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PubMed1997

[The Wolfram syndrome: diabetes mellitus, hypacusis, optic atrophy and short stature in STH deficiency].

HISTORY AND CLINICAL FINDINGS: A 43-year-old man was known for 3 years to have diabetes mellitus. For 2 months before admission he had symptoms of hyperglycaemia with polyuria, polydipsia, weight loss, as well as impairment of vision and declining fitness. In addition to bilateral deafness he was clearly of normally proportioned short stature (150 cm). INVESTIGATIONS: The levels of blood sugar (221 mg/dl), HbA1c(10.2%), triglycerides (496 mg/dl) and cholesterol (323 mg/dl) were raised, while the concentration of somatotropic hormone was diminished, both before and after arginine administration. Fundoscopy revealed concentric diminution of the visual fields with left amblyopia. Visual evoked potentials and colour sense testing revealed bilateral optical atrophy, and the audiogram demonstrated deafness. These findings provided the diagnosis of Wolfram syndrome, namely insulin-dependent diabetes mellitus, deafness, optical atrophy and small stature with somatotropic hormone deficiency. TREATMENT AND COURSE: On insulin treatment the metabolic state became normal (HbA1c 7.5%, normal lipid profile). It was decided that the deficiency in somatotropic hormone regulation did not require treatment. CONCLUSION: Cardinal symptoms of the autosomally recessive Wolfram syndrome are insulin-dependent diabetes and optic nerve atrophy. Several types of hormonal abnormalities are associated with it, including a deficiency in the somatotropic axis. To obtain early and adequate hormonal substitution requires extensive endocrinological diagnosis of a disease which frequently becomes manifest in childhood or adolescence.

Adult↗
PubMed1995

[Recurrent immune thrombocytopenia: a rare complication after contrast medium injection].

HISTORY AND CLINICAL FINDINGS: In a 66-year-old woman with unstable angina, treated with 20,000 IU heparin daily for 6 days, platelet count fell dramatically from 310,000 to 1000/microliters 8 hours after injection of 90 ml of contrast medium (Iopromide) during coronary angiography. In addition to a marked tendency towards spontaneous bleeding she developed a large haematoma at the site of the arterial puncture, with a fall in haemoglobin to 9 g/dl, and acute renal failure. TREATMENT AND COURSE: Red blood cell and platelet infusions were given, together with cortisone, 1000 mg, and immunoglobulins. Platelet count returned to within normal limits after 8 days. Two haemodialyses initiated polyuria, followed by rapid normalization of kidney function. No antibodies against iopromide, iopamidol, heparin or heparinoids were found. At an emergency coronary balloon angioplasty 3 weeks later iopamidol was injected (45 ml). Again there was a profound fall in platelets to 1000/microliters, associated with acute renal failure. Treatment identical to that after the first episode brought about complete normalization. CONCLUSION: The reported reactions were most likely due to immune thrombocytopenia after administration of contrast medium.

Acute Kidney Injury↗
PubMed1991

[Kimura disease with minimally proliferative glomerulonephritis].

A 45-year-old Turk had a year ago noticed a submandibular and a retroauricular node-like swelling, about 2 cm in diameter each, firm and freely mobile. During the preceding two months he had polydipsia and polyuria. Recently he developed a nephrotic syndrome with lower-leg oedema and proteinuria (14 g albumin in 24-hour urine). The concentrations of IgE (250 IE/ml) and IgA (745 mg/dl) were raised, and there was eosinophilia of 14%. Renal needle biopsy revealed glomerulonephritis with minimal proliferation. Excision of part of the nodular tumour revealed histologically the typical signs of Kimura's disease (eosinophilic follicular lymphadenitis of the skin; subcutaneous angiolymphoid hyperplasia with eosinophilia). During treatment with prednisolone, 20 mg daily by mouth, the clinical and biochemical findings regressed within two weeks. But eight weeks later, after dose reduction to 10 mg daily, the nephrotic syndrome recurred so that the dosage had to be increased again to 20 mg prednisolone daily. On this treatment the patient has now been symptom-free for six months. This case demonstrates the unusual association of Kimura's disease with minimally proliferative glomerulonephritis.

Angiolymphoid Hyperplasia with Eosinophilia↗
PubMed1988

[Alcoholic ketoacidosis. An important differential diagnosis from diabetic ketoacidosis].

