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At least 1,135 records · Page 63Linked to original sources
PubMed2005

Efficacy of COX-2 inhibitors in a case of congenital nephrogenic diabetes insipidus.

A 17-month-old boy presented with failure to thrive, polyuria, and vomiting. He had been diagnosed clinically with nephrogenic diabetes insipidus and treated by amiloride and hydrochlorothiazide combination without a satisfactory outcome at another center since 1 year of age. The diagnosis was confirmed by genetic analysis (AVPR2mutation), and the treatment was modified to include rofecoxib (a selective cyclooxygenase-2 inhibitor) in addition to hydrochlorothiazide and amiloride. This combination along with a low-salt diet resulted in a dramatic decrease in urinary free-water loss, while no side effect was noted. Because of prohibition of rofecoxib, it had to be substituted first by indomethacin and then by ibuprofen. However, both drugs were ineffective in controlling water diuresis. Thus, we had to replace these drugs by celecoxib (another selective cyclooxygenase-2 inhibitor). We conclude that the combination hydrochlorothiazide/amiloride/cyclooxygenase-2 inhibitor could be successfully used to treat congenital nephrogenic diabetes insipidus.

Amiloride↗
PubMed2005

A compound heterozygous mutation in the BSND gene detected in Bartter syndrome type IV.

Bartter syndrome is a genetic disorder with hypokalemic metabolic alkalosis and is classified into five types. Type IV Bartter syndrome is a type of neonatal Bartter syndrome with sensorineural deafness and has been recently shown to be caused by mutations in the BSND gene. Owing to the rarity of this disease, only a limited number of mutations have been reported. We analyzed the BSND gene in a patient with type IV Bartter syndrome. The patient was delivered at 37 weeks, with normal body weight, and his neonatal course was uneventful. He was examined for developmental delay and polyuria at age 1 year 8 months and was found to have hypokalemia, metabolic alkalosis, hyperreninemic hyperaldosteronism, and sensorineural deafness. He developed end-stage renal failure at age 15 years, and renal transplantation was performed. We identified compound heterozygous mutations (Q32X and G47R) in the BSND gene. Each mutation was inherited from the parents. The Q32X mutation is a novel mutation and the first nonsense mutation identified in this gene. The mild perinatal clinical features of the patient were similar to those of a patient reported with a homozygous G47R mutation. However, the severity of renal failure suggested that factors other than this gene might affect the manifestation of renal abnormalities.

Bartter Syndrome↗
PubMed2006

Fabry disease and nephrogenic diabetes insipidus.

Fabry disease is a lysosomal storage disorder with kidney involvement. The initial manifestation of kidney disease is often impaired urinary concentrating ability in adolescence or young adulthood. We describe a boy diagnosed prenatally with Fabry disease who presented with polyuria, polydipsia, hypertension, hypokalaemia and proteinuria at 7 years of age. A formal water-deprivation test followed by vasopressin challenge confirmed nephrogenic diabetes insipidus. A renal biopsy revealed findings typical of Fabry disease. Angiotensin converting-enzyme therapy resulted in rapid improvement of symptoms, normalization of blood pressure and resolution of hypokalaemia and proteinuria. This child is the youngest reported Fabry disease patient with documented renal pathology and clinical manifestations of hypertension, proteinuria and nephrogenic diabetes insipidus.

Child↗
PubMed2006

Lack of evidence of hypervolemia in children with insulin-dependent diabetes mellitus.

Hypervolemia is considered to play a major role in the pathogenesis of diabetic vasculo- and nephropathy. The aim of our study is to determine whether children and adolescents with insulin-dependent diabetes mellitus (IDDM) experience alterations in blood volume (BV) before onset of apparent nephropathy. BV (calculated as the sum of measured plasma volume (PV) and red cell volume (RCV)) was determined in 31 children (9-16 yr) with a mean duration of IDDM of 6.6 yr and without microalbuminuria. Due to dependence of these values on age, size and sex, all data were normalised for body size parameters. While no statistical difference for BV normalised for lean body mass (LBM) (86.98+/-9.5 ml/kg) was found in diabetic children compared with our control population (84.91+/-12.08 ml/kg), a difference could be shown when normalised for body surface area (BSA) (diabetic children 2.37+/-0.3 L/m(2); control population 2.15+/-0.38 L/m(2), p=0.002). Increased BV is only present when normalising for BSA and not for the theoretical superior LBM-index. Because the study population exhibited a poor glycemic control (HbA1c 10.2+/-2.4 %), an influence of glucosuria-induced polyuria on BV cannot be excluded. Taking into account these limitations our data do not confirm the presence of hypervolemia before onset of diabetic nephropathy.

