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PubMed1983

Polyuria and inappropriate secretion of arginine vasopressin in hypothalamic sarcoidosis.

Inappropriate arginine vasopressin release and polyuria with excessive thirst were found in a patient with hypothalamic sarcoidosis subsequently confirmed at autopsy. He became intensely thirsty during a 5% saline infusion at a plasma osmolality of 274 mosmol/liter. The normal thirst threshold under these conditions is 294 +/- 3 mosmol/liter (+/- SD). An increase in radioimmunoassayable arginine vasopressin was detected at an inappropriately low plasma osmolality, and free water clearance was negative despite a plasma osmolality of 265 +/- 5 mosmol/liter with ad libitum fluid intake. The syndrome of inappropriate antidiuresis has not been described previously in combination with hypothalamic sarcoidosis. Demeclocycline therapy was associated with an exacerbation of the patient's polyuria. Propranolol administration, however, was associated with a reduction of urine output and an increase in plasma osmolality to 279 mosmol/liter on one and 299 mosmol/liter on another occasion.

Adult↗
PubMed1984

Marked hypotonic polyuria resulting from nephrogenic diabetes insipidus with partial sensitivity to vasopressin.

We studied two women with severe hypotonic polyuria whose symptoms dated from infancy. We eliminated the possibility of central diabetes insipidus (DI) and primary polydipsia, and established the presence of nephrogenic DI on the basis of: 1) the interrelationships between plasma osmolality, urine osmolality, and urinary AVP; and 2) impaired antidiuretic responses to AVP and 1 deamino-8-D-arginine vasopressin. Though 25-50 times as resistant to 1 deamino-8-D-arginine vasopressin nasal spray as patients with central DI, these patients could be treated effectively with large doses of the nasal spray. One patient has been so treated for more than a year with dramatic improvement in her polydipsia, polyuria, and sense of well-being.

Administration, Intranasal↗
PubMedDate not supplied

Constipation, polyuria, polydipsia, and edema associated with orlistat.

OBJECTIVE: To report the occurrence of a novel group of adverse effects associated with initiation and rechallenge of orlistat. CASE SUMMARY: A 42-year-old white woman developed symptoms of constipation, polyuria, polydipsia, and increased lower-leg edema after 2 weeks of treatment with orlistat 120 mg 3 times daily. The drug was discontinued for 4 days and the symptoms resolved. On reinstitution of the orlistat treatment, the symptoms reappeared within 2 days. Thereafter, the medication was permanently discontinued. DISCUSSION: Common gastrointestinal adverse reactions associated with orlistat use include fecal urgency and abdominal pain and discomfort. Pedal edema has also been reported to occur, although less frequently. No reports were discovered documenting the occurrence of constipation, polydipsia, and polyuria associated with the use of orlistat. Despite careful consideration of other possible causes of these symptoms, the temporal association between initiation, discontinuation, and rechallenge of orlistat and the patient's symptoms suggest a medication-related adverse event. Based on the Naranjo probability scale, the likelihood that orlistat was the cause of this cluster of adverse effects is possible. CONCLUSIONS: It is important for the healthcare provider to be aware of these adverse effects to promptly evaluate and differentiate between possible causes of similar reactions.

Adult↗
PubMed1986

Neural lobe function in aged Wistar/Tw strain rats showing polydipsia and polyuria.

Neural lobe function in male rats of the Wistar/Tw strain was studied at 3, 7 and 16-18 months of age. A significant rise in the serum arginine vasopressin (AVP) level was noted in 16-18-month-old rats showing polydipsia and polyuria. The content and concentration of AVP in the neural lobe of aged rats were significantly less than those of younger animals (3 and 7 months). These results point out an enhancement of AVP release from the neural lobe of aged rats. The reduction in urinary volume in aged rats subjected to 24 hours of water deprivation was less than those in younger animals. No increase in urinary sodium, potassium and chloride concentrations was observed in aged rats, and the decrease in electrolyte excretion from urine during the dehydration period was less in aged rats than younger ones. These results suggest that the antidiuretic response to osmotic stimuli was reduced in aged rats. The administration of AVP to aged rats resulted in a significant decrease in water intake and urinary volume, but AVP administration did not induce any change in the electrolyte balance. Therefore, it is concluded that the main cause of the development of polydipsia and polyuria is the decline in renal function but not in neurosecretory activity, although exogenous AVP can effectively reduce water intake and urinary output in aged rats.

Aging↗
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↗
PubMed1987

Mechanism of polyuria and natriuresis associated with paroxysmal supraventricular tachycardia.

Changes in plasma levels of atrial natriuretic peptide (ANP) and arginine vasopressin (AVP) were studied in 8 patients during a 30 min period of induced supraventricular tachycardia (SVT). The mean plasma ANP concentration increased immediately after the onset of SVT, peaked at 30 min and gradually returned to the control level. The mean plasma AVP concentration, on the other hand, was suppressed during SVT and rebounded above the control level in the post-SVT period. In 4 patients, SVT was associated with polyuria and natriuresis. The mean urine volume in these patients increased to 580% of the control and the mean urinary sodium excretion to 278% of the control, respectively. It was concluded that both a stimulation of ANP secretion and an inhibition of AVP release, elicited by an increase in atrial pressure, may be responsible for polyuria and natriuresis associated with SVT.