Ketoacidosis developed in two patients, a woman aged 36 and a man aged 55 years, 48 and 36 hours, respectively, after a bout of drinking alcohol to excess. Both were dehydrated with hyperventilation and signs of cachexia. Other findings were polydipsia, polyuria, loss of weight and (in the woman) abdominal pain. Biochemical tests revealed a marked metabolic acidosis (pH 7.00 and 7.09, respectively), base deficit of -25 and -20 mmol/l, hyperglycaemia (210 and 297 mg/dl) and hyperkalaemia (6.3 and 6.0 mmol/l). Treatment with insulin and fluids, as well as normalization of the electrolytes, brought about rapid regression of the metabolic disorder and restoration of the carbohydrate metabolism. Both patients were discharged without medication or dietary prescription, other than abstinence from alcohol.

Acidosis↗
PubMed1983

[Candida meningitis. Case report].

Subacute meningitis caused by Candida albicans was confirmed by culture and immunoserologically in a 19-year-old girl. Combined administration of amphotericin B and flucytosine only slowly affected the course of the disease despite impressive improvement in clinical symptoms. Pleocytosis (1000/mm3) in cerebrospinal fluid persisted. Falling Candida antibody titre in serum and CSF, however, pointed to an improvement in the acute infection. Treatment had to be discontinued after 42 days because of side-effects such as rigor, fever and polyuria with low concentration. Under serial clinical observations with occasional CSF punctures complete cure occurred with normal CSF findings. There was an additional and unusual neurological-otological condition of intermittent inner-ear deafness, left more than right, before treatment. Recording of early auditory evoked potentials pointed to an involvement of the cranial nerves as part of the inflammatory process.

Adolescent↗
PubMed1984

The clinical information value of the glycosylated hemoglobin assay.

We evaluated the clinical information value of the glycosylated hemoglobin assay by comparing it with practitioners' estimates of glucose control over the preceding 10 weeks in 216 patients with diabetes. Twenty-four per cent of the practitioners' estimates, which were based on historical and laboratory data collected during a routine office visit, differed by more than +/- 75 mg per deciliter from the actual mean blood glucose levels calculated with the glycosylated hemoglobin assay. One third of the mean blood glucose concentration fell outside the confidence intervals physicians used to bound their estimates. When examined individually or in the aggregate, historical information, such as polyuria, nocturia, or home urine testing for glucose, and laboratory information, such as fasting or random blood glucose levels, were weak predictors of the actual mean concentration of blood glucose. We conclude that the glycosylated hemoglobin assay provides information about the degree of long-term glucose control that is not otherwise obtainable in the usual clinical setting.

Blood Glucose↗
PubMed2001

Nocturia in women.

Frequent episodes of nocturnal voiding disturb the sleep and well-being of women. The prevalence of nocturia is more common in parous women and shows a linear increase with age, occurring in more than 50% of women > or =80 years old. Nocturia has a multifactorial origin that develops through a pathophysiologic mechanism of nocturnal polyuria or low functional bladder capacity or through a combination of both. Nocturia is also one of the most bothersome lower urinary tract symptoms and has a significant impact on quality of life. However, most women accept symptoms of nocturia as part of the aging process and few seek medical help. Treatments for nocturia (behavior modification and pharmacologic treatment) are effective in many cases, although it is important to tailor treatment to the underlying pathophysiology. This review discusses the impact of nocturia on women and reviews the current situation regarding the definition, prevalence, diagnosis, and treatment of this condition in this patient population.

Aged↗
PubMed2002

Urinary habits among asymptomatic women.

OBJECTIVE: The purpose of this study was to determine normal ranges for voiding diary variables for a racially diverse sample of women without lower urinary tract symptoms in the United States. STUDY DESIGN: Three hundred women without lower urinary tract symptoms completed a 24-hour log of fluid intake and volumes voided. We used linear regression to analyze diary data according to patient characteristics, which included race, age, body mass index, and parity. RESULTS: The following races were represented: black, 118 women (39%); white, 117 women (39%); Hispanic, 36 women (12%); Asian, 28 women (9%); and mixed race, 1 woman (<1%). Subjects voided a median of 8 times in 24 hours; 95% of the subjects recorded fewer than 13 voids per 24 hours. Subjects recorded a median of 4 voids per liter of fluid intake (95% recorded fewer than 9 voids per liter intake) and a median of 5 voids per liter urine output (95% recorded fewer than 12 voids per liter output). Nighttime voids were recorded by 133 subjects (44%). According to current definitions, polyuria was present in 54 subjects (18%). Linear regression showed that the number of voids per 24 hours was related to patient age (beta =.2, P <.001) and fluid intake (beta =.39, P <.001). Mean (beta = -.31, P <.001) and maximum (beta = -.2, P =.003) voided volumes were lower among black women. Voids per liter of fluid intake varied with age (beta =.19, P =.002) and were higher among parous women (beta =.12, P =.003) and Asian women (beta =.17, P =.002). Voids per liter output were lower among black women (beta =.34, P <.001). The number of nighttime voids depended only on patient age (beta =.23, P <.001). CONCLUSION: The results of this multiracial study differ materially from other studies of asymptomatic women. It is probably inappropriate to apply a single set of normative values to all women in the United States because of the significant variability in regional climates and populations.

