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PubMed2005

Desmopressin: in adults with nocturia.

Desmopressin, a synthetic antidiuretic hormone analogue, is the only drug currently approved for the treatment of nocturia associated with nocturnal polyuria or multiple sclerosis (MS). Compared with vasopressin, desmopressin has a longer lasting and more potent antidiuretic effect and is devoid of vasopressor and uterotonic effects. In two large, randomised, double-blind phase III trials in adults with nocturia associated with nocturnal polyuria, 3 weeks of oral desmopressin therapy was significantly more effective than placebo in reducing the mean number of nocturnal voids and in normalising the rate of nocturnal urine production. Beneficial effects of desmopressin on nocturia were maintained and increased in patients completing 10 or 12 months of further treatment in a nonblind extension of short-term trials. In randomised, double-blind trials in MS patients with nocturia, nasal desmopressin reduced the mean number of nocturnal voiding episodes by 31-54%. In both patient populations, desmopressin increased the initial sleep period or mean maximum period of uninterrupted sleep by approximately 2 hours, an outcome significantly greater than that achieved with placebo. In trials of < or =6 weeks duration in adults with nocturia, desmopressin was generally well tolerated. Most desmopressin-related adverse events were transient and mild or moderate in severity. Clinically significant hyponatraemia was reported in approximately 5% and required withdrawal from studies in < or =3% of patients.

Adult↗
PubMed2005

Amphotericin B-induced nephrogenic diabetes insipidus in a case of cryptococcemia.

A 66-year-old woman with malignant lymphoma became neutropenic during chemotherapy and developed cryptococcemia. After amphotericin B had been commenced, she developed significant hypokalemia and polyuria, though her renal function remained stable. The laboratory findings showed no evidence of renal tubular acidosis. With vigorous water and potassium replacement, amphotericin B had been continued until the cumulative dose reached 2.5 g. After the cessation of amphotericin B, the hypokalemia and polyuria resolved promptly. Based on theses findings, she was diagnosed as nephrogenic diabetes insipidus with hypokalemia and without renal tubular acidosis due to amphotericin B. This complication is usually reversible, and vigorous water and potassium replacement may allow completion of treatment by amphotericin B, though careful monitoring of body water balance and renal function is of importance.

Aged↗
PubMed1995

[A case of Sjögren's syndrome complicated with cryoglobulinemia, nephrogenic diabetes insipidus, and renal tubular acidosis].

A 68-year-old woman had been complained of xerostomia since she was 30 years old. Further symptoms of polyuria, polyposia and insomnia had been developed since she was 35 years old. The biopsy material from a minor salivary gland demonstrated the infiltration of lymphocytes into mesenchyme which was compatible with Sjögren's syndrome. She admitted to our hospital because of myalgia in bilateral gastrocnemius and petechiae in both lower extremities in addition to the complaints described above. Complete blood cell counts on admission revealed hemoglobin 9.7 g/dl, platelet count 12.5 x 10(4)/microliters, and white blood cell count 3,300/microliters. Marked polyuria, polyposia (more than 5,000 ml/day, respectively) and low urine gravity (1.005) were observed, although the serum creatinine level showed normal value. Serologic examination showed that the elevation of total serum protein concentration (9.5 g/dl) with marked elevation of serum IgG level (6,190 mg/dl). Her immunoglobulins contained cryoglobulin (cryocrit 20%), and immunoelectrophoresis demonstrated the existence of IgG-kappa monoclonal protein. A positive anti-nuclear antibody at 1:320 dilution, a positive rheumatoid factor and a positive antibody to SS-A (Ro) were also observed. The serial studies of blood gas analysis could not demonstrated the presence of metabolic acidosis. Together with the result of elevated plasma antidiuretic hormone level and results of vasopressin test, Fishberg's concentrating test and the tests of the overload of NH4Cl or bicarbonate, she was diagnosed Sjögren's syndrome with both diabetes insipidus and subclinical renal tubular acidosis. She was initially medicated with prednisolone (40 mg/day, orally), then she was given six courses of intravenous cyclophosphamide (750 mg/body/month).(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗
PubMed1988

Depression and the reporting of diabetes symptoms.

