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PubMed2006

[Nephrogenic diabetes insipidus].

Nephrogenic diabetes insipidus which can be inherited or acquired, is characterized by an inability to concentrate urine despite normal or elevated plasma concentrations of the antidiuretic hormone, arginine-vasopressine (AVP). Polyuria, with hyposthenuria and polydipsia are the cardinal clinical manifestations of the disease. Hypercalcemia, hypokaliemia, lithium administration and chronic renal failure are the principal causes of acquired nephrogenic diabetes insipidus. About 90 percent of patients with congenital nephrogenic diabetes insipidus are males with X-linked recessive nephrogenic diabetes insipidus who have mutations in the arginine-vasopressin receptor 2 (AVPR2) gene that codes for the vasopressin V2 receptor. The gene is located in chromosome region Xq28. In about 10 percent of the families studied, congenital nephrogenic diabetes insipidus has an autosomal recessive or autosomal dominant mode of inheritance. In these cases, mutations have been identified in the aquaporin-2 gene (AQP2), which is located in chromosome region 12q13 and codes for the vasopressin-sensitive water channel. Other inherited disorders with mild, moderate or severe inability to concentrate urine include Bartter's syndrome and Cystinosis. Identification of the molecular defect underlying congenital nephrogenic diabetes insipidus is of immediate clinical significance because early diagnosis and treatment of affected infants can avert the physical and mental retardation associated with episodes of dehydration.

Diabetes Insipidus, Nephrogenic↗

PubMed2005

Metabotropic glutamate receptor (mGluR5) antagonist MPEP attenuated cue- and schedule-induced reinstatement of nicotine self-administration behavior in rats.

Previous studies suggested that metabotropic glutamate 5 (mGlu5) receptors play an important role in the reinforcing effects of abused drugs. The present experiments evaluated the effects of the mGlu5 receptor antagonist, MPEP (2-methyl-6-(phenylethynyl)-pyridine hydrochloride; 1-10 mg/kg, salt, i.p.), in rat models of nicotine-seeking behavior that may have relevance to relapse to drug-taking. Male Wistar rats (with restricted access to food) were trained to nose-poke to receive intravenous infusions of nicotine (0.03 mg/kg per infusion, base) under a fixed ratio 5 time out 60 s schedule of reinforcement. After stable nicotine self-administration was acquired, nose-poking behavior was extinguished in the absence of nicotine-associated cues. During the reinstatement test phase, independent groups of animals were exposed to: (a) response-contingent nicotine-associated cues (cue-induced reinstatement); or (b) response-noncontingent presentations of 45-mg food pellets under fixed time 2 min schedule (schedule-induced reinstatement). Additional control experiments were conducted to demonstrate that in nicotine-naïve animals MPEP does not affect cue-induced reinstatement of food-seeking behavior and has no effects on operant behavior maintained by a simple fixed interval 2 min schedule of food reinforcement. Pretreatment with MPEP (10 mg/kg) significantly attenuated the reinstatement of nicotine-seeking in both experiments. Further, MPEP (10 mg/kg) significantly attenuated polydipsia induced by a fixed time 2 min food schedule. In conclusion, the present findings indicate that the blockade of mGlu5 receptors attenuates cue-induced reinstatement of nicotine self-administration behavior (but not food-seeking) and may produce a general inhibition of schedule-induced behaviors, including schedule-induced nicotine-seeking.

Analysis of Variance↗

PubMed2004

Inflammatory pseudotumor of the pituitary: case report.

BACKGROUND: Inflammatory pseudotumor of the pituitary is a very rare nonneoplastic lesion. We describe a case of a patient with past history of lymphocytic meningitis. CASE DESCRIPTION: A 32-year-old man presented with polyuria, polydipsia, anorexia, abdominal discomfort, and panhypopituitarism. He had 2 episodes of lymphocytic meningitis in the last two years. Magnetic resonance image (MRI) disclosed a sellar and suprasellar mass with extension to the pituitary stalk. The patient underwent transnasal-transsphenoidal surgery to remove the lesion. Histopathological findings revealed mixed inflammatory cells composed mainly of lymphocytes, macrophages and extensive fibrosis. CONCLUSIONS: Inflammatory pseudotumor of the pituitary, although rare, should be included in the differential diagnosis of a sellar and suprasellar mass.

Adult↗

PubMed1997

Epidemiology, pathophysiology, and management of hyponatremic encephalopathy.

