What is the pathogenetic mechanism for the development of prerenal polyuria. A constant companion to the development of diabetes mellitus, also known as polyuria: causes, associated symptoms and treatment. Treatment of polyuria using folk remedies

Often specific symptoms indicate the presence of a particular disease. Polyuria in diabetes mellitus is one of the most common manifestations of this disease. This unpleasant symptom causes serious discomfort and requires adequate therapy. To do this, it is necessary to determine the exact cause of the pathology, as well as differentiate it from other anomalies that are expressed in a similar way.

What it is?

Polyuria quite often is not only one of the manifestations diabetes mellitus, and also its complication.

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Polyuria is excessive urine production, which is manifested by a very frequent urge to urinate. This is one of the main symptoms of diabetes that can occur in people of different ages and gender. The pathogenesis of polyuria, which is characterized by the following features in the body:

• changes in kidney secretion abilities;
• the influence of the hormone vasopressin, which has an antidiuretic effect;
• decrease in renal concentration function;
• insufficient reabsorption of water from the renal collecting ducts;
• disruption of normal kidney function;
• copious urine production.

The severity of polyuria in diabetes mellitus depends on many components:

• protein breakdown products;
• electrolytes;
• nucleic acids;
• glucose content;
• ketone bodies.

Cause of pathology

The occurrence of polyuria can be caused by various reasons, the main of which are listed in the table:

Types by etiology	Groups of provoking factors	Causes
Pathological	Diabetes of various types	Diabetes
		Diabetes insipidus
		Uncompensated diabetes mellitus, which is accompanied by significant hyperglycemia
	Kidney diseases	Pyelonephritis
		Nephrosis
		Chronic renal failure
		Hyperparathyroidism
		Nephritis
		Nephrosclerosis
		Polycystic
		Nephropathy
	Inflammatory process	Urinary ducts
		Reproductive system
		Urethritis
		Bladder walls
		Cystitis
	Brain abnormalities	Hypoxia
		Trauma to the hypothalamic-pituitary zone
		Ischemia
		Tumor
		Hemorrhage
	Psychogenic polyuria	Schizophrenia
		Severe stress
		Psychical deviations
	Diseases of the endocrine glands	Pancreas
		Adrenal glands
		Epithelial body
	Surgical intervention	Brain surgery
		Kidney transplant
	Other abnormal processes in the body	Hypertension
		Genetic diseases
		Hyperaldosteronism
		Prostatitis
		Swelling
		Amyloidosis
		Diseases of the cardiovascular system
		Hyperparathyroidism
		Alcoholism
Physiological	Excessive fluid intake	Kvass, carbonated drinks
		Alcohol
		Caffeine
	Limiting salt	Specific low protein diet
	Pregnancy	The bladder experiences pressure from the uterus as it enlarges
	Medications	Taking diuretics when there is glucose in the urine

Etiology and pathogenesis of polyuria in diabetes mellitus

The amount of sugar in the blood, the amount and frequency of urination are strongly interrelated, they increase in parallel and proportionally.

Polyuria is an increased production of urine.

In diabetes mellitus, polyuria is very common and is called diabetes mellitus. The development of this pathology is caused by:

• increased glucose levels in urine;
• decreased reabsorption of water by kidney tubules;
• inability of the renal tubular epithelium to absorb fluid normally;
• removal from the body of almost all consumed fluid;
• excessive urine production.

Polyuria that accompanies diabetes mellitus dangerous phenomenon and without proper treatment in most cases it becomes the cause of serious pathologies, such as:

• renal tubular dysfunction;
• hypertension, hypertension, hypertensive crisis;
• pathologies of the cardiovascular system;
• diabetic coma;
• diseases of the central nervous system;
• chronic renal failure.

Symptoms

Polyuria during diabetes is not difficult to determine, since it is accompanied by pronounced characteristic symptoms, such as:

• significantly increased nocturnal diuresis, nocturia;
• urine has low density;
• convulsions do not always occur;
• constant strong thirst;
• excretion of significant volumes of urine;
• arrhythmia, manifests itself sometimes;
• urinary incontinence, especially in young children;
• dry mouth;
• too frequent urge to go to the toilet;
• weight loss;
• sudden coma;
• increased body temperature;
• general weakness.

Polyuria is a dramatic and often confusing problem that arises in a variety of clinical situations.

It may be a normal homeostatic reaction, or it may reflect profound metabolic disorders. Polyuria resulting from oral administration or intravenous infusions large quantity fluid and electrolytes, is benign, temporary and should not cause great diagnostic difficulties. On the other hand, persistent polyuria as a result of primary polydipsia, diabetes insipidus (DI), acquired kidney disease, or osmotic diuresis may be diagnostically questionable and life-threatening. Accurate differential diagnosis of polyuria requires a detailed understanding of the physiological mechanisms of water excretion. The reason we emphasize the basic physiology of water excretion is the importance of this fundamental information in recognizing and treating the numerous disorders that lead to polyuria.

Polyuria, or the production of excess urine, is usually obvious to both the patient and the doctor. Since there is no generally accepted definition of polyuria, we arbitrarily define a urine volume greater than 3.5 L/day (or 150 ml/h) as excessive.

Typically, in normal adults, diuresis ranges from 1 to 2 L/day, and its value depends on the amount of fluid consumed orally. It has been established that the desire to urinate is felt when 100-200 ml of urine accumulates in the bladder (the capacity of the bladder is from 300 to 450 ml) and urination in adults occurs 4-7 times a day. If diuresis increases to 3.5 l/day, the frequency of urination increases to 10 or more times. Increased frequency of urination and nocturia without increased urine output are not considered polyuria and are not discussed in this article.

MAIN INDICATORS OF URINARY LEVEL

In a healthy adult with an average body weight of 70 kg, urine formation begins with the production of 150 l/day of glomerular filtrate. About 80% of filtered salts and water are reabsorbed by the proximal nephron. The major determinant of final urine volume is the fraction of water reabsorbed from the remaining 20% ​​of the filtrate as it passes through the distal nephron. This process is regulated by the renal concentrating mechanism and antidiuretic hormone (ADH) produced by the pituitary gland. In the presence of ADH, more water is reabsorbed in the distal nephron, resulting in less concentrated urine being produced. Accordingly, in the absence of ADH, it is reabsorbed less water, which leads to the production of large volumes of dilute urine.
The physiological limits of urine concentration range from 50 to 1400 mOsm/kg (specific density - from 1000 to 1040). Within these limits, more than 25-fold fluctuations in urine volume are allowed at a constant level of salt excretion (Fig.).

Level of urine output at different meanings urine concentration and salt excretion level.

Renal regulation of the level of excretion of salts and water is aimed at maintaining a constant composition of body fluids and their volume. U healthy individuals The composition and volume of urine reflect dietary intake and extrarenal losses of salts and water.

Electrolyte balance

Substances that are excreted in the kidneys are sodium, potassium, chlorine and end products of protein breakdown (nitrogenous products - urea, creatinine, uric acid and ammonia, as well as inorganic acids - phosphoric and sulfuric). For example, a diet containing 6 g sodium chloride and 60 g protein produces approximately 600 mOsm/day of salts that must be excreted through the kidneys. Given the physiological limits of urine concentration, these substances can be excreted in urine volumes ranging from 12 L/day to 400 ml/day (see Fig. 1). Despite dietary diversity, the salt load requiring renal excretion usually ranges from 400 to 1200 mOsm/day. Thus, it is clear that water reabsorption in the distal nephron, which is determined by the level of ADH secretion and the renal concentrating mechanism, is a more important clinical determinant of urine volume than the amount of salts that the kidneys need to excrete.

Water balance

Regulation of the overall water balance is carried out in order to maintain normal blood plasma osmolarity values ​​of 280-295 mOsm/kg. Within these limits, water balance is established mainly due to changes in the level of renal excretion of water under the influence of ADH and the renal concentration mechanism. The relationships between blood plasma osmolarity, ADH concentration and urine osmolarity are shown in Fig. 2. The main stimulus leading to a change in the level of ADH secretion by the pituitary gland is a change in the osmolarity of body fluids. With an initial osmolarity of 287 mOsm/kg (solid arrow in Fig. 2, a), intake of 0.5 l of water, an amount sufficient to reduce the osmolarity of blood plasma by only 1% (3 mOsm/kg), is perceived by the osmoreceptors of the anterior hypothalamus , leads to a decrease in the secretion of ADH by the posterior lobe of the pituitary gland and a drop in the plasma concentration of ADH from 2 to 1 pg/ml. The urine concentration decreases from approximately 500 to 250 mOsm/kg (Fig. 2b). Assuming that the salt load remains constant at 600 mOsm/day, urine volume should double from 1.2 to 2.4 L/day (see Figure 1).

Rice. 2. Schematic representation of the effect of small changes in plasma osmolarity on plasma vasopressin (ADH) concentrations and urine osmolarity in healthy adults.

Conversely, if enough water is lost to increase blood osmolarity by 1%, plasma ADH concentration increases by 1 pg/mL, urine concentration increases from approximately 500 to 700 mOsm/kg, and urine volume decreases from 1.2 L/day to 850 ml/day. If plasma osmolarity exceeds the normal limit, thirst occurs, which leads to increased water consumption. Drinking water is retained as a result of increased ADH levels and dilutes body fluids, ultimately leading to the restoration of normal plasma osmolarity.

Within the normal range of plasma osmolarity, the amount of water consumed is determined by social and cultural traditions, and not by the feeling of thirst. A change in blood plasma osmolarity as a result of drinking water in turn leads to a change in the level of ADH secretion, concentration and volume of urine. Thus, it is clear that under normal conditions the main determinant of urine volume is the amount of water consumed.

