Abstract
Ectopic lipid accumulation in the kidney (fatty kidney) is a potential driver of diabetic kidney disease, and tight glycemic control can reduce risk of diabetic nephropathy. We assessed whether glycemic control influences renal triglyceride content (RTGC). Furthermore, we compared glucagon-like peptide-1 receptor agonist liraglutide versus standard glucose-lowering therapy. In this single-center parallel-group trial, patients with type 2 diabetes mellitus were randomized to liraglutide or placebo added to standard care (metformin/sulfonylurea derivative/insulin). Changes in RTGC after 26weeks of glycemic control measured by proton spectroscopy and difference in RTGC between treatment groups were analyzed. Fifty patients with type 2 diabetes mellitus were included in the baseline analysis (mean age, 56.5±9.1years; range, 33-73years; 46% males). Seventeen patients had baseline and follow-up measurements. Mean glycated hemoglobin was 7.8±0.8%, which changed to 7.3±0.9% after 26 weeks of glycemic control irrespective of treatment group (P=.046). Log-transformed RTGC was -0.68±0.30% and changed to -0.83±0.32% after 26 weeks of glycemic control irrespective of treatment group (P=.049). A 26-week-to-̶baseline RTGC ratio (95% confidence interval) was significantly different between liraglutide (-0.30 [-0.50, -0.09]) and placebo added to standard care (-0.003 [-0.34, 0.34]) (P=.04). In this exploratory study, we found that 26weeks of glycemic control resulted in lower RTGC, in particular for liraglutide; however, larger clinical studies are needed to assess whether these changes reflect a true effect of glycemic control on fatty kidney.
Highlights
ROUGHLY, A THIRD of patients with type 2 diabetes mellitus (T2DM) will develop diabetic kidney disease (DKD) depending on age, ethnicity, diabetes duration, and/or extent of hyperglycemia exposure.[1]
Log-transformed renal triglyceride content (RTGC) was significantly lower after 26 weeks of glycemic control compared with baseline (P 5 .049)
Nine patients with T2DM randomized to liraglutide, and 8 patients with T2DM randomized to placebo, added to usual glycemic care had both baseline and follow-up 1H-MRS data available that met the quality criteria
Summary
ROUGHLY, A THIRD of patients with type 2 diabetes mellitus (T2DM) will develop diabetic kidney disease (DKD) depending on age, ethnicity, diabetes duration, and/or extent of hyperglycemia exposure.[1]. With the Angiontensin II Antagonist Losartan (RENAAL)[4] and Irbesartan Diabetic Nephropathy Trial (IDNT)[5] showed that treatment of hypertension and proteinuria in particular when using renin-angiotensin-aldosterone system inhibitors conveyed a 30% risk reduction for ESKD. In spite of these cornerstone therapies, the incidence of ESKD by DKD continues to rise,[6] indicating possible involvement of other (nonproteinuric) pathways related to, e.g., hyperfiltration and metabolic regulation.[7]
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