Polyuria

POLYURIA, an increase in the amount of urine excreted per day, represents an important clinical symptom of a number of diseases of both the kidneys themselves and the neuroendocrine apparatus. The pathogenesis of polyuria appears to be extremely diverse, as is its diagnostic significance. Secondary polyuria may occur with the administration of large quantities of water (urina ex potu), both under physiological conditions and as a result of psychogenically increased drinking (polydipsia). Transient polyurias occurring during the resolution of edema and in convalescents after certain infections also belong to the group of secondary polyurias. Significantly more important, however, are persistent polyurias, sometimes independent either of increased fluid intake or the use of diuretic agents. Such a "primary" pathological polyuria represents a formidable symptom of many renal diseases, indicating the loss of the kidneys' ability to concentrate urine. The appearance of polyuria indicates that a significant part of the renal parenchyma is excluded from function, in connection with which the second phase of urine secretion—the possibility of water reabsorption in the tubules—has decreased (see Diuresis, physiology). A necessary condition for the occurrence of renal polyuria is, however, the preservation of the water-excreting capacity of the renal glomeruli. Changes in the kidneys causing polyuria can be of a most diverse character. The cause of polyuria can be: 1) a decrease in the functioning renal parenchyma due to cystic degeneration, shrinkage (nephrocirrhosis, nephrosclerosis), or partial destruction of renal tissue (hydronephrosis); 2) a violation of pressure and nutrition conditions in the renal tubules, which occurs with prostate hypertrophy, compression of the urinary excretion system by tumors, and in mild degrees of intoxication by renal poisons (e.g., sublimate). The latter group of polyurias is of a more transient nature and may disappear with the removal of the cause conditioning it. The second group of "primary" polyurias, resulting from lesions of the vegetative-nervous metabolism centers and the endocrine system, is observed in people with a normal urinary excretion apparatus. In such cases, polyuria is caused either by the loss of the influence of the vegetative system regulating diuresis from the so-called "water" center in the diencephalon, or by the absence or decrease in the function of the pituitary gland, which produces in its posterior lobe the antidiuretic hormone that is part of pituitrin. Clinically, polyuria from a disturbance of neuroendocrine diuresis regulation occurs in diabetes insipidus and diabetes mellitus. From a differential-diagnostic standpoint, it is important to take into account that primary renal and central polyurias (with the exception of diabetes mellitus) are as a rule accompanied by the persistent excretion of urine of low specific gravity (hyposthenuria), whereas in secondary polyurias the specific gravity of the urine depends mainly on the amount of solid components introduced with food or their reserve in the body's tissues.

M. Vovei.