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A case of transient vasopressin-resistant diabetes insipidus is reported, which developed during the seventh month of pregnancy and remitted postpartum. The patient was resistant to large doses of deamino-D-arginine vasopressin as well as to aqueous pitressin. She was treated with hydrochlorothiazide. Evidence that prostaglandins may play a role in this syndrome is discussed.
A 20-yr-old male was found to have diabetes insipidus is association with panhypopituitarism but without any focal neurological lesion being identified. He was initially treated with steroid supplements, the features of diabetes insipidus being controlled with a thiazide diuretic. Eighteen months later the patient lost thirst sensation and stopped treatment, subsequently being re-admitted with severe dehydration, oliguria and focal neurological signs. Further investigation, including brain biopsy, confirmed the presence of an atypical pinealoma which was considered inoperable. Measurements of plasma antidiuretic hormone (ADH) and angiotensin II (AII) concentrations during the severe dehydration showed very high levels of AII, but inappropriately low plasma ADH levels for the severity of dehydration. We consider that the evidence obtained from this case supports the view that the oliguria with hypertonic urine present during severe dehydration was due to a direct renal action of the very high AII levels, possibly supplemented by the residual ADH secretion.
Thiazides have been used in patients with nephrogenic diabetes insipidus (NDI) to decrease urine volume, but the mechanism by which it produces the paradoxic antidiuretic effect remains unclear. Previous studies have reported that downregulation of aquaporin-2 (AQP2) is important for the development of lithium-induced (Li-induced) polyuria and that hydrochlorothiazide (HCTZ) increases renal papillary osmolality and Na(+) concentration in Brattleboro rats. For elucidating the molecular basis of the antidiuretic action of HCTZ in diabetes insipidus, whether administration of HCTZ may affect the expression of AQP2 and major renal Na(+) transporters in Li-induced NDI rats was investigated, using semiquantitative immunoblotting and immunohistochemistry. After feeding male Sprague-Dawley rats Li chloride-containing rat diet for 4 wk, HCTZ or vehicle was infused subcutaneously via osmotic minipump. Urine output was significantly decreased by HCTZ treatment, whereas it was not changed in vehicle-treated rats. Urine osmolality was also higher in HCTZ-treated rats than in vehicle-treated rats. Semiquantitative immunoblotting using whole-kidney homogenates revealed that HCTZ treatment caused a significant partial recovery in AQP2 abundance from Li-induced downregulation. AQP2 immunohistochemistry showed compatible findings with the immunoblot results in both cortex and medulla. The abundances of thiazide-sensitive NaCl co-transporter and alpha-epithelial sodium channel were increased by HCTZ treatment. Notably, HCTZ treatment induced a shift in molecular weight of gamma-epithelial sodium channel from 85 to 70 kD, consistent with previously demonstrated aldosterone stimulation. The upregulation of AQP2 and distal renal Na(+) transporters in response to HCTZ treatment may account for the antidiuretic action of HCTZ in NDI.
The juxtaglomerular apparatus (JGA) of rats with hereditary hypothalamic diabetes insipidus (DI) was studied. Plasma concentration of renin and angiotensin II, as well as serum sodium concentration and serum osmolality of DI rats are elevated. The morphological examination reveals no characteristic alteration of the epitheloid cells. The results show that the epitheloid cells are sufficiently adapted for the higher release of renin.
