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At least 613 records · Page 34Linked to original sources
PubMed1998

Suprachiasmatic nucleus in a patient with multiple system atrophy with abnormal circadian rhythm of arginine-vasopressin secretion into plasma.

We performed a quantitative investigation of arginine-vasopressin (AVP) immunopositive neurons in the suprachiasmatic nucleus (SCN), which is the endogenous clock of the brain of a patient with multiple system atrophy (MSA) who exhibited nocturnal polyuria associated with decreased urinary specific gravity and depression of nocturnal AVP secretion. Eleven age- and sex-matched subjects were used as controls. Although, the number of AVP-positive neurons was decreased in neither the supraoptic nucleus nor the paraventricular nucleus, the number of AVP-positive neurons in the SCN was decreased and gliosis was present in the SCN. The cytoplasmic area of AVP-immunopositive neurons in the SCN was smaller in the patient than in the control subjects. These findings raise the possibility that SCN is involved in MSA and the neurodegeneration in the SCN results in altered circadian rhythm of AVP secretion and nocturnal polyuria.

Adult↗
PubMed2002

The valve bladder syndrome: pathophysiology and treatment with nocturnal bladder emptying.

PURPOSE: We determine the etiology and treat the specific pathophysiology of the valve bladder syndrome. MATERIALS AND METHODS: Defined as persisting or progressive severe hydroureteronephrosis without residual or recurrent obstruction, the valve bladder syndrome developed in 18 boys who underwent successful ablation of the posterior urethral valve. Serial radiographic, renal function, renographic, urodynamic and perfusion studies were performed for a mean time of 11 years. RESULTS: The cause of the valve bladder syndrome proved to be sustained bladder over distention due to a combination of polyuria with 24-hour urine volume greater than 2 l. in 10 boys, impaired bladder sensation in 18 and residual urine volume in 14. Treatment of over distention during the daytime alone was unsuccessful. Nocturnal bladder emptying was performed with an indwelling nighttime catheter, intermittent nocturnal catheterization and/or frequent nocturnal double voiding. Hydronephrosis markedly improved once nocturnal bladder emptying was started and was comparable to the results after urinary diversion. CONCLUSIONS: The valve bladder syndrome is not due to a permanent prenatal alteration in bladder anatomy and function. Instead, it appears to result from sustained postnatal bladder over distention due to a combination of polyuria, impaired bladder sensation and residual urine volume, which represent sequelae of prenatal valve injury. These factors synergize to prevent bladder normalization after valve ablation and progressively reduce functional bladder capacity to maintain bladder over distention. Bladder decompensation, upper tract dilation, and renal injury develop and characterize the valve bladder syndrome. Because current therapy, including intermittent catheterization, leaves the bladder full throughout the night, it remains markedly over distended. Nocturnal bladder emptying is the specific antidote for this pathophysiological situation, and results in prompt and impressive improvement or elimination of hydronephrosis in these and similar groups of patients. This response to nocturnal bladder emptying suggests that the bladder is not the primary cause for the valve bladder syndrome.

Child↗
PubMed1980

Polyuric megalocystis.

We diagnosed and treated 5 children with huge bladders and hydroureteronephrosis secondary to polyuria, resulting from either familial nephrogenic diabetes insipidus, medullary cystic disease, central diabetes insipidus secondary to panhypopituitarism or psychogenic polydipsia. Polyuria was documented by the measurement of 24-hour urine volumes. The possibility of anatomic and physiologic outlet obstruction was eliminated by flowmetry, voiding cystourethrography and endoscopy.

Adolescent↗
PubMed1994

Multiple manifestations of renovascular hypertension.

We report a case of hyponatremia, polyuria-polydipsia, hypokalemia, nephrotic syndrome, and hypertension caused by unilateral renal ischemia, and the resolution after nephrectomy of the ischemic kidney. The renin-angiotensin-aldosterone axis seems to play an essential role in the pathogenesis of these features. Mechanisms by which angiotensin II, hypokalemia, and proteinuria can affect salt and water balances, and the role of angiotensin II as a cause of heavy proteinuria are discussed. Renovascular hypertension should be considered in the differential diagnosis of hyponatremia, hypokalemia, and polyuria-polydipsia.

