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At least 19 recordsLinked to original sources

[Massive natriuresis and polyuria after triple craniocervical subarachnoid hemorrhage: cerebral salt wasting syndrome?].

A thirty-year-old male patient suffered subarachnoidal haemorrhage from an angioma positioned in the cranio-cervical transition. After rebleeding twice the patient developed a hydrocephalus internus malresorptivus and excessive natriuresis and polyuria, accompanied by depressed renin activity and extremely low aldosterone plasma levels. Neither fluid restriction and sodium substitution, nor administration of hydro-chlorothiazide/indomethacin affected natriuresis and polyuria. It was only after treatment with fludrocortisone-acetate/hydrocortisone that hyponatraemia and polyuria were resolved. At the same time a ventriculo-peritoneal shunt was applied. Differential diagnosis excluded the syndromes of inadequate antidiuretic hormone secretion, renal and cerebral diabetes insipidus, osmotic receptor hypofunction, chronic renal dysfunction and tubular necrosis. Natriuresis and polyuria developed under dexamethasone therapy. Since patient history, physical examination and laboratory criteria could not explain the electrolyte and fluid imbalance, this might be attributed to the hydrocephalus. Similar disturbances have been reported from other patients with intracranial disorders. Mechanical pressure exercised on the hypothalamus might cause the disturbance of fluid and sodium balance. Assuming a cerebral salt wasting syndrome, a putative natriuretic factor coming from the brain or an imbalance in the cerebral renin-angiotensin-system, as described in rats and dogs, must be discussed.

Adult

Mechanism of inappropriate polyuria in septic patients.

Inappropriate polyuria leading to hypovolemia and hypotension occurs frequently in severely septic patients. It's etiology was studied in three patients with polyuria and systolic hypotension. Glomerular filtration rate and renal blood flow were measured by the standard renal clearance techniques. Renal blood flow distribution to the outer cortex, inner cortex-outer medulla, and the inner medulla were measured by radioactive xenon. The glomerular filtration rate, renal blood flow, and renal blood flow distribution were normal. Polyuria does not result from a maldistribution of renal blood flow. Antidiuretic hormone did not alter the polyuric syndrome. These data suggest that sepsis produces a blockade at either the distal tubule or the collecting duct, thereby preventing salt and water conservation. This blockade may be due to either a toxin or a toxic metabolic breakdown product of sepsis.

Adult

On the mechanism of polyuria in potassium depletion. The role of polydipsia.

The association of potassium (K) depletion with polyuria and a concentrating defect is established, but the extent to which these defects could be secondary to an effect of low K on water intake has not been systematically investigated. To determine whether hypokalemia has a primary effect to increase thirst and whether any resultant polyuria and polydipsia contribute to the concentrating defect, we studied three groups of rats kept in metabolic cages for 15 days. The groups were set up as follows: group 1, normal diets and ad lib. fluids (n = 12); group 2, K-deficient diet on ad lib. fluids (n = 12); and group 3, K-deficient diet and fluid intake matched to group 1 (n = 14). Daily urine flow and urinary osmolality of groups 1 and 3 were not significantly different throughout the study. In contrast, as of day 6, group 2 rats consistently had a higher fluid intake (P < 0.0025), higher urine flow (P < 0.001), and lower urinary osmolality (P < 0.001) than the other two groups. These alterations in fluid intake and urine flow preceded a defect in maximal concentrating ability. On day 7, maximal urinary osmolality was 2,599+/-138 msmol/kg in rats on K-deficient intake and 2,567+/-142 msmol/kg in controls. To determine whether this primary polydipsia is itself responsible for the development of the concentrating defect, the three groups of rats were dehydrated on day 15. Despite different levels of fluid intake, maximal urinary osmolality was impaired equally in groups 2 and 3 (1,703 and 1,511 msmol/kg, respectively), as compared to rats in group 1 (2,414 msmol/kg), P < 0.001. We therefore conclude that K depletion stimulates thirst, and the resultant increase in water intake is largely responsible for the observed polyuria. After 15 days of a K-deficient diet, the impaired maximal urinary concentration in hypokalemia, however, was not related to increased water intake, since fluid restriction did not abolish the renal concentrating defect.

Animals

Polyuria in childhood.

Polyuria may result from either a water or a solute diuresis. Although the history and physical examination may provide clues to the cause of the polyuria, the definitive diagnosis requires laboratory tests which focus on the osmolality of the urine and serum in combination with the urine volume and the rate of excretion of osmoles. An isoosmolar or hyperosmolar urine is found in children with a solute diuresis or in normal children, whereas a hypoosmolar urine is found in children with a water diuresis. In the latter case, a low serum osmolality suggests primary polydipsia whereas a high serum osmolality suggests antidiuretic hormone (ADH) deficiency or insensitivity. A water deprivation test is necessary when the initial evaluation fails to establish the cause of polyuria. A vasopressin test enables the differentiation between neurogenic and nephrogenic diabetes insipidus (DI).