Adult↗
PubMed1980

Failure of infusion of prostaglandin A2 to restore the response to antidiuretic hormone in rats with polyuria induced by lithium.

Male Wistar rats were fed a lithium diet for 2--3 months producing marked polyuria (greater than 75 ml/100 g in 24 h) and a plasma Li concentration of 0.7 mmol/l. In acute experiments animals were anaesthetized with 5-ethyl-5-(1-methylpropyl)-2-thiobarbituric acid and infused with hypotonic glucose-saline (15 ml/h). Addition of prostaglandin A2 (PGA2; 0.2 ng/min) for 180 min to the infusate did not restore the impaired antidiuretic response to arginine-vasopressin (AVP) whether this agent was infused continuously (150 micromicron./min) or given as bolus injections (2500 micromicron.). In long-term experiments animals were kept in metabolism cages and Alzet osmotic minipumps were implanted for intravenous infusion of drugs at 1 microliter/h. Again, PGA2 infusion at 0.2 ng/min failed to restore the impaired antidiuretic response to AVP (150 micromicron./min). It was therefore concluded that in rats with severe polyuria induced by long-term administration of lithium, infusion of PGA2 at 0.2 ng/min cannot restore the impaired response to antidiuretic hormone as has been reported by others.

Animals↗
PubMed1995

A case of non-Hodgkin's lymphoma presenting with polyuria and acute renal insufficiency.

A case of non-Hodgkin's lymphoma presenting with polyuria, enlarged kidneys, and renal insufficiency is reported. The diagnosis was made by percutaneous needle biopsy of the kidney. Renal failure reversed and the kidneys regressed in size on exhibition of the first cycle of chemotherapy. The rarity of polyuria at presentation, the role of renal biopsy in the diagnosis, and the response of renal failure to specific chemotherapy are discussed.

Acute Kidney Injury↗
PubMed1992

[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↗
PubMed2002

[Diagnostic image (80). A men with thirst and polyuria. Bladder retention].

A 69-year-old man was admitted because of polyuria and renal insufficiency. At physical examination a huge bladder retention was found (31). The polyuria was explained by the decreased concentrating ability of the kidney due to impaired tubular function; this was caused by hydronephrosis due to prostate hypertrophy.

Aged↗
PubMed2002

Diuresis pattern, plasma vasopressin and blood pressure in healthy elderly persons with nocturia and nocturnal polyuria.

BACKGROUND: Nocturia, a common symptom in the elderly, is often caused by increased urine production at night. METHODS: The present study comprised 17 men and six women aged 68.1 +/- 4.7 (mean +/- SD) years with nocturia (> or = 2 nocturnal voids) and nocturnal polyuria (nocturnal urinary output of > or = 0.9 mL min(-1)). A physical examination, measurements of recumbent blood pressure after a 15-minute rest, plasma AVP assay at noon and midnight, and urine collection performed during a 24-hour period. RESULTS: The daytime urine output was 1358 +/- 664 mL, and the nocturnal urine output 796 +/- 312 mL. The AVP level was lower at midnight than at noon in 17 persons, and higher at midnight in six persons. Blood pressure was 142.0 +/- 15.7/87.4 +/- 9.1 mmHg. Systolic (but not diastolic) blood pressure increased with decreasing nocturnal plasma AVP. Increasing nocturnal diuresis rate (r2= 0.26; p < 0.01) but not plasma AVP was associated with increasing systolic blood pressure. CONCLUSION: In elderly persons with nocturia and nocturnal polyuria, the plasma AVP is low and does not rise nocturnally. The systolic blood pressure is increased with increasing diuresis but unaffected by plasma AVP.

Aged↗
PubMedDate not supplied

[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↗
PubMed1992

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↗
PubMed2005

[Efficacy of intranasal desmopressin in the treatment of nocturia due to nocturnal polyuria].

Older adults often cite nocturia as one of the most bothersome lower urinary tract symptoms (LUTS). We investigated the efficacy and safety of intranasal desmopressin in the treatment of nocturia due to nocturnal polyuria on 12 patients (ten men, two women) ranging in age from 53 to 77 years (mean 67 years). All patients experienced more than two episodes of nocturia per night, and had a nocturnal urine volume greater than 35% of the daily voided volume, measured using a 3-day voiding diary with a frequency-volume chart. They began taking intranasal desmopressin (10 microg) at bedtime. When compared with the baseline data, the nocturnal urine volume, (928 +/- 307 versus 469 +/- 251 ml, p = 0.0007) and nocturnal frequency (4.8 +/- 2.0 versus 2.8 +/- 1.8, p = 0.0009) were significantly decreased. The daytime urine volume (1,008 +/- 458 versus 930 +/- 419 ml, p = 0.49) did not change significantly. The unine osmolarity (420 +/- 143 versus 598 +/- 158 mOsm/kg, p = 0.0065), and urine sodium levels (100 +/- 32 versus 140 +/- 60 mEq/l, p = 0.007) increased significantly, whereas the serum sodium levels (141 +/- 3 versus 135 +/- 7 mEq/l, p = 0.048) decreased significantly. Among the 12 patients, 5 (41.6%) patients reported side effects, including headache in 1, edema in 1 and hyponatremia in 3. The patient with edema discontinued medication, but the other 4 patients continued their medication and the side effects subsided. In conclusion, desmopressin is an effective treatment for adult patients complaining of nocturia due to nocturnal polyuria. One should be aware of the potential side effects including hyponatremia.

