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Published on: July 18, 2017
Urinary aquaporin-2 in children with acute pyelonephritis
Elena A Rodionova1, Alla A Kuznetsova, Elena I Shakhmatova
1Laboratory of Renal Physiology, IM Sechenov Institute of Evolutionary Physiology and Biochemistry, St. Petersburg, Russia.
Insights
Children with acute pyelonephritis experience increased polyuria, linked to higher urinary levels of aquaporin-2 (AQP2). This suggests a compensatory kidney response to infection, impacting water balance.
Area of Science:
- Pediatric Nephrology
- Renal Physiology
- Molecular Biology
Background:
- Acute pyelonephritis in children often causes polyuria and impaired urine concentrating ability.
- The water channel aquaporin-2 (AQP2) in renal collecting ducts is crucial for water reabsorption and regulated by arginine vasopressin (AVP).
- Urinary AQP2 excretion is considered an indicator of AVP signaling activity in the kidney.
Purpose of the Study:
- To investigate the association between polyuria in children with acute pyelonephritis and altered urinary excretion of aquaporin-2 (AQP2).
- To assess changes in AQP2 excretion during the acute phase and after treatment of pyelonephritis compared to controls.
Main Methods:
- Studied children aged 5-14 with acute pyelonephritis and age-matched controls.
- Measured urinary flow rate, creatinine clearance, urine osmolality, and ion excretion.
- Quantified urinary AQP2 excretion using dot immunoblotting; also assessed aquaporin-3 excretion.
Main Results:
- Children with acute pyelonephritis exhibited increased urinary flow rate and solute excretion, with unchanged urine osmolality.
- Urinary AQP2 levels and excretion were significantly elevated during acute pyelonephritis and decreased after treatment.
- Aquaporin-3 excretion remained unchanged, ruling out generalized shedding of collecting duct cells.
Conclusions:
- The polyuria in pediatric acute pyelonephritis may stem from mechanisms upstream of the collecting duct.
- Elevated urinary AQP2 suggests a compensatory upregulation of AQP2 targeting to the apical membrane in response to pyelonephritis.
- These findings highlight a role for AQP2 regulation in the pathophysiology of pediatric pyelonephritis.
Abstract:
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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