Suppressed urinary excretion of aquaporin-2 in an infant with primary polydipsia

Matsumoto, Tatsuro; Takeya, Mitsue; S, Takuwa; Hiquchi, E; Fujimatsu, Akiko; Maeshiro, Hiroko; Ito, Yuhei; Kanno, Kazuo; Sasaki, Sei; Kato, Hirohisa

doi:10.1007/s004670050012

Cited by 6 publications

(3 citation statements)

References 19 publications

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“…Urinary excretion of AQP2 has previously been shown to increase in response to dehydration, NaCl infusion, and treatment with exogenous AVP or V2 receptor agonist, and to decrease in response to hydration and V2 receptor antagonist therapy [8,10,12,15,16,17,18,19,20]. In acute pyelonephritis, which is known to increase renal cell death [21], the increase in urinary AQP2 excretion might also be a result of increased shedding of collecting duct cells into the urine.…”

Section: Discussionmentioning

confidence: 94%

Urinary aquaporin-2 in children with acute pyelonephritis

Rodionova

et al. 2005

Pediatr Nephrol

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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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Section: Discussionmentioning

confidence: 94%

Urinary aquaporin-2 in children with acute pyelonephritis

Rodionova

et al. 2005

Pediatr Nephrol

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“…23 The slope of the regression line was used to describe the sensitivity of the osmoregulatory system (reference range, 0.24-2.47 pg/mL per mOsm/kg), and the intercept with the 5-pg/mL line provided a measure of its threshold value (reference range, 276-309 mOsm/kg). If the correlation coefficient of the regression line was less than 0.8, VP peaks were excluded from the regression analysis, and the VP response was termed nonlinear (dogs [8][9][10][11][12][13][14][15][16][17][18]. Dogs in which the VP response reached very high values compared to responses in healthy dogs 23 and in which the sensitivity of the response was high were termed hyperresponsive (dogs 1-3).…”

Section: Hypertonic Saline Infusionmentioning

confidence: 99%

“…8,9 Primary polydipsia is a less common disorder, but may be more prevalent in young children than previously recognized. [9][10][11][12] It is not always easy to distinguish among central diabetes insipidus, Submitted November 12, 2003; Revised March 15, 2004, April 19, 2004; Accepted June 11, 2004. Copyright ᭧ 2004 by the American College of Veterinary Internal Medicine 0891-6640/04/1806-0001/$3.00/0 primary polydipsia, and nephrogenic diabetes insipidus as causes of polyuria in children. 9 The most powerful diagnostic tool for differentiation of these conditions is the hypertonic saline infusion test, with measurement of Posm and plasma VP concentration, 13 but interpretation of the test results may pose problems.…”

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confidence: 99%

Vasopressin Response to Osmotic Stimulation in 18 Young Dogs with Polyuria and Polydipsia

Vonderen

Kooistra

Timmermans-Sprang

et al. 2004

Veterinary Internal Medicne

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Common disorders of water homeostasis leading to polyuria include a variety of endocrine, metabolic, and renal disturbances. After exclusion of most of these conditions, the diagnostic dilemma of differentiating between central diabetes insipidus, primary polydipsia, and nephrogenic diabetes insipidus may remain. Here, we report on 18 young dogs with polyuria that had been present in most cases since the dogs were puppies. The conditions were categorized according to the plasma vasopressin (VP) response to hypertonicity. The VP response to osmotic stimulation was tested by IV infusion of 20% NaCl for 2 hours. The VP response in all dogs was abnormal. Three categories could be distinguished: an exaggerated response (n = 3), a subnormal response (n = 4), and a nonlinear response with high plasma VP concentrations unrelated to increases in plasma osmolality (n = 11). The VP response to hypertonicity did not consistently distinguish among different clinical entities. In the 9 dogs with variations in urine osmolality compatible with primary polydipsia, exaggerated, subnormal, and nonlinear responses were observed. Examination of the present data questions the generally accepted notion that VP measurements during hypertonic saline infusion are the "gold standard" for the diagnostic interpretation of causes of polydipsia and polyuria. Studies of the peripheral reflection in plasma of the pulsatile VP release in healthy and polyuric individuals, with and without osmotic provocation, should be performed.

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