Administration, Intranasal↗
PubMed1977

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↗
PubMed1989

[Renal function in experimental potassium depletion. I. Effects of lysine-8-vasopressin in hypotonic polyuria].

Renal function has been studied by the clearance (cl.) method during hypotonic polyuria--four 15-min cl. periods--and successive antidiuresis--two 60-min cl. periods (A1, A2)--induced by lysine-8-vasopressin (LVP), 5 mU in bolus followed by infusion at a rate of 0.04 mU/min. The endogenous creatinine cl. (Cc) and the osmotic cls. (Cosm, CH2O) were determined by the usual methods as well as the absolute and fractional urinary excretions of water, sodium, chloride and potassium. The urinary concentrations of PGE2, 6-keto-PGF1 alpha and TxB2 were determined by the RIA method. This study protocol has been applied to 28 healthy women either in normal potassium balance (N, n = 14) or after potassium depletion (KD) induced by low potassium dietary intake (less than or equal to 10 meq/d) plus natriuretic treatment according to two different time patterns: two KD groups were obtained with potassium cumulative deficit of 160 +/- 43 (D2, n = 8) and 198 +/- 22 meq (D3, n = 6). The early % effects of LVP, i.e. (A1-P)% of P (mean polyuria), were significantly different only in D3 as compared to N. Precisely, the LVP-effect to reduce Cc was blunted; moreover a LVP-effect to reduce renal sodium and chloride fractional excretions and a tendentiously enhanced LVP-effect to reduce water fractional excretion were observed. These tubular effects are likely related to the inhibited renal synthesis of prostanoids in the D3 group.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

[Renal function in experimental potassium depletion. II. Indomethacin and effects of lysine-8-vasopressin in hypotonic polyuria].

Renal function has been studied by the clearance (cl.) method during hypotonic polyuria--four 15-min cl. periods--and successive antidiuresis--two 60-min cl. periods (A1, A2)--induced by lysine-8-vasopressin (LVP), 5 mU in bolus followed by infusion at a rate of 0.04 mU/min. The endogenous creatinine cl. (Cc) and the osmotic cls. (Cosm, CH2O) were determined by the usual methods as well as the absolute and fractional urinary excretions of water, sodium, chloride and potassium. The urinary concentrations of PGE2, 6-keto-PGF1 alpha and TxB2 were determined by the RIA method. This study protocol has been applied to 20 healthy women submitted to paired functional explorations in both the absence and presence of indomethacin (100 mg i.m.); the drug effects have been evaluated in both normal potassium balance (N2, n = 6) and in two groups of potassium depletion (KD) with potassium cumulative deficit of 160 +/- 43 (D2, n = 8) and 198 +/- 22 meq (D3, n = 6), respectively. As regards the early % effects of LVP, i.e. (A1-P)% of P (mean polyuria), the inhibition of prostanoid synthesis with indomethacin produced significant changes: 1) an enhanced reduction in renal chloride excretion in all experimental groups; 2) a reduction in renal sodium and chloride fractional excretions in both KD groups; 3) an enhanced antidiuretic effect in D3 only, i.e. in the experimental condition with inhibition of prostanoid renal synthesis present during the control study.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

[Plasma levels of atrial natriuretic peptide (ANP) in patients with paroxysmal supraventricular tachycardia and concomitant polyuria (urina spastica)].

A concomitant diuresis and natriuresis has been reported to occur in 30-50% of patients with paroxysmal supraventricular tachycardia. While the increase of the diuresis may be secondary to an inhibition of vasopressin, the etiology of the natriuresis is presently not well understood. To determine the role of atrial natriuretic peptide (ANP) in the pathogenesis of tachycardia-induced polyuria, we measured ANP levels in two female patients (aged 59 and 68 years) with recurrent episodes of paroxysmal supraventricular tachycardia during such attacks, as well as after conversion to a normal sinus rhythm. In both patients, episodes of supraventricular tachycardia were associated with both a large increase in ANP plasma levels (560 resp. 1.208 pg/ml; normal range: 50 +/- 10 pg/ml) and polyuria. Despite elevated ANP plasma levels, no diuretic and natriuretic response to tachycardia could be observed during episodes of shorter duration, some of which occurred in the older patient studied. After restoration of a normal sinus rhythm, ANP plasma levels decreased to baseline levels (107 resp. 32 pg/ml). The results of this study show that the secretion of ANP is increased during episodes of paroxysmal supraventricular tachycardia, suggesting that ANP might contribute to the pathogenesis of natriuresis and diuresis frequently associated with supraventricular tachycardia.

Aged↗