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PubMed2000

Identification and monitoring of disordered water balance: bioelectrical impedance analysis as an alternative to the target weight procedure.

Many psychiatric patients present with disorders of water balance manifested by polydipsia or polyuria. Multiple frequency bioelectrical impedance analysis (MFBIA) was investigated as a suitable method for the assessment of body water in such patients. Whole body bioelectrical impedance, total body water and extracellular water and serum sodium were measured in 10 chronic psychiatric inpatients with polydipsia. Fluid volumes predicted by MFBIA correlated significantly (P < 0.002) with those obtained by reference methods but the relatively high limits of agreement (2.2 L) suggest that the method is not yet sufficiently accurate for random screening purposes. However, owing to the simplicity and non-invasive nature of the technique, it warrants further investigation and development, particularly for routine patient monitoring.

Adult↗
PubMed2005

A history of diabetes mellitus or how a disease of the kidneys evolved into a kidney disease.

Diabetes mellitus has a long history during which it was considered to be a disease of the kidneys well into the middle of the 19th century. Recognized in antiquity from its excessive urine output and described as a disease of the urinary tract, its clinical features and fatal outcome were quite accurately recorded by the 1st century ad . Galen (129-200) described it as a disease specific to the kidneys because of a weakness in their retentive faculties. The sweet taste of diabetic urine, which is described in ancient Indian texts and noted by Avicenna (980-1037) and Morgagni (1635-1683), was attributed to the passage of absorbed water and nutrients unchanged into the urine. In 1674, Thomas Willis (1621-1675) first differentiated diabetes from other causes of polyuria by the sweet taste (quasi melle) of diabetic urine and suggested that the sweetness first appears in the blood. A century later, Matthew Dobson (1732-1784) showed that the urine sweetness was because of sugar and was preceded and accompanied by sugar in the blood. Although diabetes then came to be ascribed to increased sugar in the blood, the presence of sugar in the urine continued to be attributed to the decreased retentive properties of the kidneys. The experimental production of diabetes in pancreatectomized dogs that could be reversed by subcutaneous pancreatic transplantation in 1889, and ultimate isolation of insulin in 1922 clearly established diabetes as an endocrine disease. The stage of diabetes as a disease of the kidneys was now over but that of diabetes as a cause of kidney disease was yet to come. Diabetes as a cause of end stage kidney disease was first described in 1936 and extensively documented shortly thereafter, whereas the evidence of its increasing prevalence as a cause of chronic kidney disease continues to accrue.

Diabetes Mellitus↗
PubMed1997

Atherosclerosis, aortic stenosis and sudden onset central diabetes insipidus.

The majority of cases of central diabetes insipidus are still pathogenetically unclear (idiopathic). Atherosclerotic cholesterol emboli might be partly responsible for some of these idiopathic cases. A 54-year-old woman with known aortic valve stenosis and a history of a transitory ischemic attack presented with sudden-onset polyuria and polydipsia of up to eight l/d, which had started acutely with headaches. She had been treated with lithium for 3 years because of cyclothymic depression. Plasma sodium was in the upper normal range (142-148 mmol/l). Hypertonic saline infusion during lithium therapy revealed a normal threshold of thirst and resetting of vasopressin secretion (osmotic threshold > 300 mosmol/l), whereas vasopressin reserve was normal. Lithium withdrawal led to an even greater delay of vasopressin release upon hypertonic saline infusion (> 310 mosmol/l). Pituitary function tests revealed a normal anterior pituitary function. MR imaging of the hypothalamo-hypophyseal region showed a normal hypothalamic region and a highly intensive neurohypophyseal signal in the T1-weighted image. The patient responded well to desmopressin. We suggest that in this rare case clinical symptoms as well as biochemical findings like impairment of AVP release might be related to a minor structural hypothalamic damage by a vascular lesion, caused, for example, by an atheromatous (cholesterol) embolism in the hypothalamic region responsible for integration of osmoreceptor function and AVP-secretion. The patient's atherosclerosis and aortic stenosis might be responsible for this event.

Aortic Valve Stenosis↗
PubMed2000

Diabetes insipidus in a patient with a highly malignant B-cell lymphoma and stomatitis.

