Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032617 (polyuria)
 3,056 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nephrogenic Diabetes Insipidus (NDI) is characterised by the inability of the kidneys to concentrate urine in response to arginine vasopressin (AVP). Such patients typically experience polyuria and polydipsia because of this inability to autoregulate their water balance. This provides a perioperative challenge that could lead to a life-threatening situation. This article documents a patient with NDI who underwent an elective bowel re-anastomosis. Two peak serum sodium values were attained. The first when the patient was retaining sodium due to an inappropriate fluid regimen and the second due to hypovolaemia. The literature is reviewed and principles for NDI perioperative management are proposed.
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PMID:The perioperative challenge of nephrogenic diabetes insipidus: a multidisciplinary approach. 1586 43

Children with acute pyelonephritis develop polyuria and have reduced maximum urinary concentration capacity. We studied whether these abnormalities are associated with altered urinary excretion of the water channel aquaporin-2 (AQP2) in the renal collecting duct. AQP2 is the main target for antidiuretic action of arginine vasopressin (AVP), and the urinary excretion of this protein is believed to be an index of AVP signaling activity in the kidney. Children with acute pyelonephritis, aged 5-14 years, were examined for urinary flow rate, creatinine clearance, unchallenged urine osmolality, and urinary ion excretion. Urinary excretion of AQP2 was measured by dot immunoblotting technique. Studies were performed in the acute phase of pyelonephritis, in the same children after treatment, and in control patients. At the onset of pyelonephritis, urinary flow rate and solute excretion were increased, but the urinary osmolality was unchanged. The urinary level and urinary excretion of AQP2 was increased in acute pyelonephritis and decreased after treatment. Excretion of aquaporin-3 was unchanged, suggesting that the increase in AQP2 urinary excretion was not due to a shedding of collecting duct cells. The results suggest that a mechanism proximal to the collecting duct may be responsible for the polyuria observed in children with acute pyelonephritis. Increased urinary AQP2 levels suggest that a compensatory activation of apical plasma membrane targeting of AQP2 may occur in pyelonephritis.
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PMID:Urinary aquaporin-2 in children with acute pyelonephritis. 1638 24

Thrombotic thrombocytopenic purpura (TTP) is a rare and often fatal disorder characterized by thrombocytopenia, microangiopathic hemolytic anemia, mental status changes, and renal dysfunction. Central diabetes insipidus (CDI) is a rare disease due to anatomic lesions of the hypothalamicpituitary system associated with various underlying diseases, or trauma. We present an unusual case of TTP and CDI in a 47 year-old African American female who was admitted to our hospital with crampy abdominal pain and nausea. The patient had tachycardia, fever and hypotension. The patient subsequently became confused, developed seizures, and her renal function deteriorated. Bone marrow analysis showed adequate megakaryocytes while a peripheral smear revealed severe thrombocytopenia, polychromasia and schistocytes. The diagnosis of thrombotic thrombocytopenic purpura (TTP) was made and plasmapharesis initiated. Over the next few days, the patient developed severe polyuria with a rise in serum sodium. Central diabetes insipidus was diagnosed and DDAVP (desmopressin acetate, 1-deamino-8-D-arginine vasopressin) was given. However, DDAVP was stopped several times due to worsening thrombocytopenia. Renal function worsened and the patient expired. A review of the literature revealed only one case of report of TTP and central diabetes insipidus. Our case was the only one reporting the use of DDAVP in such a setting.
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PMID:Unique case of thrombotic thrombocytopenic purpura and diabetes insipidus. 1641 83