Renal concentration mechanism

Wide physiological limits of water excretion are associated with wide variations in urine concentration, ranging from 50 to 1400 mOsm/kg. To adequately assess the clinical situation in cases of polyuria, a clear understanding of the renal concentration mechanism is mandatory. Urine formation begins with the production of isotonic ultrafiltrate blood plasma in the glomeruli. As the fluid passes through subsequent segments of the nephron, its composition and osmolarity change due to the selective reabsorption of salts and water. In the wide medullary ascending limb of the loop of Henle, sodium and chloride are reabsorbed without being accompanied by water reabsorption, resulting in hypotonic tubular fluid entering the cortical distal collecting ducts and hypertonic interstitial fluid of the renal medulla. This critical selective reabsorption of salts without water, resulting in the formation of hypertonic renal medulla, is known as the “isolation effect.” This effect is enhanced by the parallel countercurrent function of the ascending and descending limbs of the loop of Henle, called the countercurrent multiplier.

A very schematic representation of the functioning of the countercurrent mechanism is shown in Fig. 3. An example of a countercurrent multiplier is the loop in Fig. 3, a, illustrating the mechanism by which, due to processes occurring in the loop of Henle, a high concentration of salts is achieved in the medullary part of the loop. In this model, the transport of salts from the ascending limb is not accompanied by the release of water. Since the membrane of the descending limb is permeable to both salts and water, the concentration of salts in it begins to progressively increase immediately after the tubular fluid reaches a sharp turn. In fact, the transport of salts from the ascending limb is directed primarily not directly to the descending limb, but to the cerebral interstitium surrounding the loop of Henle. Moreover, the tonicity of the tubular fluid increases, most likely as a result of the reabsorption of water from this segment into the hypertonic medulla. The net effect of this mechanism is to achieve a concentration gradient along the cerebral interstitium, from isotonicity at the corticomedullary junction to maximum concentration at the papilla. At the apex of the papilla, osmolarity is 1200-1400 mOsm/kg. In Fig. 3b, the collecting duct (“flow element”), containing hypotonic fluid, is shown lying directly behind the loop. ADH increases the permeability of the collecting duct to water. In the presence of ADH, water is reabsorbed by osmosis from the tubular fluid as it passes through the hypertonic medulla. In the absence of ADH, the collecting tract is relatively impermeable to water, which remains in the tubule and is excreted in the urine.

Rice. 3. Diagram of the renal concentration mechanism.
a - a pumping mechanism in a membrane impermeable to water leads to the transport of salt from the ascending limb of the loop of Henle to the descending one (isolated effect), b - a “flow element”, which is a collecting duct of the medulla, compared with the competitive system shown in Fig. A. The fluid flowing down the collecting duct gradually becomes concentrated as the water passes through osmosis into the countercurrent loop.

A simplified illustration of the transport of salts and water in the nephron is shown in Fig. 4; the filtrate formed in the glomerulus is isotonic with respect to blood plasma (its osmolarity is close to 300 mOsm/kg). Of the approximately 150 L produced each day, approximately 120 L is adsorbed under isotonic conditions by the proximal tubule. Consequently, the descending limb of the loop of Henle reaches about 30 liters of isotonic fluid. Adsorption of water occurs as it descends into the hypertonic medulla region; The osmolarity of the tubular fluid is maximum in the region of the sharp turn. The salts are then absorbed through primary active transport of chloride ions and passive reabsorption of sodium ions. As a result of salt reabsorption, the tubular fluid reentering the nephron cortex is hypotonic. As shown in Fig. 4a, in the presence of ADH, an equilibrium occurs between the osmolarity of the tubular fluid and the renal interstitium, resulting in the formation of the most concentrated urine. In the absence of ADH (Fig. 4b), the distal part of the nephron is relatively impermeable to water. As a result of subsequent sodium reabsorption, urine osmolarity progressively decreases, reaching minimum values ​​of 50–60 mOsm/kg in the collecting duct.

Rice. 4. Simplified diagram of the renal concentration mechanism.

In conclusion, to concentrate urine, it is necessary to establish and maintain hypertonicity in the medulla, as well as the presence of ADH. Polyuria occurs in situations where the secretion of ADH or the sensitivity of the canalicular membrane to it is reduced or the transport of salts in the nephron is impaired, which leads to a decrease in the hypertonicity of the cerebral interstitium.

Relationship between urine concentration, salt load and urine volume

In Fig. Figure 1 shows the values ​​of urine volume at various levels of urine osmolarity and salt load. If the salt load is normal (about 600 mOsm/day), as long as the urine osmolarity does not fall below 200 mOsm/kg, the urine volume does not exceed 3.5 liters. In such cases, mostly water is lost in the urine without a significant amount of salts (“water diuresis”). If the process of urine concentration is disrupted and its maximum omolarity is 300 mOsm/kg, polyuria occurs only in cases where the daily salt load exceeds the usual 600 mOsm/kg. In these cases, both salts and water are lost in the urine (“salt diuresis”). Diuresis exceeding 5 l/day is observed only with a very low urine concentration (50-100 mOsm/day) or an extremely high salt load (more than 1500 mOsm/day).

Polyuria caused by water diuresis is characterized by urine osmolarity below 200 mOsm/kg without significant loss of salts. A significant volume of urine may be produced, and in some cases, high levels of urine output may lead to the development of hydronephrosis and bladder enlargement.

Habitual excess water consumption (primary polydipsia). An increase in the total water content in the body due to its excess consumption leads to a decrease in salt concentration as a result of dilution and a temporary decrease in blood plasma osmolarity. Suppression of ADH secretion is accompanied by a decrease in its concentration in the blood plasma and a decrease in water reabsorption in the distal nephron. As a result, until plasma osmolarity increases to normal values, large volumes of dilute urine are excreted. It has been established that insensible water loss in adults is 500 ml/day, and for polyuria to occur, as defined here, the amount of water consumed must exceed 4 L/day. Hypoosmolarity of blood plasma does not occur until the amount of water consumed exceeds the normal reserves of its excretion, which is approximately 12 l/day. However, patients with mental disorders may drink enormous amounts of water over a short period of time and thus cut off normal water excretion reserves. In such cases, blood plasma osmolarity ranges from 240 to 290 mOsm/kg. Severe hypoosmolarity can lead to cramping abdominal pain, nausea, vomiting, diarrhea and metabolic encephalopathy, characterized by headache, impaired consciousness, irritability and epileptiform seizures. This syndrome can be difficult to diagnose because severely ill patients may deny drinking water. In addition, if the patient is in a comatose state and, as a result, the flow of water stops, due to the excretion of water by the kidneys, by the time of examination, plasma osmolarity can be restored to normal values.

Neurogenic diabetes insipidus (ID). Complete and partial violations. Polyuria can occur as a result of absolute or relative deficiency of ADH in diseases of the central nervous system. As stated previously, if urine output exceeds 3.5 L/day during normal salt loading, urine osmolarity should be below 200 mOsm/kg, which means that the plasma ADH concentration is below 1 pg/ml (see Fig. 1 and 2). For such a significant decrease in ADH levels to occur, the loss of more than 90% of the cells producing it in the hypothalamus is necessary. Lesser damage leads to partial impairment of the concentrating ability of the kidneys and a less pronounced increase in urine volume.

Water diuresis from excess water consumption leads to an increase in the concentration of body fluids. The resulting hypertension stimulates the feeling of thirst, and the consumption of increasing amounts of water is accompanied by replenishment of its losses. Consequently, a patient with neurogenic diabetes insipidus who has access to water, with the mechanism of thirst still intact, will experience polyuria, polydipsia and normal blood plasma osmolarity values. However, if water does not enter the body, progressive depletion of its reserves leads to severe hypertonicity of fluid spaces and metabolic encephalopathy. The decrease in intravascular volume is insignificant, since less than 10% of water is lost due to this space.

The main disorders leading to neurogenic ND are listed in Table. Most of them can be identified by concomitant neurological or endocrinological disorders, including headache and visual field impairment or hypopituitarism. The most common causes of ND appear to be head trauma or neurosurgical interventions in the pituitary gland or hypothalamus. After hypophysectomy, DI occurs in 28-84% of patients. Disturbances in ADH secretion result from retrograde degeneration of neurons in the supraoptic and paraventricular nuclei of the hypothalamus after transection of the pituitary stalk. Damage occurs less frequently and is more likely to be temporary after a low pedicle intersection, while after a high pedicle intersection the likelihood of permanent damage is greater. Idiopathic ND is still one of the most common disorders, most often found in young adults, but can also occur in patients of other age categories. In several cases, postmortem examination of the brain in idiopathic ND has revealed selective but ultimately complete destruction of hypothalamic neurons that produce ADH. Familial ND occurs in only 2% of cases.

Causes of neurogenic diabetes insipidus
Head trauma, including neurosurgical
Idiopathic neurogenic
ND
Brain tumors
Pituitary adenoma
Kr aniof arshin a
Metastases
Infiltrative lesions
Sarcoidosis
Disease
Hand-Schüller-Christian
Medicines and ethyl alcohol
Postpartum pituitary neurosis
Encephalitis
Heredity

Taking ethyl alcohol is accompanied by reversible suppression of ADH secretion and short-term polyuria. Water diuresis occurs 30-60 minutes after taking 25 g of alcohol, the alcohol content in the blood ranges from 50 to 80 mg%. The volume of urine depends on the amount of alcohol taken in a single dose. Continuous use does not lead to sustained urination, despite the existence of a constant concentration of alcohol in the blood.

Nephrogenic diabetes insipidus. In contrast to patients with neurogenic ND, in nephrogenic ND, the plasma concentration of ADH corresponds to the osmolarity of the blood plasma. The cause of polyuria in this case is associated either with the impermeability of the renal collecting ducts to water, which exists despite the presence of ADH, or with the insufficiency of the function of the renal concentration mechanism aimed at maintaining adequate hypertonicity of the cerebral interstitium. Damage to renal function in this pathology ranges from selective impairment of the response to ADH to global disorders of nephron function. With the exception of cases of congenital nephrogenic ND, the damage to the concentrating function of the kidneys is incomplete, so the osmolarity of urine exceeds the osmolarity of the blood plasma. Consequently, with a normal salt load in these patients, diuresis usually does not exceed 3.5 l/day and severe polydipsia is not observed, which distinguishes them from patients with complete neurogenic ND.