Hyponatremia is the most common electrolyte abnormality among hospitalized patients. Death or brain damage associated with hyponatremia has been described since 1935, and it is now evident that hyponatremia can lead to death in otherwise healthy individuals. In the past, it had been assumed that the likelihood of brain damage from hyponatremia was directly related to either a rapid decline in plasma sodium or a particularly low level of plasma sodium. Recent studies have demonstrated that other factors may be more important. These factors include the age and gender of the individual, with children and menstruant women the most susceptible. Although many clinical settings are associated with hyponatremia, those most often associated with brain damage are postoperative, polydipsia, pharmacological agents, and heart failure. Morbidity and mortality associated with hyponatremia are primarily a result of brain edema, hypoxemia, and associated hormonal factors. Management of hyponatremia is largely determined by symptomatology. If the patient is asymptomatic, discontinuation of drugs plus water restriction is often sufficient. If the patient is symptomatic, active therapy to increase the plasma sodium with hypertonic NaCl is usually indicated. Although inappropriate therapy of hyponatremia can lead to brain damage, such an occurrence is rare. Thus, the risk of not treating a symptomatic patient for exceeds that of improper therapy.

Brain Diseases, Metabolic↗

PubMed1998

Nephrogenic diabetes insipidus.

In nephrogenic diabetes insipidus, the kidney is unable to concentrate urine despite normal or elevated concentrations of the antidiuretic hormone arginine vasopressin (AVP). In congenital nephrogenic diabetes insipidus (NDI), the obvious clinical manifestations of the disease, that is polyuria and polydipsia, are present at birth and need to be immediately recognized to avoid severe episodes of dehydration. Most (>90%) congenital NDI patients have mutations in the AVPR2 gene, the Xq28 gene coding for the vasopressin V2 (antidiuretic) receptor. In <10% of the families studied, congenital NDI has an autosomal recessive inheritance and mutations of the aquaporin-2 gene (AQP2), ie, the vasopressin-sensitive water channel, have been identified. When studied in vitro, most AVPR2 mutations lead to receptors that are trapped intracellularly and are unable to reach the plasma membrane. A minority of the mutant receptors reach the cell surface but are unable to bind AVP or to trigger an intracellular cyclic adenosine-monophosphate (cAMP) signal. Similarly AQP2 mutant proteins are trapped intracellularly and cannot be expressed at the luminal membrane. The acquired form of NDI is much more common than the congenital form, is almost always less severe, and is associated with downregulation of AQP2. The advances described here are examples of "bedside physiology" and provide diagnostic tools for physicians caring for these patients.

Aquaporins↗

PubMed1995

Combined fractional excretion of sodium and urea better predicts response to saline in hyponatremia than do usual clinical and biochemical parameters.

BACKGROUND: The treatment of hyponatremic patients requires physicians to make a therapeutic choice between saline infusion and water restriction. Therefore, they need readily available and reliable parameters to facilitate making that choice. This study was designed to determine whether the use of clearance ratios can help clinicians recognize saline-responding hyponatremic patients. PATIENTS AND METHODS: Thirty-five nonedematous, hospitalized, hyponatremic patients were classified according to their history and saline response into four groups: diuretic-taking patients, polydipsic patients, saline responders, and saline nonresponders. Within these four groups, clinical and biochemical volume-related parameters, including clearance ratios, were prospectively evaluated before infusion of 2 L isotonic saline. Clearance ratios as well as usual clinical and biochemical parameters were tested for their accuracy in predicting saline responsiveness. RESULTS: Both positive (70%) and negative (54.5%) predictive values for hypovolemia were unsatisfactory; clinical prediction of hypovolemia was also characterized by low sensitivity (41.1%), but acceptable specificity (80%). In the polydipsia and saline-nonresponder groups, plasma urea and uric acid values tended to be lower than in the diuretic and saline-responder groups. However, the usefulness of these parameters was limited by too large an overlap among the different groups. In both polydipsic patients and saline responders, urinary sodium concentration was low. The combined amount of urinary sodium and potassium in relation to plasma sodium did not discriminate among the different groups. Most helpful in distinguishing among the groups was a combination of several clearance ratios (fractional excretions of sodium, potassium, urea, and uric acid), since the predictive use of each parameter on its own was restricted. The best indicator of saline responsiveness was a low fractional excretion of filtered sodium (< 0.5%) combined with a low fractional excretion of urea (< 55%). CONCLUSION: The accuracy of clinical evaluation for predicting the state of extracellular fluid volume in hyponatremia is low. The combination of low fractional sodium excretion (< 0.5%) and low fractional urea excretion (< 55%) is the best biochemical way to predict saline response, whereas high fractional potassium excretion (> 20%) indicates diuretic intake.

