POLYURIA (polyuria; grech, poly is a lot of + uron wetting) — increase in release of urine (for the adult of St. 1800 ml per day).
Excess water consumption (psychogenic P.), disturbance of a water salt metabolism and its regulation (extrarenal P.), patol, processes in kidneys (renal P.) can be P.'s reasons. The mechanism P. of any origin is connected with reduction of a reabsorption in tubules of kidneys of the filtered substances and waters or only waters. In the first case P. is caused by osmotic diuresis (see) or salurezy, in the second — a water diuresis. The item can reach 10 — 30 l and be the cause of lethal dehydration.
Psychogenic P. as result polydipsias (see) can be a consequence of disturbances of c. N of page — a hyperexcitability of the center of thirst, especially in connection with encephalitis (see). To distinguish not diabetes mellitus and primary polydipsia, measure osmolarity of blood serum: at not diabetes mellitus it higher than 300 mosm/l, at a polydipsia — less than 270 mosm/l. At a polydipsia deprivation of the patient of water within several hours leads to increase in osmolarity of urine and P.'s reduction, at not diabetes mellitus osmolarity of urine significantly does not change. If test with xerophagia is inefficient, apply test with antidiuretic hormone: at normal function of kidneys intramuscular introduction of 5 PIECES of vasopressin or Pituitrinum increases the osmotic pressure of urine to 800 — 1200 mosm/l. Drop introduction of a pitres-sin or an intramuscular injection of an oil suspension of drug of antidiuretic hormone is more preferable than a single injection of Pituitrinum since because of a long absence of antidiuretic hormone in an organism reaction of kidneys decreases and P.'s reduction is usually short-term and trudnoulovimo. Test with antidiuretic hormone is contraindicated at pregnancy, epilepsy, heavy arterial hypertension, coronary insufficiency.
The item of an extrarenal origin can accompany the painful and vegetative crises which are followed by excess emission in blood catecholamines (see). One of extrarenal P.'s types is the so-called urina spastica developing after migraine, hypertensive crisis, a Bouveret's disease, acute vegetative crisis with allocation during 1 — 4 hour to 8 l of urine with a low ud. it is powerful. Extrarenal P. can be observed at a convergence hypostases (see), at the same time P.'s genesis is connected with change of a cordial and renal hemodynamics, reduction of secretion of antidiuretic hormone and Aldosteronum.
The item arises also at a number of endocrine diseases: hyperparathyreosis, hyperthyroidism, Cushing's syndrome, Conn's syndrome, diabetes mellitus.
The item at an osmotic diuresis it is caused by hit from blood in an ultrafiltrate of badly reabsorbiruyemy substances (e.g., Mannitolum) or so-called threshold substances (see. Urine ) in the concentration considerably exceeding reabsorbtsionny ability of renal tubules (e.g., glucose at a hyperglycemia). Increase in a diuresis is promoted by the urea and amino acids which are also filtered from blood that happens at a high-protein diet or administration of solution of amino acids. The item of an osmotic origin can be followed by hyper osmolarity and reduction of volume of the circulating blood. The osmotic diuresis is used at treatment poisonings (see).
