[Diabetes insipidus: etiology, diagnosis, and therapy].
Diabetes insipidus is a disorder of the water retaining ability of the organism. It is a polydipsic-polyuric syndrome caused by partial or complete vasopressin deficiency (central diabetes insipidus) or vasopressin resistance of the kidney tubules (nephrogenic diabetes insipidus) or increased water intake due to oversensitivity of the thirst centre (dipsogenic diabetes insipidus = primary polydipsia). The pathogenetic factors may affect the osmoreceptors, the vasopressinergic magnocellular nuclei of the hypothalamus, the median eminence, the pituitary stalk, the vasopressin release from the neurohypophysis, the vasopressin inactivating mechanisms and the renal structures mediating the antidiuretic effect of vasopressin. In the evaluation of the results of the diagnostic procedures, it is to be considered that long-term overhydration of any origin suppresses the vasopressin secretion and the "washout" effect of the long-term water-diuresis decreases the concentration gradient of the renal medulla leading to blunted sensitivity towards vasopressin. This is, why the differential diagnostics of central, nephrogenic and dipsogenic diabetes insipidus seems sometimes to be enigmatic. Central diabetes insipidus can be excluded only on the basis of proportional parallel increase of plasma osmolality and plasma vasopressin level. Similarly, nephrogenic diabetes insipidus will be excluded when plasma vasopressin increases proportionately with the increase of urinary osmolality. In equivocal cases T1-weighted MRI of the pituitary may be of help in the establishment of an exact diagnosis. As far as possible, the therapy is to be focused on the diabetes insipidus evoking basal diseases. In central diabetes insipidus, diuresis can be decreased by vasopressin substitution. The first choice compound for this purpose is 1-desamino-8-D-arginine-vasopressin. The non-vasopressin containing oral antidiuretics have become outdated in the treatment of central diabetes insipidus. There is no specific treatment for nephrogenic and dipsogenic diabetes insipidus, so far. Nephrogenic diabetes insipidus can be influenced by non-steroidal antiinflammatory agents or diuretics. Their combined administration is even more effective, however, still does not exceed a 50-percent mitigation in diuresis.
Laczi
Ferenc
F
Szegedi Tudományegyetem, Altalános Orvostudományi Kar, Szent-Györgyi Albert Orvos- és Gyógyszerésztudományi Centrum, Endokrinológiai Onálló Osztály és Kutató Laboratórium.
D003894:Deamino Arginine Vasopressin / Q000627:therapeutic use; D003919:Diabetes Insipidus / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism / Q000628:therapy; D006801:Humans; D008279:Magnetic Resonance Imaging; D009994:Osmolar Concentration; D010904:Pituitary Gland, Posterior / Q000378:metabolism*; D012076:Renal Agents / Q000627:therapeutic use; D014667:Vasopressins / Q000097:blood / Q000172:deficiency / Q000378:metabolism*
D012076:Renal Agents; D014667:Vasopressins; D003894:Deamino Arginine Vasopressin