar positive, easy to identify, need to pay attention to some cases of diabetes insipidus, diabetes.

(2) hypercalciuria: seen in hyperparathyroidism, sarcoidosis, vitamin D poisoning, multiple myeloma, cancer bone metastasis and other diseases, with primary symptoms to identify.

(3) hyperuricemia: seen in primary aldosteronism, potassium loss nephropathy, renal tubular acidosis, Fanconi syndrome, Liddle syndrome, Bartter syndrome.

(4) hyperosmotic polyuria: urine specific gravity greater than 1.020, urine osmotic pressure greater than 300mOsm / kgH20, seen in: 1 urine sugar increased. 2 Urea is elevated (high protein, high energy nutrition). 3 elevated urinary sodium (such as when adrenal insufficiency).

(5) hypotonic polyuria: urine specific gravity is less than 1.006, urine osmotic pressure <280mOsm / kgH20, seen in: 1 renal dysfunction. 2 potassium loss nephropathy. 3 renal diabetes insipidus. 4 high calcium uremia. 5 central diabetes insipidus. 6 spiritual polydipsia and so on.

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