A 37-year-old male patient with a diffuse pleomorphic B-cell-lymphoma, which has been diagnosed two month earlier with the primary site at the pterygopalatine fossa on both sides with infiltration of the clivus and cavernous sinus was referred to our hospital for continuation of the third course of CHOP chemotherapy. At admission he reported about a recent history of painful swallowing and intermittent substernal chest pain. Alleviation of the pain on swallowing and the chest pain was apparently only possible by drinking 10 to 15 l of cold coca cola throughout the day and night, a regimen that resulted in polyuria. Physical examination revealed extensive thrush stomatitis and soor esophagitis. Despite successful treatment with fluconazole, polydipsia continued unabated. The classic osmotic test of dehydration and exogenous vasopressin revealed hypothalamic diabetes insipidus (DI). Basal hormones and stimulated endocrine function tests of the adenohypophysis were found to be normal. MRI-scan revealed lymphoma infiltration of the neurohypophysis. After the third course of CHOP chemotherapy the patient surprisingly recovered completely from his excessive thirst. The present report shows that clinical disorders such as thrush stomatitis can mask diabetes insipidus caused by an early relapsing lymphoma.

Adult↗
PubMed2005

Clinical characteristics of type 2 diabetes mellitus in overweight European caucasian adolescents.

AIM: To present the clinical features of Type 2 diabetes mellitus (T2DM) in overweight European Caucasian children and adolescents. METHODS: We report the clinical characteristics of 16 non-syndromal overweight European Caucasian adolescents with T2DM (10 boys, 6 girls, SDS-BMI in median +2.8, range +1.6 to +3.4) treated in 5 specialised centres for obesity and diabetes. RESULTS: None of the adolescents manifested with ketoacidosis. 13 were asymptomatic (3 adolescents with polyuria), 12 showed features of metabolic syndrome (dyslipidaemia or hypertension), 8 demonstrated acanthosis nigricans and 12 had relatives with T2DM. 11 adolescents were extremely obese and all patients were pubertal. Mean age at diagnosis was 14.2 years (range 11.0 - 16.9). Median insulin was 19 microU/ml, insulin resistance index (HOMA) 8.5, C-peptide 2.3 ng/ml, HbA1c 6.9 %, fasting blood glucose 176 mg/dl and blood glucose at 2 hours with the oGTT 229 mg/dl at manifestation. Fasting blood glucose and HBA1c were in the normal range in 4 and 6 adolescents respectively, while oGTT always fitted the diagnosis of T2DM. CONCLUSION: Since T2DM occurred in Caucasian overweight adolescents and is frequently asymptomatic, it is essential that clinicians perform diagnostic procedures to identify T2DM in high-risk groups of overweight Caucasian adolescents (extreme obesity, features of metabolic syndrome, relatives with T2DM).

Acanthosis Nigricans↗
PubMed1986

[Primary polyuric kidney failure and acute yellow liver dystrophy following infusion of glucose substitutes in children].

Four children (aged 2 1/2-14 years) were given infusions of fructose, sorbitol and xylitol after sustaining head trauma (n = 3) or after attempted suicide with carbromal (n = 1). After transitory polyuria renal failure of varying severity set in three to five days after onset of the infusion treatment. Serum osmolality fell to 265-274 mosm/kg, haematocrit to 0.25-0.31, and hyponatraemia developed. Serum creatinine rose to maximally 256-930 mumol/l. Liver damage developed in parallel to the renal failure, two children dying with acute yellow liver atrophy. Two children--given symptomatic treatment with balanced equalization of the hyponatraemia, administration of frusemide and adjusted carbohydrate substitution--were discharged after four to eight weeks with normal renal and hepatic functions. Dialysis was not required. The hepatic and renal abnormalities must have been due to the high amounts of fructose, sorbitol and xylitol, to a total of 7.1-23.0 g/kg on the first day, well above recommended levels.

Acute Kidney Injury↗
PubMed1980

Disordered control of thirst in hypothalamic-pituitary sarcoidosis.

We evaluated water metabolism in 11 patients with hypothalamic-pituitary sarcoidosis. Seven patients had abnormal water metabolism: one had partial antidiuretic hormone (ADH) deficiency, one had severe ADH deficiency, one had severe ADH deficiency and deficient thirst, one had only deficient thirst, and three had excessive thirst. In four of the five with thirst disturbances, there was loss of congruence of osmotic thresholds for thirst and ADH release. Five of our patients presented with polyuria and polydipsia, but only two had true diabetes insipidus, whereas three had organic primary polydipsia with adequate endogenous ADH. That disordered thirst resulting in polydipsia was more common than true diabetes insipidus is at odds with previously held views on the prevalence of ADH deficiency in this condition.

Adolescent↗
PubMed2006

Congenital progressive hydronephrosis (cph) is caused by an S256L mutation in aquaporin-2 that affects its phosphorylation and apical membrane accumulation.

