Urinary adiponectin excretion rises with increasing albuminuria in type 1 diabetes

Anders Jorsal*, Emilie Hein Petersen, Lise Tarnow, Georg Hess, Dietmar Zdunek, Jan Frystyk, Allan Flyvbjerg, Maria Lajer, Peter Rossing

*Corresponding author af dette arbejde

    Publikation: Bidrag til tidsskriftArtikelForskningpeer review

    Abstrakt

    Aim Urinary adiponectin (u-adiponectin) excretion has been suggested to reflect early glomerular damage. Inspired by this, we studied the levels of u-adiponectin in type 1 diabetic patients with different levels of urinary albumin excretion (UAE). Methods U-adiponectin was analysed by ELISA in type 1 diabetic patients: Fifty-eight with normoalbuminuria (< 30 mg albumin/24 h), 43 with persistent microalbuminuria (30-300 mg/24 h) and 44 with persistent macroalbuminuria (> 300 mg/24 h). For comparison, a control group of 55 healthy individuals was included. Results U-adiponectin increased with increasing levels of UAE (p < 0.01). U-adiponectin median (interquartile range): Normoalbuminuria 0.38 (0.14-1.31), microalbuminuria 1.12 (0.20-2.68), macroalbuminuria 9.20 (1.10-23.35) and controls 0.09 (0.06-0.24) μg/g creatinine. Levels were unrelated to sex, age, cholesterol, diastolic BP and BMI. U-adiponectin was weakly associated with increasing systolic BP and HbA1c (r2 < 0.1, p < 0.05), but strongly related to increasing UAE (r2 = 0.57, p < 0.001) and decreasing eGFR (r 2 = 0.26, p < 0.001). The relationship between UAE and u-adiponectin was significant in all groups and independent of eGFR, BMI, BP and HbA1c. Furthermore, u-adiponectin was associated with markers of tubular damage (p < 0.01). Conclusion U-adiponectin rises with increasing levels of UAE in patients with type 1 diabetes. This is in accordance with the hypothesis that loss of adiponectin may reflect glomerular and/or tubular damage.

    OriginalsprogEngelsk
    Sider (fra-til)604-608
    Antal sider5
    TidsskriftJournal of Diabetes and its Complications
    Vol/bind27
    Udgave nummer6
    DOI
    StatusUdgivet - 1 nov. 2013

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