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
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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 |
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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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