The relationship of diabetes symptoms to current mood and general metabolic control was studied. Symptoms commonly associated with poorly controlled diabetes (e.g., thirst, polyuria, weight loss) were measured in 114 patients with diabetes mellitus (type 1 = 57, type 2 = 57). Scores for these individual symptoms were correlated with glycosylated hemoglobin (HbA1) and depression as measured by the Beck Depression Inventory (BDI). HbA1 was poorly correlated (r less than 0.2) with nine of the eleven symptoms and made a significant independent contribution only to the reporting of polyuria (p = 0.04). In contrast, depression was moderately correlated with nine symptoms and had a significant effect on the reporting of two of three hyperglycemic symptoms, five of six hypoglycemic symptoms, and both nonspecific symptoms of poor control (p less than 0.05 for each). We conclude that many reported symptoms often attributed to diabetes are more related to depressive mood than to a conventional clinical measure of blood glucose control. Diabetes symptoms may be unreliable indicators of poor metabolic control when features suggestive of depression are present.

Adult↗
PubMed1977

The spontaneously diabetic Wistar rat. Metabolic and morphologic studies.

A new, spontaneously diabetic syndrome has been recognized in nonobese outbred Wistar rats of both sexes. The age at detection of first glycosuria has varied from 48 to 120 days, with a mean of 67 days. Eighteen rats have been studied, 14 untreated and four during and after cessation of insulin treatment. The affected animals have demonstrated a spectrum of severity, with hyperglycemia (252-732 mg./dl.), hypoinsulinemia (0-1 ng./ml.), and hyperketonemia. The severely ketotic rats, with total blood ketone body levels between 6 and 13 mM, showed rapid loss in weight and dehydration over one to six days. The moderately ketotic (1-5 mM) declined gradually in weight over 15 days, with marked polyuria and glycosuria. The stable rats, with ketonemia less than 1 mM, sustained their weights, polyuria, and glycosuria for longer than 40 days. A relative or absolute increase in plasma immunoreactive glucagon and elevated levels of free fatty acids and branched-chain amino acids were observed in relation to the severity of the syndrome. Intraperitoneal arginine or tolbutamide elicited no insulin response, but the glucagon response to arginine was exaggerated. Pancreatic insulin content was normal or moderately decreased. Light-microscopic examination of pancreases of ketotic animals at the end stage of the disease showed islets to be very small and rare, consisting virtually of non-beta cells. In stable and earlier ketotic rats, the islets were small, with reduction in beta-cell number and a striking inflammatory cell infiltration. Surviving beta cells showed variable degranulation. This model of spontaneous diabetes in nonobese rats displays insulin deficiency, glucagon excess, and ketosis, with a dramatic inflammatory lesion during active beta-cell destruction.

Aging↗
PubMed1991

New inbred strain of Long-Evans Tokushima lean rats with IDDM without lymphopenia.

Spontaneously diabetic rats with remarkable polyuria, polyphagia, and polydipsia were discovered in 1983 in an outbred colony of Long-Evans rats purchased from Charles River Canada in 1982. They have since been maintained at the Tokushima Research Institute (Otsuka Pharmaceutical, Tokushima, Japan). A strain of rats (Long-Evans Tokushima Lean [LETL]) with diabetes was bred from these rats. The characteristic features of the disease in LETL rats are 1) sudden onset of polyuria, polyphagia, hyperglycemia, and weight loss; 2) no sex differences in the rate of onset or severity; 3) lymphocyte infiltration into islets followed by destruction of beta-cells and disappearance of lymphocytes at the onset of diabetes; 4) no significant T lymphopenia; 5) lymphocyte infiltration into the salivary glands and lacrimal glands; and 6) at least two recessive genes involved in the pathogenesis of insulitis, one of which is closely linked with RT1u. These characteristics closely resemble those of human insulin-dependent diabetes mellitus (IDDM). Results suggest that the LETL rat is a useful animal model for analysis of genetic and immunologic factors relating to the pathogenesis of human IDDM.

Animals↗
PubMed1982

Hydramnios and observations in Bartter's syndrome.