Congenital progressive hydronephrosis (cph) is a spontaneous recessive mutation that causes severe hydronephrosis and obstructive nephropathy in affected mice. The mutation has been mapped to the distal end of mouse chromosome 15, but the mutated gene has not been found. Here, we describe the identification of a single base pair change in aquaporin-2 (Aqp2) in cph mutants through genetic linkage mapping. The C-T change led to the substitution of a Ser (S256) by a Leu in the cytoplasmic tail of the Aqp2 protein, preventing its phosphorylation at S256 and the subsequent accumulation of Aqp2 on the apical membrane of the collecting duct principal cells. The interference with normal trafficking of Aqp2 by this mutation resulted in a severe urine concentration defect. cph homozygotes demonstrated polydipsia and produced a copious amount of hypotonic urine. The urine concentration defect could not be corrected by [deamino-Cys1,D-Arg8]-vasopressin (DDAVP, a vasopressin analog), characteristic of nephrogenic diabetes insipidus. The nephrogenic diabetes insipidus symptoms and the absence of developmental defects in the pyeloureteral peristaltic machinery in the mutants before the onset of hydronephrosis suggest that the congenital obstructive nephropathy is most likely a result of the polyuria. This study has revealed the genetic basis for the classical cph mutation and has provided direct genetic evidence that S256 in Aqp2 is indispensable for the apical accumulation, but not the general glycosylation or membrane association, of Aqp2.

Amino Acid Sequence↗
PubMed1970

Renal damage associated with silicon compounds in dogs.

A number of oral preparations of various forms of silicon were fed to young adult Beagle dogs and young rats of both sexes for a period of four weeks. During the test period the animals were observed for clinical symptoms and urine and blood measurements were made. At the end of the experimental period all animals were sacrificed and subjected to a complete necropsy and histopathologic study. Polydipsia, polyuria, and soft stools in some animals fed sodium silicate and magnesium trisilicate were the only untoward clinical signs observed; all clinical tests on blood and urine were within normal limits. Gross and microscopic renal lesions were observed in dogs fed sodium silicate and magnesium trisilicate but no changes were seen in those animals fed silicon dioxide or aluminium silicate. Lesions were not observed in any of the rats. In view of the large number of commercial preparations which contain sodium silicate and magnesium trisilicate used in human medicine, these compounds deserve further study.

Aluminum Silicates↗
PubMed2000

Clinical aspects of nephropathia epidemica (Puumala virus infection) in Europe: a review.

Nephropathia epidemica (NE) is a prevalent zoonosis throughout Europe and is caused by the Puumala type of hantavirus. The incidence of NE varies in a cyclic fashion, with peaks occurring every 3rd to 4th year, coinciding with peaks in vole populations. The clinical course of NE is generally milder than haemorrhagic fever with renal syndrome caused by hantaviruses in other parts of the world. Typically, NE has a sudden onset with fever, headache, backpain and gastrointestinal symptoms. However, severe complications, e.g. gastrointestinal haemorrhage, occur and fatal cases have been reported. Renal involvement is prominent and manifests as initial oliguria and later as marked polyuria. Tests of renal function show pronounced glomerular and tubular involvement. Vaccine against Puumala virus infection as well as specific treatment for NE are still lacking.

Animals↗
PubMed2004

Tubulopathy consecutive to tenofovir-containing antiretroviral therapy in two patients infected with human immunodeficiency virus-1.

Tenofovir disopril fumarate, a new nucleotide analogue against human immunodeficiency virus-1 (HIV-1), can induce hypophosphataemia, the mechanism of which is unclear. Moreover, a renal tubulopathy can occur in long-term treated patients, as observed in 2 HIV-1-infected patients after 12 months of tenofovir therapy, with polyuria-polydipsia, proteinuria, glycosuria and amino-aciduria, which resolved after discontinuation of tenofovir. The risk of renal tubulopathy symptoms in patients on long-term tenofovir therapy should be noted.

Adenine↗
PubMed2004

Nocturia: a new perspective on an old symptom.

The purpose of this review is to make urologists aware of the fact that nocturia among elderly men has a multifactorial aetiology and does not always depends on bladder outlet obstruction. After diagnosis of the underlying cause, specific treatments can be offered to the patient, one of which is transurethral resection of the prostate. Nocturia, defined as waking up at night to void, is a very common and bothersome symptom, affecting >50% of both men and women aged >60 years. Nocturnal polyuria is one reason for nocturia. Recent studies have shown that this condition can now be treated successfully with desmopressin acetate, a synthetic analogue of arginine vasopressin, which for many years has been used in the treatment of enuresis in children.

Deamino Arginine Vasopressin↗
PubMed1989

Lack of a modifying effect by the diuretic drug furosemide on the development of neoplastic lesions in rat two-stage urinary bladder carcinogenesis.

The effect of the diuretic drug furosemide on two-stage urinary bladder carcinogenesis in F344 rats initiated by N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) was investigated with regard to possible promoting activity. BBN was administered at 2 doses, 0.01 or 0.05%, in drinking water for 4 wk, and thereafter furosemide was given by gavage 3 times weekly for 32 wk, 250 mg/kg body weight. Furosemide ingestion induced diuresis with an alkaline, hypotonic urine. No significant difference with regard to incidences of bladder lesions were apparent between furosemide and control groups. The present investigation indicated that neither furosemide nor its related polyuria acted as a promoter in two-stage urinary bladder carcinogenesis.

