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Vasopressin associated with renal vascular resistance in adults with
longstanding type 1 diabetes with and without diabetic kidney disease.
Authors Piani F, Reinicke T, Lytvyn Y, Melena I, Lovblom LE, Lai V, Tse J, Cham L,
Orszag A, Perkins BA, Cherney DZI, Bjornstad P
Submitted By Petter Bjornstad on 5/5/2021
Status Published
Journal Journal of diabetes and its complications
Year 2021
Date Published 3/1/2021
Volume : Pages 35 : 107807
PubMed Reference
Abstract Arginine vasopressin (AVP) and its surrogate, copeptin, have been implicated in
diabetic kidney disease (DKD) pathogenesis, which develops in a subset of people
with longstanding type 1 diabetes, but not in others (DKD Resistors). We
hypothesized that patients with DKD would exhibit higher copeptin concentrations
vs. DKD Resistors., Participants with type 1 diabetes (n?=?62, duration
=50?years) were stratified into 42 DKD Resistors and 20 with DKD (eGFR
=60?mL/min/1.73m2 or =30?mg/day urine albumin), and age/sex-matched controls
(HC, n?=?74) were included. Glomerular filtration rate (GFR) and effective renal
plasma flow (ERPF) were calculated by inulin and p-aminohippurate clearance
before and after angiotensin II (ang II) infusion. Renal vascular resistance
(RVR) was calculated as mean arterial pressure/renal blood flow. Plasma
copeptin, renin, aldosterone, neutrophil gelatinase-associated lipocalin (NGAL),
and urea concentrations were measured, along with 24-h urine volume., DKD
resistors had lower copeptin (95% CI: 4.0 [3.4-4.8] pmol/l) compared to DKD (5.8
[4.5-7.6] pmol/l, p?=?0.02) and HC (4.8 [4.1-5.5] pmol/l, p?=?0.01) adjusting
for age, sex and HbA1c. In type 1 diabetes, higher copeptin correlated with
lower GFR (r: -0.32, p?=?0.01) and higher renin concentration (r: 0.40,
p?=?0.002) after multivariable adjustments. These relationships were not evident
in HC. Copeptin inversely associated with RVR change following exogenous ang II
only in participants with type 1 diabetes (脽?卤?SE: -6.9?卤?3.4, p?=?0.04)., In
longstanding type 1 diabetes, copeptin was associated with intrarenal
renin-angiotensin-aldosterone system (RAAS) activation and renal hemodynamic
function, suggesting interplay between AVP and RAAS in DKD pathogenesis.

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