A boy was born after a pregnancy complicated by a hydramnios. He appeared to suffer from Bartter's syndrome, a disease characterized by hyperreninemia, hyperaldosteronism and excess prostaglandin production resulting in hypokalemia, normotension, impaired urine concentration ability, polyuria and renal sodium loss. Other children with Bartter's syndrome, and also a different syndrome characterized by polyuria and hydramnios, are reviewed. In the evaluation of gross hydramnios of unknown etiology, Bartter's syndrome might also be considered.

Adult↗
PubMed1991

Nephrotoxicity of an ellipticine derivative (N2-methyl-9-hydroxyellipticinium acetate) in rat: a defect of urinary concentrating ability.

The antitumor drug celiptium (N2-methyl-9-hydroxyellipticinium) is an ellipticine derivative effective in experimental tumors and in man. The major side effect is nephrotoxicity. The impairment of renal function is studied in rats following a single i.v. dose of 20 mg/kg celiptium and a long-term study (day 2 to day 60). A loss of body weight is noted in celiptium-treated animals between day 4 and day 15, and recovery occurs between day 15 and day 60. Histologic study shows cortical lesions characterized by focal necrosis of proximal tubules without any glomerular, interstitial, and vascular alterations on day 8. It is to be noted that any medullary lesions were not shown. A polyuria and a decreased creatinine clearance are reported on day 8. We were interested in a special study of this polyuria. For this study, rats were water deprived between day 6 and day 8 following celiptium administration. The decrease of urinary osmolality is not recovered after dehydration and exogenous vasopressin derivative (dD AVP) does not correct the renal concentration defect. AVP plasma levels increase after dehydration. These results suggest a pitressino-resistant urinary concentrating inability in celiptium-treated rats.

Acute Kidney Injury↗
PubMed2000

A case of nephrogenic diabetes insipidus caused by obstructive uropathy due to prostate cancer.

Nephrogenic diabetes insipidus (DI) secondary to chronic urinary tract obstruction is a rare disease. The exact cause is unknown but it is likely that increased collecting duct pressures cause damage to the tubular epithelium, resulting in insensitivity to the action of arginine-vasopressin (AVP). A 77-year-old man complaining of polyuria and polydipsia was treated with alpha glucosidase inhibitor under the impression of polyuria due to diabetes mellitus. But his symptoms did not improve. Water deprivation and AVP administration study revealed that the patient had nephrogenic DI. Urinary tract obstruction due to an enlarged prostate was suggested as a principal cause of nephrogenic DI. The patient underwent transurethral resection of the prostate and bilateral subcapsular orchiectomy. After surgery, the urine osmolarity was normalized and the patient became symptom-free. We report a case of nephrogenic DI due to obstructive uropathy which was cured by surgery eliminating obstruction.

Adenocarcinoma↗
PubMed1993

[Development of bladder capacity, nocturnal urinary volume and urinary behavior in nonenuretic and enuretic children].

Bladder capacity, nocturnal urinary volume and nocturnal urinary behavior were investigated in 1751 nonenuretic and 282 enuretic children in two primary schools and four kindergartens. The results were as follows: 1. A statistically significant linear correlation was observed between the age and the bladder capacity in the morning and daytime, as well as nocturnal urinary output, in nonenuretic children. 2. The bladder capacity of enuretic children was smaller in the ages below 6 but larger in the ages over 7 than that of noneuretic children. It was not likely from this evidence that an immature bladder capacity was a primary cause of enuresis. 3. For the estimation of the maximum bladder capacity in the study of enuresis, urinary output in the morning immediately after awakening with sufficient urinary sensation was thought to be more reasonable than that in the daytime, because output in the morning was approximately 50% more than that of the daytime. 4. Ten to 15% of nonenuretic children showed nocturnal polyuria with nocturnal urination after complete awakening more than one time every week. It was also not likely from this evidence that polyuria was a primary cause of enuresis. 5. The overall occurrence rate of enuresis was 14%, higher in males up to the ages of 9, and almost equal in males and females after the ages of 10. 6. The average age for the spontaneous disappearance of enuresis was 7.3 y.o., therefore, adequate treatments for enuresis should be instituted after the age of 8.