Adolescent↗
PubMed2006

A novel PCLN-1 gene mutation in familial hypomagnesemia with hypercalciuria and atypical phenotype.

Familial hypomagnesemic hypercalciuria and nephrocalcinosis (FHHNC [MIM 248250]) is a rare renal tubular disorder characterized by impaired reabsorption of magnesium and calcium in the thick ascending limb of Henle's loop (tALH), causing renal magnesium wasting and hypercalciuria. Patients with FHHNC usually present with recurrent urinary tract infections, polyuria, nephrolithiasis (NL) and nephrocalcinosis (NC) with many progressing to chronic renal failure (CRF). We have shown recently that loss of function mutations in paracellin-1 PCLN-1/claudin-16, a renal tight junction protein located in the TAL, are causative of FHHNC. We present clinical and molecular studies on a highly inbred family with FHHNC in association with an unusual phenotype in that all affected members were extremely short. Affected individuals were found to be homozygous for marker D3S1314 on chromosome 3q. Sequencing of the PCLN-1/claudin-16 gene revealed a previously unknown point mutation at S235Y on exon 4 on the 4th transmembrane domain, providing additional evidence that inactivating mutations in the PCLN-1/claudin-16 gene result in FHHNC.

Adolescent↗
PubMed2007

A case of nephrogenic diabetes insipidus with a novel missense mutation in the AVPR2 gene.

We describe a pediatric case of nephrogenic diabetes insipidus (NDI) with a novel missense mutation in the arginine vasopressin receptor 2 (AVPR2) gene. The patient, a 3-year-old boy, had polyuria (4357 ml/day, 7230 ml/m(2)/day) and polydipsia. Water deprivation testing demonstrated no decrease of urine volume, and urinary volume did not respond to subcutaneous injection of 0.1 U/kg pitressin. Molecular genetic analysis demonstrated that the patient had an AVPR2 missense mutation involving substitution of phenylalanine for tyrosine at position 205 (Y205F). It was also found that the patient's mother was heterozygous for this Y205F mutation. Analysis of the intermolecular interaction of the Tyr-205 hydrogen group by molecular modeling showed that Tyr-205 was located in transmembrane domain (TM) 5, and that its hydroxy group formed a hydrogen bond with Leu-169 main-chain =O located in TM 4. The mutation of Tyr-205 to phenylalanine would cause loss of this hydrogen bond and decrease or change the interaction between these TM coils, thus affecting the ability of AVP to bind to the receptor. According to this molecular model of AVPR2, the Y205F mutation would cause nephrogenic diabetes insipidus.

Base Sequence↗
PubMed1998

Bartter and related syndromes: the puzzle is almost solved.

It is now evident that the term Bartter syndrome does not represent a unique entity but encompasses a variety of disorders of renal electrolyte transport. Application of molecular biology techniques has permitted a better understanding of these "Bartter-like syndromes," which at present can be divided into three different genetic and clinical entities. Neonatal Bartter syndrome is observed in newborn infants and characterized by polyhydramnios, premature delivery, life-threatening episodes of fever and dehydration during the early weeks of life, growth retardation, hypercalciuria, and early-onset nephrocalcinosis. Two molecular defects have been identified: either at the gene encoding the renal bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2) or the gene encoding an ATP-sensitive inwardly rectifying K channel (ROMK). "Classic" Bartter syndrome is mostly observed during infancy and childhood and is characterized clinically by polyuria and growth retardation. Nephrocalcinosis is not present. Very recently, either deletions or mutations at the gene encoding a renal chloride channel (ClC-Kb) have been identified. Gitelman syndrome is observed in older children and adults presenting with intermittent episodes of muscle weakness and tetany, hypokalemia, and hypomagnesemia. Mutations at the gene encoding the thiazide-sensitive Na-Cl cotransporter have been identified in the majority of patients studied. Obviously the validity of this classification must be confirmed in the near future when all mutations have been described and genotypic-phenotypic correlations are better defined.

Bartter Syndrome↗
PubMed1999

Hypercalciuria and recurrent urinary tract infection in Venezuelan children.