Congenital nephrogenic ND. This rare hereditary pathology predominantly affects men.
Severe polyuria and polydipsia are observed immediately after birth, and episodes of hypertensive dehydration are often observed in the neonatal period. In connection with this disease, there is often a delay in mental and physical development.

Metabolic disorders. Hypokalemia and hypercalcemia are accompanied by slight disturbances in the concentration function of the kidneys, which disappear after correction of electrolyte disturbances. In both cases, small changes in the tubules and interstitium are noted, which may play an important role in the pathogenesis of concentration disorders.

Parenchymal kidney diseases. There are a number of kidney diseases in which, even before a decrease in glomerular filtration (GF), pronounced damage to the tubules and renal interstitium is observed (Table 2).

Table 2. Parenchymal kidney diseases leading to nephrogenic diabetes insipidus

Diuresis in these cases usually does not exceed 3.5 l/day, and polyuria is observed only with increased water consumption. Disturbances in the mechanism of urine concentration are multifactorial in nature, and include a decrease in the transport of salts in the loop of Henle, structural changes in the tubules and vessels of the medulla, in which the countercurrent mechanism is realized, a violation of the permeability of the collecting ducts for water, as well as a decrease in sensitivity to ADH. For glomerular and interstitial kidney diseases leading to progressive renal failure, additional factor, which reduces the ability to concentrate urine is a decrease in the delivery of salts to the loop of Henle as a result of a decrease in the level of CP. Although parenchymal kidney disease does not usually result in the production of more than 3.5 L of urine per day, it is the most common cause of nephrogenic DI.

Medications. Lithium and demeclocycline interfere with the sensitivity of the collecting ducts to ADH. Impaired ability to concentrate urine is observed in 10% of patients receiving lithium preparations. In some patients, after long-term use of such drugs, irreversible changes were found in the form of interstitial fibrosis and renal failure. A decrease in the concentrating ability of the kidneys as a result of the use of a tetracycline derivative, demeclocycline, depends on the dose of the drug and is reversible; this side effect of the drug has been successfully used for long-term treatment of ADH deficiency syndrome.

Amphotericin B and the anesthetic methoxyflurane cause a decrease in handwriting concentration in most patients. The use of high doses of these drugs can lead to disorders of various tubular functions and acute renal failure.

Salt diuresis

Polyuria as a result of salt diuresis is characterized by urine osmolarity values ​​approaching 300 mOsm/kg and significant losses of salts and water.

Consumption of salts. In contrast to polyuria caused by water load, for patients with salt diuresis, plasma osmolarity values ​​that are at the upper limit of normal or clearly exceed it are typical. Additional use salts increases the osmolarity of blood plasma, which stimulates the feeling of thirst and leads to the consumption of water. The resulting increase in extracellular fluid volume increases renal blood flow and glomerular filtration rate and decreases proximal tubular reabsorption. As a result, the delivery of salts to the distal parts of the nephron increases. As shown in Fig. 1, if urine osmolarity is 300 mOsm/kg, diuresis will exceed 3.5 L/day only when the salt load exceeds 1200 mOsm/day.

A common cause of polyuria in inpatients is the use of large doses of saline and protein solutions (total parenteral nutrition). Sodium chloride, sodium bicarbonate and nitrogenous products resulting from salt loading are excreted in the final urine. In patients, careful clinical and laboratory examination reveals, respectively, an increase in extracellular fluid volume, metabolic alkalosis (or alkaline urine) or azotemia. Urine is usually no more concentrated than blood plasma because there is no incentive to retain water or salts. It is obvious that polyuria in these cases is simply a normal homeostatic reaction aimed at maintaining the overall salt balance, and that the excretion of large volumes of urine will continue until the administration of saline solutions stops. Diagnostic difficulties arise in cases where polyuria is regarded as a reflection of primary renal failure in the implementation of sodium retention and if intravenous infusions are continued to avoid a decrease in the volume of extracellular fluid. As discussed below, renal sodium loss sufficient to cause polyuria (as defined here) is rare.

Osmotic diuresis. Causes of prolonged osmotic diuresis that have important clinical significance are diabetic hyperglycemia (ketoacidosis or non-ketocidotic hyperosmolar coma), as well as prolonged mannitol infusion. Central to the pathophysiology of this condition are the characteristic properties of osmotic substances. Mannitol is an inert sugar that does not pass through cell membranes. By slowing the transport and metabolism of glucose in the absence of insulin, it has the same properties. These low molecular weight substances are freely filtered by the glomeruli and pass from the plasma directly into the tubular fluid. Mannitol is not reabsorbed by the renal tubules at all, and tubular reabsorption of glucose with increased levels in the blood is blocked due to a large filtration load. Substances with poor permeability (both mannitol and glucose) increase the osmolarity of the tubular fluid and reduce the reabsorption of sodium and water in the proximal tubules, thereby increasing the flow of salts and water into the distal nephron and secondary urine. In addition, the presence of these substances and the high flow rate of tubular fluid limit the reabsorption of water and salts in the distal parts of the nephron, reducing the hypertonicity of the cerebral interstitium and preventing both the concentration and dilution of urine. As a result, urine osmolarity is close to that of blood plasma, typically 310-340 mOsm/kg, and large amounts of sodium chloride and water (as well as glucose and mannitol) are lost in the urine. This can lead to an extreme decrease in the volume of extracellular fluid and the development of hypertonicity. Hypertonicity of the extracellular fluid is the result of two factors:
1) the presence of high concentrations of glucose or mannitol and
2) disturbances in the concentrating ability of the kidneys.
Both of these factors lead to increased renal water loss. Despite the fact that the effect of hypertonicity may be blunted with an increase in water consumption, which is stimulated by the feeling of thirst, the progressive loss of salts from the extracellular fluid leads to a pronounced decrease in its volume. Clinical expressions of this situation are metabolic encephalopathy, arterial hypotension, tachycardia, decreased skin turgor and prerenal azotemia.
Kidney diseases. Inability to retain sodium (salt depletion) is a symptom of some renal diseases that occur with severe tubulointerstitial damage, as well as all diseases that cause progressive renal failure. However, sodium loss rarely leads to an increase in urine volume - more than 3.5 l / day (see Fig. 1).

However, such a pronounced degree of salt diuresis can be observed with cystic lesions of the renal medulla, during recovery from acute tubular necrosis, as well as during the recovery period after bilateral renal obstruction. In these situations, salt diuresis can lead to a rapid decrease in extracellular fluid volume. In addition, it should be noted that with these changes, the sensitivity of the tubules to ADH is impaired. Thus, excess water loss can accompany salt diuresis and lead to hypertonicity of the blood plasma.
Cystic lesion of the medulla and kidneys (congenital nephronophthisis). This rare genetic disorder affects adults at a young age and leads to progressive kidney failure. In the region of the corticomedullary junction of the kidneys there is big number small cysts, and renal biopsy reveals interstitial fibrosis. An early and pronounced symptom of this disease, often providing a clue to diagnosis, is salt depletion.
Recovery from acute tubular necrosis. When the level of glomerular filtration is restored, pronounced salt diuresis may occur with the release of large volumes of urine, reaching 6-8 l/day (“diuretic phase” of acute tubular necrosis). Obviously, polyuria is caused by the excretion of salts accumulated in the body during the oliguric phase, and, as a rule, disappears after about a week. Minor disturbances in the concentrating ability of the kidneys can be observed for many months after acute tubular necrosis; recovery usually occurs within a year.

Post-obstruction diuresis. The pathogenesis of severe salt diuresis that occurs during the recovery period after bilateral renal obstruction remains unknown. At least 3 factors are involved:
1) an increase in the volume of extracellular fluid as a result of salt retention during the period of renal obstruction;
2) osmotic diuresis as a result of excretion of accumulated urea and other nitrogenous products;
3) persistent impairment of tubular function.

The absence of pronounced salt depletion in the recovery period after unilateral ureteral obstruction in the experiment indicates that the triggering factor for post-obstructive diuresis is salt retention.
Use of diuretics. The intended and desired effect of diuretic therapy is loss of water and salts. A significant decrease in the volume of extracellular fluid usually does not occur, since when it decreases, renal blood flow and the level of glomerular filtration decrease, renal tubular reabsorption increases and the flow of sodium and chlorine into secondary urine is limited. However, ongoing losses of sodium and water may occur with the use of osmotic diuretics (eg, mannitol, discussed earlier), as well as strong diuretics that affect loop of Henle function (furosemide and ethacrynic acid). Despite the fact that the use of osmotic diuretics causes hyperosmolarity of the blood plasma, the use of diuretics that affect the function of the loop of Henle can lead to increased urine concentration (by reducing its volume), water retention and hypoosmolarity of the blood plasma.

History of polyuria

By identifying the clinical conditions in which polyuria occurs, the range of possible diagnoses leading to this syndrome can be quickly narrowed. First of all, it is important to determine the following factors: whether polyuria represents an independent clinical problem or just one of many existing problems; does diuresis exceed 5-6 liters per day; whether polyuria is temporary or permanent.

The most important anamnestic factor in patients with polyuria is detailed information about the clinical situation in which polyuria appeared. Polyuria that appears after head trauma or neurosurgical procedures, as well as polyuria in patients with focal neurological symptoms and signs of pituitary diseases, is most likely due to neurogenic ND. Polyuria in patients receiving large intravenous infusions, such as parenteral nutrition or saline, is apparently due to salt and water load. In patients with kidney disease, polyuria is usually nephrogenic ND, and in those recovering from acute tubular necrosis and bilateral renal obstruction, it is associated with excretion of previously accumulated salts. In patients with diabetes mellitus, polyuria is usually caused by hyperglycemia and glycosuria. In patients receiving treatment for manic-depressive psychosis, polyuria usually occurs as a result of the use of lithium drugs. Polyuria in newborns is most likely caused by familial neurogenic or nephrogenic ND.