Child↗
PubMed1999

Congenital renal dysplasia and psychogenic polydipsia in a Bernese mountain dog.

Congenital renal dysplasia was tentatively diagnosed, based on ultrasound and an intravenous urogram, in a 5-month-old female with polyuria and polydipsia. Creatinine clearance measurement revealed that the renal dysplasia was not the cause of the polyuria. A modified water deprivation test eliminated other differential diagnoses and confirmed psychogenic polydipsia.

Animals↗
PubMed1999

[Marked hypernatremia in suprasellar germinoma lacking a sense of thirst].

We here report a 17-year-old high school boy having suprasellar germinoma who presented marked hypernatremia probably due to damages of both the osmoregulation and thirst centers. He was in good health until July, 1996, when he noticed slight general malaise and complained of dryness of the mouth, but without polyuria. He was found to have hypernatremia of mild degree (serum Na 151 mEq/l), but dropped out from the follow-up. In April, 1997, he was admitted to our hospital with complaints of general malaise and weakness of the upper and lower extremities. Serum Na was high at 202 mEq/l with a plasma osmolality of 390 mOsm/kg H2O. He completely lacked a sense of thirst and polydipsia/polyuria. Computed tomography and magnetic resonance imaging indicated a suprasellar tumor, possibly a germinoma. Hypernatremia was first treated with intravenous infusion of a half-normal saline solution, followed by immediate polyuria of 3 to 6 l/day. Subsequently, nasal administration of desamino-D-arginine vasopressin (DDAVP) induced stabilization of serum Na to a range between 140 and 160 mEq/l. The tumor disappeared following steroid pulse therapy and irradiation of 50 Gy to the brain. At the time of discharge, he and his family were instructed to record the urine volume, amount of water intake, body weight and amount of DDAVP used. The patient was instructed to drink water corresponding to the urine volume while maintaining the dose of DDAVP. One year after treatment, the water balance reverted to a positive direction, leading to a normal range of serum Na probably because of partial recovery of the osmoreceptors and/or trained drinking habit. This case illustrates the so-called adipsic hypernatremia which is attributed to partial osmoreceptor destruction by a suprasellar germinoma.

Adolescent↗
PubMed2000

Normal voiding patterns and determinants of increased diurnal and nocturnal voiding frequency in elderly men.

PURPOSE: We determined the normal value of diurnal and nocturnal voiding frequency, and its determinants in a population based sample of elderly men. MATERIALS AND METHODS: We collected data on 1,688 men 50 to 78 years old recruited from the population of Krimpen, The Netherlands. Measurements consisted of self-administered questionnaires, including the International Prostate Symptom Score (I-PSS), a 3-day frequency-volume chart, transrectal prostatic ultrasound, uroflowmetry and post-void residual urine volume measurement. RESULTS: Diurnal voiding frequency is independent of age and more frequent in men with benign prostatic hyperplasia (BPH). Nocturia 2 or more times is present in 30% of men 50 to 54 and in 60% of those 70 to 78 years old, while nocturia 3 or more times is present in 4% and 20%, respectively. In addition, nocturia is strongly associated with BPH and nocturnal polyuria but apparently not with cardiovascular symptoms, hypertension or diabetes mellitus. We noted poor agreement of the responses on the frequency-volume charts and the I-PSS question on nocturia. Using the I-PSS leads to a higher prevalence of nocturia. CONCLUSIONS: Diurnal frequency is independent of age (median 5 voids, interquartile range 4 to 6) but higher in men with BPH. Nocturia increases with advancing age and is more frequent in men with nocturnal polyuria. BPH is an independent risk factor for nocturia and increased diurnal voiding frequency. In those with nocturia there is a great difference in subjective symptoms and objective data, indicating that the weight of the I-PSS question on nocturia for making treatment decisions should be reconsidered.

Aged↗
PubMed2000

[Magnetic resonance imaging in central diabetes insipidus in children and adolescents. findings at diagnosis and during follow-up].