Aged↗

PubMed2005

[Pituitary tuberculosis: a case report].

Through a case of sellar and suprasellar tuberculoma which presented with central diabetes insipidus, the authors report the frequency of pituitary tuberculoma, its physiopathology, clinical presentation hormonal and radiological findings thus management and evolution. A 42 years old woman, with a history of erythema nodosum, presented with polyuria polydipsia (PUPD), amenorrhea and galactorrhea. Endocrine investigations showed central diabetes insipidus, elevated serum prolactin levels and cortisol failure. Magnetic resonance imagining scans (MRI) revealed a nodular thickening of the pituitary enlargement and loss of posterior pituitary hypointensity signal. Etiologic inquiry has removed the diagnosis of sarcoidosis, Langerhan's histosis, autoimmune hypophysitis and sellar metastasis. The history of erythema nodosum, the positivity of tuberculin skin test and the presence of koch bacillus in the bronchial fluid after culture led to a diagnosis of tuberculosis. Treatment was started with four drug antitubercular chemotherapy regimen for 2 months, and tow drug antitubercular chemotherapy regimen for 16 months. This treatment is associated with hydrocortisone, desmopressin nasal spray and bromocriptine. Under treatment, there was an improvement in clinical condition, disapearence of headache, PUPD and galactorrhea thus normalization of prolactin. A follow-up MRI, 8 months later, showed that pituitary lesion has been completely removed, suggesting our clinical and biology presumption. Pituitary tuberculosis is rare, however, when encountered, they may present a diagnostic difficulty. Accurate diagnosis and management is important because pituitary tuberculoma is curable.

Adult↗

PubMed2006

[Panhypopituitarism revealing metastasis of small-cell lung carcinoma associated with sarcoidosis].

Pituitary metastasis and sarcoidosis are two causes of pituitary stalk thickening. Their association has been described ago three decades. In this setting, we report a case of panhypopituitarism revealing pituitary metastasis from a small-cell lung carcinoma associated with sarcoidosis. A 49 year-old smoking patient with type 2 diabetes was admitted for acute adrenal failure with polyuria polydipsia syndrome and a pituitary tumor syndrome. Hormone explorations confirmed anterior pituitary insufficiency. Water restriction revealed central diabetes insipidus. The hypothalamic-pituitary MRI revealed a 1-cm sellar mass with nodular thickening of the stalk. The chest radiograph showed a heterogeneous opacity in the left lung. The thoraco-abdominal scan demonstrated a mass in the left lung highly suggestive of malignancy and many enlarged mediastinal nodes, hepatic nodules, and hypertrophy of the left adrenal. Bronchoscopy was performed three times and showed infiltration of the left bronchial tree but histological examination of the bronchial biopsies was negative for all samples. Ultrasound-guided biopsy of the liver was achieved and histology demonstrated sarcoidosis. The diagnosis of sarcoidosis was incompatible with the deterioration of the patient's general status. Subsequent radiographic explorations showed an increase in the size of the tumor mass and histological evaluation of a scan-guided trans-thoracic biopsy demonstrated small-cell carcinoma. Small-cell lung carcinoma is the most common cancer with pituitary metastasis. The proposed link between sarcoidosis and malignancy has remained controversial but has not been proven false.

Adrenal Gland Diseases↗

PubMed1996

Characterization of endothelin receptors in streptozotocin-induced diabetic rat vas deferens.

As there is increasing evidence that diabetes induces changes in the plasma levels of endothelins (ETs) and in the properties of ET receptors in peripheral tissues, and as there are reports indicating the presence of significant amounts of ET receptors in mammalian vasa deferentia, we studied possible alterations in ET receptor characteristics in the vasa deferentia of the following groups of rats: 8 weeks diabetic (D8), 8 weeks age-matched control (C8), 16 weeks diabetic (D16), 16 weeks diabetic-insulin-treated (started 8 weeks after the onset of diabetes) (DI16), and 16 weeks age-matched control (C16). Diabetes was induced by the i.v. injection of 65 mg/kg streptozotocin (STZ). Diabetic rats had hyperglycemia, hypoinsulinemia, glucosuria, polydipsia, and polyuria and had smaller vasa deferentia than control and diabetic-insulin-treated animals. Receptor binding experiments with [125I]ET-1 demonstrated that the densities of ET receptors in vasa deferentia from D8, C8, D16, DI16, and C16 animals were 377 +/- 11, 255 +/- 24, 315 +/- 18, 210 +/- 12, and 214 +/- 7 fmol/mg of protein, respectively. [125I]ET-1 binding to the ET receptors was inhibited by ET-1 (non-selective), BQ 610 (ETA selective), ET-3 (ETC selective), and IRL 1620 (ETB selective) with the following rank order of Ki values: ET-1 < BQ 610 < ET-3 < < IRL 1620. The pharmacological profile of the ET receptors was similar in all groups and was consistent with the predominance of the ETA receptor subtype in the rat vasa deferentia. Our data indicate that experimental diabetes up-regulates the density of ET receptors in the rat vasa deferentia and that the receptor up-regulation is reversed by insulin treatment.

