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At least 217 records · Page 12Linked to original sources
PubMed2001

Perioperative management of central diabetes insipidus in kidney transplantation.

Central diabetes insipidus is clinically masked in dialysis patients. We report a 12-year-old girl receiving a living-related donor graft for renal failure from Alport syndrome, in whom a craniopharyngioma had been resected 6 months before transplantation. Pretransplant evaluation had documented central hypothyroidism, growth hormone deficiency, and presumptive hypogonadotropic hypogonadism. The corticotropin-releasing factor test had been normal. Four hours after transplantation, urine output exceeded 1,000 ml/h without diuretic therapy. Serum sodium concentration was 155 mmol/l, serum osmolality 333 mmol/kg, and plasma antidiuretic hormone 4.9 ng/l, while urine osmolality was 233 mmol/kg. Desmopressin acetate was started by continuous intravenous infusion at 1 microgram/day. Serum electrolytes rapidly normalized, urine output stabilized at 2 l/day. The patient was discharged 4 weeks after transplantation with good allograft function, receiving intranasal desmopressin acetate 10 micrograms twice daily. Pre-existing central diabetes insipidus is unmasked after successful kidney transplantation, leading to rapid dehydration and hypernatremia, which can be prevented by prompt institution of desmopressin therapy.

Child↗
PubMedDate not supplied

Sleep deficits in rats with hereditary diabetes insipidus.

Interest in the Brattleboro diabetes insipidus rat has resurged with the recent increase in research on brain peptides. Various reports have suggested that in these rats, the impaired ability for memory consolidation is due essentially to a chronic lack of vasopressin. On the other hand, sleep stages and particularly the paradoxical phase of sleep have been shown to have a key role in the processes of learning and memory consolidation. Curiously, the possible involvement of sleep deficits in the impairment of memory function in the Brattleboro rat has never been suspected. Here I report a significant reduction (38%) in the daily duration of paradoxical sleep (PS) in the homozygous diabetes insipidus (HODI) rat compared to the heterozygous Long Evans strain. Normal or increased durations of PS were observed after intravenous (i.v.) administration of vasopressin but also when the normal daily water intake (240 ml) was infused i.v. These results provide direct evidence that PS deficits in the HODI rat are not due to the absence of vasopressin. They also suggest that the impaired ability for learning and memory processes are probably due to the impairment of PS rather than to some direct consequence of the hereditary lack of vasopressin.

Animals↗
PubMed1999

Nephrogenic diabetes insipidus in a dog with intestinal leiomyosarcoma.

Nephrogenic diabetes insipidus was diagnosed in a dog with an intestinal leiomyosarcoma. The diagnosis of nephrogenic diabetes insipidus was made on the basis of results of serum biochemical tests, urinalyses, and a water-deprivation test, along with a lack of response to exogenous administration of vasopressin following the water-deprivation test. The temporal association between resection of the intestinal mass and resolution of clinical signs of diabetes insipidus (i.e., polyuria and polydipsia) and between recurrence of clinical signs and detection of metastatic disease suggests that there may have been a causal relationship, and nephrogenic diabetes insipidus may have developed as a paraneoplastic syndrome in this dog.

Animals↗
PubMedDate not supplied

Diabetes insipidus and spinal cord injury: a challenging combination.

Diabetes insipidus is a life-threatening condition in which the kidneys excrete huge quantities of diluted urine. Diabetes insipidus as a sequela of head trauma is unusual, but not rare. When it arises in conjunction with a spinal cord injury (SCI), diabetes insipidus not only is life threatening but also raises challenges for bladder retraining. This article describes the pathogenesis, diagnosis, and management of diabetes insipidus. A case study is used to demonstrate the patient course and nursing implications, with emphasis on two nursing diagnoses: fluid volume deficit and alterations in urinary elimination.

Adult↗
PubMed1998

[Nephrogenic diabetes insipidus].