Female↗
PubMed2001

Activation of hypothalamic neuronal nitric oxide synthase in lithium-induced diabetes insipidus rats.

The expression of the neuronal nitric oxide synthase (nNOS) gene in the paraventricular (PVN) and supraoptic nuclei (SON) in rats with lithium (Li)-induced polyuria was examined by using in situ hybridization histochemistry. The state of the thyroid axis in these rats was also examined by in situ hybridization histochemistry for thyrotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH) mRNAs and radioimmunoassay for circulating thyroid hormones. Adult male Wistar rats consuming a diet that contained LiCl (60 mmol/kg) for 4 weeks developed remarkable polyuria. The urine in the Li-treated rats was hypotonic and had a large volume and low ionic concentration. The nNOS mRNA in the PVN and SON was significantly increased in the Li-treated rats in comparison with that in control. The increased levels of the nNOS mRNA in the PVN and SON were confirmed by NADPH-diaphorase histochemical staining. There were no differences of TRH mRNA in the PVN, TSH mRNA in the anterior pituitary and plasma concentrations of free T3 and free T4 between Li-treated rats and control rats. These results suggest that Li-induced diabetes insipidus may activate nNOS in the PVN and SON without change of the thyroid axis.

Animals↗
PubMed1998

Nephrogenic diabetes insipidus and tethered cord syndrome with a lipoma of the cauda equina.

The tethered cord syndrome is characterized by sensory and motor disturbances of the lower extremities and incontinence. We report a 12-year-old girl with a cauda equina lipoma and a tethered spinal cord, whose chief complaints were polyuria and polydipsia. She was diagnosed as having nephrogenic diabetes insipidus. This unusual complication of the tethered cord syndrome was most likely due to a hydronephrosis secondary to a neurogenic bladder. Thus, spinal lesions have to be considered in patients with polyuria and polydipsia.

Cauda Equina↗
PubMed2006

Management of the valve-bladder syndrome and congenital bladder obstruction: the role of nocturnal bladder drainage.

Valve-bladder syndrome often develops after the resolution of posterior urethral valves, but is also found after the resolution of congenital bladder obstruction. The features of this syndrome include the persistent dilation of the upper urinary tracts, a thick-walled, noncompliant urinary bladder, urinary incontinence, and polyuria secondary to nephrogenic diabetes insipidus. Nocturnal bladder management, which involves timed emptying of the bladder or continuous drainage, has been recommended in conjunction with diurnal timed voiding therapy as an adjunct to the treatment of valve-bladder syndrome. This treatment is derived from the hypothesis that valve-bladder syndrome is caused by congenital obstruction, and that the resultant changes in detrusor muscle are associated with a persistent bladder dysfunction characterized by chronic overdistention of the urinary bladder. Such overdistention is exacerbated by polyuria, and can be a cause of secondary hydronephrosis. Bladder dysfunction and overdistention is usually treated during waking time, but occasionally this is not effective on its own, and nocturnal therapy is used as well. To date, there are a few sets of data that suggest overnight bladder drainage can bring about profound improvements in the degree of upper-tract hydronephrosis, renal function, or bladder function. Nocturnal bladder drainage seems, in these initial reports, to be a simple and safe therapeutic maneuver. This review discusses the etiology of valve-bladder syndrome and examines each of the studies which have investigated nocturnal bladder drainage in its treatment.

Circadian Rhythm↗
PubMed2003

Beneficial effects of continuous overnight catheter drainage in children with polyuric renal failure.

