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PubMed1995

Newly discovered familial juvenile gouty nephropathy in a Japanese family.

Our attention was initially called to 2 young Japanese sisters with gout and renal insufficiency, which led to an investigation of members of their family with similar conditions. One sister, a 26-year-old woman who had suffered from polyuria since infancy, suffered from gout and renal insufficiency. Her younger sister also had a history of polyuria, hyperuricemia, and moderately reduced renal function. Their urinary uric acid levels were reduced but purine enzyme activities in the erythrocytes were normal. A renal biopsy specimen from the younger sister showed severe interstitial fibrosis with tubular atrophy. An investigation of the family revealed an autosomal dominant transmission pattern. We believe these are new familial cases of juvenile gouty nephropathy found in a Japanese family.

Adult↗

PubMedDate not supplied

Hypopituitarism and hyponatremia in a case with nasopharyngeal carcinoma.

We report a case of nasopharyngeal carcinoma (NPC) accompanied by hyponatremia and polyuria which was induced by tumor invasion into the pituitary gland. Magnetic resonance imaging showed the pituitary gland pushed upward by NPC. Hypopituitarism due to an intracranial tumor and the extracellular volume excess due to chemotherapy caused hyponatremia and polyuria. As the intracranial tumor was diminished by chemotherapy and irradiation, pituitary hormones were normalized. In patients with T4 NPC, pituitary-adrenocortical function should be endocrinologically evaluated before treatment.

Algorithms↗

PubMed1991

Diabetes insipidus due to pituitary metastasis from bladder cancer.

We report a 41-year-old man with bladder cancer who developed polyuria following successful treatment of hypercalcemia and who was found to have a transitional cell carcinoma within the pituitary gland at autopsy. He also had widespread bone metastases. Although primary urogenital cancers rarely metastasize to the pituitary, the patient's clinical course led us to suspect metastatic disease from the bladder cancer. Metastasis to the pituitary gland is more common than generally thought and should be considered in patients with advanced cancer who develop polyuria and polydipsia.

Adult↗

PubMed1994

Treatment system for nocturnal enuresis according to an original classification system.

Our department has reported recent studies for nocturnal enuresis. The morning bladder capacity in enuretic children was smaller in the 3- and 4-year-old age range but larger in the 7-year and over age range than that in nonenuretic children. 15% of nonenuretic children showed nocturnal polyuria with nocturnal urination after complete awakening more than once per week. It was not likely from this evidence that an immature bladder capacity or nocturnal polyuria was the primary cause of enuresis. Patients with enuresis were classified into three types based on overnight simultaneous monitoring by electroencephalography and cystometry. The pathogenesis of enuresis type I and type IIa was a disturbance of awakening, while that of type IIb was a disturbance of bladder function not shown in the daytime but only at night. An original systematic therapeutic plan was established with the development of an original therapeutic machine primarily for enuresis type I.

Child↗

PubMed1985

Pathogenesis of nephrogenic diabetes insipidus due to chronic administration of lithium in rats.