Recurrent urinary tract infection (UTI) has not been widely recognized as a clinical manifestation of hypercalciuria in children. We studied 59 children with two or more episodes of UTI, a normal urinary tract, and with hypercalciuria. Clinical manifestations were fever, dysuria, straining with micturition, hematuria, polyuria, abdominal pain, and failure to thrive. Urinary calcium/creatinine ratio was 0.36+/-0.15 mg/mg. Renal function studies included serum bicarbonate (21+/-3 mmol/l), urinary/blood PCO2 difference (11+/-11 mmHg), urinary net acid excretion (63+/-3 micromol/min per 1.73 m2), uric acid fractional excretion (13%+/-12%), and maximal urinary osmolality (920+/-236 mosmol/kg). Treatment included promotion of fluid intake, avoiding excessive salt and protein, and keeping dietary calcium between 900 and 1,200 mg/day. Potassium citrate or hydrochlorothiazide were indicated if hypercalciuria persisted. With this treatment, in 95% of the children, no further episodes of UTI occurred once normocalciuria was achieved. It is possible that hypercalciuria may play a predisposing role for recurrent UTI in children by promoting the formation of microcrystals which damage the uroepithelium. We advocate the investigation of urinary calcium excretion in children with recurrent UTI and a normal urinary tract.

Acidosis, Renal Tubular↗
PubMed2001

Intracranial aneurysms in a child with autosomal recessive polycystic kidney disease.

Intracranial aneurysms (ICA) are a well-known feature of autosomal dominant polycystic kidney disease. There is only one report about ICA in an adult patient with autosomal recessive polycystic kidney disease (ARPKD). We observed a 2-year, 6-month old girl with ARPKD and multiple ICA. The family history is negative for kidney disease. The diagnosis of ARPKD was based on the typical findings in ultrasonography and computed tomography. Cystic ectasia of biliary ducts 6.3/4.8 cm in diameter was found in the liver. Arterial hypertension in a range of 140/100-170/120 mm Hg was registered. The child has polyuria, polydipsia and enuresis. Blood urea was 15 mmol/l, creatinine in a range of 120 to 75 micromol/l. One episode of vomiting, dizziness and lethargy was the reason for a brain magnetic resonance imaging. Multiple fusiform and saccular aneurysms in the branches of middle and posterior cerebral arteries were seen bilaterally. The girl is growing well without neurological symptoms during an observation period of 1.5 years. Blood pressure is well controlled with an ACE inhibitor (Enalapril 2.5 mg daily). It was concluded that ICA can be found in patients with ARPKD. Blood pressure control is essential to reduce the risk of intracranial hemorrhage.

Child, Preschool↗
PubMed2006

Parathyroid carcinoma: A rare case with mandibular brown tumor.

Parathyroid carcinoma constitutes less than 1 % of primary hyperparathyroidism. The male to female ratio is approximately equal and the mean age at presentation is 40 years. In about half of the patients there is a palpable cervical mass, and serum calcium level is usually above 14 mg/dl. In a case report we present a 21-year-old man with a non-tender, non-mobile bulging mandibular mass. He suffered from fatigue, recent weight loss, hoarseness, polydipsia, polyuria, hematuria, recurrent renal stones and bouts of constipation and diarrhea. A mandibular biopsy confirmed brown tumor. Serum calcium level was 15.4 mg/dl. Cervical ultrasound revealed a hypoecho area suspicious of parathyroid adenoma. Parathyroid carcinoma was later confirmed and en bloc resection was performed. During a two-year follow up there has been no evidence of recurrence or hypercalcemia. This unique case of parathyroid carcinoma in conjunction with brown tumor is the second reported case worldwide.

Adenoma↗
PubMedDate not supplied

Placental pathology in fetal bartter syndrome.

Bartter syndrome, which presents clinically with polyuria, urinary potassium loss, hypokalemia, hypercalciuria, and alkalosis, is an autosomal recessive disorder with mutations in genes encoding the Na-K-2Cl cotransporter, the chloride channel CLC-NKB, and the potassium channel ROMK. Prenatal diagnosis of Bartter syndrome is now possible; however, there are no reports of the placental pathology associated with fetal Bartter syndrome. We present the placental pathologic findings in two siblings with fetal Bartter syndrome. Both pregnancies were complicated by polyhydramnios and preterm delivery. The first pregnancy delivered at 30 weeks, and Bartter syndrome was diagnosed in the perinatal period. The subsequent pregnancy required periodic therapeutic amniocentesis secondary to massive polyhydramnios and delivered at 32 weeks gestation. The suspicion of fetal Bartter syndrome was very high in this second pregnancy, and the infant was confirmed to have Bartter syndrome subsequently. Both placentas were large for gestational age, weighing greater than the 95th percentile. Microscopic examination showed extensive subtrophoblastic basement membrane mineralization (special stains positive for iron and calcium) in the chorionic villi. This striking finding was present in both placentas. Subtrophoblastic mineralization has been described in the literature in placentas of fetuses with abnormalities including anencephaly, trisomy 21, and other congenital abnormalities; however, it has also been described in normal pregnancies. Mechanisms of calcification in the placenta are not well understood, but these striking cases suggest that defects in fetal renal excretion of ions can lead to dystrophic calcification within the placenta, particularly in a subtrophoblastic pattern.