OBJECTIVE: To determine the possible beneficial effect of providing decompression of the collecting system by continuous overnight catheter drainage (COCD) in children with progressive renal disease and dysfunctional bladder syndrome, commonly associated with polyuria which may overwhelm bladder capacity. PATIENTS AND METHODS: COCD was used in seven patients (four boys) with progressive polyuric kidney failure associated with dysfunctional bladders (current age 18.7 years, SD 5; age at COCD 12 years, SD 6). Five children had surgical bladder augmentation and all were prescribed daytime intermittent catheterization (IC) for a mean (SD) of 4.7 (3.4) years before COCD. All had significant polyuria, with a mean (SD) urine output of 2370 (971) mL/m2 per day. RESULTS: The mean (SD) glomerular filtration rate at the start of COCD was 48 (21) mL/min/1.73 m2, which is currently stable in the five patients continuing treatment. The mean (SD) duration of COCD was 4.9 (2) years. One patient showed no improvement and had a pre-emptive transplant within 1.2 years; another was transplanted after 5.5 years. Six patients showed evidence of benefit from COCD, with significant attenuation in the slope of renal functional decay (P = 0.02) and a mean (sd) prolongation of the predicted time to end-stage renal disease of 12.2 (5.6) years (P < 0.002). Hospitalization for febrile urinary tract infections was decreased from a mean (sd) of 1.7 (1.4) to 0.4 (0.7) times (P = 0.03) in the first year of COCD and eliminated by the second year (P < 0.01). CONCLUSION: COCD of the dysfunctional bladder in patients with progressive polyuric renal failure appears to offer the potential for preserving kidney function in selected patients. It does not replace surgical bladder augmentation or daytime IC in the core management.

Child↗
PubMed2001

A patient with partial central diabetes insipidus: clarifying pathophysiology and designing treatment.

Studies were undertaken in a 32-year-old man who developed polyuria (4 L/d) a few days after a basal skull fracture; the condition persisted 1 year after the accident. The other major features were thirst, a plasma sodium of 143 mmol/L, 24-hour urine osmolality of 221 mOsm/kg H(2)O, and levels of vasopressin in plasma that were less than 0.5 pg/mL on 20 separate occasions. The 24-hour urine volume implied that the diagnosis was partial rather than complete central diabetes insipidus; however, several random urine samples had a much higher osmolality. An infusion of hypertonic saline led to the release of vasopressin and the excretion of concentrated urine. We propose that the basis for the lesion may be the transection of some, but not all, of the fibers connecting the osmostat and vasopressin release center. This partial transection could permit vasopressin to be secreted in response to a larger rise in plasma sodium concentration. This pathophysiologic analysis provided the basis for therapy to minimize the degree of polyuria.

Adult↗
PubMed2001

Islet cell antibodies and glutamic acid decarboxylase antibodies, but not the clinical phenotype, help to identify type 1(1/2) diabetes in patients presenting with type 2 diabetes.

This study was undertaken to determine which type 1 diabetes-associated autoantibodies and what clinical characteristics are most useful to identify patients with type 1(1/2) diabetes. We studied 125 patients, recently diagnosed clinically with type 2 diabetes for the presence of islet cell antibodies (ICA), insulin autoantibodies (IAA), antibodies to glutamic acid decarboxylase(GADAb), and IA-2a (IA-2Ab). Patients with a diagnosis of type 2 diabetes who met all of the following criteria at diagnosis were studied: age > or = 30 years, no history of ketonuria or ketoacidosis, and not requiring insulin treatment. Thirty-six patients (29%) were positive for at least 1 antibody. Thirty-two (26%) were ICA positive and 20 (16%) GADAb positive. Insulin autoantibodies and IA-2Ab occurred less frequently in 2 (1.6%) and 8 (6.4%) patients, respectively. There was no significant difference in the ages at diagnosis between the Ab(+) and Ab(-) patients, age in years (range) 47.2 (32 to 64) versus 51.2 (31 to 77), respectively, P =.06. Body mass index (BMI) was different in the 2 groups, with Ab(+) patients being less obese, BMI (range) 28.3 kg/m(2) (17.6 to 54.9) versus 32.0 kg/m(2) (19.2 to 68.8), respectively, P =.01. Clinical presentation of diabetes was more commonly symptomatic with polyuria and polydipsia in Ab(+) patients, while in Ab(-) patients, diagnosis was more often incidental, P =.002. However, more than 95% of patients overlapped in both age and BMI irrespective of antibody status. Similarly, 42% of Ab(+) patients had their diabetes diagnosed incidentally, while 29% of Ab(-) patients presented with polyuria and polydipsia. We therefore conclude that screening with antibodies, mainly ICA and GAD, but not age, BMI, or clinical presentation should be used to identify type 1(1/2) diabetes.