Diuresis exceeding 5-6 l/day is usually uncharacteristic even for conditions that occur with severe impairment of the concentration function of the kidneys. Such severe polyuria most often occurs with primary polydipsia, saline infusions, complete neurogenic ND, or osmotic diuresis. Of course, these disorders can occur with polyuria, in which 3.5 to 5 liters of urine are released per day.

Polyuria that occurs after ingesting large quantities of water and salt, as well as excessive diuresis after ingesting a large, salty, protein-rich meal together with large amounts of alcohol, are well known. Short-term polyuria is usually caused by the use of diuretics and radiocontrast agents. Diabetes insipidus after head trauma and neurosurgical procedures may also be transient.

The greatest diagnostic difficulties arise with moderate polyuria (diuresis within 3.5-4 l/day), not accompanied by severe symptoms of concomitant diseases. Differential diagnosis in these cases includes consideration of new-onset diabetes mellitus, pituitary and renal disease, hypokalemia, hypercalcemia, and primary polydipsia.

Physical examination

Pathological physical symptoms in patients with polyuria can be either primary (caused by disorders causing polyuria) or secondary (caused by disturbances in water-mineral balance caused by loss of water and salts).

Indicators of a decrease in the volume of intravascular fluid are acute loss of body weight, arterial hypotension, decreased skin turgor, postural changes in heart rate and blood pressure. In these cases, an adequate renal response consists of salt and water retention. Consequently, a patient with arterial hypotension and polyuria has serious impairments in the concentrating ability of the kidneys. The decrease in fluid content in the body is most pronounced in patients with osmotic diuresis, during the period of recovery from acute tubular necrosis or bilateral renal obstruction, as well as in cystic lesions of the renal medulla. A decrease in body weight without changes in blood pressure and heart rate often indicates salt-free water losses that occur with diabetes insipidus, hypercalcemia, hypokalemia and most parenchymal kidney diseases. Extreme depletion of the body's water reserves does not develop in these patients until the thirst mechanism is disrupted or the patient is deprived of access to water.

Acute weight gain, arterial hypertension and edema indicate excessive salt intake. An increase in body weight without the occurrence of arterial hypertension can be caused by excessive consumption of both salts and water.

The presence of focal neurological symptoms indicates neurogenic ND caused by neoplasms, such as a pituitary tumor, or infiltrative lesions. General symptoms such as drowsiness, psychosis and agitation have no diagnostic value.

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For laboratory examination of a patient with polyuria, only a small set of routine blood and urine tests are needed. With some exceptions, the final diagnosis in a patient with polyuria can be obtained by careful study of clinical data in conjunction with adequate interpretation of laboratory results. Sometimes it becomes necessary to perform an overnight dehydration test to determine the level of ADH in the blood plasma.

ANALYSIS OF URINE

Glucosuria in a patient with polyuria (with or without ketonuria) indicates hyperglycemia and osmotic diuresis. Proteinuria and the presence of tubular cells or large granular casts in the urine indicate parenchymal kidney disease. However, the main value of urine analysis in a patient with polyuria is to determine its relative density and osmolarity. The relationship between urine osmolarity and its relative density is shown in Fig. 1. Urine osmolarity of 300 mOsm/kg (corresponding to approximately 0.3 osm/l), which actually indicates that urine is isotonic to the blood plasma, means the absence of a concentration of glomerular filtrate and corresponds to a relative density of urine of 1010. The molecular weight of glucose (180) is higher than osmotically active substances contained in normal urine (urea - 60, sodium chloride - 58); therefore, in patients with glucosuria at all levels of measurement, urine osmolarity values ​​will correspond to higher relative to normal values ​​of its relative density (measured using a hygrometer). In practice, it is not always necessary to measure urine osmolarity.

In most cases of polyuria, the diagnosis can be made with appropriate interpretation of the results of determining the relative density of urine, especially if it is determined using a refractometer.

Rice. 1. Relationship between specific gravity and osmolarity of urine.
The following urine test options are shown: small dots - sugar or protein are not detected; large dots - glycosuria, squares - proteinuria, crosses - after oral administration of 25 g of urea.

A relative density of urine exceeding 1012 (urine osmolarity above 300 mOsm/day) in patients with polyuria indicates the excretion of a large amount of salts, which occurs with polyuria caused by the infusion of saline solutions (saline or fluids for total parenteral nutrition), osmotic diuresis, diuretic use, cystic renal medulla disease, or recovery from tubular necrosis or bilateral renal obstruction. A relative density of urine less than 1005 (urine osmolarity less than 150 mOsm/kg) in a patient with polyuria means the virtual absence of ADH secretion, which is observed in complete neurogenic ND, primary polydipsia and in infants with congenital nephrogenic ND. Relative density of urine, ranging from 1005 to 1012 (urine osmolarity in the range of 200-300 mOsm/kg), can be observed with polyuria of any etiology.

BLOOD TEST

The necessary studies are to determine the blood levels of sodium, potassium, chlorine, total CO2, urea nitrogen, creatinine, glucose, calcium, as well as plasma osmolarity. In the absence of radiopaque substances, mannitol, ethyl and methyl alcohol, as well as ethyl glycol in the blood, the osmolarity of blood plasma can be determined using the following formula:

Plasma osmolarity = 2(Na+) + urea nitrogen glucose / 2.8 + glucose / 18

Osmolarity is measured in mOsm/kg, concentration - sodium in meq/l, urea nitrogen and glucose - in mg%. Osmolarity values ​​calculated in this way usually differ from measured ones by 10-15 mOsm/kg.

Hyperosmolarity of blood plasma in a patient with polyuria means loss of water and a violation of the thirst mechanism or insufficient intake of water into the body and indicates that primary polydipsia in this case cannot be the cause of polyuria. The presence of hyperosmolarity in blood plasma, indicating excess salts, provides important diagnostic information. Hyperosmolarity due to hyperglycemia indicates untreated diabetes mellitus and osmotic diuresis, while hyperosmolarity due to hypernatremia indicates water loss or the use of hypertonic sodium chloride solution. Azotemia (increased concentration of urea nitrogen) indicates that hyperosmolarity is due to the use of high-protein nutritional solutions (eg, enteral tube feeding or total parenteral nutrition) and the presence of renal failure. If the measured plasma osmolarity exceeds the calculated osmolarity by more than 15 mOsm/kg, there must be some substance present in the blood plasma, such as mannitol or alcohol, that is causing the polyuria.

If the plasma osmolarity of a patient with polyuria is normal, this means that he retains an adequate sense of thirst and has access to water. Normal blood plasma osmolarity values ​​have little diagnostic value unless the measured osmolarity exceeds the calculated one, which happens in cases where the cause of polyuria is the presence of an unknown substance in the blood.

Hypoosmolarity of blood plasma in a patient with polyuria means dilution of body fluids as a result of the introduction or retention of water. Detection of hypoosmolarity of blood plasma has a valuable diagnostic value, since this fact narrows the list possible reasons polyuria to two conditions: primary polydipsia and iatrogenic water intoxication.
In addition to calculating the osmolarity of blood plasma, determining the content of electrolytes in it allows us to identify hypokalemia and hypercalcemia as possible causes of polyuria. Determination of serum creatinine concentration should be performed in all patients with polyuria in order to assess renal function.

NIGHT DEHYDRATION TEST

The main application of this test is to determine the integral response of the pituitary secretion of ADH and the renal concentration mechanism to water restriction. In normal individuals, insensible water losses during an anhydrous diet result in a slight increase in plasma osmolarity, accompanied by an increase in ADH secretion and concentrated urine output. During 12-16 hours of anhydrous diet, the normally insensible water loss of 300-400 ml leads to an increase in blood osmolarity by 1%, and this stimulus is sufficient for a significant increase in ADH secretion. Naturally, any renal water losses occurring at this time will lead to a more pronounced increase in blood plasma osmolarity and ADH secretion. In normal subjects, during the period of anhydrous diet, diuresis decreases and there is a gradual increase in urine osmolarity, which reaches a plateau at values ​​​​of 900-1400 mOsm/kg, which is an indicator of maximum urine concentrating ability. Body weight loss is usually less than 1 kg, and during this period the osmolarity of the blood plasma remains within normal values. Based on the dependence presented in Fig. 2, it can be predicted that the ADH content in the blood plasma will be 3-5 pg/ml. Indeed, the administration of exogenous ADH - 5 units of water-soluble vasopressin (pitressin) - in this situation in healthy individuals will not lead to a further increase in urine concentration. In hospitalized patients, the maximum urine osmolarity is lower and reaches only 400-1200 mOsm/kg, however, as in healthy individuals, the maximum urine concentration in response to the administration of 5 units of water-soluble vasopressin does not increase in them.

In practice, a dehydration test can be performed in an outpatient clinic or department if the volume of urine excreted is less than 4-5 l/day. The anhydrous diet begins at 20:00 on the first day; starting at 8 o'clock next day(12 hours later), hourly urine samples are collected to determine its relative density. In patients with severe polyuria (diuresis more than 5 l/day), an overnight dehydration test should be carried out in a hospital setting and it is better to start it in the morning rather than in the evening. Frequent measurements of blood pressure, heart rate and body weight are taken. Loss of more than 3% of body weight (this is an indicator of the amount of fluid lost) should not be allowed. After the relative density of urine reaches maximum values, blood and urine samples are taken to determine their osmolarity and 5 units of water-soluble vasopressin are injected under the skin. After 1 hour, urine is collected again to determine its osmolarity. An insufficient increase in osmolarity or relative density of urine, despite a 3% loss of body weight, or an increase in plasma osmolarity inversely proportional to the decrease in body weight is considered pathological, indicating damage to the hypothalamic-pituitary-renal system.