The syndrome of polyuria and polydipsia is practically identical in three very different disorders (central diabetes insipidus, nephrogenic diabetes insipidus, primary polydipsia). In congenital nephrogenic diabetes insipidus both the thirst mechanism and the production of the antidiuretic hormone are intact, but the hormone is ineffective in the kidney. The acquired form of the disease is caused most frequently by tubulointerstitial and urinary tract obstructive disorders as well as among the several drugs, lithium. In the differential-diagnosis the results of determinations related to the nomograms of normal interrelationships between osmolality and vasopressin in urine and plasma are used, besides the classical Carter-Robbins and indirect dehydration (Miller) tests. It has been postulated recently that in many cases the resistancy toward vasopressin is not absolute and these partially vasopressin sensitive patients can be treated successfully by thiazide, and potassium sparing compounds, antiprostaglandin pain killers (non-steroid antiinflammatory drugs) and first of all dDAVP as well as combinations of these preparations.

Diabetes Insipidus, Nephrogenic↗
PubMedDate not supplied

Diabetes insipidus as a presenting symptom of acute myelogenous leukemia.

This report describes a case of diabetes insipidus associated with acute myelogenous leukemia. An 11-year-old boy presented with fatigue, polydipsia and polyuria. His evaluation revealed a diagnosis of acute myelogenous leukemia FAB-M2, and a water deprivation test confirmed the diagnosis of central diabetes insipidus. His brain magnetic resonance imaging (MRI) showed a thickened, enhancing pituitary stalk with absence of the normal hyperintense signal in the posterior pituitary. He was treated with systemic chemotherapy, intensive intrathecal therapy, and 1,000 cGy to the pituitary. The patient achieved a remission but continued to need desmopressin therapy to control his diabetes insipidus. Diabetes insipidus is a rare complication of acute myelogenous leukemia that can be caused by leukemic infiltration of the pituitary. The diabetes insipidus is irreversible despite intensive systemic and central nervous system chemotherapy and radiation.

Child↗
PubMed1994

Nephrogenic diabetes insipidus associated with bilateral ureteral obstruction.

Nephrogenic diabetes insipidus associated with ureteral obstruction is rare. We report a case of nephrogenic diabetes insipidus associated with ureteral obstruction caused by ileal leiomyosarcoma in a 32-year-old man. The treatment with trichlorothiazide and diclofenac sodium reduced urine output from 8 L/day to 4 L/day. Six months after nephrostomy, urine output decreased to 2.5 L/day without any drug administration. This case suggests that ureteral obstruction may cause an increase in urine output to 8 L/day and that surgical treatment for ureteral obstruction is effective in reducing urine output in nephrogenic diabetes insipidus patients with ureteral obstruction.

Adult↗
PubMed1992

Diabetes insipidus.

OBJECTIVES: To review the pathophysiology, diagnosis, and treatment of the syndromes of diabetes insipidus with an emphasis on those situations likely to be encountered in the critical care setting. DATA SOURCES: Extensive clinical experience and relevant publications from the English literature identified via MEDLINE search, citation in reviews, publications of original data, and endocrine texts. STUDY SELECTION AND DATA EXTRACTION: Landmark papers pertaining to all aspects of diabetes insipidus were selected. Reviews, primary articles, and case reports pertaining to diabetes insipidus in the critical care setting were identified and selected according to their content of clinically useful information. DATA SYNTHESIS AND CONCLUSIONS: Diabetes insipidus may result from impaired synthesis and release of vasopressin from the hypothalamic-pituitary unit (neurogenic) or renal insensitivity to circulating vasopressin (nephrogenic). A number of interventions, diseases, and drugs commonly encountered in the critical care setting may result in the development or exacerbation of diabetes insipidus. The diagnosis of diabetes insipidus requires the exclusion of other causes of polyuria and a systematic demonstration of the response of homeostatic mechanisms to controlled dehydration. The treatment of diabetes insipidus depends on many factors, including the clinical setting, degree and pathophysiologic classification, ability of the patient to compensate for free water losses, and expected duration of the abnormality. Underlying disorders should be treated appropriately whenever possible.

Blood Volume↗
PubMed1993

Pathophysiology of transient cranial diabetes insipidus during pregnancy.