Animals↗

PubMed1997

Anterior medial temporal lobe volumes in polydipsic schizophrenic patients with and without hypo-osmolemia: a pilot study.

The volume of certain brain structures, particularly those in the anterior medial temporal lobe, may be reduced to a greater extent in hyponatremic/hypo-osmolemic polydipsic schizophrenics than other schizophrenic patients. To explore if volume reduction is specific to this particular brain region, and if it is fundamentally associated with polydipsia, we imaged the anterior hippocampi/subicula and adjacent temporal lobes in normal males (n = 10) and polydipsic schizophrenic patients with (n = 7) and without (n = 6) hypo-osmolemia. Bilateral hippocampal/subicular (p < .01), but not temporal lobe (p < .30), volumes were diminished in the hypo-osmolemics relative to the other two groups, who resembled each other on these measures. No recognized or putative factor could explain these findings. Thus anterior medial temporal lobe structures appear to be preferentially diminished in hypo-osmolemic polydipsic schizophrenics. Additional studies are needed to more precisely define these anatomic differences and their relationship to these patients' impaired water excretion and severe mental illness.

Adult↗

PubMed1997

Atropine decreases drinking but not feeding and induces less hypothalamic acetylcholine release in diabetic rats.

Drinking, feeding and hypothalamic extracellular acetylcholine (ACh) release was measured before and after the administration of several doses of atropine sulfate in streptozotocin (STZ)-diabetic and normal rats. Drinking but not feeding was dose-relatedly decreased by i.p. or intrahypothalamic injections of atropine in STZ-diabetic rats. Hypothalamic ACh release, as measured by microdialysis, increased less (dose-related) in diabetic than normal rats following an i.p. administration of atropine. Ach basal levels were the same in both groups. These results are discussed in terms of a hyperactive hypothalamic cholinergic (muscarinic) system involved in the diabetic polydipsia.

Acetylcholine↗

PubMed2001

Clozapine-induced Fos-protein expression in rat forebrain regions: differential effects of adrenalectomy and corticosterone supplement.

Unlike classical antipsychotic drugs, clozapine activates the hypothalamo-pituitary-adrenal axis and induces a specific regional pattern of Fos-protein expression in the rat forebrain. Whether corticosterone plays a role in the clozapine-induced Fos response is the subject of this study. Some rats were adrenalectomized and in a number, including intact animals, a corticosterone pellet (100 mg s.c.) was implanted; after 1 week, a single dose of clozapine (20 mg kg(-1) i.p.) was administered. The clozapine-induced Fos response was not affected by adrenalectomy, apart from the nucleus accumbens shell, the subfornical organ and the supraoptic nucleus; there was an increased response in the nucleus accumbens shell, while other regions showed less Fos immunoreactivity. Implantation of the corticosterone pellet in both sham-operated and adrenalectomized animals, reduced the clozapine-induced Fos responses strongly in the hypothalamic paraventricular nucleus, the subfornical organ and possibly in the prefrontal cortex; in the supraoptic nucleus, this effect was seen only in intact animals. The effect of clozapine on plasma corticosterone levels was also diminished by supplemental corticosterone treatment. These results imply that the effects of clozapine are partially dependent upon hypothalamo-pituitary-adrenal axis integrity and activation. The efficacy of clozapine in the treatment of polydipsia and hyponatremia in chronic psychiatric patients may involve clozapine-mediated activation of the cellular activity in the subfornical organ.

Adrenalectomy↗

PubMed1996

Conn syndrome in a child, caused by adrenal adenoma.

Hyperaldosteronism owing to aldosterone-producing adenoma (Conn syndrome) is a rare but potentially curable form of pediatric hypertension. The authors report on a 5-year-old girl who had symptoms of polyuria, polydipsia, and fatigue, and for whom the diagnosis of hyperaldosteronemia was suggested by a low serum potassium level and persistent hypertension. The diagnosis was confirmed by increased levels of plasma aldosterone and decreased levels of plasma renin. The tumor was localized with ultrasonography and computed tomography, which showed a 2-cm mass in the left adrenal gland. The left adrenal gland was excised, and pathological assessment showed an adenoma. Only 14 other pediatric cases (< 16 years of age) have been reported in the English-language literature.