A polyuric syndrome with nephrogenic diabetes insipidus (NDI) is a frequent consequence of prolonged administration of lithium (Li) salts. Studies in the past, mainly the acute and in vitro experiments, indicated that Li ions can inhibit hydroosmotic effect of [8-arginine]vasopressin (AVP) at the step of cAMP generation in vitro. However, the pathogenesis of the NDI due to chronic oral administration of low therapeutic doses of Li salts is not yet clarified. We conducted a comprehensive study to clarify the mechanism by which Li administered orally for several weeks induces polyuria and NDI in rats. Albino rats consuming a diet which contained Li (60 mmol/kg) for 4 wk developed marked polyuria and polydipsia; at the end of 4 wk the plasma Li was 0.7 +/- 0.09 mM (mean +/- SEM; n = 36). Li-treated rats had a significantly decreased (-33%) tissue osmolality in papilla and greatly reduced cortico-papillary gradient of urea (cortex--43%; medulla--64%; papilla--74%). Plasma urea was significantly (P less than 0.001) lower in Li-treated rats (5.4 +/- 0.2 mM) compared with controls (6.8 +/- 0.3 mM). Medullary collecting tubules (MCT) and papillary collecting ducts (PCD) microdissected from Li-treated animals had higher content of protein than MCT and PCD from the control rats. The cAMP accumulation in response to AVP added in vitro was significantly (delta = -60%) reduced. Also, the cAMP accumulation in MCT and PCD after incubation with forskolin was markedly lower in Li-treated rats. Addition of 0.5 mM 1-methyl,3-isobutyl-xanthine did not restore the cAMP accumulation in response to AVP and forskolin in MCT from Li-treated animals. In collecting tubule segments from polyuric rats with hypothalamic diabetes insipidus (Brattleboro homozygotes) the AVP-dependent cAMP accumulation was not diminished. The activity of adenylate cyclase (AdC) in MCT of Li-treated rats, both the basal and the activity stimulated by AVP, forskolin, or fluoride, was significantly (delta approximately equal to -30%) reduced, while the activity of cAMP phosphodiesterase (cAMP-PDIE) in the same segment showed no significant difference from the controls. Also, the content of ATP in MCT microdissected from Li-treated rats and incubated in vitro did not differ from controls. The rate of [14C]succinate oxidation to 14CO2 in MAL was inhibited (-77%) by 1 mM furosemide, which indicates that this metabolic process is coupled with NaCl cotransport in MAL. The rate of (14)CO(2) production from [14C]succinate in MAL was not significantly different between control and Li-treated rats. In MCT of control rats, the rate of [14C]succinate oxidation was approximately 3 times lower than in MAL. The rate of (14)CO(2) production from [(14)C]succinate in MCT of Li-treated rats was significantly (delta +33%) higher than in MCT dissected from control rats. Based on these results, we conclude that at least two factors play an important role in the pathogenesis of NDI consequent to chronic oral administration of Li: (a) decreased ability of MCT and PCD to generate and accumulate cAMP in response to stimulation by AVP; this defect is primarily due to diminished activity of AdC in these tubular segments caused by prolonged exposure to Li; and (b) lower osmolality of renal papillary tissue, due to primarily to depletion of urea, which decreases osmotic driving force for water reabsorption in collecting tubules. On the other hand, NaCI reabsorption in MAL is apparently not affected by chronic Li treatment.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1988

Polydipsia and hyponatremia in psychiatric patients.

Many psychiatric patients have polydipsia and polyuria without identifiable underlying medical causes. Hyponatremia develops in some polydipsic patients and can progress to water intoxication with such symptoms as confusion, lethargy, psychosis, and seizures or death. This syndrome is sometimes called "compulsive water drinking," "psychogenic polydipsia," and "self-induced water intoxication." Although the underlying pathophysiology of the syndrome is unclear, several factors have been implicated in producing polydipsia and symptomatic hyponatremia. These include a possible hypothalamic defect, the syndrome of inappropriate secretion of ADH (SIADH), and neuroleptic medication. Evaluation of psychiatric patients with polydipsia includes a search for other medical causes of polydipsia, polyuria, hyponatremia, and SIADH. Treatment modalities currently available include fluid restriction and medications.

Adult↗

PubMed1977

Plasma levels of antidiuretic hormone in patients receiving prolonged lithium therapy.

Among 18 patients receiving prophylactic, long-term lithium treatment for manic-depressive psychosis, a high incidence of increased thirst and frequency of micturition (60-70 per cent) was noted on direct questioning. Symptoms arose at varying times after the start of lithium therapy; in no patient did symptoms antedate the use of the drug. Plasma levels of antidiuretic hormone were found, on average, to be higher than in normal control subjects for a given level of plasma osmolality, although the scatter of results was wide. It is suggested that elevation of antidiuretic hormone occurs as a compensatory mechansims for the polyuria which is a common feature of long-term lithium treatment. The more florid form of nephrogenic diabetes insipidus occasionally seen in lithium takers seems likely to be due to a different mechanism from the more common mild polyuria.