Child

[Transient polyuria in pregnancy in diabetes insipidus and gestational diabetes].

Two pregnant women developed overt polyuria (up to 11 l/day) and polydipsia during their second and third trimesters of pregnancy. In one patient hydronephrosis was present. Both patients suffered from mild gestational diabetes mellitus. Plasma sodium was 145 and 162 mmol/l. Polyuria and urinary hypo-osmolality responded well to desmopressin acetate. After delivery, polyuria and polydipsia disappeared in one patient and significantly improved in the other. Infusion of hypertonic saline one and two weeks respectively after delivery led to plasma hyper-osmolality (294 mosmol/kg and 305 mosmol/kg) without detectable stimulation of arginine vasopressin (AVP). Anterior pituitary function was normal. No stimulation of AVP occurred following insulin-induced hypoglycemia. AVP plasma disappearance after i.v. pulse injection of 1 microgram AVP as well as AVP plasma concentration after continuous infusion of 10 ng AVP/min was studied two weeks after delivery in one patient. The results suggested markedly elevated degradation of AVP compared to control subjects, probably due to an increased vasopressin activity. Eight months after delivery, hypertonic saline infusion in one patient led to a plasma-osmolality of 312 mosmol/kg without stimulation of AVP. In the second patient, AVP was not detectable (less than 0.2 pg/ml) six months after delivery when plasma osmolality was 290 mosmol/kg. Our studies demonstrate that a subclinical compensated diabetes insipidus was preexistent in both patients. Exacerbation occurred due to an increased AVP-clearance and presumably due to the hemodynamic and hormonal alterations during pregnancy, including a mild gestational diabetes mellitus.

Adult

Atrial regulation of intravascular volume: observations on the tachycardia-polyuria syndrome.

The atria, strategically located at the junction of the venous and arterial circulation, contain a network of neural and humoral structures by which they sense and regulate intravascular volume. Atrial receptors, most commonly consisting of complex unencapsulated nerve endings discharging into myelinated vagal fibers, are located in the intrapericardial portions of the caval and pulmonary veins and the adjacent atrial walls. Receptor activation by atrial distension results in increased afferent vagal fiber discharge, which in turn leads to tachycardia (Bainbridge's reflex) and decreased renal sympathetic nerve activity, renal vasomotor tone, and antidiuretic hormone activity. In addition, atrial distension also releases ANF, a peptide with potent diuretic, natriuretic, and vasorelaxant actions. The combined effect of these neurohumoral changes is the production of a large hypotonic diuresis. In the clinical setting the volume-regulating role of the atria is demonstrated by the tachycardia-polyuria syndrome. Laboratory and clinical evidence points to the activation of atrial neurohumoral mechanisms in response to atrial distension as the mediators of the polyuria that often accompanies paroxysmal tachycardias. The involvement of these mechanisms in other forms of cardiac congestion and the capability to easily measure in the blood an index of atrial distension, namely ANF, provide the opportunity to elucidate the pathophysiology and hence to open new therapeutic avenues in many cardiac disorders.

Animals

Different mechanisms of polyuria and natriuresis associated with paroxysmal supraventricular tachycardia.

The mechanism of polyuria associated with paroxysmal supraventricular tachycardia (SVT) was investigated in 8 patients. SVT was induced artificially and sustained for 60 minutes. Urine and blood samples were collected every 30 minutes. During the latter half of SVT, urine flow increased twofold in the control subjects before SVT. Urinary sodium excretion increased significantly (p less than 0.01) within 30 minutes after SVT. Urinary excretion of antidiuretic hormone (ADH) decreased (p less than 0.01) during the latter half of SVT and increased (p less than 0.01) after SVT, respectively. Plasma level of ADH did not change during SVT but increased (p less than 0.05) after SVT. The concentration of plasma atrial natriuretic polypeptide (ANP) increased significantly (p less than 0.05) before SVT ended. Urinary excretion of prostaglandin E2 increased significantly (p less than 0.05) after termination of SVT. The percent changes in the urinary excretion of prostaglandin E2 were correlated (r = 0.713, p less than 0.001) with those of ADH. There was also a correlation (r = 0.6, p less than 0.001) between the percent changes in the urinary excretion of prostaglandin E2 and those of sodium. Their findings suggest that the polyuria during SVT is attributed mainly to the inhibition of ADH release and that the natriuresis after SVT is due not only to the increased ANP but also to the increased renal prostaglandin E2 probably stimulated by ADH.