AIM: The absence of the hyperintense signal of the posterior pituitary in magnetic resonance imaging (MRI) is considered by some authors to be evidence of neurohypophyseal dysfunction. To evaluate the utility of MRI as a complementary diagnostic aid in patients with central diabetes insipidus (CDI), we studied the MR images of pediatric patients at diagnosis and during follow-up. METHODS: MR images from 14 patients (4 females, 10 males; mean age 8.5 years) who were referred for polyuria and polydipsia and whose diagnosis was central diabetes insipidus (CDI) were analyzed. Mean time of evolution from onset of polyuria until the first MRI was 1.5 years. In 11 patients more than one MR image was obtained during follow-up. Mean time of follow-up was 2.8 years. RESULTS: In 10 patients CDI was idiopathic, in 3 it was secondary to a hypothalamic tumor and in 1 it was secondary to histiocytosis. In one patient with idiopathic CDI, the hyperintense signal was present at diagnosis but disappeared during the following 15 months. Four of the patients with idiopathic CDI developed thickening of the pituitary stalk, some at their diagnosis and others during follow-up. Of the three patients in whom CDI was secondary to a germinoma, the hyperintense signal was absent in two of them, while in one the signal was ectopic and associated with a thickened pituitary stalk. In the patient with histiocytosis, the hyperintense signal was absent at diagnosis. CONCLUSIONS: 1. In most of the patients with CDI the hyperintense signal of the posterior pituitary was absent at diagnosis; however in one patient this signal disappeared during follow-up and consequently its presence does not rule out a diagnosis of CDI. 2. Although a thickened pituitary stalk could reflect only a non-specific, transient inflammatory process, its presence makes ruling out tumoral or infiltrative disease obligatory.

Adolescent↗
PubMed2001

[A case of congenital nephrogenic diabetes insipidus accompanied by hypertension].

Congenital nephrogenic diabetes insipidus is a rare disorder in which the kidney is insensitive to the antidiuretic hormone, vasopressin. In most cases, a mutation in the vasopressin type 2(V2) receptor gene is the genetic cause of the disease. So far, few cases of congenital nephrogenic diabetes insipidus with hypertension have been reported. We report one male case of congenital nephrogenic diabetes insipidus accompanied by hypertension. The patient was a 24-year-old man who had suffered from polyuria and polydipsia since infancy and had been found to have hypertension at about 16 years. He was admitted to hospital in May 2000 for investigation of polyuria and hypertension with a high plasma level of renin activity of 10.4 ng/ml/hr. On physical examination, the blood pressure was 150/90 mmHg and the daily urinary output was 18.5 l. There was no change in urine volume and urine osmolality after an intramascular injection of vasopressin and water deprivation. The blood pressure and plasma renin activity were increased from 127/73 mmHg to 146/87 mmHg and from 4.9 ng/ml/hr to 6.1 ng/ml/hr, respectively, by a 4-hour dehydration test. He was found to have a C-to-T transition at nucleotide position 675 by sequencing analysis of the V2 receptor gene. After administration of hydrochlorothiazide, both the blood pressure and urine volume were reduced. Consequently, it was suggested that activation of the renin-angiotensin system by dehydration, at least in part, contributed to high blood pressure in this case.

Adult↗
PubMedDate not supplied

[Chronic interstitial nephritis caused by analgesics].

Interstitial nephritis secondary to analgesic ingestion is apparently an uncommon subject in pediatric literature. Two cases are reported in this article: case 1 is a girl followed for the last fifteen years when she had lipoid nephrosis which was treated initially with corticosteroids; she responded satisfactorily, but presented frequent relapses. After 8 years, she was given cyclophosphamide plus prednisone and lately, she responded and has remained well. Further on, her urinalysis showed specific gravity of 1,033 and no proteinuria. Five years ago, because of protracted headache due to psychological disturbance, she started to ingest a variety of analgesics in progressively increasing doses. For the last 2 years, abdominal pains, paleness, polydipsia and polyuria have been observed; at present, her blood pressure, serum chemistry, and urine sediment are normal, but there is a marked failure in the renal concentration capacity, as well as marked sodium urinary losses. A percutaneous renal biopsy showed tubulo-interstitial fibrosis and edema with normal glomeruli. Case 2 is a girl with rheumatoid arthritis which appeared 3 years ago; for over one year, the patient was given 15 mg/day prednisone plus 1.5 g. acetylsalycilic acid. She was admitted to the hospital because her osteoarticular problem did not improve. Her blood pressure, blood chemistries and urinary sediment were also normal. LE tests were negative. Renal concentrating capacity was reduced and the renal biopsy showed tubular atrophy; there was intestinal edema and mononuclear infiltration. Chronic interstitial nephritis, secondary to analgesics is supported in both cases; polyuria and a marked defect of renal concentrating capacity are the earliest and most characteristic features. Normal urinary sediment is a common finding leading to erroneous assessment of a lack of renal involvement. Pathological lesions are located in the interstice of the renal medulla and sometimes in the papilla. Early arrest of analgesic ingestion may stop and even reverse the renal lesion and the renal insufficiency.