Arginine Vasopressin↗

PubMed1993

Experimental diabetes mellitus in a teleost fish. I. Effect of complete isletectomy and subsequent hormonal treatment on metabolism in the goby, Gillichthys mirabilis.

The anatomical feature of a single pancreatic endocrine (islet) organ devoid of exocrine tissues and separated from other vital organs in the goby, Gillichthys mirabilis, allowed a relatively simple surgical isletectomy to be performed. Isletectomized (Ix) fish were then evaluated to determine whether the lack of islet hormones would cause the development of symptoms of insulin-dependent diabetes mellitus (IDDM) in a teleost fish. Isletectomy resulted in several symptoms typical of untreated IDDM in mammals. Plasma glucose was 3.5-fold higher in Ix animals (approximately 23 mmol/liter) than in intact and sham-Ix controls (6-7 mmol/liter), while urinary glucose was increased from less than 4 mmol/liter in controls to greater than 40 mmol/liter in Ix animals. Isletectomy also resulted in a significant elevation of plasma beta-hydroxybutyrate (from 0.7-0.8 to 1.0 mmol/liter). The severity of the metabolite imbalances was directly correlated with the degree of food consumption in Ix individuals, suggesting a reduced ability to assimilate dietary nutrients. In addition, distension of the abdomen due to increased food intake and a marked swelling of the urinary bladder suggested hyperphagia and polyuria, respectively, in the Ix animals. Insulin replacement therapy over 2 weeks corrected the glycosuria, polyuria, and hyperphagia and resulted in dose-related reductions in plasma glucose and beta-hydroxybutyrate levels. Injection of Ix animals with GH, on the other hand, produced no significant changes in any of the metabolic parameters measured. The establishment of this unique model of IDDM in an ectothermic vertebrate should prove valuable for future comparative studies on the role of insulin and other pancreatic factors in the regulation of metabolic and growth processes.

Animals↗

PubMed1981

Hormonal and metabolic abnormalities associated with central nervous system germinoma in children and adolescents and the effect of therapy: report of 10 patients.

We describe the results of clinical and endocrinological investigations performed on 10 children and adolescents (5 males and 5 females) with a primary central nervous system germinoma. Eight of 10 patients were between 10-20 yr of age at the time of initial presentation. Polyuria (7 of 10) and a decrease in or cessation of linear growth (5 of 10) were the most common presenting symptoms, while only 2 of 10 patients complained of visual problems. Two patients presented with the syndrome of polyuria, adipsia, hypernatremia, profound muscle weakness, and hyperlipidemia. Initial physical exam revealed abnormal eye findings in 60%, short stature (greater than or equal to 2.5 SD) in 50%, and abnormal pubertal development in 30% of the patients. The neoplasm was located in the suprasellar-hypothalamic region in 8, caudate nucleus in 1, and pineal region in 1. Biopsy performed in 7 patients revealed the classic two-cell germinoma in all cases. Assessment of endocrine function before radiotherapy documented pituitary deficits in all patients studied. Antidiuretic hormone was deficient in 8 of 10 patients and was associated with hypoadipsia in 4. GH was deficient in al patients tested (7 of 7). TSH (5 of 8), ACTH (3 of 7), and gonadotropin (1 of 1) deficiencies were also common before treatment. Plasma PRL concentrations were elevated in 5 of 8 patients, all with suprasellar tumors. The hCG values were elevated only in the patient with sexual precocity (1 of 10). Endocrine evaluation during the postirradiation period revealed additional instances of GH (1), ACTH (1), and gonadotropin (5) deficiencies. All 10 patients are alive without evidence of active disease 6 months to 10 yr after radiation therapy (4500-5100 R). Evidence of hypothalamic-pituitary dysfunction is an early and almost universal feature of central nervous system germ cell tumors. The importance of careful evaluation and follow-up of children with acquired anterior or combined anterior and posterior pituitary dysfunction for a suprasellar tumor is stressed.

Adolescent↗

PubMed2002

[Fundamental and applied studies on transport and metabolism of electrolytes and glucose--aim to contact with molecular biology].