In the next section, we describe the reaction to a dehydration test in patients with polyuria of various etiologies.
Excessive consumption of salts and water. Polyuria due to salt intake is usually easily diagnosed based on clinical findings and urine relative gravity values ​​of about 1010; as a rule, in patients of this category there is no need to perform a dehydration test. However, diagnosing polyuria caused by water consumption is often difficult, since patients may hide the fact of excessive water consumption or complain of increased thirst. The quantitative response of patients with primary polydipsia to a dehydration test is similar to that of healthy individuals, but there are the following exceptions. First, it may take a longer period of time to reach maximum urine osmolarity values ​​(usually about 16 hours), and the weight loss may be large as a result of previous overhydration (about 2 kg). Secondly, the maximum urine concentration is lower than normal (500-900 mOsm/kg). As in healthy individuals, plasma osmolarity remains within normal values, and the addition of exogenous ADH does not exceed urine osmolarity (Fig. 5).

Rice. 5. Osmolarity and specific gravity of urine during a dehydration test in patients with polyuria caused by various disorders.

Neurogenic ND. Patients with severe neurogenic ND experience rapid dehydration within 4-12 hours, during which urine osmolarity reaches maximum values ​​of only 100-250 mOsm/kg (see Fig. 5). During this time, body weight decreases by 2-3 kg and blood osmolarity increases to 300 mOsm/kg. Despite these changes, the level of ADH in the blood plasma remains low. A characteristic diagnostic sign is the reaction to the administration of exogenous ADH. The osmolality of urine increases on average by 2 times compared with the initial level before the administration of ADH, and this means that the cause of polyuria is ADH deficiency, and not a dysfunction of the renal tubules. The possibility of rapid dehydration in these patients emphasizes the need for strict medical monitoring during the study.
In patients with partial ADH deficiency, maximum urine osmolarity is higher (300-600 mOsm/kg) and is achieved after a longer period of dehydration, usually after 8-16 hours (see Fig. 152). The decrease in body weight is usually less than 2 kg, and plasma osmolarity increases slightly, to approximately 295 mOsm/kg.

Nephrogenic ND. As discussed earlier, with the exception of cases of congenital pathology, most patients with nephrogenic DI have moderate damage to the concentration function of the kidneys, and they retain the ability to increase urine osmolarity to values ​​​​exceeding the osmolarity of blood plasma. The administration of ADH does not lead to a further increase in urine concentration, which makes it possible to differentiate this state of partial neurogenic ND. The largest subgroup of patients with nephrogenic ND are those with tubulointerstitial kidney disease - this diagnosis becomes obvious after examining urine sediment and determining serum concentrations of creatinine and electrolytes. To confirm the diagnosis of nephrogenic ND in these patients, there is usually no need to perform a dehydration test.

Osmotic diuresis. Since the conditions leading to osmotic diuresis are usually easily diagnosed (diabetic hyperglycemia and long-term use of mannitol), a dehydration test is performed in rare cases. Osmotic diuresis is characterized by urine osmolarity values ​​close to the osmolarity of blood plasma (usually in the range of 310-340 mOsm/kg); During the dehydration test, the osmolarity of urine increases slightly or does not change, and after the administration of ADH it no longer increases.

Salt diuresis as a result of kidney disease or diuretic use. In patients with salt diuresis, there is usually no need to perform a dehydration test, since the diagnosis is usually easy to make based on clinical data, urinary sediment examination, and serum creatinine concentration. It can be assumed that after a dehydration test and administration of ADH, the osmolarity of urine in these patients will either not change at all or increase slightly.

DETERMINATION OF ADH (VASOPRESSIN) CONTENT IN BLOOD PLASMA

It is possible to directly measure the content of ADH in blood plasma using a radioimmunoassay method, which uses antibodies to active human ADH.

Rice. 6. Relationship between plasma GDP, plasma osmolarity and urine osmolarity in normal adults at various stages of hydration and in patients with polyuria due to various disorders (see text).
Solid circles are the norm (n=25); squares—primary polydipsia (n=2); triangles - nephrogenic diabetes insipidus; circles with dots—neurogenic diabetes insipidus (n=8).

Although this technique is not currently performed in most clinical chemistry laboratories, it is likely to find widespread use in the near future. Moreover, preliminary results indicate that the combination of this technique with a dehydration test allows a more accurate classification of patients with polyuria.

The content of water-soluble vasopressin (WVP) in the blood plasma of patients with polyuria is examined after the relative density or molarity of urine reaches a plateau during a dehydration test (Fig. 6). If the content of GDP in the blood plasma does not increase in accordance with plasma osmolarity, the patient most likely has neurogenic ND. An increase in the level of plasma GDP without an increase in urine osmolarity indicates the presence of nephrogenic ND. A parallel increase in blood plasma GDP and urine osmolarity during a dehydration test suggests the presence of primary polydipsia. The results of measuring blood plasma GDP during a dehydration test in patients with polyuria caused by water diuresis coincide with those in patients with complete neurogenic ND. However, differences in the study results can be observed when comparing them with patients with partial neurogenic ND, nephrogenic ND and primary polydipsia in 1/2-1/3 of cases. When routine testing of blood plasma GDP becomes possible, the use of this method in combination with a dehydration test will lead to a more accurate diagnosis of polyuria.

Renal failure is a serious complication of various renal pathologies, and a very common one. The disease can be treated, but the organ cannot be restored. Chronic renal failure is not a disease, but a syndrome, that is, a set of signs indicating impaired renal function. The causes of chronic failure can be various diseases or injuries, as a result of which the organ is damaged.

Stages of kidney failure

Water, nitrogen, electrolyte and other types of metabolism in the human body depend on the functioning of the kidney. Kidney failure is evidence of failure to perform all functions, leading to disruption of all types of balance at once.

Most often, the cause is chronic diseases, in which the kidney parenchyma is slowly destroyed and replaced by connective tissue. Kidney failure becomes the last stage of such ailments - urolithiasis and the like.

The most indicative sign of pathologies is the daily volume of urine - diuresis, or minute. The latter is used when examining the kidneys using the clearance method. With normal kidney function, daily urine output is about 67–75% of the volume of fluid drunk. In this case, the minimum volume required for the organ to function is 500 ml. Therefore, the minimum volume of water that a person should consume per day is 800 ml. With standard water consumption of 1–2 liters per day, daily diuresis is 800–1500 ml.

In renal failure, urine volume changes significantly. In this case, there is both an increase in volume - up to 3000 ml, and a decrease - up to 500 ml. The appearance of daily diuresis of 50 ml is an indicator of kidney failure.

There are acute and chronic renal failure. The first is characterized by the rapid development of the syndrome, pronounced symptoms, and severe pain. However, most of the changes that occur with acute renal failure are reversible, allowing renal function to be restored within a few weeks with appropriate treatment.

The chronic form is caused by the slow irreversible replacement of the kidney parenchyma with connective tissue. In this case, it is impossible to restore the functions of the organ, and in later stages surgical intervention is required.

Acute renal failure

Acute renal failure is a sudden, severe disruption of the functionality of an organ associated with suppression of excretory function and the accumulation of nitrogen metabolism products in the blood. In this case, a disorder of water, electrolyte, acid-base, and osmotic balance is observed. Changes of this kind are considered potentially reversible.

ARF develops within a few hours, less often within 1–7 days, and becomes so if the syndrome is observed for more than a day. Acute renal failure is not an independent disease, but a secondary one, developing against the background of other diseases or injuries.

The causes of acute renal failure are:

• low blood flow rate;
• tubular damage;
• obstruction of urine flow due to obstruction;
• destruction of the glomerulus with loss of capillaries and arteries.

The cause of acute renal failure serves as the basis for appropriate qualifications: according to this criterion, prerenal acute failure is distinguished - 70% of all cases, parenchymal - 25% and obstructive - 5%.

According to medical statistics, the causes of such phenomena are:

• surgery or trauma – 60%. The number of cases of this kind is constantly growing, as it is associated with an increase in the number of operations under artificial circulation;
• 40% are treatment related. The use of nephrotoxic drugs, necessary in some cases, leads to the development of acute renal failure. This category also includes acute poisoning with arsenic, mercury, and mushroom poison;
• 1–2% appear during pregnancy.

Another classification of the stages of the disease is used, related to the patient’s condition; 4 stages are distinguished:

• elementary;
• oligoanuric;
• polyuric;
• recovalescence.

Causes of acute renal failure

initial stage

Signs of the disease depend on the cause and nature of the underlying disease. Caused by stress factors - poisoning, blood loss, injury.

• Thus, with an infectious lesion of an organ, the symptoms coincide with the symptoms of general intoxication - headache, lethargy, muscle weakness, and possible fever. If an intestinal infection becomes complicated, vomiting and diarrhea may occur.
• If acute renal failure is a consequence of poisoning, then anemia, signs of jaundice, and possible seizures are observed.
• If the cause is acute kidney disease - for example, there may be blood in the urine and severe pain in the lower back.

Changes in diuresis at the initial stage are unusual. Pallor, a slight decrease in blood pressure, and a rapid pulse may be observed, but there are no characteristic signs.

Diagnosis at the initial stage is extremely difficult. If acute renal failure is observed against the background of an infectious disease or acute poisoning, the disease is taken into account during treatment, since kidney damage due to poisoning is a completely natural phenomenon. The same can be said for those cases when the patient is prescribed nephrotoxic drugs.

A urine test at the initial stage indicates not so much acute renal failure as it does the factors that provoke the deficiency:

• the relative density for prerenal OPN is higher than 1.018, and for renal OPN is lower than 1.012;
• slight proteinuria and the presence of granular or cellular casts are possible in renal acute renal failure of nephrotoxic origin. However, in 20–30% of cases this sign is absent;
• in case of injury, tumor, infection, urolithiasis, a greater number of red blood cells is detected in the urine;
• a large number of leukocytes indicates an infection or allergic inflammation of the urinary tract;
• if uric acid crystals are found, urate nephropathy can be suspected.

At any stage of acute renal failure, a bacteriological urine test is prescribed.

A general blood test corresponds to the primary disease; a biochemical test at the initial stage can provide evidence of hyperkalemia or hypokalemia. However, mild hyperkalemia – less than 6 mmol/l, does not cause changes.