Adult↗
PubMed1977

[Hyperreninism without hyperaldosteronism in diuretic abuse: a report of a case with identification of mefruside and ethacrynic acid in urine (author's transl)].

A 46-year-old nurse had been hospitalized 16 times during the preceding five years because of episodes of excessive hypokalaemia. On admission to hospital there was hypokalaemia, polyuria, excessive plasma renin activity but no increased aldosterone secretion rate. Diuretic abuse was confirmed by gas-chromatography and mass spectrometry of mefruside and ethacrynic acid in the patient's urine. Apart from other interesting aspects of this case there was the demonstration of hyperreninism without hyperaldo-steronism. The stimulating effect of renin on aldosterone secretion was obviously lower than the inhibiting effect of hypokalaemia. The general term "renin-angiotensin-aldosterone system" is, therefore, misleading because it mentions only one pathway of aldosterone regulation. The combination of hypokalaemia, polyuria, hyperreninism without hyperaldosteronism is apparently the principal but not widely recognised feature of diuretic abuse.

Aldosterone↗
PubMed2005

[Autoimmune hypophysitis--two case reports].

HISTORY AND CLINICAL FINDINGS: Two young female patients presented with polyuria and polydipsia. In one patient we additionally found idiopathic vitiligo, there were no relevant previous diseases. The gynaecological history was unremarkable. INVESTIGATIONS: In both cases a water deprivation test confirmed the diagnosis of central diabetes insipidus, the MRI investigation of the pituitary region showed a prominent and thickened pituitary stalk. DIAGNOSIS: After exclusion of a systemic granulomatous inflammation we diagnosed an autoimmune hypophysitis based on the typical morphological lesions of the pituitary gland and stalk. TREATMENT AND FOLLOW-UP: High-dose glucocorticoid therapy was without any beneficial effect on the central diabetes insipidus. Desmopressin treatment was initiated and led to a normalization of the pre-existing polyuria and polydipsia. CONCLUSION: Autoimmune hypophysitis is a very rare disease and the diagnosis is mostly achieved by excluding other causes. Systematic evaluations on large patient cohorts are lacking in the literature with respect to diagnostic procedures, therapy and outcome, the existing knowledge and experience is largely based on case reports. For this reason it appears desirable to create a central register to collect and to evaluate the course of disease in patients with autoimmune hypophysitis.

Adult↗
PubMed1998

Central diabetes insipitus in a patient with congenital toxoplasmosis.

A 33-day-old male infant who developed central diabetes insipitus as a complication of congenital toxoplasmosis is presented. He had polyuria and hypernatremia on admission and responded to Intranasal desmopressin acetate with the normalization of above mentioned findings. Computed tomographic (CT) scan of the brain showed obstructive hydrocephaly with periventricular and right basal ganglion calcification. CT scan of the pituitary gland, thyroid function tests, and serum cortisol levels were all normal. This is the first report of isolated diabetes insipitus with congenital toxoplasmosis in literature and central diabetes insipitus should be remembered if polyuria and hypernatremia develops in a patient with congenital toxoplasmosis.

Diabetes Insipidus↗
PubMed1977

Role of diet in the management of vasopressin-responsive and -resistant diabetes insipidus.

Dietary protein and NaCl are the precursors of about 60% of the urinary osmoles (urea and NaCl). This investigation tested the hypothesis that in patients with dieabetes insipidus, intake of dietary protein and salt will directly influence the degree of polyuria. Four subjects with pituitary and one with nephrogenic diabetes insipidus were studied. All medications were discontinued. To provide diets ranging between "low-solute" and "high-solute," protein was varied in increments from 40 to 130 g/day and NaCl was varied simultaneously from 0.5 to 10 g/day. In all patients, each increment in protein and salt caused a prompt increase in 24-hr urinary osmoles in the form of urea, Na+, and Cl-. The 24-hr urine volume likewise increased progressively. Average increase in urine osmoles and volume from low- to high-solute diet was +224% and +127%, respectively. In four of the five patients, Reduction of protein/salt intake from habitual dietary at home to the recommedded daily allowance caused a 50 to 100% reduction in the magnitude of polyuria.