The authors' research focuses on polyuria, natriuresis, glucosuria, glycemia, and renal calcification in occupational lead poisoning and endemic fluorosis. Changes in electrolyte mobilization and in glucose metabolism and transport following the administration of lead compounds or fluoride were examined to elucidate these mechanisms. The results suggest fundamental approaches to the mechanism of aging and life style diseases. Our results show that: 1) Natriuresis and polyuria in lead poisoning and fluorosis are due to a decrease in renal Na/K-ATPase activity; 2) Renal calcification in fluorosis is due to stimulation of parathyroid function and activation of the renal phosphatidylinositol cascade; 3) Glycemia in fluorosis is due to elevation of renal and hepatic glucose-6-phosphatase activities; 4) Glusosuria in fluorosis is due to decreased renal Na/K-ATPase activity (but fluoride administered directly did not damage the renal Na/glucose cotransporter (SGLT); 5) Renal calcification in fluorosis is due to stimulation of parathyroid function; and 6) The decrease in renal Na/K-ATPase and SGLT activities with aging and hypertension is due to a decrease in phosphorylation activity by protein kinase C (PKC) etc. (decrease in PKC productivity with aging and hypertension).

Aging↗

PubMed2004

Clinical characteristics of eight patients with congenital nephrogenic diabetes insipidus.

Congenital nephrogenic diabetes insipidus (NDI) is characterized by the insensitivity of the distal nephron to arginine vasopressin. Clinical knowledge of this disease is based largely on case reports. For this study, we investigated the clinical findings of eight patients in terms of age at onset, age at diagnosis, main complaint, results of physical examination, the diagnosis, the effect of treatment, kidney function, and presence or absence of gene defects. The main complaints of all eight cases at initial examination were unknown fever, failure to thrive, and short stature. Polyuria and polydipsia are not always the chief complaints with congenital NDI. In one case, diabetes insipidus could be diagnosed based only on the results of a 5% hypertonic saline test. In six cases, we found abnormalities in the V2 receptor gene. Initially, trichlormethiazide therapy was shown to have a significant effect on polyuria; however, this effect decreased over time. In one patient with partial NDI, the addition of trichlormethiazide twice a day to 1-desamino-8-D-arginine vasopressin increased urine osmolality in the morning and caused nocturia to disappear. Results of 99mTc-diethylenetriamine pentaacetic acid kidney scintigraphy revealed a slight decrease in glomerular filtration rate in three patients. No patient experienced serious renal dysfunction.

Adolescent↗

PubMed1996

Manifestation of subclinical diabetes insipidus due to pituitary tumor during pregnancy.

We describe a case of diabetes insipidus (DI) due to a pituitary tumor in a 33-year-old pregnant woman who developed a sudden onset of polyuria (over 8 l/day) and polydipsia at 30 weeks of gestation. Her plasma concentration of vasopressin (AVP) was low compared with high serum osmolality (298 mOsm/kg), and her urine output was well controlled by treatment with desmopressin acetate (DDAVP). Cranial magnetic resonance imaging (MRI) demonstrated a 1.8 x 1.2-cm pituitary tumor, but she did not have any disturbance in the release of anterior pituitary hormones. The serum concentration of cystine aminopeptidase (CAP) was within the normal range for a woman at 34 weeks of gestation. After an uncomplicated delivery of a healthy girl, her polyuria gradually resolved. The size of the pituitary tumor gradually decreased in parallel to a reduction in her urine output, but a silent hemorrhage was detected in her pituitary gland 4 weeks after the delivery. Although pregnancy is sometimes associated with central DI, the occurrence of DI due to pituitary tumor under pregnancy is rare. The basal AVP recovered to within the normal range, but the low response of AVP secretion to high osmolality persisted. In this case, pregnancy may affect the manifestation of subclinical DI. This case may therefore enhance our understanding of the mechanisms of DI during pregnancy.

Adenoma↗

PubMed1999

An elderly patient with transient diabetes insipidus associated with lymphocytic infundibulo-neurohypophysitis.