Adult↗
PubMed2002

Identification of mutations in the arginine vasopressin receptor 2 gene causing nephrogenic diabetes insipidus in Chinese patients.

Congenital nephrogenic diabetes insipidus (NDI) is, in most instances, a rare X-linked recessive renal disorder (MIM 304800) characterized by the clinical symptoms of polyuria, polydipsia, and dehydration. The X-linked NDI is associated with mutations of the arginine vasopressin receptor type 2 (AVPR2) gene, which results in resistance to the antidiuretic action of arginine vasopressin (AVP) in the renal tubules and collecting ducts. Identification of mutations in the AVPR2 gene can facilitate early diagnosis of NDI, which can prevent serious complications such as growth retardation and mental retardation. We analyzed three unrelated Chinese NDI families and identified three mutations: R106C, F287L, and R337X. In addition, an A/G polymorphism at cDNA nucleotide position 927 (codon 309L) was identified. A functional expression assay of the R106C and F287L mutants in COS-7 cells revealed that both mutants show significant dysfunction and accumulate intracellular cyclic adenosine monophosphate in response to AVP hormone stimulation. These results facilitate the diagnosis of NDI at the molecular level in the Chinese population, and provide insight into the molecular pathology of NDI.

Amino Acid Sequence↗
PubMed2006

Safety of nifedipine GITS in stable angina: the ACTION trial.

AIM: We describe the safety profile of nifedipine GITS as assessed from adverse events reported in the ACTION trial in which 7,665 patients with stable, symptomatic coronary artery disease were randomly assigned nifedipine GITS or placebo and followed for a mean of 4.9 years. METHODS: All adverse events were coded using the COSTART coding dictionary. The incidence rate for each event was calculated as the number of patients with the event concerned divided by the total time 'at risk'. Hazard ratios comparing nifedipine with placebo and their 95% confidence intervals were obtained by Cox proportional-hazards analysis. RESULTS: As reported previously, nifedipine significantly reduced the incidence of cardiovascular events and procedures [hazard ratio (HR) 0.89, 95% confidence interval (CI) 0.83-0.95]. Apart from the known side effects of nifedipine, which include peripheral oedema, vasodilatation, hypotension, asthenia, constipation, leg cramps, non-specific respiratory complaints, impotence and polyuria, and which were reported more frequently in patients assigned nifedipine, the incidence rates of most other adverse events were similar. There were no differences in the occurrence of gastrointestinal haemorrhage, myocardial infarction and suicide. The rate of occurrence of death or new cancer excluding non-melanoma skin cancer for patients with no history of cancer at baseline was 2.53/100 patient years for patients assigned nifedipine and 2.37/100 patient years for patients assigned placebo (HR 1.06, 95% CI 0.93-1.22). CONCLUSION: Overall nifedipine GITS was well tolerated by patients with stable symptomatic angina.

Adverse Drug Reaction Reporting Systems↗
PubMed2005

Diabetes insipidus caused by isolated intracranial metatstases in patient with breast cancer.

We present a case of late recurrence of breast cancer manifested with diabetes insipidus caused by isolated intracranial metastases. A 57-year-old postmenopausal woman was diagnosed with breast cancer and underwent radical mastectomy, without any adjuvant therapy. Seventeen years later, she presented with polyuria, polydipsia, weight loss, weakness, diffuse bone pain, hoarseness and mild dyspnoea. Cranial CT revealed several dural masses in the frontal, parietal and occipital lobes and along the falx cerebri. The diagnosis of central diabetes insipidus without impairment of anterior pituitary function was based on the clinical symptoms, laboratory tests and imaging findings. The patient was successfully treated with desmopressin acetate and letrozole, and remained alive and ambulating 22 months after initial presentation with diabetes insipidus.

Antineoplastic Agents↗
PubMed2005

Intracranial aggressive fibromatosis presenting as panhypopituitarism and diabetes insipidus.