Adenoma↗

PubMed1992

Use of calcium excretion values to distinguish two forms of primary renal tubular hypokalemic alkalosis: Bartter and Gitelman syndromes.

Clinical or biochemical findings were reevaluated in 34 pediatric patients with primary renal tubular hypokalemic metabolic alkalosis. The patients were subdivided into two groups. Bartter syndrome (primary renal tubular hypokalemic metabolic alkalosis with normocalciuria or hypercalciuria) was diagnosed in 18 patients with molar urinary calcium/creatinine ratios greater than 0.20, and Gitelman syndrome (primary renal tubular hypokalemic metabolic alkalosis with magnesium deficiency and hypocalciuria) was diagnosed in 16 patients with molar urinary calcium/creatinine ratios less than or equal to 0.20 and plasma magnesium levels less than 0.75 mmol/L. Some clinically important differences between the groups were observed. Patients with Bartter syndrome were often born after pregnancies complicated by polyhydramnios (8/18) or premature delivery (7/18) and had short stature (11/18) or polyuria, polydipsia, and a tendency to dehydration (16/18) during infancy (12/18) or before school age (18/18). Patients with Gitelman syndrome had tetanic episodes (12/16) or short stature (3/16) at school age (14/16). We conclude that the Bartter and Gitelman syndromes represent two distinct variants of primary renal tubular hypokalemic metabolic alkalosis and are easily distinguished on the basis of urinary calcium levels.

Alkalosis↗

PubMed1994

Nephrocalcinosis in pseudohypoaldosteronism and the effect of indomethacin therapy.

We report four patients with pseudohypoaldosteronism, aged 5 months to 5 years. All patients had hypercalciuria and three had nephrocalcinosis. Two patients with nephrocalcinosis were treated with indomethacin. Polydipsia decreased and appetite and weight gain improved within 14 days of therapy. Hypercalciuria, polyuria, and creatinine clearance decreased 30% to 50% and urinary prostaglandin E2 levels decreased fourfold to eightfold.

Calcium↗

PubMed1994

Temporal changes in rabbit urinary bladder function and DNA synthesis during chronic treatment with furosemide.

In a preliminary study we showed that 14 days of furosemide infusion in rabbits caused increases in bladder mass and contractile responses of bladder body strips to field stimulation, bethanechol, ATP and KCl. The present study investigated the temporal effects of furosemide-induced diuresis on micturition, bladder mass, bladder wall proliferation activity and DNA synthesis. In addition, contractile responses of bladder body strips were monitored. Furosemide-containing osmotic pumps were implanted in male New Zealand White rabbits. Micturition was monitored for 7 days. Biochemical analyses were done 3, 7 and 14 days after implantation. Contractile responses were measured at 3 and 7 days. Polyuria and polydipsia started within 1 day after implantation of furosemide-containing osmotic pumps and continued at the same level for 7 days. Bladder mass was significantly increased at 3 and 7 days. Diuresis stimulated 3H-thymidine uptake and caused an increase in bladder DNA concentration at 3 days. However, both DNA concentrations and 3H-thymidine levels returned to control levels by 7 days. Contractile responses to field stimulation and agonists were increased at 7 days but unchanged at 3 days. The data confirm that modest increases in bladder mass and the ensuing increases in contractile function are a normal and beneficial physiological response to diuresis.

Adenosine Triphosphate↗

PubMed1988

Polyuric urinary tract dilatation with renal damage.

Polyuria of diabetes insipidus and psychogenic polydipsia can produce massive dilatation of the urinary tract in the absence of any mechanical obstruction. Renal failure in these cases is rare. We report the second case of nephrogenic diabetes insipidus with nonobstructive hydronephrotic renal damage. Temporary suprapubic drainage restored renal function to normal and decreased the upper tract dilatation. Renal function has been preserved for more than 10 years. Surgical intervention beyond temporary vesical drainage is unnecessary.

Child↗

PubMed1980

Polyuric megalocystis.

We diagnosed and treated 5 children with huge bladders and hydroureteronephrosis secondary to polyuria, resulting from either familial nephrogenic diabetes insipidus, medullary cystic disease, central diabetes insipidus secondary to panhypopituitarism or psychogenic polydipsia. Polyuria was documented by the measurement of 24-hour urine volumes. The possibility of anatomic and physiologic outlet obstruction was eliminated by flowmetry, voiding cystourethrography and endoscopy.

Adolescent↗