Adult

A patient with monosomy 7 and polyuria.

Diabetes insipidus (DI) is a rare complication of leukaemia. An association between monosomy 7 and DI in leukaemias has been proposed. We present a case of Ph1-positive CML who developed polyuria at the time of lymphoid blast transformation associated with loss of chromosome 7. Biochemical results were not diagnostic of DI and a therapeutic trial of DDAVP was unsuccessful. Post-mortem showed a peripituitary and renal leukaemic infiltrate and although DI is a possibility, the cause of his polyuria remains unresolved.

Blast Crisis

Polydipsia, polyuria, and hypertension associated with renin-secreting Wilms tumor.

A 16-month-old black male infant had unusual thirst, polyuria, hyponatremia, and hypertension. His polyuria was unresponsive to vasopressin therapy, and his high blood pressure was not effectively controlled by antihypertensive drugs. Radiographic examinations revealed an occult Wilms tumor in the right kidney. After removal of the tumor, the signs and symptoms were relieved. The tumor had a renin activity about 280 times that of the adjacent renal cortex, and many intracytoplasmic secretory granules were found on electron microscopy. The pathogenesis of these clinical manifestations appears to be mediated through the physiologic pathways of renin-angiotensin II and renin-aldosterone.

Humans

[A case of late-onset Pick's disease with polyuria].

A 72-year-old male was admitted to our hospital with a 2-year history of polyuria, prosopagnosia and aphasia. He showed characteristic clinical features of Pick's disease such as stereotyped verbal output and behavior and personality changes. CT and MRI scans showed marked atrophy in the bilateral anterior temporal lobes mild atrophy of the bilateral frontal lobes. SPECT scans revealed perfusion abnormalities in corresponding areas. A 6-hour-water deprivation test resulted in decrease in the urine volume and in concentration of the urine, suggesting abnormality of his secondary drinking behavior. Polyposia resulting in polyuria as a clinical manifestation may be due to stereotypic behavior which is often seen in Pick's disease.

Aged

[Pathogenesis of lithium polyuria].

An attempt is made to elucidate the pathogenesis of polyuria arising consequent upon medication of affective states with lithium salts. Experiments conducted with 54 male-rats showed that changes in the neurosecretion of supraoptic nuclei of the hypothalamus and neurohypophysis that take place after a course-wise intraperitoneal administration in amounts of 200 mg/kg (2/9DL20) of lithium chloride per 24 hours for a duration of 6 days occur parallel with histochemical changes of renal acid muconpolysaccharides and they accord with the nature of diuresis disorders. By the 5th day of the experiment the compound perverts the antidiuretic effect of a single subcutaneous injection of pituitrin (10 U/kg). The authors infer therefrom that polyuria emerging after introduction of lithium salts is caused by a deranged synthesis and secretion of the diuretic hormone and also by the ability of lithium to mitigate the action of this hormone on the kidneys.

Animals

Polyuria during Guillain-Barré syndrome.

Severe Guillain-Barré syndrome (GBS) usually results in life-threatening autonomic disturbances requiring a close monitoring of the patient in an Intensive Care Unit. Besides dangerous cardiac manifestations, neuroendocrine changes are also reported and could induce electrolytes and fluid balance impairments. Polyuria has been observed in a severe case of GBS occurring in a 16-year-old boy. Consecutive blood samples were obtained for renin, aldosterone, antidiuretic hormone and atrial natriuretic factor measurements. Polyuria in GBS is multifactorial and would be partly due to a dysregulation of osmoreceptors.

Adolescent

Antidiuretic and urinary cyclic AMP response of vasopressin in normal rats and in rats with lithium-polyuria.

The antidiuretic and urinary cyclic AMP response to supramaximal vasopressin infusion was studied in normal rats and in rats with lithium-polyuria. The animals were anaesthetized and then infused with a solution designed to produce excessive water diuresis and to lower basal cyclic AMP excretion. In 6 control animals not infused with vasopressin (1) urinary cyclic AMP excretion decreased during the infusion period. Vasopressin infusion (300 muU/min.) consistantly induced antidiuresis in all of 13 control rats (II); but the urinary cyclic AMP response varied individually from a significant increase in 6 animals to either no change or to a decrease in the remaining animals. The antidiuretic response to vasopressin was inhibited by 85% in 10 animals with marked polyuria induced by lithium administration (III). None of the animals in this group showed a significant increase of cyclic AMP excretion in response to vasopressin. The average rate of cyclic AMP excretion, which was equal in the two groups before vasopressin, was signifimantly lower in group III than in group II during vasopressin infusion. It is suggested that the increase in cyclic AMP excretion during vasopressin antidiuresis, although not consistant, most likely reflects hormone-induced changes of intracellular cyclic AMP levels in the renal medulla. Thus, the data suggest that the nephrogenic diabetes insipidus syndrome produced by lithium is associated with a defect in the renal formation of cyclic AMP in response to vasopressin.