Adrenal Cortex Hormones↗
PubMed2001

Lithium isotopes: differential effects on renal function and histology.

OBJECTIVES: Reduction in renal concentrating ability has been reported in patients undergoing chronic lithium treatment. Prior work has demonstrated differences in physiological effects of the stable lithium isotopes, 6Li and 7Li. Here, we measured the degree of polyuria, polydipsia and kidney histological changes induced in rats by equimolar amounts of 6LiCl, 7LiCl and the commercially available mixture of both isotopes. METHODS: Rats were given 1.0 mEq/kg of either 6LiCl, 7LiCl or 'nLiCl' (isotope mixture, 93% 7LiCl) by subcutaneous injection twice daily for up to 49 days. Twenty-four-hour urine volume and water intake were measured daily. Kidneys from rats treated for 7 days with 1.5 mEq/kg 6LiCl, 7LiCl and vehicle were examined under light microscopy and histopathologic changes graded on a 4-point scale of severity. RESULTS: All rats showed loss in renal concentrating ability manifested by increasing urine volume and water intake. Peak effects occurred after 9-13 days treatment, then declined to stable levels at two to three times pre-treatment level. Mean peak effect was significantly greater for 6LiCl than for 7LiCl. Chronic effects of 6LiCl (weeks 3-7 of treatment) on polyuria and polydipsia were persistently higher than that of 7LiCl. nLiCl effect was intermediate. Kidneys from rats treated for 7 days with 6LiCl showed more frequently severe lesions in renal tubules than did 7LiCl-treated rats. CONCLUSIONS: Our current data and prior studies suggest that elimination or reduction of 6Li from pharmaceutical preparations may merit further evaluation as a possibly less potentially nephrotoxic form of lithium treatment.

Animals↗
PubMedDate not supplied

[Bartter's syndrome: new classification, old therapy].

We report on two cases of Bartter's syndrome, together with the review of current literature on the aetiology, development and treatment of Bartter's syndrome. Bartter's syndrome belongs to a group of hypokalaemic renal channelopathies, which are caused by a molecular hereditary disorder of ion channels in renal tubules. These channels are located in the lipid layer of cell membranes where they exist as water channels through which ion transport is performed. Based on the type of genetic disorder and clinical presentation, Bartter's syndrome is classified as neonatal, classical and Gitelman's syndrome. Neonatal form is found in newborns and is characterized by foetal polyuria, premature birth, postnatal episodes of severe dehydration, growth retardation, hypercalciuria and early nephrocalcinosis. It is the result of mutation of a gene responsible for renal tubular Na-K-2Cl cotransport or another gene which controls the ATP-dependant potassium channel (ROMK). Classic form is found in young children with polyuria, hypokalaemia and growth retardation. This type is caused by a defect of a gene for chloride channel (CIC-Kb) in the distal tubule. Gitelman's syndrome is found in late childhood or adolescence. It is caused by mutation in the gene for Na-Cl co-transport in the distal tubule. Children with Gitelman's syndrome occasionally have muscle weakness or tetany, hypokalaemia and hypomagnesaemia. Even though there have been advances in understanding the aetiology and pathogenesis of Bartter's syndrome in the recent years, the possibilities and strategies for its management remained almost the same. Treatment is based on prostaglandin inhibitors, potassium sparing diuretics and substitution therapy.

Bartter Syndrome↗