Adult↗
PubMed2003

Transient neonatal hyperkalemia in the antenatal (ROMK defective) Bartter syndrome.

OBJECTIVE: Identification of neonatal hyperkalemia as a complication of Bartter syndrome (BS), a disorder usually characterized by hypokalemic metabolic alkalosis. Study design Case-series description of a group of 12 infants with mutations in the renal potassium channel ROMK, causing one of the antenatal variants of BS. RESULTS: Prematurity, postnatal polyuria, and dehydration were seen in all cases. Plasma potassium was as high as 9.0 +/- 1.2 mmol/L and sodium as low as 124 +/- 3.5 mmol/L, appearing usually at day 3 of life and normalizing by the end of the first postnatal week. No hyperkalemia was found in 12 neonates with the variant of BS and deafness. The mean plasma potassium level during the first week of life among a group of very low-birth-weight infants with similar relative azotemia was 4.9 +/- 1 mmol/L (P <.001). The postneonatal period in the ROMK-defective children with BS was characterized by failure to thrive, hypercalciuria, nephrocalcinosis, and minimal-to-no hypokalemia. CONCLUSIONS: Early postnatal hyperkalemia, sometimes severe, may complicate antenatal BS associated with ROMK mutations. Its association with hyponatremia and hyperreninemic hyperaldosteronism may erroneously suggest the diagnosis of pseudohypoaldosteronism type 1. The expression of ROMK in both the thick ascending limb and cortical collecting duct may explain this apparently tubular maturation phenomenon.

Adolescent↗
PubMed2005

Nephrogenic diabetes insipidus in mice lacking all nitric oxide synthase isoforms.

Nitric oxide (NO) is produced in almost all tissues and organs, exerting a variety of biological actions under physiological and pathological conditions. NO is synthesized by three different isoforms of NO synthase (NOS), including neuronal, inducible, and endothelial NOSs. Because there are substantial compensatory interactions among the NOS isoforms, the ultimate roles of endogenous NO in our body still remain to be fully elucidated. Here, we have successfully developed mice in which all three NOS genes are completely deleted by crossbreeding singly NOS-/- mice. NOS expression and activities were totally absent in the triply NOS-/- mice before and after treatment with lipopolysaccharide. Although the triply NOS-/- mice were viable and appeared normal, their survival and fertility rates were markedly reduced as compared with the wild-type mice. Furthermore, these mice exhibited marked hypotonic polyuria, polydipsia, and renal unresponsiveness to an antidiuretic hormone, vasopressin, all of which are characteristics consistent with nephrogenic diabetes insipidus. In the kidney of the triply NOS-/- mice, vasopressin-induced cAMP production and membranous aquaporin-2 water channel expression were reduced associated with tubuloglomerular lesion formation. These results provide evidence that the NOS system plays a critical role in maintaining homeostasis, especially in the kidney.

Analysis of Variance↗
PubMed2000

Nephrogenic diabetes insipidus in mice lacking aquaporin-3 water channels.