Adolescent↗
PubMed1998

Pathophysiology of aquaporin-2 in water balance disorders.

The recent identification of aquaporin water channel proteins has provided detailed information about the molecular basis for transepithelial water transport. At least five aquaporins have been identified in the kidney; they have provided detailed molecular insight into the fundamental physiology of water balance. This article focuses primarily on the physiology and pathophysiologic significance of the vasopressin-regulated water channel aquaporin-2 (AQP2) in a number of conditions where body water balance is disturbed. AQP2 is regulated by vasopressin by both short- and long-term mechanisms. Acutely, vasopressin induces exocytic insertion of AQP2 into the apical plasma membrane to increase collecting duct water reabsorption. Moreover, long-term regulation of body water balance is achieved by changes in total collecting duct levels of AQP2. Recent studies have documented that both vasopressin and vasopressin-independent regulation play important roles in this. In conditions with acquired nephrogenic diabetes insipidus (eg, lithium treatment, hypokalemia, postobstructive polyuria), AQP2 expression and targeting have been found to be markedly reduced, providing an explanation for the polyuria and the inability to concentrate urine associated with these conditions. Conversely, in conditions with water retention (eg, heart failure, pregnancy), it has been shown that AQP2 levels and plasma membrane targeting are increased. Continued analysis of aquaporins is providing detailed molecular insight into the physiology and pathophysiology of water balance disorders.

Animals↗
PubMed1984

Massive diuresis after acute renal failure.

Polyuria, peaking at 2000 ml/h, was seen in a patient after resuscitation of hemorrhagic shock and a brief period of oliguria. This unusual polyuria appears to be a consequence of renal tubular dysfunction that persisted after glomerular filtration rate had returned to normal.

Acute Kidney Injury↗
PubMed1976

Lithium and the antidiuretic hormone.

The effect of lithium on the urine concentrating response to antidiuretic hormone (ADH) and the excretion of ADH has been studied in rats and man. The maximum urine osmolarity following 18 h dehydration and Pitressin (5 u) was decreased in three out of four patients during lithium treatment compared to their response to the same test in the absence of lithium. In a fifth patient, tested only during lithium treatment, the urine remained hypotonic to plasma throughout this test. Lithium increased the excretion of ADH in non-polyuric patients from 9-22 mu/24 h in the absence of lithium to 36-202 mu/24 - during lithium treatment. In four patients with lithium-induced polyuria, a diuretic acting on the distal tubules, clorexolone, reduced the polyuria. Lithium increased urine volume and the excretion of ADH in four rats receiving lithium in their diet. The response to exogenous ADH was decreased during lithium administration.

Animals↗
PubMed2004

Clinical presentation of childhood type 1 diabetes mellitus in the Al-Madina region of Saudi Arabia.

AIM: To describe the clinical pattern and the laboratory characteristics at presentation of childhood type 1 diabetes mellitus in the Al-Madina region of the north-west province of Saudi Arabia. METHODS: The clinical and laboratory data of a total of 230 children who presented with diabetes during a 10-year period (1992-2001) were retrospectively analyzed based on hospital records. RESULTS: Polyuria and polydipsia were by far the most frequent symptoms at presentation (96%); three quarters of the children (76.6%) had weight loss at presentation. One hundred and twenty-seven children (55.2%) of 230 presented with ketoacidosis. The mean age at diagnosis was 6.9 yr. The average duration of presenting symptoms before the hospital encounter was 17.1 d ranging from 3.0 to 45.0 d, with an average of 16.2 d in boys and 17.7 d in girls, a difference which was not significant. CONCLUSION: Polyuria, polydipsia, and weight loss are the most common symptoms at presentation of childhood diabetes mellitus in our region. The frequency of diabetic ketoacidosis was relatively high. The commonly recognized symptoms of diabetes were present in most of the children for a relatively long duration before the diagnosis. This calls for a collaboration of efforts for the early recognition of symptoms by patients and physicians to avoid the more severe types of presentation.

Adolescent↗