Animals

Dopamine-related polyuria in patients with gram-negative infection.

Two patients developed polyuria with natriuresis while receiving intravenous dopamine hydrochloride for the treatment of hypotension. Both patients had Gram-negative pneumonia and both had evidence of extracellular volume depletion that was considered to be a result of the dopamine-induced polyuria. Following restoration of extracellular volume and withdrawal of dopamine therapy, both patients became normotensive and required no vasopressors. The diuretic action of dopamine, which persisted despite the severe intravascular volume contraction and perpetuated the hypotensive state in these two patients, is not well understood. The Gram-negative infection could play an important role possibly by enhancing the effect of dopamine on the renal vasculature.

Aged

Polyuria associated with an antibody to vasopressin.

1. A patient with polyuria in whom diabetes insipidus had been diagnosed was treated with Pitressin. Resistance to this therapy developed after 18 months and a circulating antibody to vasopressin was then demonstrated. Withdrawal of therapy led to a fall in titre of the antibody and an increase in maximal urinary concentration. 2. The antibody to vasopressin was associated with the IgA fraction of the serum immunoglobulins and its characteristics are described.

Adult

Effect of carbamazepine in polyuria associated with lithium therapy.

Ten patients, suffering from affective disorders, were treated with carbamazepine for polyuria and polydipsia associated with long-term lithium therapy. Oral carbamazepine (300--600 mg daily for six weeks) was observed to have no beneficial effect in alleviating these symptoms when compared with placebo tablets in a double blind crossover study. Plasma and urinary osmolality were observed to be within normal range in these patients and there was no antidiuretic response following subcutaneous Pitressin injection. There was 50% drop-out due to severe side-effects like ataxia, dizziness, restlessness and confusional states. It appears that lithium exacerbates carbamazepine induced CNS side-effects or vice versa, the mechanism of which is not very clear. It may be due to their mutual effect on sodium metabolism or on nervous conduction velocity. Hence, simultaneous administration of these two drugs should preferably be avoided.

Adult

Polyuria and imparied ADH release following medial preoptic lesioning in the rat.

Studies were carried out in the rat to detemine if hypothalamic lesions which caused polydipsia and polyuria had their effect mediated through an alteration of the ability of the neurohypophyseal system to release ADH. Rats with medial preoptic lesions hadincreased water intake while on ad libitum access to water and slightly impaired ability to conserve water following dehydration, but with no impairment of urine-concentrating ability. These were associated with an increase in plasma osmolality both during ad libitum fluid intake and after dehydration. Urinary ADH excretion was at leastas great as in shamoperated controls during ad libitum water intake, but failed to increase during dehydration in spite of a marked increase in plasma osmolality. Pituitary ADH content did not differ from control animals either during ad libitum water intake of after dehydration. Animals with lesions in the lateral preoptic and septal areas did not differ from control animals during ad libitum fluid intake and after dehydration even though lateral preoptic lesions produced polydipsia. In all animals, lesions were remote from the supraoptic nuclei, which showed no histological evidence of damage. It is concluded thatareas of the central nervous system away from the supraoptic nuclei are involved in the regulation of both water intake and ADH release.

Animals

Studies of the mechanism of contralateral polyuria after renal artery stenosis.

Acute renal artery stenosis in hydropenic dogs caused a contralateral increase in urine volume and free water clearance without change in glomerular filtration, renal blood flow, or osmolar clearance. The increase in urine volume was not dependent on the development of hypertension since it occurred in animals pretreated with trimethaphan but was dependent upon angiotensin since it was presented with angiotensin blockade with Saralasin. The effect was not caused by angiotensin inhibiting antidiuretic hormone release since the polyuria occurred in hypophysectomized animals receiving a constant infusion of 10 muU/kg per min of aqueous Pitressin. Since the rise in urine volume was associated with an increase in renal vein prostaglandin E concentration and was prevented by pretreatment with indomethacin (5 mg/kg) the results suggest that the rise in plasma angiotensin after renal artery stenosis causes an increase in contralateral prostaglandin E synthesis with resultant antagonism to antidiuretic hormone at the collecting tubule.

Animals