OBJECTIVE: We investigated the possible mechanisms underlying transient cranial diabetes insipidus during pregnancy. DESIGN AND PATIENTS: A woman who developed clinical diabetes insipidus during the third trimester of pregnancy was studied through a total of three pregnancies and postpartum. MEASUREMENTS: Plasma AVP, urine and plasma osmolality, urine volume and specific gravity were measured during water deprivation tests and hypertonic saline infusion. Plasma and urine osmolality were measured after subcutaneous injection of AVP. The water deprivation and AVP test were repeated after proven inhibition of urinary PGE2 with aspirin. Serum vasopressinase activity was measured during one of the pregnancies affected with diabetes insipidus and compared with that obtained between 26 and 38 weeks from 13 normal pregnancies. RESULTS: The patient was found to have cranial diabetes insipidus which responded to low dose intranasal 1-desamino-8-D-arginine vasopressin. Inhibition of PGE2 with aspirin did not enhance urine concentrating ability or the response to a test dose of subcutaneous AVP. Plasma levels of vasopressinase remained within the physiological range for normal pregnancy. CONCLUSIONS: These studies indicate that subclinical cranial diabetes insipidus may be unmasked in late pregnancy. This effect is not related to AVP resistance resulting from PGE2 production or excessive vasopressinase activity, but may be due to a combination of physiological vasopressinase secretion with reduced AVP secretory capacity and reduction in the thirst threshold that accompanies normal pregnancy. We relate these findings to a previously described group of women with transient diabetes insipidus during pregnancy who had impaired liver function.

Adult↗
PubMed1983

A comparison of diagnostic methods to differentiate diabetes insipidus from primary polyuria: a review of 21 patients.

Direct measurement of plasma AVP and indirect assessment of antidiuretic activity during standard dehydration tests were made in 21 polyuric and polydipsic patients to establish the efficacy of each method in determining the cause of polyuria. Patients with acquired nephrogenic diabetes insipidus (e.g. diabetes mellitus, renal failure, hypercalcaemia) were excluded from the study. Cranial diabetes insipidus was diagnosed by plasma AVP responses to osmotic stimulation during infusion of hypertonic 5% saline which were subnormal in 13 patients, 4 of whom had undetectable plasma AVP and 3 who had reduced but osmoregulated AVP release. Standard water deprivation tests confirmed cranial diabetes insipidus in all but 2 patients who were diagnosed as partial nephrogenic diabetes insipidus. The remaining 8 patients had normal, osmoregulated AVP secretion; the cause of their polyuria was determined by their renal response to desmopressin. Two patients had nephrogenic diabetes insipidus and 6 had primary polydipsia. The majority of polyuric patients could be accurately diagnosed by carefully performed dehydration tests. We suggest that direct measurements of plasma AVP during osmotic stimulation are only necessary to distinguish mild forms of cranial from nephrogenic diabetes, or to define precisely the characteristics of AVP secretion.

Adolescent↗
PubMed1981

Diabetes insipidus following cardiorespiratory arrest.

Diabetes insipidus (DI) and other features of hypothalamic dysfunction were observed in two patients resuscitated following cardio-respiratory arrest (CRA). Both patients also developed marked hyperglycemia probably related to hypertonic dehydration. The development of DI in survivors of CRA suggests severe hypothalamic hypoxic injury and poor prognosis.

Adult↗
PubMed1979

Diabetes insipidus in a cow.

Diabetes insipidus was diagnosed in a 6-year-old Holstein-Friesian cow with a history of recurrent fever, ketosis, lymphadenopathy, and inappetence. The diagnosis was based on the clinical findings, response to exogenous vasopressin, and lack of urine concentration in a water deprivation test. The disease gradually regressed over a period of 1 year and did not recur.

Animals↗
PubMed1989

Transient diabetes insipidus of pregnancy.

Transient diabetes insipidus (DI) is a disease of late pregnancy, that has been reported with increasing frequency. Although initially thought to be nephrogenic, the etiology of this syndrome is most likely excess vasopressinase activity. The disease is associated with preeclampsia with liver involvement. Infants of mothers with the syndrome are predominantly male. Management may be with deamino D arginine vasopressin (dDAVP) during gestation and postpartum since vasopressinase does not break down dDAVP. The copious urine output may disguise preeclampsia. Fluid restriction should be avoided as it will lead to dehydration and hemoconcentration.

Adult↗
PubMed1983

Reversal of 6-hydroxydopamine-induced hypotension in Long Evans and diabetes insipidus (Brattleboro) rats.