Aquaporin-3 (AQP3) is a water channel expressed at the basolateral plasma membrane of kidney collecting-duct epithelial cells. The mouse AQP3 cDNA was isolated and encodes a 292-amino acid water/glycerol-transporting glycoprotein expressed in kidney, large airways, eye, urinary bladder, skin, and gastrointestinal tract. The mouse AQP3 gene was analyzed, and AQP3 null mice were generated by targeted gene disruption. The growth and phenotype of AQP3 null mice were grossly normal except for polyuria. AQP3 deletion had little effect on AQP1 or AQP4 protein expression but decreased AQP2 protein expression particularly in renal cortex. Fluid consumption in AQP3 null mice was more than 10-fold greater than that in wild-type litter mates, and urine osmolality (<275 milliosmol) was much lower than in wild-type mice (>1,200 milliosmol). After 1-desamino-8-d-arginine-vasopressin administration or water deprivation, the AQP3 null mice were able to concentrate their urine partially to approximately 30% of that in wild-type mice. Osmotic water permeability of cortical collecting-duct basolateral membrane, measured by a spatial filtering optics method, was >3-fold reduced by AQP3 deletion. To test the hypothesis that the residual concentrating ability of AQP3 null mice was due to the inner medullary collecting-duct water channel AQP4, AQP3/AQP4 double-knockout mice were generated. The double-knockout mice had greater impairment of urinary-concentrating ability than did the AQP3 single-knockout mice. Our findings establish a form of nephrogenic diabetes insipidus produced by impaired water permeability in collecting-duct basolateral membrane. Basolateral membrane aquaporins may thus provide blood-accessible targets for drug discovery of aquaretic inhibitors.

Amino Acid Sequence↗
PubMed2001

Erythrocyte water permeability and renal function in double knockout mice lacking aquaporin-1 and aquaporin-3.

Aquaporin (AQP) water channel AQP3 has been proposed to be the major glycerol and non-AQP1 water transporter in erythrocytes. AQP1 and AQP3 are also expressed in the kidney where their deletion in mice produces distinct forms of nephrogenic diabetes insipidus. Here AQP1/AQP3 double knockout mice were generated and analyzed to investigate the functional role of AQP3 in erythrocytes and kidneys. 53 double knockout mice were born out of 756 pups from breeding double heterozygous mice. The double knockout mice had reduced survival and impaired growth compared with the single knockout mice. Erythrocyte water permeability was 7-fold reduced by AQP1 deletion but not further reduced in AQP1/AQP3 null mice. AQP3 deletion did not affect erythrocyte glycerol permeability or its inhibition by phloretin. Daily urine output in AQP1/AQP3 double knockout mice (15 ml) was 9-fold greater than in wild-type mice, and urine osmolality (194 mosm) was 8.4-fold reduced. The mice remained polyuric after DDAVP administration or water deprivation. The renal medulla in most AQP1/AQP3 null mice by age 4 weeks was atrophic and fluid-filled due to the severe polyuria and hydronephrosis. Our data provide direct evidence that AQP3 is not functionally important in erythrocyte water or glycerol permeability. The renal function studies indicate independent roles of AQP1 and AQP3 in countercurrent exchange and collecting duct osmotic equilibration, respectively.

Animals↗
PubMed2002

Impaired renal NaCl absorption in mice lacking the ROMK potassium channel, a model for type II Bartter's syndrome.

ROMK is an apical K(+) channel expressed in the thick ascending limb of Henle (TALH) and throughout the distal nephron of the kidney. Null mutations in the ROMK gene cause type II Bartter's syndrome, in which abnormalities of electrolyte, acid-base, and fluid-volume homeostasis occur because of defective NaCl reabsorption in the TALH. To understand better the pathogenesis of type II Bartter's syndrome, we developed a mouse lacking ROMK and examined its phenotype. Young null mutants had hydronephrosis, were severely dehydrated, and approximately 95% died before 3 weeks of age. ROMK-deficient mice that survived beyond weaning grew to adulthood; however, they had metabolic acidosis, elevated blood concentrations of Na(+) and Cl(-), reduced blood pressure, polydipsia, polyuria, and poor urinary concentrating ability. Whole kidney glomerular filtration rate was sharply reduced, apparently as a result of hydronephrosis, and fractional excretion of electrolytes was elevated. Micropuncture analysis revealed that the single nephron glomerular filtration rate was relatively normal, absorption of NaCl in the TALH was reduced but not eliminated, and tubuloglomerular feedback was severely impaired. These data show that the loss of ROMK in the mouse causes perturbations of electrolyte, acid-base, and fluid-volume homeostasis, reduced absorption of NaCl in the TALH, and impaired tubuloglomerular feedback.

Animals↗
PubMed1991

Diurnal variation of plasma atrial natriuretic peptide in normals and patients with enuresis nocturna.