Clinical picture of the initial stage of acute renal failure

Oligoanuric

This stage in acute renal failure is the most severe and can pose a threat to both life and health. Its symptoms are much better expressed and characteristic, which makes it possible to quickly establish a diagnosis. At this stage, nitrogen metabolism products quickly accumulate in the blood - creatinine, urea, which in a healthy body are excreted in the urine. Potassium absorption decreases, which destroys the water-salt balance. The kidney does not perform the function of maintaining the acid-base balance, resulting in metabolic acidosis.

The main signs of the oligoanuric stage are:

• decreased diuresis: if the daily urine volume drops to 500 ml, this indicates oliguria, if it drops to 50 ml, anuria;
• intoxication with metabolic products - skin itching, nausea, vomiting, tachycardia, rapid breathing;
• a noticeable increase in blood pressure, conventional antihypertensive drugs do not work;
• confusion, loss of consciousness, possible coma;
• swelling of organs, cavities, subcutaneous tissue. Body weight increases due to fluid accumulation.

The stage lasts from several days - an average of 10-14 - to several weeks. The duration of the period and methods of treatment are determined by the severity of the lesion and the nature of the primary disease.

Symptoms of the oligoanuric stage of acute renal failure

Diagnostics

At this stage, the primary task is to separate anuria from acute urinary retention. To do this, catheterization of the bladder is performed. If no more than 30 ml/hour is still excreted through the catheter, it means that the patient has acute renal failure. To clarify the diagnosis, an analysis of creatinine, urea and potassium in the blood is prescribed.

• With the prerenal form, there is a decrease in sodium and chlorine in the urine, the rate of fractional excretion of sodium is less than 1%. With calcium necrosis in oliguric acute renal failure, the rate increases from 3.5%, in non-oliguric acute renal failure - to 2.3%.
• For differentiation, the ratio of urea in blood and urine, or creatinine in blood and urine is specified. In the prerenal form, the ratio of urea to plasma concentration is 20:1, in the renal form it is 3:1. For creatinine, the ratio will be similar: 40 in urine and 1 in plasma with prerenal acute renal failure and 15:1 with renal acute renal failure.
• In case of renal failure, a characteristic diagnostic sign is a low chlorine content in the blood - less than 95 mmol/l.
• Microscopy data of urinary sediment allows us to judge the nature of the damage. Thus, the presence of non-protein and erythrocyte casts indicates damage to the glomeruli. Brown epithelial casts and loose epithelium indicate. Hemoglobin casts are detected with intratubular blockade.

Since the second stage of acute renal failure provokes severe complications, in addition to urine and blood tests, it is necessary to resort to instrumental methods of analysis:

• , Ultrasound is performed to detect urinary tract obstruction, analyze the size, condition of the kidney, and assess the blood supply. Excretory urography is not performed: radiopaque angiography is prescribed for suspected arterial stenosis;
• chromocystoscopy is prescribed for suspected obstruction of the ureteral orifice;
• Chest radiography is performed to determine pulmonary edema;
• to assess renal perfusion, isotope dynamic scanning of the kidney is prescribed;
• a biopsy is performed in cases where prerenal acute renal failure is excluded and the origin of the disease has not been identified;
• An ECG is prescribed to all patients, without exception, to detect arrhythmia and signs of hyperkalemia.

Treatment of acute renal failure

Treatment is determined by the type of acute renal failure - prerenal, renal, postrenal, and the degree of damage.

The primary task in the prerenal form is to restore blood supply to the kidney, correct dehydration and vascular insufficiency.

• In the renal form, depending on the etiology, it is necessary to stop taking nephrotoxic drugs and take measures to remove toxins. In case of systemic diseases, the administration of glucocorticoids or cytostatics will be required as the cause of acute renal failure. With pyelonephritis, infectious diseases Therapy includes antiviral drugs and antibiotics. In conditions of a hypercalcemic crisis, large volumes of sodium chloride solution, furosemide, and drugs that slow down the absorption of calcium are administered intravenously.
• The condition for the treatment of postrenal acute insufficiency is the elimination of obstruction.

The water-salt balance must be corrected. Methods depend on the diagnosis:

• for hyperkalemia above 6.5 mmol/l, a solution of calcium gluconate is administered, and then glucose. If hyperkalemia is refractory, hemodialysis is prescribed;
• To correct hypervolemia, furasemide is administered. The dose is selected individually;
• It is important to observe the total intake of potassium and sodium ions - the value should not exceed daily losses. Therefore, in case of hyponatremia, the volume of fluid is limited, and in case of hypernatremia, sodium chloride solution is administered intravenously;
• the volume of fluid, both consumed and administered intravenously, should generally exceed losses by 400–500 ml.

When the concentration of bicarbonates decreases to 15 meq/l and the blood pH reaches 7.2, acidosis is corrected. Sodium bicarbonate is administered intravenously over 35–40 minutes and then monitored during treatment.

With the non-oliguric form, they try to do without dialysis therapy. But there are a number of indicators for which it is prescribed in any case: symptomatic uremia, hyperkalemia, severe stage of acidemia, pericarditis, accumulation of a large volume of fluid that cannot be removed by medication.

Basic principles of treatment of acute renal failure

Restorative, polyuric

The stage of polyuria appears only with sufficient treatment and is characterized by a gradual restoration of diuresis. At the first stage, the daily volume of urine is fixed at 400 ml, at the stage of polyuria - more than 800 ml.

At the same time, the relative density of urine is still low, the sediment contains a lot of proteins and red blood cells, which indicates restoration of glomerular functions, but indicates damage to the tubular epithelium. The blood remains high in creatinine and urea.

During the treatment process, potassium levels are gradually restored and accumulated fluid is removed from the body. This stage is dangerous because it can lead to hypokalemia, which is no less dangerous than hyperkalemia and can cause dehydration.

The polyuric stage lasts from 2–3 to 10–12 days, depending on the degree of organ damage and is determined by the rate of restoration of the tubular epithelium.

Activities carried out during the oliguric stage continue during recovery. In this case, the doses of drugs are selected and changed individually depending on the test results. Treatment is carried out against the background of a diet: the consumption of proteins, liquids, salt, and so on is limited.

Recovery stage of acute renal failure

Recovery

At this stage, normal diuresis is restored, and, most importantly, the products of nitrogen metabolism are removed. If the pathology is severe or the disease is detected too late, nitrogen compounds may not be eliminated completely, and in this case, acute renal failure may become chronic.

If treatment is ineffective or too late, the terminal stage may develop, which poses a serious threat to life.

The symptoms of the thermal stage are:

• spasms and muscle cramps;
• internal and subcutaneous hemorrhages;
• cardiac dysfunction;
• bloody sputum, shortness of breath and cough caused by the accumulation of fluid in the lung tissues;
• loss of consciousness, coma.

The prognosis depends on the severity of the underlying disease. According to statistics, with an oliguric course the mortality rate is 50%, with a non-oliguric course - 26%. If acute renal failure is not complicated by other diseases, then in 90% of cases complete restoration of kidney function is achieved over the next 6 weeks.

Symptoms of recovery from acute renal failure

Chronic renal failure

CRF develops gradually and represents a decrease in the number of active nephrons - the structural units of the kidney. The disease is classified as chronic if a decrease in functionality is observed for 3 or more months.

Unlike acute renal failure, chronic renal failure is difficult to diagnose even at later stages, since the disease is asymptomatic, and up to the death of 50% of nephrons, it can only be detected during functional load.

There are many causes of the disease. However, about 75% of them are , and .

Factors that significantly increase the likelihood of chronic renal failure include:

• diabetes;
• smoking;
• obesity;
• systemic infections, as well as acute renal failure;
• infectious diseases of the urinary tract;
• toxic lesions - poisons, drugs, alcohol;
• age-related changes.

However, for a variety of reasons, the mechanism of damage is almost the same: the number of active ones gradually decreases, which provokes the synthesis of angiotensin II. As a result, hyperfiltration and hypertension develop in intact nephrons. In the parenchyma, the renal functional tissue is being replaced by fibrous tissue. Due to the overload of the remaining nephrons, a violation of water-salt balance, acid-base, protein, carbohydrate metabolism, and so on gradually arises and develops. Unlike acute renal failure, the consequences of chronic renal failure are irreversible: it is impossible to replace a dead nephron.

The modern classification of the disease distinguishes 5 stages, which are determined by the glomerular filtration rate. Another classification is related to the level of creatinine in the blood and urine. This sign is the most characteristic, and from it you can quite accurately determine the stage of the disease.

The most commonly used classification is related to the severity of the patient's condition. It allows you to quickly determine what measures need to be taken first.

Stages of chronic renal failure

Polyuric

The polyuric or initial stage of compensation is asymptomatic. Signs of the primary disease prevail, while there is little evidence of kidney damage.

• Polyuria is the excretion of too much urine, sometimes exceeding the volume of fluid consumed.
• Nocturia is an excess of nocturnal diuresis. Normally, urine is released at night in smaller quantities and is more concentrated. Excretion of more urine at night indicates the need for renal-hepatic tests.
• Even at the initial stage, chronic renal failure is characterized by a decrease in the osmotic density of urine - isosthenuria. If the density is above 1.018, CRF is not confirmed.
• Arterial hypertension is observed in 40–50% of cases. Its difference is that in case of chronic renal failure and other kidney diseases, conventional antihypertensive drugs have little effect on blood pressure.
• Hypokalemia can occur at the stage of polyuria with an overdose of saluretics. It is characterized by severe muscle weakness and changes in the ECG.

Sodium wasting syndrome or sodium retention may develop, depending on tubular reabsorption. Anemia is often observed, and it progresses as other symptoms of chronic renal failure increase. This is due to the fact that when nephrons fail, a deficiency of endogenous epoetin is formed.

Diagnosis includes urine and blood tests. The most revealing of them include the assessment of creatinine content in the blood and urine.

Glomerular filtration rate is also a good determining sign. However, at the polyuric stage, this value is either normal - more than 90 ml/min or slightly reduced - to 69 ml/min.

At the initial stage, treatment is mainly aimed at suppressing the primary disease. It is very important to follow a diet with restrictions on the amount and origin of protein, and, of course, salt intake.

