demeclocycline and Diabetes-Insipidus

Topics: Animals; Anti-Bacterial Agents; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Benzeneacetamides; Body Water; Demeclocycline; Diabetes Insipidus; Dogs; Humans; Kidney; Liver Cirrhosis; Liver Cirrhosis, Experimental; Loop of Henle; Pyrrolidines; Rats; Receptors, Opioid; Vasopressins; Water-Electrolyte Balance

In congenital NDI, the failure of the renal tubules to respond to antidiuretic hormone is caused by mutation of the arginine vasopressin receptor gene. Two dozen different mutations have been identified to date--all with the same clinical consequences. Several causes of acquired NDI, of which lithium is the most common, are also discussed.

Topics: Arginine Vasopressin; Base Sequence; Chromosome Mapping; Demeclocycline; Diabetes Insipidus; DNA; Female; Genetic Linkage; Heterozygote; Humans; Lithium; Male; Molecular Sequence Data; Mutation; Pedigree; Receptors, Vasopressin; Signal Transduction; X Chromosome

Topics: Acne Vulgaris; Animals; Anura; Cyclic AMP; Demeclocycline; Diabetes Insipidus; Dose-Response Relationship, Drug; Humans; In Vitro Techniques; Osmosis; Urinary Bladder; Vasopressins

To examine a possible role for atrial natriuretic peptide (ANP) in water and sodium metabolism disturbances associated with abnormal vasopressin (AVP) secretion, we measured plasma ANP concentrations in 15 patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and in 17 patients with central diabetes insipidus (DI). The mean plasma ANP concentration (30.2 +/- 10.4 pmol/L) in SIADH patients who had hyponatremia, plasma hypoosmolality, hyperosmolar urinary compared to plasma sodium levels, and increased plasma AVP levels relative to plasma osmolality was significantly higher than that in normal subjects (12.6 +/- 4.9 pmol/L), although there was a considerable individual variation in plasma ANP ranging from normal to clearly elevated levels (15.1-47.0 pmol/L). When hyponatremia was corrected by water restriction or demeclocycline administration, plasma ANP levels decreased significantly and fell into the normal range (12.5 +/- 4.3 pmol/L). DI patients who complained of polyuria and polydipsia and had hypoosmolar urine, normal or elevated plasma sodium concentrations, and decreased plasma AVP levels relative to plasma osmolality, on the other hand, had a significantly lower mean plasma ANP level (7.6 +/- 2.9 pmol/L) than normal subjects. There was, again, a considerable overlap between plasma ANP levels in individual DI patients (4.2-13.9 pmol/L) and those in normal subjects. Treatment with 1-desamino-8-D-arginine vasopressin resulted in a significant increase in the mean plasma ANP level (18.6 +/- 8.0 pmol/L). There were no significant correlations between plasma ANP and AVP levels in either group of patients. The results indicate that ANP secretion is modulated by changes in plasma volume consequent to abnormal AVP secretion, which may have a pathophysiological significance in maintaining volume homeostasis.

Topics: Adolescent; Adult; Aged; Atrial Natriuretic Factor; Blood Volume; Deamino Arginine Vasopressin; Demeclocycline; Diabetes Insipidus; Female; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Polyuria; Sodium; Vasopressins; Water-Electrolyte Balance

The hypothalamic-neurohypophyseal system functions to maintain plasma osmolality within narrow limits. It also is an important mechanism in maintaining normal body fluid volume. The system exerts its influence via release or inhibition of vasopressin (antidiuretic hormone, ADH) which acts on the kidney to decrease water excretion. Deficiency of ADH is usually due to hypothalamic-neurohypophyseal lesions (central diabetes insipidus) or insensitivity of the kidney to ADH (nephrogenic diabetes insipidus). These patients, if untreated, have the predictable result of dehydration, hyperosmolality, hypovolemia, and eventual death in severe cases. On the other hand, ADH excess of the syndrome of inappropriate ADH secretion due to a variety of causes promotes water retention, hypoosmolality and hyponatremia which, if untreated, may progress to convulsions, coma, and death. It is obviously important to diagnose accurately these pathologic states of hydration. Not only is initiation of treatment in general dependent upon recognition of the disease, but each type of pathologic hydration state has specific treatment which rewards both patient and physician with effective correction of the problem.

Topics: Demeclocycline; Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Kidney; Pituitary Gland, Posterior; Vasopressins

Topics: Adult; Aged; Bronchiectasis; Chlorambucil; Cyclophosphamide; Demeclocycline; Diabetes Insipidus; Female; Humans; Lymphoma; Male; Pulmonary Fibrosis

Nephrogenic diabetes insipidus occurred in a 7-year-old child who had received a high dose of demethylchlortetracycline hydrochloride (DMC). The patient had a relatively elevated urinary sodium concentration in addition to isosthenuria. The nephrogenic diabetes insipidus was completely reversible within one month after cessation of DMC administration.