The circadian variation of plasma atrial natriuretic peptide (ANP) in relation to urinary excretion of sodium (UNa) and potassium (UK) as well as clearance of creatinine (Ccrea) was assessed in 15 juvenile patients with enuresis nocturna and compared with 11 age-, sex-, and weight-matched normal subjects. Normal juveniles showed a highly significant diurnal variation (p less than 0.001) of plasma ANP with diurnal peak levels at midnight (0000 hours) and minimum levels at 0400 hours. Enuretic patients showed a similar diurnal rhythmicity with normal levels during day and night. In normals both UNa and UK showed significant diurnal rhythmicity with a marked reduction from daytime to night-time. Although the total diurnal excretions of UNa and UK were similar to normals, patients with enuresis showed abnormal diurnal variation in both UNa (p less than 0.05) and UK (p less than 0.01). The abnormal circadian rhythm of UNa and UK in enuretics seemed to be caused by abnormal tubular handling as similar abnormalities were found in the fractional excretions and as the circadian variation of Ccrea was normal. Especially during the first hours of sleep (2200 hours to 0000 hours), the patients showed polyuria (230 +/- 138 ml vs 116 +/- 58 ml, p less than 0.01), natriuresis (20.9 +/- 16.3 mmol l-1 vs 10.7 +/- 6.8 mmol l-1, p less than 0.01), and kaliuresis (7.3 +/- 6.3 mmol l-1 vs 3.7 +/- 2.3 mmol l-1, p less than 0.05), despite normal levels of plasma ANP. In conclusion, the study describes the diurnal variation of plasma ANP in relation to urinary excretion of sodium and potassium in a juvenile normal population. Patients with nocturnal enuresis show abnormal diurnal rhythmicity in the urinary excretion of sodium and potassium that is not correlated to the plasma levels of ANP.

Adolescent↗
PubMed2005

Diuretic treatment of nocturnal enuresis.

OBJECTIVE: Nocturnal polyuria is considered a major pathogenetic factor in nocturnal enuresis, and the antidiuretic drug desmopressin, given at bed-time, is consequently recognized as a first-line treatment alternative. The aim of this open, non-randomized study was to see whether diuretic medication, given in the afternoon, could give similar therapeutic benefit. MATERIAL AND METHODS: Sixty-three children suffering from primary, monosymptomatic, nocturnal enuresis were included in the study by their primary care paediatrician. After 14 days without any treatment and 14 days for which 0.4 mg of desmopressin was given orally at bed-time, the children were given furosemide 1 mg/kg in the afternoon for 14 consecutive days. The numbers of wet and dry nights were recorded. RESULTS: The numbers of wet nights at baseline, during desmopressin treatment and during furosemide treatment were 10.2+/-3.5, 6.4+/-4.6 and 8.2+/-4.5, respectively. Both drugs were significantly better than no treatment, but only a small proportion of patients became completely dry: 24% on desmopressin and 12% on furosemide. Desmopressin was significantly better than furosemide. Three children who showed no therapeutic effect on desmopressin treatment had a favourable response to furosemide. CONCLUSION: Furosemide, given in the afternoon, has minor therapeutic potential in nocturnal enuresis.

Administration, Oral↗
PubMed1999

Sleep disturbance and bladder dysfunction in enuretic children with treatment failure: fact or fiction?

To document the occurrence of sleep disturbance and bladder dysfunction in enuretic children, 25 children (21 boys, 4 girls, mean age 9.9 years) with monosymptomatic nocturnal enuresis were studied. All children had significant enuretic symptoms (> 4 wet nights per week) which persisted after treatment failure. The investigation protocol included cystometry during the day, simultaneous polysomnographic and cystometric monitoring during the night and recording of diurnal and nocturnal urine output. None of the patients had nocturnal polyuria. According to the presence or absence of sleep disturbance and/or bladder dysfunction, five different patterns could be recognized. These patterns were grouped as having normal and abnormal daytime urodynamics. In conclusion, sleep disturbances and bladder dysfunction are common among enuretic children, especially those who fail to respond to treatment.

Adolescent↗
PubMed1990

Chronic renal failure in young Old English Sheepdogs.

Chronic renal failure was diagnosed in three young Old English Sheepdogs. Clinical signs were characterised by ill-thrift, polydipsia, polyuria, nervous signs and behavioural changes. Laboratory findings showed azotaemia, non-regenerative anaemia, hyperphosphataemia and isosthenuria. The kidneys were characterised histologically by interstitial fibrosis, and thickening and calcification of the tubular and glomerular basement membrane. A familial incidence could not be confirmed in these cases.

Journal Article↗