Symptoms of the polyuric stage of chronic renal failure

Stage of clinical manifestations

This stage, also called azotemic or oligoanuric, is distinguished by specific disturbances in the functioning of the body, indicating noticeable damage to the kidneys:

• The most characteristic symptom is a change in urine volume. If at the first stage more fluid was excreted than normal, then at the second stage of chronic renal failure the volume of urine becomes less and less. Oligouria develops - 500 ml of urine per day, or anuria - 50 ml of urine per day.
• Signs of intoxication increase - vomiting, diarrhea, nausea, the skin becomes pale, dry, and in later stages acquires a characteristic jaundiced tint. Due to the deposition of urea, patients are bothered by severe itching; scratched skin practically does not heal.
• There is severe weakness, weight loss, lack of appetite, even anorexia.
• Due to an imbalance in nitrogen balance, a specific “ammonia” odor appears from the mouth.
• At a later stage, it forms, first on the face, then on the limbs and torso.
• Intoxication and high blood pressure cause dizziness, headaches, and memory impairment.
• A feeling of chills appears in the arms and legs - first in the legs, then their sensitivity decreases. Movement disorders are possible.

These external signs indicate the addition of concomitant diseases and conditions caused by kidney dysfunction to chronic renal failure:

• Azotemia – occurs when there is an increase in nitrogen metabolic products in the blood. Determined by the amount of creatinine in plasma. The uric acid content is not so indicative, since its concentration increases for other reasons.
• Hyperchloremic acidosis is caused by a violation of the mechanism of calcium absorption and is very characteristic of the stage of clinical manifestations; it increases hyperkalemia and hypercatabolism. Its external manifestation is the appearance of shortness of breath and great weakness.
• Hyperkalemia is the most common and most dangerous symptom of chronic renal failure. The kidney is able to maintain the function of potassium absorption until the terminal stage. However, hyperkalemia depends not only on the functioning of the kidney and, if it is damaged, develops in the initial stages. When the potassium content in the plasma is excessively high - more than 7 meq/l, nerve and muscle cells lose their ability to excitability, which leads to paralysis, bradycardia, central nervous system damage, acute respiratory failure, and so on.
• With a decrease in appetite and against the background of intoxication, a spontaneous decrease in protein intake occurs. However, its too low content in food for patients with chronic renal failure is no less destructive, since it leads to hypercatabolism and hypoalbuminemia - a decrease in albumin in the blood serum.

Another characteristic symptom for patients with chronic renal failure is an overdose of drugs. For chronic renal failure side effects of any drug are much more pronounced, and overdose occurs in the most unexpected cases. This is due to kidney dysfunction, which is unable to remove waste products, which leads to their accumulation in the blood.

Diagnostics

The main goal of diagnosis is to distinguish chronic renal failure from other kidney diseases with similar symptoms, and especially from the acute form. To do this, they resort to various methods.

Of the blood and urine tests, the most informative are the following indicators:

• the amount of creatinine in the blood plasma is more than 0.132 mmol/l;
• – a pronounced decrease is 30–44 ml/min. At a value of 20 ml/min, urgent hospitalization is required;
• urea content in the blood is more than 8.3 mmol/l. If an increase in concentration is observed against the background of normal creatinine levels, the disease most likely has a different origin.

Among instrumental methods, ultrasound and x-ray methods are used. Characteristic sign Chronic renal failure is a reduction and shrinkage of the kidney; if this symptom is not observed, a biopsy is indicated.

X-ray contrast research methods are not permitted

Treatment

Until the end stage, treatment of chronic renal failure does not include dialysis. Conservative treatment is prescribed depending on the degree of kidney damage and associated disorders.

It is very important to continue treatment of the underlying disease, while eliminating nephrotoxic drugs:

• A mandatory part of treatment is a low-protein diet - 0.8-0.5 g/(kg*day). When the albumin content in the serum is less than 30 g/l, the restrictions are weakened, since with such a low protein content the development of nitrogen imbalance is possible; the addition of keto acids and essential amino acids is indicated.
• When GFR is around 25–30 ml/min, thiazide diuretics are not used. With more low values are assigned individually.
• For chronic hyperkalemia, ion-exchange polystyrene resins are used, sometimes in combination with sorbents. In acute cases, calcium salts are administered and hemodialysis is prescribed.
• Correction of metabolic acidosis is achieved by administering 20–30 mmol of sodium bicarbonate intravenously.
• For hyperphosphatemia, substances are used that prevent the absorption of phosphates by the intestine: calcium carbonate, aluminum hydroxide, ketosteryl, phosphocitrile. For hypocalcemia, calcium preparations - carbonate or gluconate - are added to therapy.

Stage of decompensation

This stage is characterized by deterioration of the patient’s condition and the appearance of complications. The glomerular filtration rate is 15–22 ml/min.

• Headaches and lethargy are accompanied by insomnia or, conversely, severe drowsiness. The ability to concentrate is impaired and confusion is possible.
• Peripheral neuropathy progresses - loss of sensation in the arms and legs, up to immobilization. Without hemodialysis, this problem cannot be solved.
• Development of gastric ulcer, appearance of gastritis.
• Chronic renal failure is often accompanied by the development of stomatitis and gingivitis - inflammation of the gums.
• One of the most severe complications of chronic renal failure is inflammation of the serous membrane of the heart - pericarditis. It is worth noting that with adequate treatment this complication is rare. Myocardial damage due to hyperkalemia or hyperparathyroidism is observed much more often. The degree of damage to the cardiovascular system is determined by the degree of arterial hypertension.
• Another common complication is pleurisy, that is, inflammation of the pleural layers.
• With fluid retention, blood stagnation in the lungs and swelling are possible. But, as a rule, this complication appears already at the stage of uremia. The complication is detected by x-ray.

Treatment depends on the complications that arise. Possibly connection to conservative hemodialysis therapy.

The prognosis depends on the severity of the disease, age, and timeliness of treatment. At the same time, the prognosis for recovery is questionable, since it is impossible to restore the functions of dead nephrons. However, the prognosis for life is quite favorable. Since the relevant statistics are not kept in the Russian Federation, it is quite difficult to say exactly how many years patients with chronic renal failure live.

In the absence of treatment, the stage of decompensation passes into the terminal stage. And in this case, the patient’s life can only be saved by resorting to kidney transplantation or hemodialysis.

Terminal

The terminal (last) stage is uremic or anuric. Against the background of retention of nitrogen metabolism products and disruption of water-salt, osmotic homeostasis, etc., autointoxication develops. Dystrophy of body tissues and dysfunction of all organs and systems of the body are recorded.

• Symptoms of loss of sensation in the limbs are replaced by complete numbness and paresis.
• There is a high probability of uremic coma and cerebral edema. Against the background of diabetes mellitus, a hyperglycemic coma is formed.
• In the terminal stage, pericarditis is a more frequent complication and is the cause of death in 3–4% of cases.
• Gastrointestinal lesions - anorexia, glossitis, frequent diarrhea. Every 10 patients experience gastric bleeding, which is the cause of death in more than 50% of cases.

Conservative treatment at the terminal stage is powerless.

Depending on the general condition of the patient and the nature of the complications, more effective methods are used:

• – blood purification using an “artificial kidney” device. The procedure is carried out several times a week or every day, has different durations - the regimen is selected by the doctor in accordance with the patient’s condition and the dynamics of development. The device performs the function of a dead organ, so diagnosed patients cannot live without it.

Hemodialysis today is a more affordable and more effective procedure. According to data from Europe and the USA, the life expectancy of such a patient is 10–14 years. Cases have been recorded where the prognosis is most favorable, since hemodialysis prolongs life by more than 20 years.

• - in this case, the role of the kidney, or, more precisely, the filter, is performed by the peritoneum. The fluid introduced into the peritoneum absorbs the products of nitrogen metabolism and is then removed from the abdomen to the outside. This procedure is carried out several times a day, since its effectiveness is lower than that of hemodialysis.
• – most effective method, which, however, has a lot of limitations: peptic ulcers, mental illness, endocrine disorders. It is possible to transplant a kidney from either a donor or a cadaveric one.

Recovery after surgery lasts at least 20–40 days and requires the most careful adherence to the prescribed regimen and treatment. A kidney transplant can prolong a patient's life by more than 20 years, unless complications arise.

Stages of creatinine and degree of glomerular filtration reduction

The concentration of creatinine in urine and blood is one of the most characteristic distinctive features chronic renal failure. Another very telling characteristic of a damaged kidney is the glomerular filtration rate. These signs are so important and informative that the classification of chronic renal failure by creatinine or by GFR is used more often than the traditional one.

Classification by creatinine

Creatinine is a breakdown product of creatine phosphate, the main source of energy in muscles. When a muscle contracts, the substance breaks down into creatinine and phosphate, releasing energy. Creatinine then enters the blood and is excreted by the kidneys. The average norm for an adult is considered to be a blood level of 0.14 mmol/l.

An increase in creatinine in the blood causes azotemia - the accumulation of nitrogen breakdown products.

Based on the concentration of this substance, 3 stages of disease development are distinguished:

• Latent - or reversible. Creatinine levels range from 0.14 to 0.71 mmol/L. At this stage, the first uncharacteristic signs of chronic renal failure appear and develop: lethargy, polyuria, and a slight increase in blood pressure. There is a decrease in the size of the kidney. The picture is typical for a condition when up to 50% of nephrons die.
• Azotemic - or stable. The level of the substance varies from 0.72 to 1.24 mmol/l. Coincides with the stage of clinical manifestations. Oligouria develops, headaches, shortness of breath, swelling, muscle spasms, etc. appear. The number of working nephrons decreases from 50 to 20%.
• Uremic stage - or progressive. Characterized by an increase in creatinine concentration above 1.25 mmol/l. Clinical signs are pronounced, complications develop. The number of nephrons is reduced to 5%.