Renal P. is more often caused renal failure (see) and an osmotic overload functioning, or so-called intact, nephrons products of metabolism. In this case P. has compensatory value since identical removal of osmotically active agents at the reduced concoction is possible at the expense of the bigger volume of the removed urine. Reaction of tubules to antidiuretic hormone at the same time is lowered. At tubulointerstitsialny defeats kidneys (see) P. it is caused preferential by disturbance of process of concoction. One of renal P.'s options is the nephrogenic not diabetes mellitus (inborn and acquired), at Krom nonsensitivity of cells of renal tubules to antidiuretic hormone is observed. Are the cornerstone of areactivity of kidneys to antidiuretic hormone disturbance of interaction with hormone of cellular receptors, insufficient activation of adenylatecyclase, reduced education in a cell of tsAMF (cyclic adenozinmo-nofosforny to - you) and disturbance of the subsequent intracellular processes, from to-rykh depends increase in permeability of tubules for water. At a family not diabetes mellitus antidiuretic hormone does not increase excretion of tsAMF with urine. Salts lity (see) at prolonged use cause in 12 — 30% of sick Items. Activation by antidiuretic hormone of adenylatecyclase is broken at a hypercalcemia, a high level of catecholamines in blood, increase in concentration of prostaglandin E in blood. Acetphenetidiene, dimethyl-chlortetracyclin, diuretics at prolonged use, and also hron, pyelonephritis, tubular acidosis, a hyper aldosteronism, resulting in deficit of potassium in cells of renal tubules, break ability of tsAMF to increase permeability of tubules for water. Deficit of magnesium is followed by loss of potassium and also leads to disturbance of concentration function of kidneys. There is a form of a renal not diabetes mellitus, at Krom lack of reactions to antidiuretic hormone and P. is caused by disturbance of secretion of hyaluronidase cells of tubules.
Can lead disturbance of regulation of water secretory function of kidneys to P.'s emergence, napr, at pathology of osmoreceptors which do not react to increase in osmotic pressure of blood; at the same time secretion of antidiuretic hormone decreases (see. Vasopressin ). For differentiation of a false and true not diabetes mellitus (see. Diabetes not sugar ) enter 0,5 — 1,0 mg of the nicotine (to the smoking persons increase a dose to 3 mg) stimulating secretion of antidiuretic hormone with a hypophysis into a vein. At pathology of osmoreceptors, an intact neurohypophysis and preservation of functions of kidneys of P. stops.
Also other pathogenetic mechanisms P are possible. Optimum speed of the movement of canalicular liquid and blood on direct vessels provides concoction of osmotically active agents in marrow of a kidney, creating conditions for a reabsorption of water. Acceleration of a blood-groove leads to washing away from vessels, an interstitium and tubules of sodium, chlorine, urea owing to what ability of kidneys to absorption of water and osmotic concoction of urine decreases. Such conditions are created, e.g., at the idiopathic hypertensia with a so-called malignant current which is followed by P. and nocturia (see). The accelerated course of provisional urine on tubules and disturbance of its concoction take place at a family nephrogenic not diabetes mellitus in connection with hereditary shortening of proximal department of a tubule. The polycystosis, an amyloidosis of kidneys, a hypopotassemia break accumulation of osmotically active agents in an interstitium and a reabsorption of water. Considerable reduction of a blood-groove on direct vessels of marrow of kidneys, in particular at a sickemia, is followed by the Item. Decrease in a tone and delay of a blood-groove on direct vessels are observed also at a chronic hypercalcemia that in combination with insufficient reactivity of tubules to antidiuretic hormone leads to
P. P. is observed also in the recovery period of an acute renal failure (see) and later renal transplantations (see).
P.'s treatment is carried out taking into account a basic disease and the reasons of the broken concoction of urine. Symptomatic therapy of effects of P. includes compensation of fluid losses, electrolytes, the bases. Small fluid losses (2 — 3 l a day) are offset in the peroral way, at more considerable losses applied infusional therapy (see).
The forecast at P. depends on character of a basic disease, expressiveness and duration of the Item.
Bibliography: Yu. V is ground. Physiological bases of differential diagnosis of polyurias and disturbances of concentration ability of kidneys, Rubbed. arkh., t. 47, Kya 4, page 13, 1975, bibliogr.; Rat-n e r M. Ya., Serov V. V. and Tomilina N. A. Renal dysfunctions (kliniko-morphological characteristic), M., 1977, bibliogr.; A n d r e o-1 i T. E. The polyuric syndromes, in book: Physiology of membrane disorders, ed. by T. E. Andreoli a. o., p. 1063, N. Y., 1978; The kidney, ed. by B. M. Brenner a. F. C. Rector, v. 1, p. 553, Philadelphia, 1976; Wardener H. E. The kidney, Edinburgh, 1973.
Yu. V. Natochin.