We present the eldest case ever reported of central diabetes insipidus (DI) associated with infundibulo-neurohypophysitis. A 77-year old woman, who complained of recent development of excessive thirst, polyuria and polydipsia, was referred to our hospital. The daily urine volume was markedly increased to 6 L. DDAVP administration effectively reduced urine volume and increased urine osmolality. The loading test using high-osmolar sodium chloride showed impaired excretion of vasopressin discordant with plasma osmolar changes. The anterior pituitary function was normal. Pituitary magnetic resonance imaging (MRI) showed thickening of the pituitary stalk and a lack of high-intensity signal of the neurohypophysis on T1-weighted images, suggestive of lymphocytic infundibulo-neurohypophysitis. The thickness of pituitary stalk on MRI improved 6 months later. DI was controlled with DDAVP for 40 days. This was followed by stabilization of the daily urine volume to less than 2.5 L without DDAVP. Our case is the eldest case of central DI associated with infundibulo-neurohypophysitis. The rapid remission of pituitary changes on MRI provides an insight that spontaneously partial remission of central DI may occur, resulting in transient polyuria and polydipsia.

Aged↗

PubMed2003

A case of a novel mutant vasopressin receptor-dependent nephrogenic diabetes insipidus with bilateral non-obstructive hydronephrosis in a middle aged man: differentiation from aquaporin-dependent nephrogenic diabetes insipidus by response of factor VII and von Willebrand factor to 1-diamino-8-arginine vasopressin administration.

We describe a case of a novel mutant vasopressin 2 receptor (V2R)-dependent nephrogenic diabetes insipidus (NDI) with bilateral non-obstructive hydronephrosis in a middle aged man. This could be distinguished from aquaporin 2 (AQP2)-dependent NDI by the response of factor VIII and von Willebrand factor (vWF) to 1-deamino-8-D-arginine vasopressin (DDAVP) administration. A 47-year-old man was admitted to hospital because of polyuria, which had been present from infancy and was suspected of causing non-obstructive hydronephrosis. His mother's father, the older brother of his mother and his second daughter also all had polyuria. Sodium concentration, osmolality and vasopressin in blood were high, while sodium concentration and osmolality in urine were low. There were no changes in urine osmolality, factor VIII and vWF in response to DDAVP infusion. Neither was heart rate, diastolic blood pressure nor facial flushing affected. These findings suggested this case was V2R-dependent NDI rather than AQP2-dependent NDI. Molecular genetic analysis demonstrated that the patient had a V2R missense mutation involving a substitution of cysteine for arginine at position 104 (R104C) located in the first extracellular loop of the V2R. It was also found that the patient's mother and his second daughter were heterozygous for this R104C mutation.

Aquaporin 2↗

PubMed1987

Plasma concentration of atrial natriuretic polypeptide in patients with atrial tachycardia.

To investigate the mechanisms of polyuria associated with tachycardia, we measured plasma concentrations of alpha-human atrial natriuretic polypeptide (alpha-hANP) and cGMP in 6 patients with paroxysmal tachycardia. Plasma concentrations of immunoreactive alpha-hANP and cGMP increased by +69% (p less than 0.05) and +100% (p less than 0.05), respectively, during both paroxysmal atrial tachycardia and atrial fibrillation. To examine whether tachycardia per se raises the secretion of alpha-hANP, we also determined plasma concentrations of alpha-hANP and cGMP in 5 patients during rapid atrial pacing. The pacing-induced tachycardia also increased both of the plasma concentrations. Further, the examinations of cardiac and renal functions in patients with complete atrioventricular block during rapid pacing revealed that each of the increases in atrial pressures, urinary sodium excretion and creatinine clearance were in parallel with the change in plasma concentration of alpha-hANP. These results suggest that an increase in plasma concentration of alpha-hANP during paroxysmal tachycardia is mainly due to elevation of atrial pressure and that this increase in alpha-hANP contributes to tachycardia polyuria.

Atrial Fibrillation↗

PubMed1980

Breeding of a non-obese, diabetic strain of mice.