A transition of G to A at nucleotide position 279 in exon 1 of the vasopressin gene has been identified in patients with familial central diabetes insipidus. The mutation predicts an amino acid substitution of Thr (ACG) for Ala (GCG) at the COOH terminus of the signal peptide in preprovasopression (preproVP). Translation in vitro of wild-type and mutant mRNAs produced 19-kD preproVPs. When translated in the presence of canine pancreatic rough microsomes, wild-type preproVP was converted to a 21-kD protein, whereas the mutant mRNA produced proteins of 21 kD and 23 kD. NH2-terminal amino acid sequence analysis revealed that the 21-kD proteins from the wild-type and the mutants were proVPs generated by the proteolytic cleavage of the 19-residue signal peptide and the addition of carbohydrate. Accordingly, mutant preproVP was cleaved at the correct site after Thr-19, but the efficiency of cleavage by signal peptidase was < 25% that observed for the wild-type preproVP, resulting in the formation of a predominant glycosylated but uncleaved 23-kD product. These data suggest that inefficient processing of preproVP produced by the mutant allele is possibly involved in the pathogenesis of diabetes insipidus in the affected individuals.
A 68 year old man developed cranial diabetes insipidus 3 years after the diagnosis of myelofibrosis, coincident with a marked increase in nucleated cell count. No mass lesion was demonstrable on computed tomographic or magnetic resonance imaging. It is suggested that hypothalamic damage was caused by local infiltration or infarction, a complication of myelofibrosis which has not previously been reported.
A fourteen-year male patient presented a retrochiasmatic craniopharyngioma. Aer transcranial surgical resection, the patient had diabetes insipidus, which presented an interphase with manifestations of inadequate secretion of ADH. The patient was adequately treated with intranasal desmopresin, but aer i.v. fluid replacement was withdrawn, severe dehydration occurred. This was attributed to loss of the thirst reflex, due to surgical lesion of the lamina terminalis, where the osmoreceptor neurons are located. This case underscores the complications with body fluids and osmolality which may occur after surgery of hypothalamic lesions; i.e. diabetes insipidus (which may have a triphasic course), and adipsia, an infrequent complication due to absence of thirst.
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The etiology, diagnosis and management of lithium-induced diabetes insipidus (LIDI) is discussed, including the presentation of a case report. It is suggested that lithium provokes LIDI by decreasing the responsive ness of the kidney to the antidiuretic hormone. Lithium-induced polyuria may be managed by concomitant treatment with a thiazide diuretic or discontinuation of the lithium. Caution must be employed, however, when using thiazides with lithium as these diuretics decrease renal clearance of lithium.
Hypothalamo-hypophyseal metastases are still a relatively unfamiliar entity. Mostly they are confirmed by autopsy. Rear clinical manifestations are presented by diabetes insipidus. In general, patients with endocrine breast carcinoma metastases are young, premenopausal women, with great tumour burden and widely disseminated tumor. We report 54-year-old woman with diabetes insipidus caused by solitary breast carcinoma metastasis, eight years after primary tumour was diagnosed. The operative and radiation therapy were effective.
The triad of diabetes insipidus (DI), monosomy 7, and acute myeloid leukemia in a 7-year-old boy is described. This triad has been described in adults but not in children. The DI ran a transient, self-limiting course and required no specific therapy. The pathogenesis of DI remains unknown, and its transient nature may result in this component of the triad going unnoticed.
Langerhans' cell histiocytosis (LCH) is a proliferative disease of Langerhans' cells that has multiple clinical manifestations including diabetes insipidus (DI). This study reviews the effectiveness of hypothalamic-pituitary radiation therapy (HPRT) as a treatment of LCH-induced DI in the modern era. A retrospective review was done of 116 pediatric patients with LCH seen from 1975 to 1992. Seventeen of the 116 patients (15%) were diagnosed with complete or partial diabetes insipidus. Diagnosis was made either by water deprivation test or on clinical grounds. Fourteen patients received hypothalamic-pituitary irradiation as treatment for DI. The median interval from the onset of DI symptoms (polyuria and polydipsia) to treatment was 30 days. The median interval from the onset of diagnosis to treatment was 4 days. With a mean follow-up of 7.3 years (range, 2.4-14.3), only two patients had a complete response to therapy, as defined as no need for antidiuretic hormone (ADH) replacement therapy. No patient had a partial response, defined as a decrease in the dose of ADH replacement. Of the two responders, neither had a complete ADH deficiency, suggesting "early" disease. In addition, both received RT within 3 days. We feel that the standard treatment of RT to all patients with LCH-induced DI is no longer justified. Our series has shown no benefit in treating patients with a long history of DI. Rather, an improved rationale would be rapid initiation of hypothalamic-pituitary irradiation in patients with new symptoms of DI and an abnormal water deprivation test.