Brattleboro (diabetes insipidus) rats showed a delayed recovery from 6-hydroxydopamine (6-OHDA) hypotension as compared to Long Evans controls. A slight increase in circulating arginine vasopressin was noted in the 6-OHDA-treated Long Evans rats but no change in circulating oxytocin was apparent in either species. The haematocrit and plasma potassium suggested haemodilution in Long Evans rats following 6-OHDA treatment but no such changes were apparent in similarly treated Brattleboro rats. Since the major difference in Long Evans and Brattleboro rats is the latter's inability to synthesize arginine vasopressin (AVP), it is suggested that AVP may have a role in the restoration of homeostasis following 6-OHDA-induced hypotension. This conclusion is supported by (a) a delayed recovery from hypotension and (b) no change in blood concentration parameters, in the Brattleboro rat.

Animals↗
PubMed1987

Ultralow doses of vasopressin in the management of diabetes insipidus.

Management of postoperative diabetes insipidus (DI) frequently requires intermittent treatment with multiple subcutaneous injections of pituitrin or vasopressin, in doses averaging 20 IU/24 h. Use of a syringe pump for a continuous infusion of ultralow doses of pituitrin produced uniform, constant, and sustained reduction of urinary output, thus facilitating regular fluid replacement. Twelve patients with postoperative DI received iv pituitrin at a dose of 1.6 +/- 0.26 mIU/kg X h (1 to 2 IU/24 h). The antidiuretic effect began at the third hour of treatment, peaked by the sixth hour (diuresis of 37 ml/h, specific gravity of 1.018 +/- 0.002), and was sustained throughout infusion. Polyuria recurred 3 h after the infusion was discontinued; this rapid reversibility is highly advantageous when excessive fluid intake causes overhydration. Pressor effects were not observed during the treatment period.

Adolescent↗
PubMed1998

Diabetes insipidus in neurosurgical patients.

Diabetes insipidus (DI) is an uncommon but important complication in the neurosurgical population. This retrospective study aimed to determine the incidence, profile and outcome of patients admitted to an 18-bedded neurosurgical intensive care unit who developed DI. The overall incidence was 3.7% (29/792 admissions). Aetiologies included subarachnoid haemorrhage (12/29), severe head injury (11/29), post-surgical excision of craniopharyngioma or pituitary adenoma (5/29) and acute haemorrhagic stroke (1/29). All patients were treated with a regime of fluid replacement, electrolyte correction, parenteral or intranasal desmopressin (DDAVP), or parenteral pitressin. Overall mortality was 72.4%. There were no deaths in the patients who underwent excision of tumours. Complications included acute pulmonary oedema, hypernatremia and hypokalaemia. The development of DI was found to be associated with impending brain death and mortality in the majority of patients with subarachnoid haemorrhage and severe head injury. However, careful diagnosis and management of DI after hypothalamo-neurohypophyseal surgery did not result in any permanent neurological sequelae.

Adult↗
PubMed1982

Oral antidiuretic therapy: studies in the diabetes insipidus rat.

In hypothalamic diabetes insipidus, water balance is achieved primarily through the thirst mechanism. The administration of an antidiuretic agent in the drinking water should restore the antidiuretic response to volume and osmoregulatory drive. To test this hypothesis, homozygous Brattleboro strain rats were given arginine vasopressin (AVP) or 1-desamino-8-D-arginine vasopressin (dDAVP) in the drinking water in concentrations of 10-10,000 micrograms/l (AVP) and 5-10,000 micrograms/l (dDAVP). Oral AVP was found to be ineffective. Oral dDAVP resulted in 1) a progressive increase in dDAVP dose, from 2.3 to 2,559 micrograms.day-1.kg-1; 2) a dose-dependent increase in urine osmolality from 306 to 1,796 mosmol/kg; and 3) a dose-dependent decrease in urinary solute excretion. At each dDAVP dose level, stable physiological states were achieved within 24 h. Similar antidiuretic states were achieved when dDAVP was administered in increasing doses or when therapy was initiated at a high dose. These findings demonstrate that inclusion of an appropriate antidiuretic agent in the drinking water can restore the renal response to volume-osmoregulatory drive.

Administration, Oral↗