Aggressive fibromatosis (AF) is a rare, locally aggressive, proliferative fibroblastic lesion affecting musculoaponeurotic structures, most often, of the limbs and trunk. Intracranial AF is extremely rare and requires aggressive treatment to prevent recurrence. We present a case of a 34 year-old male with AF involving intracranial structures causing panhypopituitarism and diabetes insipidus. Patient was admitted to hospital because of polyuria, polydipsia, and loss of libido, impotence, hearing loss, and gait disturbance. On cranial magnetic resonance imaging, the lesion extended through the sphenoid sinus into the both pterygoid recesses, destroying the left lateral wall of the sphenoid sinus and invading the retroorbital area. There was also a distinct lesion in the hypothalamic area. The tumor was markedly isointense on both T2- and T1-weighted images relative to gray matter, and enhanced strongly after administration of gadolinium. The patient underwent partial resection of the lesion via a transcranial approach. The pathological examination of the mass was reported as AF. No other sites were found to be involved by thorax and abdominal tomography. Hormonal assessment of hypothalamic-pituitary dysfunction revealed panhypopituitarism with central diabetes insipidus. Replacement therapy was instituted. In this case, standard treatment of wide-field surgical resection was impossible. On the basis of reports that radiotherapy is an effective treatment for this kind of tumor, we administered radiation to the affected area, since chemotherapy and hormonal treatment of non-resectable tumors are not satisfactory. To our knowledge, this is the first reported case of AF presenting as panhypopituitarism with central diabetes insipidus.

Adult↗
PubMed2005

Protective effect of potato peel powder in ameliorating oxidative stress in streptozotocin diabetic rats.

The potential of dietary potato peel (PP) powder in ameliorating oxidative stress (OS) and hyperglycemia was investigated in streptozotocin (STZ)-induced diabetic rats. In a 4-week feeding trial, incorporation of potato peel powder (5 and 10%) in the diet of diabetic rats was found to significantly reduce the plasma glucose level and also reduce drastically the polyuria of STZ diabetic rats. The total food intake was significantly reduced in the diabetic rats fed 10% PP powder compared to the control diabetic rats. However, the body weight gain over 28 days was nearly four times greater in PP powder supplemented diabetic rats (both at 5 and 10%) compared to the control diabetic rats. PP powder in the diet also decreased the elevated activities of serum transaminases (ALT and AST) and nearly normalized the hepatic MDA and GSH levels as well as the activities of specific antioxidant enzymes in liver of diabetic rats. The result of these studies clearly establishes the modulatory propensity of PP against diabetes induced alterations. Considering that potato peels are discarded as waste and not effectively utilized, these results suggest the possibility that PP waste could be effectively used as an ingredient in health and functional food to ameliorate certain disease states such as diabetes.

Animals↗
PubMed1988

Increased circulating atrial natriuretic factor (ANF) release during induced ventricular tachycardia.

During sustained ventricular tachycardia (VT), there is usually a rise in mean atrial pressure. Atrial natriuretic factor (ANF) is a peptide released by the atria in response to increased atrial pressure or distension. ANF causes arterial vasodilation and natriuresis in man, and may contribute to the polyuria noted during tachycardia. We hypothesized that induction of sustained VT would cause elevation of right atrial pressure and lead to increased release of ANF. We measured mean arterial pressure, right atrial pressure, VT cycle length, atrial cycle length, plasma norepinephrine, and central ANF in 11 patients during 20 episodes of VT. The mean cycle length of induced tachycardia was 335 +/- 15 msec, with a mean atrial cycle length of 547 +/- 43 msec. Baseline plasma ANF was 70 +/- 11 femtomoles per milliliter and increased to 133 +/- 22 fmol/ml (p less than 0.001) after 4 minutes of VT. There was a decrease in mean arterial pressure from 87 +/- 3 to 66 +/- 3 mm Hg, and a rise in mean right atrial pressure from 4.0 +/- 0.8 to 11 +/- 1 mm Hg (p less than 0.001). The change in plasma ANF was quite variable among individual patients and was correlated with changes in mean right atrial pressure but poorly correlated with changes in mean arterial pressure, plasma norepinephrine, and atrial cycle length. Our data demonstrate that significant increased in ANF levels occur during sustained VT and are associated with increased right atrial pressure.

Atrial Function↗
PubMed1983

Transient central diabetes insipidus after aortocoronary bypass operations.

Three cases of transient central diabetes insipidus after cardiopulmonary bypass are presented. All 3 patients responded promptly to administration of vasopressin, and were completely recovered from polyuria 10 days after cardiac surgery. It is postulated that transient diabetes insipidus after cardiac operation occurred in some patients who had preexisting selective osmoreceptor dysfunction when cardiac standstill during extracorporeal circulation alters the left atrial nonosmotic receptor function, resulting in suppression of antidiuretic hormone release.

Arginine Vasopressin↗