Topics: Child; Demeclocycline; Diabetes Insipidus; Diabetic Nephropathies; Humans; Male; Vasopressins

Topics: Benzothiadiazines; Chlorpropamide; Clofibrate; Demeclocycline; Diabetes Insipidus; Diuretics; Humans; Morphinans; Osmolar Concentration; Sodium Chloride Symporter Inhibitors; Syndrome; Vasopressins

Topics: Adult; Demeclocycline; Diabetes Insipidus; Female; Humans; Infertility, Female; Kidney Concentrating Ability

Topics: Acne Vulgaris; Acute Kidney Injury; Body Weight; Chemical and Drug Induced Liver Injury; Demeclocycline; Diabetes Insipidus; Drug Eruptions; Female; Gastrointestinal Diseases; Hematologic Diseases; Humans; Infections; Photosensitivity Disorders; Pregnancy; Tetracyclines; Time Factors

The physiologic factors involved in vaseopressin (ADH) release and action are reviewed with emphasis on the interaction between osmotic and volume stimuli to the discharge of ADH. Abnormalities in reception of stimuli to ADH release, and in the impaired synthesis and release of ADH, are reviewed in relation to the causes of diabetes insipidus, and information on the biochemical changes which have been described in patients with nephrogenic diabetes insipidus is also discussed. We summarize the pathologic lesions and associated diseases found in 54 of our patients with diabetes insipidus. Criteria for establishing the diagnosis of diabetes insipdus are reviewed with emphasis on the dehydration test, including the importance of measuring plasma osmolality at the conclusion of water deprivation. Treatment of diabetes insipidus is briefly discussed with emphasis on the use of DDAVP and oral agents. The syndrome of inappropriate ADH secretion (SIADH) is reviewed including our experience with 39 patients. The differential diagnosis of SIADH, including the value of water loading and the measurement of ADH levels, is discussed. We comment on treatment of these patients including the use of investigational drugs. Lastly, we review the pharmacologic features and clinical relevance of some drugs which alter the release and action of ADH.

Topics: Analgesics; Animals; Antidepressive Agents, Tricyclic; Antineoplastic Agents; Brain; Brain Neoplasms; Carbamazepine; Craniocerebral Trauma; Demeclocycline; Diabetes Insipidus; Diuresis; Diuretics; Humans; Lithium; Osmolar Concentration; Pituitary Gland, Posterior; Sodium Chloride; Sulfonamides; Sulfonylurea Compounds; Vasopressins

Topics: Demeclocycline; Diabetes Insipidus; Diabetes Mellitus; Diuretics; Fanconi Syndrome; Humans; Hypercalcemia; Kidney Concentrating Ability; Kidney Diseases; Lithium; Methoxyflurane; Nephrocalcinosis; Potassium Deficiency

We have studied the effects of demeclocycline on the water metabolism of a patient with the syndrome of inappropriate antidiuretic hormone (ADH) secretion who presented with a serum sodium concentration of 110 meq/litre. Free water clearance was studied before, during, and after treatment with demeclocycline. This study shows that demeclocycline (900 mg/day) can at least partially inhibit the action of ADH in the setting of tumor-induced ADH secretion, with the production of a reversible, partial nephrogenic diabetes insipidus, and with few or no side effects. Demeclocycline may be useful in the treatment of chronic inappropriate ADH secretion.

Topics: Carcinoma, Small Cell; Demeclocycline; Diabetes Insipidus; Humans; Hyponatremia; Kidney Diseases; Lung Neoplasms; Male; Middle Aged; Osmolar Concentration; Syndrome; Urine; Vasopressins

Topics: Adult; Biopsy; Bronchitis; Demeclocycline; Diabetes Insipidus; Female; Humans; Kidney Diseases; Middle Aged; Pneumococcal Infections

Topics: Acne Vulgaris; Adult; Demeclocycline; Diabetes Insipidus; Female; Gonorrhea; Humans; Male; Polyuria; Vasopressins

Topics: Adenylyl Cyclases; Animals; Cell Membrane; Cyclic AMP; Demeclocycline; Depression, Chemical; Diabetes Insipidus; Enzyme Induction; Epithelium; Fluorides; Humans; Kidney Concentrating Ability; Kidney Medulla; Kidney Tubules; Lithium; Nephrons; Osmolar Concentration; Phosphoric Diester Hydrolases; Potassium; Receptors, Cell Surface; Sodium; Stimulation, Chemical; Thiazoles; Vasopressins

Topics: Adenylyl Cyclase Inhibitors; Chlortetracycline; Cyclic AMP; Cytosol; Demeclocycline; Diabetes Insipidus; Humans; In Vitro Techniques; Kidney; Kidney Medulla; Phosphodiesterase Inhibitors; Protein Kinase Inhibitors; Tetracycline; Vasopressins

Topics: Adult; Demeclocycline; Diabetes Insipidus; Drug Resistance; Humans; Male; Polyuria; Thirst; Vasopressins

Topics: Adult; Demeclocycline; Diabetes Insipidus; Female; Humans; Kidney Diseases

Topics: Demeclocycline; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diagnosis; Drug Therapy; Humans; Kidney Diseases; Photosensitivity Disorders; Toxicology; Vasopressins