We report the cases of two children with cranial diabetes insipidus who were treated with lamotrigine for seizures and who had accompanying changes in desmopressin requirements. Lamotrigine is a new anticonvulsant chemically unrelated to other existing antiepileptic drugs. Studies suggest it acts at voltage-sensitive sodium channels and also decreases calcium conductance. Both of these mechanisms of action are shared by carbamazepine, which can cause hyponatraemia secondary to inappropriate secretion of antidiuretic hormone. It is possible that the effect of lamotrigine on fluid balance in the cases described is also centrally mediated.
Brattleboro strain rats homozygous for hypothalamic diabetes insipidus (DI rat) excrete nearly their body weight per day in dilute urine and yet can form bladders stones composed of struvite and apatite. Studies were undertaken to investigate this apparent paradox. The results show that DI rat urine is indeed undersaturated with respect to struvite and apatite. However, chronic infection of DI rat urine with a urease-containing organism (Proteus mirabilis) results in the rapid formation of large struvite/apatite bladder stones. It is concluded that the Brattleboro strain DI rat, like man and unlike other rats, forms struvite/apatite calculi only in the presence at chronic urinary tract infection.
Thirteen patients aged 1 to 59 years hospitalized for diabetes insipidus (DI) were investigated by computed tomography (CT). Apart from one craniopharyngioma, CT revealed in 8 out of 12 cases several modifications in the hypothalamic-pituitary region. In this group, CT demonstrated a small, round, isodense mass in the chiasmatic cistern that enhanced after contrast medium injection. Coronal and sagittal reconstructions helped pinpoint the lesion in the infundibulum and pituitary stalk, and, in one case, in the supraoptic nuclei. These findings, and the noninvasiveness of CT, make this technique one of the most accurate means of radiological investigation of DI and also of determining the efficacy of therapy.
A case of transient vasopressin-resistant diabetes insipidus is reported which developed during the seventh gestational month. Polyuria reached 4-6 L daily and urine osmolality remained dilute despite 21 hours of water deprivation followed by 5 U intramuscularly of aqueous pitressin, as well as four days of treatment with intranasal DDAVP (0.1-0.5 mL every 12 hours). Urinary excretion of prostaglandin E2, 1384 ng/24 hours, was fourfold that in nongravid subjects and a plasma arginine vasopressin level of 12 pg/mL was recorded. Indomethacin had no effect on urine osmolality but decreased urine volume markedly. Hydrochlorothiazide, also, decreased urine volumes, and this drug was used to manage the patient until delivery. The syndrome remitted in the puerperium, the patient concentrating her urine to 938 mOsm/kg when tested several months postpartum.
More detailed examinations of the pituitary gland in central diabetes insipidus (CDI) has been possible with magnetic resonance imaging (MRI). Compared to the high signal findings in the posterior lobes of normal subjects, the absence of such signal in adults and children with primary CDI has been reported. Familial CDI is a hereditary form of primary CDI with a variety of clinical expressions among affected individuals which is said to be related to varying degrees of an arginine vasopressin (AVP) deficiency. However, the structural correlates have yet to be documented by MRI technique. This report describes the pituitary gland MRI findings (using a superconducting magnet; 3 mm-slice thickness; spinecho, repetition time 400 ms, echo time 25 ms) in five patients in one family with familial CDI. A signal of high intensity was detected in the posterior part of the pituitary gland in 2 patients but not in 3 others. We concluded that MRI of the posterior pituitary lobe in familial CDI seem to vary in members of the same family.