By glomerular filtration rate

Glomerular filtration rate is a parameter used to determine the excretory capacity of an organ. It is calculated in several ways, but the most common involves collecting urine in two hourly portions, determining minute urine output and creatinine concentration. The ratio of these indicators gives the value of glomerular filtration.

GFR classification includes 5 stages:

• Stage 1 – with a normal level of GFR, that is, more than 90 ml/min, signs of renal pathology are observed. At this stage, for cure, sometimes it is enough to eliminate the existing negative factors– smoking, for example;
• Stage 2 – slight decrease in GFR – from 89 to 60 ml/min. At both stages 1 and 2, it is necessary to adhere to a diet, accessible physical activity and periodic observation by a doctor;
• Stage 3A – moderate decrease in filtration rate – from 59 to 49 ml/min;
• Stage 3B – marked decrease to 30 ml/min. At this stage, drug treatment is carried out.
• Stage 4 – characterized by a severe decrease – from 29 to 15 ml/min. Complications appear.
• Stage 5 – GFR is less than 15 ml, the stage corresponds to uremia. The condition is critical.

Stages of chronic renal failure according to glomerular filtration rate


Kidney failure is a severe and very insidious syndrome. In a chronic course, the first signs of damage to which the patient pays attention appear only when 50% of the nephrons, that is, half of the kidneys, have died. Without treatment, the likelihood of a favorable outcome is extremely low.

An obvious confirmation that diabetic processes are in full swing in the human body is the frequent need to visit the toilet.

This phenomenon not only causes a lot of inconvenience, but also poses an undeniable danger to the patient’s health, which negatively affects the condition of the central nervous system.

Patients often confuse this abnormality with frequent urination and panic, mistaking it for an alarming symptom. However, the phenomena listed are different.

And if in the case of frequent urination the daily volume of fluid excreted by the body remains normal, then with polyuria the amount of the excreted product will noticeably exceed the norm, and its specific gravity will be greater.

What is the cause of polyuria in diabetes mellitus?

In diabetics, a similar condition occurs every time and lasts until the volume of the substance returns to normal.

In this case, water is reabsorbed in the renal tubules and complete elimination from the body.

That is, in order to reduce glucose levels and cleanse the blood, the kidneys increase their work intensity. As a result, the process of removing glucose from the body begins to intensify, and with it the fluid required for normal life.

Each gram of glucose, when excreted, will “take away” about 30-40 g of urine. If the patient does not drink large amounts of water during this period, the condition may negatively affect the quality of the kidneys, blood vessels, heart and some other organs.

In children

In children, diabetes mellitus often occurs in an acute form. Therefore, parents should be attentive to the child’s health condition.

Frequent trips to the toilet, inability to wake up and go to the toilet in time (the child regularly wakes up “wet”, although he has already learned to wake up to go to the toilet), complaints of dry mouth and severe thirst are alarming symptoms indicating the development of polyuria, which is a consequence of more serious ailments.

Polydipsia as a faithful companion of polyuria in diabetics

Polydipsia is an integral component of polyuria. This is a state of unnatural thirst that occurs as the body excretes large amounts of urine. You can get rid of this manifestation only by normalizing the level of glucose in the blood.

Video on the topic

About the causes and treatment of polyuria in diabetes in the video:

To eliminate the manifestation of polyuria, a properly organized A complex approach, which must be selected by a physician. It is not recommended to choose medications on your own to eliminate symptoms.

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

Pathogenesis of polyuria

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

When water intake increases, circulating blood volume increases, which increases renal perfusion and GFR and leads to an increase in urine volume. However, increasing water intake decreases blood osmolality, which decreases the secretion of ADH (also known as arginine vasopressin) from the hypothalamic-pituitary axis. Because ADH stimulates the reabsorption of water in the collecting ducts of the kidneys, decreasing ADH levels increases urine volume, which allows the body's water balance to return to normal.

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

Therefore, polyuria occurs in any process that includes:

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

Causes of polyuria

• Duration and severity of polyuria (nocturia, frequency of urination, fluid intake at night).
• Family history (diabetes mellitus, polycystic kidney disease, urolithiasis).
• Reception medicines(diuretics, analgesics, lithium, etc.).
• Kidney stones (hypercalcemia).
• Weakness (hypocapemia), depression (hypercalcemia).
• Presence of mental disorders.
• Endocrine disorders (impaired menstrual function, sexual function, lactation, impaired growth of pubic hair).
• Other serious illnesses.

Kidney stones: causes

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

Symptoms and signs of polyuria

• Confusion (due to hyponatremia or dehydration).
• Coma.
• Proteinuria.
• Depression or other mental disorders.

Polyuria: laboratory and instrumental research methods

• Urea and electrolytes (kidney disease, hypokalemia).
• Blood glucose.
• Calcium, phosphates and alkaline phosphatase.
• Plasma and urine osmolality [a urine-to-plasma osmolality ratio of less than 1.0 indicates diabetes insipidus, parenchymal renal disease (accompanied by hypokalemia), or excessive water intake due to hysteria].
• X-ray of the abdominal organs (nephrocalcinosis).
• If possible, determine the level of lithium drugs in the blood.
• Determination of protein fractions.

Collection of anamese. Collection of anamnesis of the present disease should include obtaining information about the volume of fluid consumed and excreted for the purpose of differential diagnosis of polyuria from pollakiuria. If polyuria is present, the patient should be asked about the age at which it began, the rate of onset (ie, sudden or gradual onset), and any clinically significant recent factors that may cause polyuria (eg, intravenous fluids, gastric feedings). tube, relief of urinary tract obstruction, stroke, head injury, surgery).

Examination of organs and systems should look for symptoms indicating a possible causative disease, including dry conjunctiva and oral mucosa (Sjögren's syndrome), weight loss, and night sweats (cancer).

When collecting a medical history, it is necessary to pay attention to diseases associated with polyuria. It is necessary to find out if there are cases of polyuria in the family. When obtaining a drug history, the use of any drugs associated with renal diabetes insipidus and the use of substances that increase diuresis (eg, diuretics, alcohol, caffeinated beverages) should be noted.

Physical examination. General examination should note signs of obesity and malnutrition or cachexia, which may indicate an underlying malignancy or an eating disorder with surreptitious diuretic use.

When examining the head and neck, note the presence of dry eyes or dry mouth (Sjögren's syndrome). When examining the skin, note any hyperpigmented or hypopigmented lesions, ulcers, or subcutaneous nodules that may indicate sarcoidosis. A complete neurological examination should note the presence of focal neurological deficits that may indicate stroke and assess mental status for signs of psychiatric disorder.

Warning signs. The following data deserve special attention:

• Sudden onset of polyuria or its onset during the first years of life.
• Night sweats, cough and weight loss, especially when there is a long history of smoking.
• Mental illness.

Data interpretation. When collecting anamnesis, it is often possible to distinguish polyuria from pollakiuria, but in rare cases, a daily collection of urine may be required.

Clinical examination may suggest a cause, but laboratory testing is usually required. Diabetes insipidus is indicated by a history of cancer or chronic granulomatous lesions (due to hypercalcemia), use of certain medications (lithium, sidofovir, foscarnet, and phosphamide), and rarer diseases (eg, renal amyloidosis, sarcoidosis, Sjögren's syndrome), which often have more brighter and earlier manifestations than polyuria.

Sudden onset of polyuria certain time, as well as the patient's tendency to drink cold or ice water, indicate central diabetes insipidus. The onset of the symptom in the first few years of life is usually associated with hereditary forms of central or renal diabetes insipidus or decompensated type 1 diabetes mellitus. Polyuria due to diuresis is indicated by a history of taking diuretics or diabetes mellitus. Psychogenic polydipsia is more common in patients with mental disorders (mainly bipolar affective disorder or schizophrenia) in the anamnesis; less often it is one of the symptoms of the onset of the disease.

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

If there is no hyperglycemia, the following studies are required:

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

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

• Hypernatremia indicates excessive loss of free water due to central or renal diabetes insipidus.
• Hyponatremia (sodium level less than 137 mEq/L) indicates excess free water intake due to polydipsia.
• Urine osmolality is usually less than 300 mOsm/kg with water diuresis and more than 300 mOsm/kg with osmotic diuresis.

If the diagnosis remains unclear, serum and urine sodium levels should be measured in response to a water deprivation test and exogenous ADH challenge. Since severe dehydration may develop as a result of the test, it should only be performed under constant medical supervision, usually requiring hospitalization. In addition, patients with suspected psychogenic polydipsia should be monitored to exclude secret fluid intake.

The test begins in the morning by weighing the patient, drawing blood from a vein to determine the concentration of electrolytes in the serum and its osmolality, as well as the osmolality of urine. Every hour the patient urinates and the urine osmolality is measured. Dehydration is continued until the onset of orthostatic hypotension and postural tachycardia, a decrease in initial body weight of 5% or more, or an increase in urine osmolality of more than 30 mOsm/kg in consecutive samples. Serum electrolyte levels and osmolality are then reassessed and 5 units of aqueous vasopressin are injected subcutaneously. To study its osmolality, urine is collected for the last time an hour after the injection, and this is where the sample ends.

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

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

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

With psychogenic polydipsia, urine osmolality is less than 100 mOsm/kg. A decrease in water load leads to a decrease in urine output, an increase in plasma osmolality and serum sodium concentration.

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

Treatment of polyuria

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

Fluid balance is carefully measured and the patient is weighed daily.

The central vein is catheterized to monitor central venous pressure.

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

They compensate for fluid deficiency with saline solutions and glucose solutions, achieving the maintenance of normal homeostasis.

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

They do not pursue the goal of completely replacing lost fluid. Once the patient is adequately rehydrated, intravenous fluid administration should be discontinued, allowing the physiological homeostasis mechanism to restore itself. water balance body.

If diabetes insipidus is suspected, a test with limited fluid intake is performed.

Polyuria. Fluid restriction test

All medications are discontinued the day before the test; The patient should not smoke or drink coffee.

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

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

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

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

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

If polyuria continues, intranasal desmopressin is prescribed at a dose of 20 mcg every 8 hours.

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

Interpretation of the results obtained:

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