title: Altered urinary excretion of aquaporin 2 in IgA nephropathy.
abstract: OBJECTIVE
  The intrarenal renin-angiotensin system (RAS) activation plays a pivotal role in immunoglobulin A nephropathy (IgAN) pathogenesis, which is still largely undefined. Recently, vasopressin (AVP) has been advocated to contribute to the genesis and progression of chronic kidney diseases (CKD) directly, and indirectly, via RAS activation. Our aim is to explore the intrarenal activity of AVP, its relationship with RAS activity, as well as its modulation by therapies in IgAN.
  
  
  METHODS
  In this observational study, we measured plasma copeptin, a surrogate marker of AVP, the urine excretion of aquaporin 2 (AQP2), a protein reflecting renal AVP action, and angiotensinogen (AGT), a parameter of renal RAS activation, and their relationship with renal function in 44 IgAN patients at the time of renal biopsy, without any drug therapy, and after 6-month treatment with ACEi or steroid+ACEi. Twenty-one patients with other CKD and 40 healthy subjects were recruited as controls.
  
  
  METHODS
  ELISAs were used to measure all variables of interest.
  
  
  RESULTS
  At baseline, IgAN patients showed higher urinary levels of AQP2, compared with controls and patients with other CKD. Urinary AQP2 and AGT levels strongly correlated with the presence of arterial hypertension. Steroids+ACEi caused the decrease of all the variables examined. The fall of urinary AQP2 and AGT following drug treatments was associated with the decrease of daily proteinuria.
  
  
  CONCLUSIONS
  Our findings would support the involvement of AVP-AQP2 axis, interacting with the RAS, in the progression of IgAN and candidate AQP2 as a possible novel marker of the disease.
authors.affiliation: Section of Nephrology and Bioagromed, Department of Biomedical Sciences, University of Foggia, 71122 Foggia, Italy.
authors.forename: Maria Teresa
authors.initials: MT
authors.lastname: Rocchetti
authors.forename: Grazia
authors.initials: G
authors.lastname: Tamma
authors.forename: Domenica
authors.initials: D
authors.lastname: Lasorsa
authors.forename: Ida Valentina
authors.initials: IV
authors.lastname: Suriano
authors.forename: Annamaria
authors.initials: A
authors.lastname: D'Apollo
authors.forename: Massimo
authors.initials: M
authors.lastname: Papale
authors.forename: Lisa
authors.initials: L
authors.lastname: Mastrofrancesco
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Grandaliano
authors.forename: Maria
authors.initials: M
authors.lastname: Svelto
authors.forename: Giovanna
authors.initials: G
authors.lastname: Valenti
authors.forename: Loreto
authors.initials: L
authors.lastname: Gesualdo
authors.forename: Salvatore
authors.initials: S
authors.lastname: Di Paolo
mesh_terms: D000328:Adult; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000808:Angiotensinogen / Q000652:urine; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D051399:Aquaporin 2 / Q000652:urine*; D001127:Arginine Vasopressin / Q000097:blood; D015415:Biomarkers; D001920:Bradykinin / Q000652:urine; D005260:Female; D005922:Glomerulonephritis, IGA / Q000188:drug therapy / Q000652:urine*; D006020:Glycopeptides / Q000097:blood; D006801:Humans; D006977:Hypertension, Renal / Q000209:etiology / Q000652:urine; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009994:Osmolar Concentration; D011507:Proteinuria / Q000209:etiology; D012084:Renin-Angiotensin System / Q000502:physiology; D013256:Steroids / Q000627:therapeutic use
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000893:Anti-Inflammatory Agents; D051399:Aquaporin 2; D015415:Biomarkers; D006020:Glycopeptides; D013256:Steroids; C048197:copeptins; D000808:Angiotensinogen; D001127:Arginine Vasopressin; D001920:Bradykinin