A female mouse spontaneously exhibiting polyuria and glucosuria accompanied by rapid weight loss waa found in one of two sublines derived from the CTS mice. Eight mating pairs were made using its offspring and selection was performed for both spontaneous diabetes and reproductive ability. After six generations of the selective breeding the diabetic (nod) and the control (non) lines were established. A marked sex difference was observed in the incidence of diabetic symptoms in the nod mouse. The cumulative incidence of the onset up to 30 weeks of age was 80% in females and less than 20% in males. The onset of diabetes was abrupt in both sexes, and spontaneous remission was not observed. However, daily administration of insulin induced an increase of body weight and a prolongation of life span. Diabetic symptoms are biochemically characterized by polyuria, polydipsia, hyperglycemia, glucosuria and hypercholesteremia. Pathological examination revealed a high frequency of lymphocyte infiltration around and/or into the Langerhans' islet. It was observed even at the prediabetic stage over five weeks of both sexes. The number and size of the islets were markedly reduced in the overt diabetic mice. Although the mechanism of the pathogenesis is not clear yet, the nod mouse may be a useful animal model for investigating the human juvenile type diabetes.

Animals↗

PubMedDate not supplied

Water transport in the kidney and nephrogenic diabetes insipidus.

Nephrogenic diabetes insipidus is caused by an inability of the kidney to concentrate urine despite adequate concentration of vasopressin in blood and is characterized by polyuria, polydipsia, and hyposthenuria in the presence of plasma hyperosmolality. Nephrogenic diabetes insipidus is the result of defects in water homeostasis in the kidney. Nephrogenic diabetes insipidus occurs when the kidneys cannot or do not respond to vasopressin. There are 2 categories of nephrogenic diabetes insipidus. Congenital nephrogenic diabetes insipidus is a rare, inherited, irreversible cause of polyuria and polydipsia in humans that is even rarer in animals. Acquired nephrogenic diabetes insipidus is more common and is often secondary to illness or medication that interferes with the action of vasopressin in the renal tubules. Unlike congenital nephrogenic diabetes insipidus, acquired or secondary nephrogenic diabetes insipidus is often reversible with correction of the associated or causative problem.

Animals↗

PubMed1981

[One month studies on the subacute toxicity of captopril in rats].

Subacute toxicity of captopril by daily oral administration at dose levels of 10 mg/kg, 30 mg/kg, 100 mg/kg, 300 mg/kg, 900 mg/kg and 2700 mg/kg for one month was studied in Sprague-Dawley rats. In the 2700 mg/kg group, 13 of 18 males and 17 of 18 females died with marked emaciation and abdominal distension. In the 900 mg/kg group, 1 of 18 males and 3 of 18 females died also during the administration period. In dead animals, a marked dilatation of gastrointestinal tract was noted showing multiple hemorrhagic erosions and/or ulcers in the glandular stomach. The remainder of these groups exhibited polydipsia and polyuria during the dosage period. In the 300 mg/kg and 100 mg/kg groups, all animals survived throughout the entire experimental period showing polydipsia and polyuria. In the 30 mg/kg and 10 mg/kg groups, all animals survived also throughout the entire dosage period without showing any toxic sign. Regarding plasma analysis, the BUN and creatinine concentration was significantly elevated in the group of 100 mg/kg or more. In the hematological examination, there was a decrease of erythrocyte counts, hemoglobin contents and hematocrit values in the group of 300 mg/kg or more. Pathological examinations revealed a marked thickening of the wall in afferent arterioles and interlobular arteries of the kidney in association with hypertrophy and hyperplasia of juxtaglomerular cells in 100 mg/kg, 300 mg/kg, 900 mg/kg and 2700 mg/kg groups. In these groups, multiple hemorrhagic erosions with or without ulcer were also noted in the glandular stomach. In the spleen, a slight increase of extramedullary hematopoiesis and hemosiderosis was noted in the 100 mg/kg, 300 mg/kg, 900 mg/kg and 2700 mg/kg groups, in which an increase of erythropoietic elements was also noted in the bone marrow. From these results, the maximum nontoxic dose was estimated as about 30 mg/kg/day by oral administration of captopril in the rats.

Angiotensin-Converting Enzyme Inhibitors↗