Nephrogenic diabetes insipidus (NDI), which can be inherited or acquired, is characterized by an inability to concentrate urine despite normal or elevated plasma concentrations of the antidiuretic hormone arginine vasopressin (AVP). Polyuria, with hyposthenuria, and polydipsia are the cardinal clinical manifestations of the disease. About 90% of patients with congenital NDI are males with X-linked recessive NDI (OMIM 304800) who have mutations in the arginine-vasopressin receptor 2 (AVPR2) gene that codes for the vasopressin V2 receptor. In about 10% of the families studied, congenital NDI has an autosomal recessive or autosomal dominant mode of inheritance (OMIM 222000 and 125800). In these families, mutations have been identified in the aquaporin-2 gene (AQP2) (OMIM 107777), which codes for the vasopressin-sensitive water channel. Most missense AVPR2 mutations lead to receptors that are trapped intracellularly; a few mutant receptors reach the cell surface but are unable to bind AVP or to properly trigger an intracellular cyclic adenosine monophosphate signal. Similarly, most AQP2 mutant proteins are also misrouted. Prior knowledge of AVPR2 or AQP2 mutations in NDI families and perinatal mutation testing is of direct clinical value because early diagnosis and treatment can avert the physical and mental retardation associated with repeated episodes of dehydration.
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PMID:Nephrogenic diabetes insipidus. 1658 Jun 9

We report a case of pituitary dwarfism and diabetes insipidus due to pituitary stalk transection in a pregnant Japanese woman, 138 cm in height, born by breech delivery with no evidence of ante- or intrapartum asphyxia. The patient had no central nervous disturbance, was diagnosed with pituitary dwarfism during childhood and was treated at another hospital with growth hormone supplement from 5 to 14 years of age. This patient was referred to our department at 17 weeks' gestation due to a change of residence. At 30 weeks' gestation, she was hospitalized for assessment of hydronephrosis and polyuria (15-20 L/day). Analysis of a 24-h urine sample showed creatinine clearance of 157 mL/min and urine osmolality of 38 mOsm/L. The patient's urine output decreased after receiving a test dose of 0.75 g of 1-desamino-8-D-arginine vasopressin (DDAVP). Cranial magnetic resonance imaging showed transection of the pituitary stalk. Subsequently, the patient's urine output was well controlled by a maintenance dose of 0.275 mL/day intranasal DDAVP. A cesarean section was performed at 37 weeks, as the patient height was 138 cm, and a pelvic X-ray showed cephalopelvic disproportion. She delivered a female baby weighing 2302 g, and both 1- and 5-min Apgar scores were 9. The patient was followed up after 4 months and showed no visual deterioration or polyuria while on DDAVP therapy, while the neonate grew favorably.
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PMID:Pregnancy complicated by multiple pituitary hormone deficiencies. 1659 33

We used the mouse nephrin promoter to express a constitutively active Galphaq [Galphaq(Q>L)] transgene in mice. As previously reported, the transgene was expressed in kidney, pancreas, and brain, and the kidney phenotype was characterized by albuminuria and reduced nephron mass. Additional studies revealed a second phenotype characterized by polyuria and polydipsia. The polyuric phenotype was not caused by abnormal glucose metabolism or hypercalcemia but was accompanied by reduced urinary concentrating ability. Additional studies found that 1) water restriction was associated with an appropriate increase in serum vasopressin levels in transgenic (TG) mice; 2) the urinary concentrating defect was not corrected by administration of desamino-d-arginine vasopressin (DDAVP); and 3) papillary length was similar in TG and non-TG mice. To examine the renal response to DDAVP at the molecular level, we monitored aquaporin 2 (AQP2) and vasopressin V2 receptor (V2R) mRNA levels in mouse kidney. Consistent with the known effects of vasopressin, administration of DDAVP caused a decrease in V2R mRNA levels and an increase in AQP2 mRNA levels in both TG and non-TG animals, suggesting an appropriate renal response to DDAVP in the TG mice. To determine whether the urine concentrating abnormality was the result of primary polydipsia, water intake by TG mice was restricted to the amount ingested by non-TG animals. After 5 days, urinary concentrating ability was similar in TG mice and non-TG littermate controls. These data are consistent with the notion that expression of the Galphaq(Q>L) transgene in the brain induced primary polydipsia in the TG mice.
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PMID:Galphaq-dependent signaling cascades stimulate water-seeking behavior. 1660 48

A 23-year-old man was admitted because of polydipsia and polyuria. As chest radiographs and computed tomography showed mediastinal and bilateral hilary lymph node swelling, and diffuse small nodules in bilateral lung fields, we suspected sarcoidosis. Sarcoidosis was diagnosed by biopsy of a cervical lymph node, and central diabetes insipidus was diagnosed by fluid restriction test and vasopressin load test. A pituitary mass was also revealed by magnetic resonance imaging. Prednisolone therapy improved all of his clinical findings except diabetes insipidus. He had to continue intranasal 1-desamino-8-D-arginine vasopressin (DDAVP) therapy.
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PMID:[A case of sarcoidosis with diabetes insipidus]. 1668 Dec 53

