02 × [serum] (CI 0 99, 1 02) across the range 0–30,000 pg/mL R-s

02 × [serum] (CI 0.99, 1.02) across the range 0–30,000 pg/mL. R-squared for the model was 0.99. The co-variates age, gender, weight, smoking status, SBP, DBP, CKD stage, GFR or diagnostic category had no significant

influence of the regression relationship. Conclusion: There is excellent correlation of Midkine levels between serum and plasma, confirming either specimen type may be used to accurately assay Midkine levels. 162 DEFECTIVE MITOPHAGY ACTIVITY IN EXPERIMENTAL DIABETIC NEPHROPATHY GC HIGGINS1,2, TV NGUYEN1, SA PENFOLD1, V THALLAS-BONKE1, BE HARCOURT3, PM ROBB1, G RAMM4, G JERUMS5, A SKENE6, R. MACISAAC7, EI EKINCI5,8, DA POWER9, KE WHITE10, RW BILOUS11, ME COOPER1,12, JM FORBES3, 5-Fluoracil chemical structure MT COUGHLAN1,12 1Glycation, Nutrition and Metabolism Laboratory, Diabetic Complications Division, Baker IDI Heart & Diabetes Institute,

Melbourne, Victoria; 2Department of Biochemistry & Molecular Biology, Monash University, Clayton, Victoria; 3Glycation & Diabetes, Mater Medical Research Institute, South Brisbane, Queensland; 4Membrane Biology Group, Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria; 5Austin Health and the University of Melbourne, Melbourne, Victoria; 6Department of Anatomical Pathology, Austin Health, Melbourne, Victoria; 7Department of Endocrinology & Diabetes, St Vincent’s Hospital, Melbourne, Victoria; 8Menzies School of Health Research, Charles Darwin University; 9Department of Nephrology, Austin check details Health and the University of Melbourne, Melbourne, Victoria, Australia;

10EM Research Services, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne; 11James Cook University Hospital, Middlesbrough, DCLK1 United Kingdom; 12Department of Medicine, Central Clinical School, Monash University, Alfred Medical Research & Education Precinct, Melbourne, Victoria, Australia Aim: Here, we aimed to determine if there was an impairment in mitophagy and changes in mitochondrial dynamics in the kidney in Diabetic Nephropathy (DN). Background: DN is the major cause of end stage renal disease in the Western world. Defects in mitochondrial bioenergetics are evident in DN and are thought to initiate renal impairment. Accumulation of fragmented mitochondria are found in the renal cortex in experimental diabetes, suggesting that in tandem with a shift in dynamics, mitochondrial clearance mechanisms may be impaired. The process of mitophagy is the selective targeting of damaged or dysfunctional mitochondria to autophagosomes for degradation through the autophagy pathway. Methods: Markers of mitophagy and mitochondrial bioenergetics and dynamics were followed in the renal cortex from rodents rendered diabetic with the beta cell toxin streptozotocin (STZ).

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