Causes of polyuria( mechanisms and syndromes)
1. Disorders of ADH secretion.
1.1.Pathology of osmoreceptors.
1.2.Violations of the synthesis of ADH.
1.3.Accelerated decay of ADH.
2. Loss of thirst.
2.1.CNS lesions( infection, trauma, leukemia).
2.2.Psychogenic polydipsia.
3. Defects in the system of urine concentration in the kidneys.
3.1.Absence of an osmotic gradient in the renal parenchyma.
3.1.1.Chronic renal failure.
3.1.2.Nephronophthisis.
3.1.3.Amyloidosis of the kidneys.
3.1.4.Osmotic diuresis.
3.1.5.Pseudo-obstructive uropathy.
3.1.6.Sickle-cell anemia.
3.1.7.Fanconi syndrome and de Toni-Debreu-Fanconi disease.
3.2.Inadequate response to ADH.
3.2.1.Nephrogenic diabetes insipidus.
3.2.2.Nephropathy with potassium deficiency syndrome.
3.2.3.Hypercalcemia nephropathy.
3.2.4.Intoxications( lithium, tetracycline, methoxyfuran).
Nephrogenic diabetes insipidus is observed exclusively in boys, but the transfer from the father to the son is not observed. This similarity to inheritance of hemophilia indicates the linkage of the mutant gene to the sex. Incomplete forms of the disease can be observed in girls. In this case, the disease occurs with a moderately increased thirst and a corresponding increase in the amount of urine per day. The girls described mild manifestations of diabetes insipidus, in which the reaction of the renal tubules to the antidiuretic hormone( thanks to it the water balance in the body is regulated) is only moderately reduced.
It is proposed to distinguish two types of disease: at type 1 in response to the introduction of ADH, there is no increase in cAMP administration by the kidneys, while in type 2 there is an increase. Description of observations of autosomal dominant type of inheritance of diabetes insipidus also indicates a genetic heterogeneity of the disease. However, in most cases, the disease is inherited in an X-linked manner.
The first task of treatment of renal diabetes insipidus is correction of dehydration and hyelectrolithy( hyperosmia).It is necessary to correct the disturbed water balance of the body, increase the water regime, respectively, diuresis. With severe loss of fluid, intravenous glucose can be administered. It is advisable to somewhat restrict the content of protein and salt in the diet. Drugs of vasopressin are ineffective, but diuretics( hypothiazide, ethacrynic acid) remain the means of choice. It is very important combination of diet therapy, water regimen and the use of diuretics.
The effect of hypothiazide is associated with the fact that the initially increasing increase in sodium excretion in the urine( sodium naresis) leads to sodium deficiency and, accordingly, to a gradual decrease in the intensity of its excretion by the kidneys. In turn, this leads to a decrease in the excretion of water. In addition, sodium deficiency stimulates the secretion of renin and angiotensin, stimulating the inverse absorption of sodium in the tubules of the kidneys.
There have been indications that inhibitors of prostaglandin synthesis are also effective in the treatment of nephrogenic diabetes insipidus. Thus, excretion of prostaglandin E decreased in the majority under the influence of indomethacin and ibuprofen, which was also associated with a decrease in diuresis. When combined with diuretics, the effect was significantly enhanced.
Non-diabetes mellitus of the central( neurohypophysis) genesis is characterized by the normal sensitivity of the kidneys of patients to the action of ADE. It is based on a disruption of the synthesis of vasopressin in supraoptic and paraventricular nuclei of the central nervous system. It is inherited by autosomal dominant type.