The transition from day to night is associated with a pronounced decline in diuresis with reductions in the amount of excreted water, electrolytes, and other end products of our metabolism. Failure to do so leads to a large urine output at night, a condition known as nocturnal polyuria, encountered in a large proportion of children with nocturnal enuresis. The aim of this study was to clarify the mechanisms responsible for the nocturnal polyuria seen in enuretics with inadequate response to desmopressin (dDAVP). Forty-six enuretics (7-14 yr of age) and fifteen age-matched controls were admitted for a 24-h protocol with standardized fluid and sodium intake, comprising urine collections, blood sampling, and blood pressure monitoring. We included patients with severe enuresis (5 +/- 1 wet nights/wk) showing <50% reduction in wet nights on dDAVP. We characterized the patients on the basis of their nocturnal urine production. The children with nocturnal polyuria excreted larger amounts of sodium and urea at night than nonpolyurics and controls. Solute-free water reabsorption as well as urinary arginine vasopressin and aquaporin-2 excretion were normal in polyurics, and no differences were found in atrial natriuretic peptide, angiotensin II, aldosterone, and renin levels. Urinary prostaglandin E2 (PGE2) excretion was significantly higher in polyurics. The nocturnal polyuria in children with dDAVP-resistant nocturnal enuresis seems to be the result of augmented sodium and urea excretion. The high urinary PGE2 levels found in these children point toward a role for increased prostaglandin synthesis in the pathogenesis of enuresis-related polyuria.
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PMID:Nocturnal polyuria in monosymptomatic nocturnal enuresis refractory to desmopressin treatment. 1680 3

Nephrogenic diabetes insipidus (NDI) is an inherited disorder characterized by renal resistance to the antidiuretic effect of arginine vasopressin (AVP), resulting in polyuria, polydipsia, and hypoosmolar urine. In the vast majority of cases, NDI is associated with germ-line mutations in the vasopressin receptor type 2 gene (AVPR2) and in about 8% of the cases with the water channel aquaporin-2 gene (AQP-2) mutations. To date, approximately 277 families with 185 germ-line mutations in the AVPR2 gene have been described worldwide. In the present study, the AVPR2 gene was genotyped in eight unrelated Brazilian kindred with NDI. In five of these NDI families, novel mutations were noted (S54R, I130L, S187R, 219delT, and R230P), whereas three seemingly unrelated probands were found to harbor previously described AVPR2 gene mutations (R106C, R137H, R337X). Additionally a novel polymorphism (V281V) was detected. In conclusion, although NDI is a rare disease, the findings of mutations scattered over the entire coding region of the AVPR2 gene are a valuable model to determine structure function relationship in G-protein-coupled receptor related diseases. Furthermore, our data indicate that in Brazil the spectrum of AVPR2 gene mutations is "family specific".
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PMID:Novel vasopressin type 2 (AVPR2) gene mutations in Brazilian nephrogenic diabetes insipidus patients. 1702 Apr 65

Gestational diabetes insipidus (GDI) is a rare disorder characterised by polyuria, polydypsia, and excessive thirst usually manifesting in the third trimester of pregnancy. The etiology is thought to depend on excessive vasopressinase activity, a placental enzyme that degrades arginine-vasopressin (AVP), but not 1-deamino-8-D: -arginine vasopressin (dDAVP), which is a synthetic form. This is a transient syndrome and may be associated with acute fatty liver of pregnancy and preeclampsia. The use of dDAVP in symptomatic cases has been proven as a safe method for both the mother and the fetus during the pregnancy. We report a case of recurrent gestational diabetes insipidus in successive pregnancies, which responded to dDAVP and subsided after delivery.
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PMID:Transient gestational diabetes insipidus diagnosed in successive pregnancies: review of pathophysiology, diagnosis, treatment, and management of delivery. 1730 61


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