Animals↗
PubMedDate not supplied

Epidemic hemorrhagic fever revisited.

Epidemic hemorrhagic fever is a disease characterized by phases of sequential fever, hypotension, oliguria, and polyuria. This disease represented a major hazard for American soldiers during the Korean War (1950-1953) and is a persistent problem in Asia, the USSR, and northern Europe. Advances in the etiology, epidemiology, and therapy of epidemic hemorrhagic fever are discussed.

China↗
PubMed2004

Mutation in saposin D domain of sphingolipid activator protein gene causes urinary system defects and cerebellar Purkinje cell degeneration with accumulation of hydroxy fatty acid-containing ceramide in mouse.

The sphingolipid activator proteins (saposins A, B, C and D) are small homologous glycoproteins that are encoded by a single gene in tandem within a large precursor protein (prosaposin) and are required for in vivo degradation of some sphingolipids with relatively short carbohydrate chains. Human patients with prosaposin or specific saposin B or C deficiency are known, and prosaposin- and saposin A-deficient mouse lines have been generated. Experimental evidence suggests that saposin D may be a lysosomal acid ceramidase activator. However, no specific saposin D deficiency state is known in any mammalian species. We have generated a specific saposin D(-/-) mouse by introducing a mutation (C509S) into the saposin D domain of the mouse prosaposin gene. Saposin D(-/-) mice developed progressive polyuria at around 2 months and ataxia at around 4 months. Pathologically, the kidney of saposin D(-/-) mice showed renal tubular degeneration and eventual hydronephrosis. In the nervous system, progressive and selective loss of the cerebellar Purkinje cells in a striped pattern was conspicuous, and almost all Purkinje cells disappeared by 12 months. Biochemically, ceramides, particularly those containing hydroxy fatty acids accumulated in the kidney and the brain, most prominently in the cerebellum. These results not only indicate the role of saposin D in in vivo ceramide metabolism, but also suggest possible cytotoxicity of ceramide underlying the cerebellar Purkinje cell and renal tubular cell degeneration.

Animals↗
PubMedDate not supplied

Monotherapy with nifedipine for essential hypertension in adult blacks.

Thirty-two adult Nigerians with mild-to-moderate essential hypertension were included in a double-blind placebo-controlled trial matching nifedipine 20 mg twice daily with placebo for 6 weeks. Nifedipine caused very significant reductions of both systolic and diastolic blood pressures in all patients. Blood pressure fell from a mean of 181.3 (SE 3.9)/114.7 (SE 2.4) to 122.8 (SE 1.9)/79.4 (SE 1.6). Mean arterial pressure fell from a mean of 136.75 (SE -2.2) to 94.19 (SE -1.39). Polyuria was a common side effect in six of the 16 patients who received nifedipine. One additional patient developed transient occipital headache. Nifedipine monotherapy would appear to be an effective first-line drug in the management of essential hypertension in adult blacks.

Adult↗
PubMed1989

Portal versus peripheral venous drainage in segmental pancreatic transplantation in diabetic rats.

The effect of the site of venous drainage in segmental pancreatic transplantation was investigated in diabetic rats with two surgical procedures anastomosing the superior mesenteric vein either on the vena cava (systemic drainage) or on the superior mesenteric vein (portal drainage). Both procedures corrected polyuria, glycosuria, and blood glucose concentration, and resulted in similar peripheral hyperinsulinemia. Intravenous glucose tolerance tests were performed 8 weeks after transplantation. In portal-grafted rats, glucose tolerance was strictly normalized, with a plasma insulin profile similar to that observed in normal rats. In caval-grafted rats, a delayed plasma insulin peak was observed with slight abnormalities in the plasma glucose profile, the late plasma glucose concentrations being higher than in portal-grafted animals. The extent of fibrosis was similar under both conditions. This study, performed in rats, of the influence of venous drainage on the metabolic outcome of segmental transplantation, demonstrating an abnormal plasma insulin profile during a glucose challenge in case of caval drainage, is consistent with other studies suggesting that the site of drainage might be important in case of reduced grafted mass.

Animals↗
PubMed1987

Control of nephroblastoma: associated hypertension and polydipsia by captopril.

A child with nephroblastoma, severe hypertension, polydipsia, and polyuria is presented. Previous reports of this association describe great difficulty in controlling the hypertension by medical means. Captopril provided prompt and continuing control of this child's hypertension and allowed for optimal preparation prior to surgery.

Captopril↗